wandering pacemaker sinus arrhythmia

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Wandering Atrial Pacemaker

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Key features, clinical presentation, diagnostic evaluation, ongoing management.

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ESSENTIALS OF DIAGNOSIS

Progressive cyclic variation in P-wave morphology

Heart rate 60–100 bpm

Variation of P-wave morphology, P-P interval, and P-R interval

GENERAL CONSIDERATIONS

This rhythm is benign

This rhythm and multifocal atrial tachycardia are similar except for heart rate

The other possible explanation is that there is significant respiratory sinus arrhythmia, with uncovering of latent foci of pacemaker activity

Usually, it is associated with underlying lung disease

In the elderly, it may be a manifestation of sick sinus syndrome

In the young and athletic heart, it may represent enhanced vagal tone

SYMPTOMS AND SIGNS

Usually causes no symptoms and is incidentally discovered

Occasional patient may feel skipped beats

PHYSICAL EXAM FINDINGS

Variable S 1

DIFFERENTIAL DIAGNOSIS

Multifocal atrial tachycardia (heart rate > 100 bpm)

Frequent premature atrial complexes and atrial bigeminy

LABORATORY TESTS

None specific

ELECTROCARDIOGRAPHY

ECG to document rhythm

CARDIOLOGY REFERRAL

Not required

MEDICATIONS

No specific treatment

Monitor and treat the underlying cause, such as sick sinus syndrome or lung disease

DIET AND ACTIVITY

No restrictions

General healthy lifestyle

Once a year if sinus node abnormality is suspected; otherwise when symptoms arise

COMPLICATIONS

May progress to sick sinus syndrome

This condition by itself is benign

PRACTICE GUIDELINES

Indications for pacemaker:

– If part of sick sinus syndrome

– If associated with documented symptomatic bradycardia

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Ectopic Supraventricular Arrhythmias

Various rhythms result from supraventricular foci (usually in the atria). Diagnosis is by electrocardiography. Many are asymptomatic and require no treatment.

(See also Overview of Arrhythmias .)

Ectopic supraventricular rhythms include

Atrial premature beats

Atrial tachycardia, multifocal atrial tachycardia, nonparoxysmal junctional tachycardia, wandering atrial pacemaker.

Atrial premature beats (APB), or premature atrial contractions (PAC), are common episodic impulses. They may occur in normal hearts with or without precipitating factors (eg, coffee, tea, alcohol, pseudoephedrine ) or may be a sign of a cardiopulmonary disorder. They are common in patients with chronic obstructive pulmonary disease (COPD). They occasionally cause palpitations.

Diagnosis is by electrocardiography (ECG—see figure Atrial premature beat ).

Atrial premature beat (APB)

Image courtesy of L. Brent Mitchell, MD.

APBs may be normally, aberrantly, or not conducted and are usually followed by a noncompensatory pause. Aberrantly conducted APBs (usually with right bundle branch block morphology) must be distinguished from premature beats of ventricular origin.

Atrial escape beats are ectopic atrial beats that emerge after long sinus pauses or sinus arrest. They may be single or multiple; escape beats from a single focus may produce a continuous rhythm (called ectopic atrial rhythm). Heart rate is typically slower, P wave morphology is typically different, and PR interval is slightly shorter than in sinus rhythm.

Atrial tachycardia is a regular rhythm caused by the consistent, rapid atrial activation from a single atrial focus. Heart rate is usually 150 to 200 beats/minute; however, with a very rapid atrial rate, nodal dysfunction, and/or digitalis toxicity, atrioventricular (AV) block may be present, and ventricular rate may be slower. Mechanisms include enhanced atrial automaticity and intra-atrial reentry.

Atrial tachycardia is the least common form (5%) of paroxysmal supraventricular tachycardia and usually occurs in patients with a structural heart disorder. Other causes include atrial irritation (eg, pericarditis

Symptoms are those of other tachycardias (eg, light-headedness, dizziness, palpitations, and rarely syncope).

Diagnosis is by electrocardiography (ECG); P waves, which differ in morphology from normal sinus P waves, precede QRS complexes but may be hidden within the preceding T wave (see figure True atrial tachycardia ).

True atrial tachycardia

Vagal maneuvers may be used to slow the heart rate, allowing visualization of P waves when they are hidden, but these maneuvers do not usually terminate the arrhythmia (demonstrating that the AV node is not an obligate part of the arrhythmia circuit).

Treatment involves managing causes and slowing ventricular response rate using a beta-blocker or calcium channel blocker. An episode may be terminated by direct current cardioversion . Pharmacologic approaches to termination and prevention of atrial tachycardia include antiarrhythmic drugs in class Ia, Ic, or III. If these noninvasive measures are ineffective, alternatives include overdrive pacing and ablation .

Multifocal atrial tachycardia (chaotic atrial tachycardia) is an irregularly irregular rhythm caused by the random discharge of multiple ectopic atrial foci. By definition, heart rate is > 100 beats/minute. On ECG, P-wave morphology differs from beat to beat, and there are ≥ 3 distinct P-wave morphologies. The presence of P waves distinguishes multifocal atrial tachycardia from atrial fibrillation . Except for the rate, features are the same as those of wandering atrial pacemaker. Symptoms, when they occur, are those of rapid tachycardia. Multifocal atrial tachycardia can be due to an underlying pulmonary disorder such as chronic obstructive pulmonary disease coronary artery disease , and electrolyte abnormalities such as hypokalemia . Treatment is directed at the underlying disorder.

Nonparoxysmal junctional tachycardia is caused by abnormal automaticity in the AV node or adjacent tissue, which typically follows open heart surgery, acute inferior myocardial infarction, myocarditis, or digitalis toxicity. Heart rate is 60 to 120 beats/minute; thus, symptoms are usually absent. ECG shows regular, normal-appearing QRS complexes without identifiable P waves or with retrograde P waves (inverted in the inferior leads) that occur shortly before ( < 0.1 second) or after the QRS complex. The rhythm is distinguished from paroxysmal supraventricular tachycardia by the lower heart rate and gradual onset and offset. Treatment is directed at causes.

Wandering atrial pacemaker (multifocal atrial rhythm) is an irregularly irregular rhythm caused by the random discharge of multiple ectopic atrial foci. By definition, heart rate is ≤ 100 beats/minute. Except for the rate, features are the same as those of multifocal atrial tachycardia. Treatment is directed at causes.

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A. KESH HEBBAR, M.D., AND WILLIAM J. HUESTON, M.D.

A more recent article on  common types of supraventricular tachycardia  is available.

Am Fam Physician. 2002;65(12):2479-2487

This is part I of a two-part article on common arrhythmias. Part II, “Ventricular Arrhythmias and Arrhythmias in Special Populations,” appears on page 2491 of this issue.

Family physicians frequently encounter patients with symptoms that could be related to cardiac arrhythmias, most commonly atrial fibrillation or supraventricular tachycardias. The initial management of atrial fibrillation includes ventricular rate control to provide adequate cardiac output. In patients with severely depressed cardiac output and recent-onset atrial fibrillation, immediate electrical cardioversion is the treatment of choice. Hemodynamically stable patients with atrial fibrillation for more than two days or for an unknown period should be assessed for the presence of atrial thrombi. If thrombi are detected on transesophageal echocardiography, anticoagulation with warfarin for a minimum of 21 days is recommended before electrical cardioversion is attempted. Patients with other supraventricular arrhythmias may be treated with adenosine, a calcium channel blocker, or a short-acting beta blocker to disrupt reentrant pathways. When initial medications are ineffective, radiofrequency ablation of ectopic sites is an increasingly popular treatment option.

Heart palpitations and cardiac arrhythmias are common problems encountered by family physicians. Patients may present with acute cardiac rhythm abnormalities. Although these arrhythmias are usually benign, they can indicate significant underlying heart disease. More often, patients have chronic arrhythmias, such as atrial fibrillation, that may require treatment to reduce the risk of future complications. The challenges for the family physician are to determine which arrhythmias are benign and which indicate probable cardiac malfunction, and to manage recurrent or chronic rhythm abnormalities.

This two-part article reviews common atrial and ventricular arrhythmias, with a focus on initial management decisions. Part I discusses supraventricular arrhythmias. Part II discusses ventricular arrhythmias and the management of rhythm abnormalities in special populations, including pregnant women, athletes, and children.

Atrial Fibrillation

Atrial fibrillation is the most common cardiac arrhythmia family physicians are likely to encounter. This rhythm abnormality affects 3 to 5 percent of patients more than 60 years of age 1 and becomes increasingly common with advancing age. The median age of patients with atrial fibrillation is 75 years, and the prevalence of the arrhythmia doubles every 10 years after the age of 55. 2 , 3 In the United States, atrial fibrillation is estimated to affect almost 9 percent of patients more than 75 years of age. 2

Most risk factors for atrial fibrillation are associated with structural or ischemic heart disease. Risk factors include hypertension, left ventricular hypertrophy, dilated and restrictive cardiomyopathies, coronary artery disease, chronic obstructive pulmonary disease, and diabetes in women. 1

The annual risk of stroke in patients with atrial fibrillation and normal valve function has been reported to be 4.5 percent per year. 4 Anticoagulation with warfarin (Coumadin) reduces the risk by about two thirds. 4 The mortality rate for stroke in patients with atrial fibrillation is approximately twice as high as the rate in patients without this rhythm abnormality. 5 Although anticoagulation is contraindicated in some elderly patients, a study in Great Britain 6 found that about 60 percent of patients identified in community screenings as having atrial fibrillation were eligible for, and would benefit from, this treatment.

The first step in managing a patient with atrial fibrillation is to decide whether there is a high likelihood of safe conversion to sinus rhythm or whether the patient should be allowed to remain in atrial fibrillation. A patient with recent onset of atrial fibrillation (within the previous 12 months) and no evidence of enlargement of the left atrium has a greater chance of achieving and maintaining sinus rhythm. If the arrhythmia is long-standing and the patient is not a suitable candidate for rate cardioversion, initial treatment should focus on ventricular rate control, with consideration given to long-term stroke prophylaxis.

Restoration of Sinus Rhythm

Patients who present within 48 hours of the onset of new atrial fibrillation are candidates for cardioversion with a low risk of embolism. Conversion to sinus rhythm can be attempted by electrical shock or with antiarrhythmic drugs. Patients who have been in atrial fibrillation for more than 48 hours or for an undetermined period are more likely to have atrial thrombi and may develop emboli with immediate electrical or medical (pharmacologic) cardioversion.

Atrial thrombi are not evident on transthoracic echocardiograms, but they can been seen on transesophageal echocardiograms. 7 If the transesophageal echocardiogram reveals thrombi, anticoagulation is recommended before cardioversion is attempted. Anticoagulation can be accomplished using warfarin, with the dosage adjusted to achieve an International Normalized Ratio (INR) between 2.0 and 3.0 for a minimum of 21 days. 8

If the transesophageal echocardiogram does not show thrombi on multiplane views, cardioversion can be attempted. Short-term anticoagulation with heparin should be started before the procedure, and warfarin therapy should be initiated after cardioversion. 8

When rhythm conversion is indicated, it can be accomplished using direct-current cardioversion or pharmacologic therapy. Synchronized cardioversion is currently considered the treatment of choice for the restoration of sinus rhythm and, in appropriately selected patients, has a success rate of at least 80 percent. 4 Cardioversion is also indicated in patients with hypotension, angina, heart failure, or other evidence of severe compromise caused by atrial fibrillation. 5

Medical cardioversion of atrial fibrillation may be achieved with class IA drugs (quinidine, disopyramide [Norpace], procainamide [Procanbid]) or with amiodarone (Cordarone). In the past, quinidine was frequently used for both cardioversion and maintenance of sinus rhythm in patients who had undergone electrical cardioversion. However, because of the proarrhythmic action of class IA agents and their detrimental effects on left ventricular function, these drugs are now used less often than amiodarone for primary therapy of atrial fibrillation. 4

Amiodarone therapy is successful in 86 percent of patients who have had atrial fibrillation for less than two years. 4 , 9 Treatment is also effective in 40 to 60 percent of patients with long-standing atrial fibrillation that has been resistant to other agents and to electrical cardioversion. 4 Amiodarone can be given in a dosage of 200 mg a day, which is lower than the dosages that have been associated with thyroid abnormalities and pulmonary fibrosis. Although there is little risk of toxicity when amiodarone is given in a low dosage, it is prudent to monitor patients for the development of thyroid, pulmonary, hepatic, and cardiac side effects.

Findings on the usefulness of various agents for the conversion of atrial fibrillation, based on the evidence-based practice program of the Agency for Healthcare Research and Quality, are summarized in Table 1 . 10 Although drugs such as digitalis preparations and sotalol (Betapace) are sometimes used for rate control, they are not effective for converting atrial fibrillation to sinus rhythm. 10 , 11

If external electrical cardioversion is unsuccessful and antiarrhythmic drug therapy fails, other measures can be used. However, these approaches are usually reserved for use in patients who cannot tolerate atrial fibrillation and patients who have associated systolic dysfunction. Techniques include internal electrical cardioversion through the application of electrical current to pulmonary veins via a transcatheter cathode 4 and radiofrequency ablation of the atrioventricular node with insertion of a ventricular pacemaker. 12 In addition, an implantable atrial defibrillator can be used to provide rapid cardioversion in patients with atrial fibrillation that cannot be controlled with medications. 13

Rate Control in Chronic Atrial Fibrillation

In patients in whom rhythm conversion is not indicated or those who have new-onset atrial fibrillation with a rapid ventricular response, treatment may be needed to control the ventricular rhythm. Excessive ventricular rates may result in diminished cardiac output because of poor filling time, and in ischemia because of increased myocardial oxygen demand. Medications used for ventricular rate control in patients with atrial fibrillation are listed in Table 2 . 14

Acute management of ventricular rates can usually be achieved with intravenously administered diltiazem (Cardizem), given in an initial bolus of 15 to 20 mg (0.25 mg per kg) over two minutes, or with an intravenously administered beta blocker such as propranolol (Inderal), given in a dose of 0.5 to 1 mg (up to 3 to 5 mg if needed).

A number of medications, including calcium channel blockers, beta blockers, and digoxin (Lanoxin), are effective for maintaining ventricular rates within acceptable ranges. Because calcium channel blockers are associated with better exercise tolerance, they may be preferable to beta blockers. 15 Digoxin is associated with a high degree of exercise intolerance; therefore, it should be reserved for use in patients who are relatively immobile, who cannot tolerate other treatment options, or who have significant ventricular dysfunction.

Paroxysmal Supraventricular Tachycardias

Based on duration, supraventricular tachycardias are usually categorized as paroxysmal, persistent, or chronic. Paroxysmal supraventricular tachycardia (PSVT) is the most common of these arrhythmias and the one that is most often encountered in the primary care setting. Longer-duration supraventricular tachycardias can be treated similarly to PSVT, but cardiology consultation is often required to identify the electrophysiologic mechanism responsible for sustaining the arrhythmia. In contrast to ventricular tachycardias (discussed in part II of this article) and atrial fibrillation, PSVT is usually a narrow-complex tachycardia with a regular rate.

Atrioventricular Nodal Reentry Causing PSVT

Atrioventricular nodal reentry, the most common mechanism of PSVT, occurs when two pathways exist with different conduction rates. A premature atrial complex that is blocked in the fast pathway and redirected through the slow pathway usually triggers the tachycardia ( Figure 1 ) . The electrical signal proceeds down the slow pathway and then reenters the fast pathway in a retrograde direction. By the time the signal has propagated down the slow pathway and back around on the fast pathway, the slow pathway is no longer refractory and is ready to conduct the signal again, completing a continuous circuit.

Reentrant tachycardias usually produce a narrow-complex tachycardia with no discernible P wave. The rate is usually between 160 and 190 beats per minute. In a less common form of atrioventricular nodal reentrant tachycardia, the circulating wavefront proceeds in an antegrade fashion down the fast pathway and in a retrograde fashion up the slow pathway. In this form, inverted P waves ( Figure 2 ) are clearly visible in lead II of the electrocardiogram (ECG).

It is important to note that atrioventricular nodal reentrant tachycardia can result in a wide-complex tachycardia if the patient has preexisting bundle branch block.

Accessory Pathways Causing PSVT

Accessory pathways (Wolff-Parkinson-White syndrome) and other bypass tracts can cause PSVT. In patients with Wolff-Parkinson-White syndrome, a shortened PR interval and a slurred upstrike to the QRS complex “delta wave” on the resting ECG indicate the presence of an accessory pathway ( Figure 3 ) .

It should be noted that the resting ECG may be normal in some patients with Wolff-Parkinson-White syndrome, because of the inability of the accessory pathway to conduct in the antegrade direction. The usual mechanism of PSVT in this setting is antegrade conduction down the normal pathways through the atrioventricular node and retrograde conduction through the accessory pathway.

The ECG in an atrial arrhythmia with an accessory pathway usually shows a narrow-complex tachycardia at rates of 160 to 240 beats per minute. Delta waves are absent because the normal pathways are used for ventricular activation. Inverted P waves may be seen in the inferior leads. In a much less common form of PSVT, antegrade conduction is down the bypass tract and results in a wide-complex tachycardia.

Increased Automaticity Causing PSVT

Increased automaticity usually occurs when the atrium is enlarged, as in patients with chronic lung disease, congestive heart failure, or electrolyte and acid-base disturbances. Usually, the stretched atria fire irregularly, producing multiple premature beats that emanate from different areas of the atria. Because the foci for the ectopic beats are in multiple sites, the P waves vary in morphology, giving rise to the term “multifocal atrial tachycardia.”

The diagnosis of multifocal atrial tachycardia depends on the identification of an irregular rhythm with three or more different P-wave morphologies. The rate is usually between 130 and 180 beats per minute. Treatment is directed at correcting the underlying cause. Antiarrhythmic drugs are usually not helpful.

In most patients, PSVT is benign and self-limited. However, some patients can have angina, hypotension, and intense anxiety. The first step in the management of PSVT is to determine whether the patient is hemodynamically stable. If PSVT is sustained and there is any indication of instability (i.e., angina, shortness of breath, decreased level of consciousness, hypotension, or congestive heart failure), electrical cardioversion should be performed urgently.

If the symptoms are restricted to discomfort (e.g., palpitations and anxiety), conservative measures should be applied. Conservative management of PSVT can include both nonpharmacologic and pharmacologic measures ( Table 3 ) . 16

Vagal maneuvers to increase parasympathetic tone and slow conduction through the atrioventricular node should be the first approach. Patients should be taught some of these maneuvers for use in future episodes. They should also be instructed to avoid inciting factors, such as caffeine, tobacco, alcohol, pseudoephedrine, and stress. Carotid sinus massage can be attempted, but its role hasbecome more limited because of the effectiveness of drug therapy and the risk of embolism from carotid pressure in some patients.

The goal of pharmacologic management is to slow or block atrioventricular nodal conduction. Agents used for this purpose include adenosine (Adenocard), calcium channel blockers (verapamil [Calan] or diltiazem), and beta blockers (e.g., esmolol [Brevibloc]).

Adenosine is an ultra–short-acting agent that is cleared quickly (half-life of 1 to 6 seconds). This agent is given intravenously in an initial dose of 6 mg, which is followed by one or two 12-mg boluses. Adenosine works by reducing conductance along the slow antegrade pathway. Side effects include flushing, dyspnea, and chest pain. Because of the short half-life of adenosine, these effects are usually very brief and do not ordinarily result in complications.

One advantage of adenosine is that it lacks the negative inotropic effects of calcium channel blockers. Adenosine can also decrease the sinus rate transiently and produce a “rebound” sinus tachycardia. Adenosine should not be used in patients with heart transplants, because such patients may be too sensitive to its effects. 17

Calcium channel blockers can also be used to disrupt a reentrant pathway. Verapamil can be given in a 5- to 10-mg bolus over 2 minutes, followed by 10 mg in 15 to 30 minutes if the initial dose does not convert the arrhythmia. 18 Verapamil and other calcium channel blockers should not be used in patients with an undiagnosed wide-complex tachycardia, because of the risk of fatal hypotension or ventricular fibrillation if the arrhythmia is actually ventricular tachycardia and not PSVT. 19

Intravenously administered diltiazem is also effective. 20 Initial treatment consists of a bolus of 0.25 mg per kg administered over two minutes. A repeat bolus of 0.35 mg per kg given over two minutes can be administered 15 minutes later.

Esmolol, a short-acting beta blocker, can be given in an intravenous bolus of 0.5 mg per kg over 1 minute or in an infusion at a rate of 0.5 mg per kg per minute after an initial loading dose of 0.5 mg per kg. An advantage of esmolol over other beta blockers is its short half-life (four to five minutes), compared with the much longer half-lives (three hours or more) of most other beta blockers. Because of a similar depressive effect on left ventricular contractility, esmolol should be used with caution if initial treatment with a calcium channel blocker is not successful.

Other antiarrhythmic drugs, including quinidine, procainamide, flecainide (Tambocor), and amiodarone, may be used in patients who do not respond to initial medications. However, selective radiofrequency ablation is rapidly becoming the treatment of choice in this situation.

Long-term control of recurrent PSVT caused by atrioventricular nodal reentry may be achieved with pharmacologic therapy or radiofrequency ablation. Patients who have infrequent, well-tolerated recurrences may manage these episodes with self-administered physiologic maneuvers.

Radiofrequency ablation is now used early in the management of patients with PSVT caused by an accessory pathway (Wolff-Parkinson-White syndrome), atrioventricular nodal reentrant tachycardia, or atrial tachycardia. 21 The success rate for radiofrequency ablation is 95 percent in patients with an accessory pathway or atrioventricular nodal reentrant tachycardia, and approximately 80 percent in patients with atrial tachycardia. 21

Other Atrial Arrhythmias

Sinus arrhythmia.

Sinus arrhythmia is usually a normal event in young persons and athletes. In fact, it occurs with such high frequency that it may considered a normal variant rather than a true arrhythmia.

There are two forms of sinus arrhythmia. In the “respiratory” form, the RR interval shortens during inspiration and slows during expiration. Breath-holding eliminates the variation. In the “nonrespiratory” form, the same phasic variation is seen in the RR interval but is not related to respirations. This form of sinus arrhythmia occurs in elderly patients, patients with digoxin overdose, and patients with increased intracranial pressure.

Sinus arrhythmia is usually asymptomatic. Sometimes, however, the long pauses can cause dizziness or syncope. Treatment is usually unnecessary.

WANDERING ATRIAL PACEMAKER

Patients with wandering atrial pacemaker are usually not symptomatic. The condition is most often an isolated finding on the ECG and requires no treatment. Sometimes it is noted on physical examination as an irregularly irregular rhythm.

With wandering atrial pacemaker, the ECG shows variable P-wave morphology and PR intervals. The atrial impulses conduct in a 1:1 fashion and usually control the rhythm for several beats before shifting to another focus. The normal heart rate in wandering atrial pacemaker differentiates this condition from multifocal atrial tachycardia.

PREMATURE ATRIAL COMPLEXES

A premature atrial complex is generated from an ectopic focus in the atria. Therefore, the P wave is usually different in morphology from the usual sinus P wave. The impulse conducts along the normal pathways, generating a narrow QRS complex followed by a pause. Sometimes the premature atrial complex is not conducted and can mimic heart block ( Figure 4 ) .

Premature atrial complexes are found in a variety of settings, including the excessive consumption of caffeine or alcohol and the use of sympathomimetic drugs. These complexes can also be present in patients with structural heart disease.

Patients with premature atrial complexes are usually asymptomatic and require no treatment. A beta blocker given in a low dosage can be tried in patients with uncomfortable symptoms, but no studies of efficacy have been reported. Patients should be counseled to decrease their intake of caffeine, tobacco, and alcohol, and their use of over-the-counter sympathomimetic substances, which are often present in cold medicines and weight-loss preparations.

It is important to note that premature atrial complexes sometimes precipitate supraventricular tachycardia, atrial flutter, or atrial fibrillation.

Sinus Nodal Arrhythmias

Sinus pause and sinoatrial exit block.

Sinus pause or arrest occurs when the sinoatrial node fails to discharge. The ECG shows a pause in the sinus rhythm, with no preceding P wave. Patients usually have no symptoms, but if the pause is prolonged, they may have lightheadedness, palpitations, syncope, and falls. In sinus arrest, the length of the pause has no relationship to the PP interval. Sinoatrial exit block is recognized by the pauses being multiples of PP intervals.

Sinus node dysfunction is usually caused by drugs such as digoxin, quinidine, or procainamide. It can also be caused by ischemia, myocarditis, or fibrosis.

From a therapeutic standpoint, it is probably not important to distinguish between sinus arrest and sino-atrial exit block. Both can occur in well-trained athletes 22 and can be a factor in sick sinus syndrome. 23

SICK SINUS SYNDROME

The term “sick sinus syndrome” encompasses a number of abnormalities, including sinus bradycardia, sinus arrest or exit block, combinations of sinoatrial and atrioventricular nodal conduction disturbances, and atrial tachyarrhythmias. More than one of these arrhythmias may be recorded in the same patient (bradycardia-tachycardia syndrome).

The abnormalities in sick sinus syndrome are usually due to ischemia, fibrosis, or drug-induced or autonomic dysfunction. Signs and symptoms are related to cerebral hypoperfusion and reduced cardiac output.

Treatment of recurrent symptomatic bradycardia or prolonged pauses requires implantation of a permanent pacemaker. 24

Levy S. Epidemiology and classification of atrial fibrillation. J Cardiovasc Electrophysiol. 1998;9(8 suppl):S78-82.

Ryder KM, Benjamin EJ. Epidemiology and significance of atrial fibrillation. Am J Cardiol. 1999;84(9A):R131-8.

Benjamin EJ, Levy D, Vaziri SM, D'Agostino RB, Belanger AJ, Wolf PA. Independent risk factors for atrial fibrillation in a population-based cohort. The Framingham Heart Study. JAMA. 1994;271:840-4.

Golzari H, Cebul RD, Bahler RC. Atrial fibrillation: restoration and maintenance of sinus rhythm and indications for anticoagulation therapy. Ann Intern Med. 1996;125:311-23.

Pritchett EL. Management of atrial fibrillation. N Engl J Med. 1992;326:1264-71.

Sudlow M, Thomson R, Thwaites B, Rodgers H, Kenny RA. Prevalence of atrial fibrillation and eligibility for anticoagulants in the community. Lancet. 1998;352:1167-71.

Falk RH. Atrial fibrillation. N Engl J Med. 2001;344:1067-78.

Manning WJ, Silverman DI, Keighley CS, Oettgen P, Douglas PS. Transesophageal echocardiographically facilitated early cardioversion from atrial fibrillation using short-term anticoagulation: final results of a prospective 4.5-year study. J Am Coll Cardiol. 1995;25:1354-61.

Santos AL, Aleixo AM, Landieri J, Luis AS. Conversion of atrial fibrillation to sinus rhythm with amiodarone. Acta Med Port. 1979;1:15-23.

Management of new onset atrial fibrillation. Summary, evidence report/technology assessment: no. 12. Rockville, Md.: Agency for Healthcare Research and Quality, May 2000; AHRQ publication no. 00-E006. Retrieved April 23, 2002, from www.ahcpr.gov/clinic/epcsums/atrialsum.htm .

Falk RH, Knowlton AA, Bernard SA, Gotlieb NE, Battinelli NJ. Digoxin for converting recent-onset atrial fibrillation to sinus rhythm. A randomized, double-blinded trial. Ann Intern Med. 1987;106:503-6.

Pappone C, Rosanio S, Oreto G, Tocchi M, Gugliotta F, Vicedo-mini G, et al. Circumferential radiofrequency ablation of pulmonary vein ostia: a new anatomic approach for curing atrial fibrillation. Circulation. 2000;102:2619-28.

Swerdlow CD, Schsls W, Dijkman B, Jung W, Sheth NV, Olson WH, et al. Detection of atrial fibrillation and flutter by a dual-chamber implantable cardioverter-defibrillator. For the Worldwide Jewel AF Investigators. Circulation. 2000;101:878-85.

Physicians' desk reference. 56th ed. Montvale, N.J.: Medical Economics, 2002.

Segal JB, McNamara RL, Miller MR, Kim N, Goodman SN, Powe NR, et al. The evidence regarding the drugs used for ventricular rate control. J Fam Pract. 2000;49:47-59.

Myerburg RJ, Kessler KM, Castellanos A. Recognition, clinical assessment, and management of arrhythmias and conduction disturbances. In: Alexander RW, Schlant RC, Fuster V, eds. Hurst's The heart, arteries and veins. 9th ed. New York: McGraw-Hill, Health Professions Division, 1998:873–942.

O'Nunain S, Jennison S, Bashir Y, Garratt C, McKenna W, Camm AJ. Effects of adenosine on atrial repolarization in the transplanted human heart. Am J Cardiol. 1993;71:248-51.

Rinkenberger RL, Prystowsky EN, Heger JJ, Troup PJ, Jackman WM, Zipes DP. Effects of intravenous and chronic oral verapamil administration in patients with supraventricular tachyarrhyth-mias. Circulation. 1980;62:996-1010.

Stewart RB, Bardy GH, Greene HL. Wide complex tachycardia: misdiagnosis and outcome after emergent therapy. Ann Intern Med. 1986;104:766-71.

Betriu A, Chaitman BR, Bourassa MG, Brevers G, Scholl JM, Bruneau P, et al. Beneficial effect of intravenous diltiazem in the acute management of paroxysmal supraventricular tach-yarrhythmias. Circulation. 1983;67:88-94.

Morady F. Radio-frequency ablation as treatment for cardiac arrhythmias. N Engl J Med. 1999;340:534-44.

Bjornstad H, Storstein L, Meen HD, Hals O. Ambulatory electrocardiographic findings in top athletes, athletic students and control subjects. Cardiology. 1994;84:42-50.

Wu DL, Yeh SJ, Lin FC, Wang CC, Cherng WJ. Sinus automaticity and sinoatrial conduction in severe symptomatic sick sinus syndrome. J Am Coll Cardiol. 1992;19:355-64.

Haywood GA, Katritsis D, Ward J, Leigh-Jones M, Ward DE, Camm AJ. Atrial adaptive rate pacing in sick sinus syndrome: effects on exercise capacity and arrhythmias. Br Heart J. 1993;69:174-8.

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INTRODUCTION

The sinoatrial (SA) node represents the integrated activity of pacemaker cells, sometimes called P cells, in a compact region at the junction of the high right atrium and the superior vena cava. Perinodal cells, sometimes called transitional or (T) cells, transmit the electrical impulse from the SA node to the right atrium. Each of these cell types has distinct expression profiles of ion channels and gap junctions.

Given the architecture of the SA node, SA nodal dysfunction typically results from either abnormalities in impulse generation by the P cells or abnormalities in conduction across the T cells. SA nodal dysfunction is more commonly an acquired condition, but in some patients it can be inherited, with gene mutations having been described in some forms of inherited SA nodal dysfunction [ 1 ]. Patients with SA nodal dysfunction may be asymptomatic or highly symptomatic as in cases of sinus node dysfunction (SND).

Sinoatrial nodal pauses, arrest, and exit block will be discussed here. Additional details regarding the anatomy and electrophysiology of the SA node, as well as a discussion of the SND, are presented separately. (See "Sinus node dysfunction: Epidemiology, etiology, and natural history" .)

Sinus pause, arrest, and exit block may arise from hyperkalemia; excessive vagal tone; ischemic, inflammatory, or infiltrative or fibrotic disease of the SA node; sleep apnea; certain drugs (eg, digitalis). The causes of SND are discussed in detail elsewhere. (See "Clinical manifestations of hyperkalemia in adults" and "Sinus node dysfunction: Epidemiology, etiology, and natural history", section on 'Etiology' and "Obstructive sleep apnea and cardiovascular disease in adults", section on 'Other arrhythmias' and "Cardiac arrhythmias due to digoxin toxicity", section on 'Sinus bradycardia, tachycardia, block, and arrest' .)

In patients receiving one or more agents that depress SA node and atrioventricular (AV) node function, a syndrome of bradycardia, renal failure, AV block, shock, and hyperkalemia (BRASH), has been described [ 2,3 ]. Patients with BRASH are generally taking therapeutic doses of SA and AV node blocking medications, and the level of hyperkalemia may be mild. However, the severity of bradycardia (caused by sinus arrest and/or AV block) is generally greater than expected for either the dose/level of SA and AV node blocker or the level of hyperkalemia.

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Electrical Injury and Wandering Atrial Pacemaker

Ranjan k singh.

1 Internal Medicine, Anti-Retroviral Therapy Centre, District Hospital, Khagaria, IND

The supply of household electricity remains a low-voltage (110-220 V) energy source, and its effects on the human body depend on several factors, including the type of contact and duration of contact, among other things. In a significant number of cases, direct contact with household electricity causes reversible cardiac arrhythmia-ventricular fibrillation, ventricular premature beats, atrial tachycardia, and atrial fibrillation.

Wandering atrial pacemaker (WAP) is a benign atrial arrhythmia observed in elderly patients suffering from obstructive pulmonary diseases that result from an ischemic heart. This report discusses WAP as observed in a patient who suffered an electrical injury.

Introduction

The effects of electrical injury vary from skin burn to internal organ damage directed especially at the cardiovascular and nervous systems. The extent of electrical injury depends on the type of electricity source, i.e., direct current (DC) or alternating current (AC), the duration of contact with the source of electricity, the state of the body whether wet or dry, the presence of calluses over the palm, the route of electrical flow, and the level of voltage [ 1 ]. The severity of an electric shock depends on the current flow (I) measured in ampere (A). It is linked to the resistance of the conductor (R, unit: ohm ‘W’) and the potential difference between the two ends of a conductor (Volt; unit V), and is derived by applying the formula based on Ohm’s law: i.e., I = V/R. The severity of an electrical burn, by contrast, depends on the energy (Watt) and is derived from Joule’s formula W=I2 x R x T (duration of exposure with the source of current).

Household electrical supply is a low-voltage (220 V) AC at 60 Hz frequency. The physiological effects of contact with a low-frequency AC (60 Hz) current vary at different amperes. For example, 1mA (1/1000 A) is barely perceptible as numbness, whereas 20 mA can cause respiratory muscle paralysis, while 100 mA reaches a threshold for ventricular fibrillation [ 1 , 2 ]. The resulting cardiac arrhythmia may take the form of ventricular fibrillation, ventricular tachycardia, ventricular premature beats, atrial premature beats, atrial arrhythmia, and/or heart block [ 2 ].

Case presentation

A 40-year-old male patient was brought into the emergency ward after suffering an accidental electrical injury that involved an entry wound in the middle of his left hand and an exit wound in the back of his chest. He was holding the hanging rod for a ceiling fan when the connection was plugged in, resulting in electric shock. He lost consciousness and fell to the ground with the rod clenched in his hand for a minute and a half. The electricity source was disconnected and cardiopulmonary resuscitation was administered to the patient by his neighbors. The patient regained consciousness and complained of aching all over the body along with general weakness. 

He had a black hole in the middle of his left palm (Figure ​ (Figure1A) 1A ) and a linear burn on the back of his chest (Figure ​ (Figure1B 1B ).

His pulse was irregularly irregular at 78/minute, and his blood pressure was 110/78 mm Hg. His total leucocyte count was 8600/cmm with neutrophils at 64%, and his hemoglobin was 13 gm/dL. Urinalysis did not show myoglobin. Serum sodium and potassium were 134 mEq/L and 4.2 mEq/L, respectively. Electrocardiography (ECG) showed occasional ventricular premature beat with wandering atrial pacemaker (Figures ​ (Figures2A 2A - ​ -2B). 2B ). Of note, the patient did not have any kind of cardiac ailment previously. The patient was hydrated with intravenous fluids and his wounds were treated with antiseptic dressings and antibiotics. He remained under observation for 48 hours and the ECG showed sinus rhythm (Figure ​ (Figure2C 2C ).

Low voltage currents cause severe electrical burns to the skin as a result of high energy output from the current flow. Dry skin with callouses over palm (resistance of 500 W) and a long contact of palm with the source of electricity attribute to severe burn in this patient (Joule formula). Thereby, the electrical energy output is dissipated and there is less internal injury [ 3 , 4 ].

Low voltage currents travel through the body along low-resistance pathway nerves and blood vessels to cause severe cardiac injury. Also, the distance between the entry and exit wounds can determine the severity of the cardiac injury. The heart remains in the central location of the electrical current’s pathway between the left palm and back of the chest. Current spikes occur in the palm and fingers of an individual holding a metal rod that is suddenly connected to an electric source [ 5 ]. The electric shock causes depolarisation of cardiac muscles and increases membrane pores of the cells resulting in arrhythmias; sinus tachycardia, ventricular premature beats, ventricular tachycardia, and atrial fibrillation are common [ 6 , 7 ]. Wandering atrial pacemaker (WAP) is a benign atrial arrhythmia that has been observed in this case study. WAP and multifocal atrial tachycardia (MAT) differ only with the heart rate - WAP has a heart rate less than 100 bpm whereas MAT has a heart rate greater than 100 bpm. In the WAP rhythm, the pacemaker wanders with the impulses originating from the sinoatrial node to the atrium, and to the atrioventricular junction with a changing focus. Hence, the P waves on an ECG are presented in different configurations. WAP is differentiated from sinus arrhythmia by the fact that heart rate variability occurs from beat-to-beat, and is not phasic. Also, in sinus arrhythmia, the P-wave morphology and the P-R interval are constant [ 7 ]. Most of the arrhythmias occur soon after electric shock and are short-lived. However, delayed arrhythmias occurring 12 hours after electric shock have been reported, too [ 8 ].

Conclusions

Household electric supply is low voltage AC of 60 Hz. It is the electric current that determines the pathophysiological effects in the body but the voltage does determine the outcome of electric shock. Even a low-voltage shock can cause ventricular fibrillation if resistance is low and current flow reaches a threshold of 100 mA. The severity of burn lesion is determined by the resistance of skin and duration of exposure with the source of current. Most cardiac arrhythmias are short-lived and do not require treatment.

The content published in Cureus is the result of clinical experience and/or research by independent individuals or organizations. Cureus is not responsible for the scientific accuracy or reliability of data or conclusions published herein. All content published within Cureus is intended only for educational, research and reference purposes. Additionally, articles published within Cureus should not be deemed a suitable substitute for the advice of a qualified health care professional. Do not disregard or avoid professional medical advice due to content published within Cureus.

The authors have declared that no competing interests exist.

Human Ethics

Consent was obtained or waived by all participants in this study. NA issued approval NA. This is a case report.

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The Wandering Atrial Pacemaker

The qt interval, boring bundle branch block, dextrocardia and reversed limb leads, unusual av wenckebach.

Today, it is unusual to see an electrocardiograph (ECG) with the diagnosis of Wandering Atrial Pacemaker , but when we do, it is often incorrect. The last one I saw was a marked sinus arrhythmia with unifocal atrial ectopics and it is important to differentiate these two diagnoses as the treatment and prognosis are very different.

Wandering atrial pacemaker, as the name implies, is an irregular ECG rhythm which wanders from sinus to at least two other different atrial ectopic foci resulting in P waves with three different morphologies.

Here is an example:

The rate is slow and there are two atrial ectopic foci: crista terminalis (looks like the sinus P wave), low atrial (inverted P waves), and not surprisingly, atrial fusion beats with maybe more than one P wave morphology. Clearly, the atrium is very irritable, and therefore the rhythm is a precursor to atrial fibrillation. The term chaotic atrial mechanism is also used. Most examples of this rhythm are difficult to diagnose because the rhythm is faster than 100 bpm and hence is called multifocal atrial tachycardia .

It is easy to see how this rhythm can be confused with atrial fibrillation with an uncontrolled ventricular response. Indeed, an ECG performed soon after this Holter monitor recording showed atrial fibrillation, confirming the transient appearance and thus rarity of this rhythm.

In the past this ECG was seen with severe cor pulmonale, cyanosis and right heart disease. The uncontrolled atrial fibrillation in such a sick patient was often a terminal event.

Dr Harry Mond

About Assoc Prof Harry Mond

In 49+ years as a practicing cardiologist, Dr Harry Mond has published 260+ published manuscripts & books. A co-founder of CardioScan, he remains Medical Director and oversees 500K+ heart studies each year.

Download his full profile here.

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Benefits and Limitations

The electrocardiogram (ECG or EKG) provides a graphic representation of the electrical depolarization and repolarization processes of the cardiac muscle, as "viewed" from the body surface. The amplitude of these electrical potential differences between various points on the body is measured in millivolts (mV) and their duration in seconds. The ECG can provide information on heart rate, rhythm, and intracardiac conduction; it may also reveal evidence of specific chamber enlargement, myocardial disease or ischemia, pericardial disease, certain electrolyte imbalances, and some drug toxicities. But note that although the ECG is a valuable part of the cardiac evaluation, it cannot determine if congestive heart failure is present, or (in itself) predict whether an animal will survive procedures requiring anesthesia, nor can it provide much information on the strength (or even presence) of cardiac contractions.

Sinus rhythm is the normal cardiac rhythm, described above. The P waves are positive in the caudal leads (II and aVF), the P-Q intervals are consistent and the R-R intervals occur regularly, with less than 10% variation in timing. Normally, the QRS complexes are narrow and upright in leads II and aVF; however, if an intraventricular conduction disturbance or ventricular enlargement pattern is present, they may be wide and abnormally shaped.

Sinus bradycardia is a rhythm that originates in the sinus node and is conducted normally but has too slow a rate, while sinus tachycardia also originates in the sinus node and is conducted normally but is too rapid.

Sinus arrhythmia is characterized by a cyclical slowing and speeding of the sinus rate, most commonly associated with respiration. The rate tends to increase on inspiration and decrease with expiration because of changes in vagal tone. Often, there is an accompanying change in P wave configuration (wandering pacemaker) with the P waves becoming taller and spiked during inspiration and flatter in expiration. Marked sinus arrhythmia occurs in some animals with chronic pulmonary disease. Sinus arrhythmia is a normal rhythm variation . It is commonly seen in dogs, but not often in the clinical setting in normal cats. However, cats frequently have sinus arrhythmia when relaxed or sleeping.

Sinus arrest is a cessation of sinus node activity lasting at least twice as long as the patient's longest expected R-R interval. The resulting pause in heart rate is interrupted by either an escape beat or resumption of sinus activity. Fainting or weakness may result during these pauses.

Conduction blocks in the major ventricular conduction system also disturb the normal activation process and result in altered QRS configurations. The portion of the ventricles served by the diseased bundle branch is activated late and slowly, resulting in widening of the QRS with the terminal forces oriented toward the area of delayed activation.

Rhythm Disturbances

Impulses originating from outside the sinus node are abnormal and create an arrhythmia (dysrhythmia). Abnormal or ectopic impulses are described based on their site of origin (atrial, junctional, supraventricular, ventricular). They are also characterized by timing , that is, whether they occur earlier than the next expected sinus impulse ( premature ) or whether they occur late ( escape ), as a rescue mechanism. Abnormal premature impulses (complexes) may occur singly or in multiples. Groups of three or more comprise an episode of tachycardia ; bouts of tachycardia may be brief (paroxysmal tachycardia) or quite prolonged (sustained tachycardia). A bigeminal pattern occurs when each normal QRS is followed by a premature complex; the origin of the premature complexes determines whether the rhythm is atrial or ventricular bigeminy.

Supraventricular (atrial, junctional) premature complexes originate above the AV node, in either the atrium or the AV junctional (near the AV node) area; however, since they are conducted through the ventricles in the normal manner, their QRS configuration is normal (unless an intraventricular conduction disturbance is also present). Atrial premature complexes are preceded by an abnormal P wave (either positive, negative or biphasic).

Ventricular premature complexes (VPCs or PVCs) originate below the AV node and do not activate the ventricles by the normal pathway; therefore, they have an abnormal ECG configuration. Ventricular ectopic complexes are also wider than the normal QRS complexes because of their slower conduction through ventricular muscle. When the configuration of VPCs or tachycardia in a patient is consistent, the complexes are described as being uniform or unifocal. When the VPCs occurring in an individual have differing configurations, they are said to be multiform. Increased electrical instability of the heart is thought to accompany multiform VPCs or tachycardia. Ventricular tachycardia defines a rapid series of VPCs (greater than 100 beats/minute in the dog, for example). The R-R interval is usually regular, although some variation is not uncommon. Sinus P waves may be seen superimposed on or between the ventricular complexes; they are unrelated to the VPCs because the AV node and/or ventricles are in the refractory period (physiologic AV dissociation).

Atrial fibrillation ("delirium cordis") is a common arrhythmia characterized by rapid, chaotic electrical activation of the atria. There are no P waves on the ECG; rather, the baseline usually shows irregular undulations (fibrillation waves). Since there is no organized electrical activity, meaningful atrial contraction is absent. The AV node, being constantly bombarded with these disorganized electrical impulses, conducts as many as possible to the ventricles. The (ventricular) heart rate is, therefore, determined by how many impulses the AV node can conduct. Atrial fibrillation results in an irregular heart rhythm, which is usually quite rapid. Most often, the QRS complexes appear normal in configuration, since the normal intraventricular conduction pathway is used. Atrial fibrillation tends to be a consequence of significant atrial disease and enlargement in small animals.

Atrio - ventricular (AV) conduction blocks may result from therapy with certain drugs, high vagal tone, and organic disease of the AV node and/or ventricular conduction system. AV blocks are also called "Heart Blocks."

Matthew W. Miller, DVM, MS, DACVIM (Cardiology) College of Veterinary Medicine and Biomedical Sciences Texas A&M University College Station, TX, USA

Thursday, March 4, 2021

Blog #200 — wandering pacemaker (vs mat).

There is no clinical information is available for the ECG and 2-lead rhythm strip shown below in  Figure-1 .

• HOW would you interpret this tracing?
• What treatment is likely to be needed? 

====================================

Editorial  Comment:

It is always challenging to interpret tracings without the benefit of clinical information. That said — this situation is common in clinical practice. My experience in this area derives from the 30 years during which I was charged with interpreting  all  ECGs ordered by 35 medical providers at a primary care clinic — as well periodic stints during which I interpreted hospital tracings without the benefit of any history. 

• The challenge lies with having to decide  which  tracings in the  “pile of ECGs to be interpreted”  were those for which I needed to pull the medical chart ( or call the provider ) because of ECG findings of immediate potential concern.
• Obvious time constraints made it impossible to pull the chart for each ECG that I was given to read ( I’d never get anything else done if I did so ).
• I therefore became well versed in the skill of limiting the charts that I would pull to those patients whose ECGs showed findings I thought were important  and  potentially indicative of an acute situation that may have been overlooked.

=====================================

MY Thoughts  on the ECG in Figure-1:

As always — systematic interpretation of  any  ECG should begin with assessing the cardiac rhythm. In general —  lead II  and  lead V1  are the 2  best  leads on a 12-lead tracing for assessing atrial activity — and we have the advantage in  Figure-1  of a  simultaneously-recorded  2-lead rhythm strip of both of these leads.  By the  Ps ,  Qs and  3R Approach:

• The rhythm in  Figure-1  is  clearly   irregular .
• The  QRS  complex is  narrow ( ie,  not  more than half a large box in duration = ≤0.10 second ) . 
• The rate  varies  from  50 /minute — to just under  100 /minute.
• More than 1 P wave morphology is present . That said — P waves  do  appear to be related to neighboring QRS complexes, because the PR interval for the P wave shapes that we see remains constant  ( See   Figure-2 ) .

MY Thoughts  on Figure-2:

There are 2 different P wave shapes in  Figure-2 .

• The tracing begins with  3  sinus  beats ( ie,  RED arrows highlight 3 similar-looking upright-in-lead-II P waves — all with the same PR interval ) .
• P wave shape then changes  for beats #4, 5 and 6  ( ie,  BLUE arrows highlighting an almost isoelectric, if not negative P wave with fixed PR interval ) .
• The atrial focus then shifts back , with return to sinus P waves for beats #7, 8, 9 and 10 (ie,  return of RED arrows highlighting similar-looking, upright P waves in lead II — albeit with variability in the R-R interval ).
• The rhythm in  Figure-2  concludes with a  slowing-down  of the ventricular rate, as  the 2nd atrial focus returns , in which the P wave is almost isoelectric (ie,  BLUE arrows for beats #11 and 12 ).

BOTTOM LINE  regarding  Figure-1:  The rhythm in  Figure-2  is most consistent with a  Wandering  Atrial  Pacemaker . This is because the change from one atrial site to the next occurs gradually over a period of several beats.

• PEARL:  The reason it is uncommon ( if not rare ) in clinical practice to see a wandering atrial pacemaker — is that most providers do not pay  long enough  attention to  beat-to-beat  change in P wave morphology needed to identify  gradual  shift between  at least  3 different atrial sites.

SUMMARY:  Review of the  KEY  features of wandering atrial pacemaker is the theme below for our  ECG  Media  Pearl #17 ( a 3:30 minute audio recording ).

• Written review of wandering pacemaker appears below in  Figure-3 .
• Review of  MAT  is covered in our  ECG Blog #199 .

Today’s   E CG  M edia   P EARL  # 17 ( 3:30 minutes   Audio )  —   What is a  Wandering  Atrial Pacemaker ( as opposed to MAT )?

A DDENDUM   ( 3/4/2021 ) :

I received the following note from  David Richley  regarding today’s tracing: “I think I would use different terminology to describe this because to me the atrial pacemaker doesn’t so much ‘wander’ as ‘jump’. I would describe this as sinus arrhythmia with junctional escape rhythm at 60-65/minute every time the sinus node discharge rate slows to below that rate. I interpret the escape beats as junctional rather than atrial, because athough the P waves, ( which are initially negative in II, aVF and V4-V6 — and positive in aVR ) precede the QRS — the PR segment is very short, suggesting an AV nodal origin. However, we describe this phenomenon — I do agree that it’s likely to be completely benign.

MY Thoughts:  Dave’s comment is one of the reasons why:  i )  The diagnosis of wandering pacemaker requires clear demonstration of shift in the atrial pacemaker in  at least  3 different sites. We  only  see 2 different sites here;  and ,  ii )  The diagnosis of wandering atrial pacemaker is  not  common. 

• It’s impossible to rule out Dave’s theory from the single tracing we have.
• That said — the BLUE arrow P wave site may or may not be of AV nodal origin ( you can see a similar, near-isoelectric P wave with short PR interval from a low atrial site ).
• I also considered the possibility of the BLUE arrow P waves representing junctional escape — but decided against it because the difference in R-R interval from what we see between beats #9-10  vs  what we see between beats #10-11 is  more  than what I’d expect based on the cadence of rate variation I see from beats #7-10.
• Bottom Line:  We both agree there is a shift in the pacemaker site in a rhythm that is likely to be benign. And, we both agree that additional monitoring would be needed for a definitive response.  THANK YOU Dave!

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• Wandering atrial pacemaker
• 2 Clinical Features
• 3.1 Palpitations
• 4.2 Diagnosis
• 5 Management
• 6 Disposition
• 8 External Links
• 9 References
• Three or more ectopic foci within the atrial myocardium serve as the pacemaker
• Rate is less than 100bpm (in contrast to MAT )
• Is irregularly irregular therefore sometimes confused with atrial fibrillation and sinus arrhythmia
• Intrinsic cardiac or pulmonary disease
• Metabolic derangements
• Drug toxicity (including Digoxin )

Clinical Features

• Often seen in the extremes of age and in athletes
• Rarely causes symptoms

Differential Diagnosis

Palpitations.

• Narrow-complex tachycardias
• Wide-complex tachycardias
• Second Degree AV Block Type I (Wenckeback)
• Second Degree AV Block Type II
• Third Degree AV Block
• Premature atrial contraction
• Premature junctional contraction
• Premature ventricular contraction
• Sick sinus syndrome
• Acute coronary syndrome
• Cardiomyopathy
• Congenital heart disease
• Congestive heart failure (CHF)
• Mitral valve prolapse
• Pacemaker complication
• Pericarditis
• Myocarditis
• Valvular disease
• Panic attack
• Somatic Symptom Disorder
• Drugs of abuse (e.g. cocaine )
• Medications (e.g. digoxin , theophylline )
• Thyroid storm
• Pulmonary embolism
• Dehydration
• Pheochromocytoma

• ECG should show three distinct P wave morphologies with a ventricular rate <100bpm
• Rarely requires treatment

Disposition

• Outpatient management
• Multifocal atrial tachycardia
• Dysrhythmia

External Links

• Richard Cunningham
• fardis tavangary
• Ross Donaldson
• Privacy policy
• Disclaimers

Atrial Rhythms ECG Interpretation

This page provides an introduction to atrial rhythms and links to training materials on this website.

Atrial rhythms originate in the atria, not from the SA node. The P wave's shape can be different from a normal sinus rhythm as the electrical impulse follows a different path. For a complete discussion of atrial rhythm ECG, use our atrial rhythms training module and our practice strips. Atrial rhythms categories:

• Atrial Fibrillation (afib)
• Atrial Flutter

Premature Atrial Complex

Multifocal atrial tachycardia, supraventricular tachycardia.

• Wandering Atrial Pacemaker

Wolff-Parkinson-White Syndrome

Atrial rhythm categories.

• Atrial Fibrillation

Sites in the atria are firing very rapidly, between 400-600 bpm. These rapid pacemaking signals cause the atria to quiver. The ventricles beat at a slower rate because the AV node blocks some of the atrial impulses.

There are two types of atrial flutter. Type I (also called classical or typical) has a rate of 250-350 bpm. Type II (also called non-typical) are faster, ranging from 350-450 bpm. ECG tracings will show tightly spaced waves or saw-tooth shaped waveforms (F-waves).

During multifocal atrial tachycardia, several (non-SA) sites are creating impulses. The P waves will vary in shape and at least three different shapes can be observed. The PR Interval varies. Ventricular rhythm is irregular.

Premature atrial complex occurs when an ectopic site within the atria fires an impulse before the next impulse from the SA node. If the ectopic site is near the SA node, the P wave will often have a shape similar to a sinus rhythm. But this P wave will occur earlier than expected.

This term covers three types of tachycardia that originate in the atria, AV junction or SA node.

Wandering atrial pacemaker is an irregular rhythm. In is similar to multifocal atrial tachycardia but the heart rate is under 100 bpm. P waves are present but will vary in shape.

Wolff-Parkinson-White Syndrome occurs when the impulse travels between the atria and ventricles via an abnormal path, called the bundle of Kent. The impulse, not being delayed by the AV node, can cause the ventricles to contract prematurely. ECG characteristics include a shorter PR Interval, longer QRS complex and a delta wave.

Training Resources

Atrial rhythm training.

After a brief review of cardiac rhythm analysis, this module explains morphologic features and qualifying criteria of atrial rhythms.

Atrial Rhythms Course

ECG Rhythm Tests

Hundreds heart rhythms in this practice test. Test can be tailored for specific learning needs.

ECG Monitor Challenge

A quiz using a simulated patient monitor. Evaluate a scrolling waveform rather than a paper tracing.

Lesson #1: Rhythm Analysis Method - 312

The five steps of rhythm analysis will be followed when analyzing any rhythm strip.

• Analyze each step in the following order.

Rhythm Regularity

• P wave morphology
• P R interval or PRi
• QRS complex duration and morphology
• Carefully measure from the tip of one R wave to the next, from the beginning to the end of the tracing.
• A rhythm is considered “regular or constant” when the distance apart is either the same or varies by 1 ½ small boxes or less from one R wave to the next R wave.

Heart Rate Regular (Constant) Rhythms

• The heart rate determination technique used will be the 1500 technique.
• Starting at the beginning of the tracing through the end, measure from one R wave to the next R wave (ventricular assessment), then P wave to P wave (atrial assessment), then count the number of small boxes between each and divide that number into 1500. This technique will give you the most accurate heart rate when analyzing regular heart rhythms. You may include ½ of a small box i.e. 1500/37.5 = 40 bpm (don’t forget to round up or down if a portion of a beat is included in the answer).

Step 2 (Cont)

Heart rate - irregular rhythms.

• If the rhythm varies by two small boxes or more, the rhythm is considered “irregular”.
• The heart rate determination technique used for irregular rhythms will be the “six-second technique”.
• Simply count the number of cardiac complexes in six seconds and multiply by ten.

P wave Morphology (shape)

• Lead II is most commonly referenced in cardiac monitoring
• In this training module, lead two will specifically be referenced unless otherwise specified.
• The P wave in lead II in a normal heart is typically rounded and upright in appearance.
• Changes in shape must be reported. This can be an indicator that the locus of stimulation is changing or the pathway taken is changing.
• P waves may come in a variety of morphologies i.e. rounded and upright, peaked, flattened, notched, biphasic(pictured), inverted and even buried or absent!
• Remember to describe the shape. This can be very important to the physician when diagnosing the patient.

PR interval (PRi)

• Measurement of the PR interval reflects the amount of time from the beginning of atrial depolarization to the beginning of ventricular depolarization.
• Plainly stated, this measurement is from the beginning of the P wave to the beginning of the QRS complex.
• The normal range for PR interval is: 0.12 – 0.20 seconds (3 to 5 small boxes)
• It is important that you measure each PR interval on the rhythm strip.
• Some tracings do not have the same PRi measurement from one cardiac complex to the next. Sometimes there is a prolonging pattern, sometimes not.
• If the PR intervals are variable, report them as variable, but note if a pattern is present or not.

QRS complex

• QRS represents ventricular depolarization.
• It is very important to analyze each QRS complex on the tracing and report the duration measurement and describe the shape (including any changes in shape).
• As discussed in step 3, when referring to P waves, remember changes in the shape of the waveform can indicate the locus of stimulation has changed or a different conduction pathway was followed. It is no different when analyzing the QRS complex. The difference is that in step 3, we were looking at atrial activity. Now we are looking at ventricular activity.
• Measure from the beginning to the end of ventricular depolarization.
• The normal duration of the QRS complex is: 0.06 – 0.10 second

Lesson #2: Interpretation - 312

Introduction.

• The previous slides presented the five-steps of rhythm analysis. These five steps must be followed regardless of how simple of complex the tracing is you are reviewing.
• The information gathered in these steps are telling a story.
• The title of that story is the interpretation.

Atrial Dysrhythmias Types

The dysrhythmias in this category occur as a result of problems in the atria. These atrial dysrhythmias primarily affect the P wave. We will be discussing the following complexes and rhythms:

• Premature Atrial Complexes (PAC’s)

Lesson #3: Premature Atrial Complex

Intro to pac.

• PAC's can occur for a number of different reasons i.e., diet, fatigue, stress, disease, ischemia to name a few.
• Premature complexes frequently occur in bradycardic rhythms, but may occur almost any time.
• PAC's occur when an early electrical impulse occurs from a location in the atria other than the SA node.

Intro to PAC 2

• This early impulse causes an early cardiac complex which disrupts the underlying rhythm.
• The locus of stimulation being different, results in a change in the morphology of the P wave.
• PAC's can occur occasionally or frequently.
• PAC's can be observed with or without a pattern
• The P wave with PAC's will always be upright

ECG Analysis

Notice the following: the R to R interval is irregular, the fifth complex is early and the P wave on the early complex is a different shape.

ECG Practice Strip

Analyze this tracing using the five steps of rhythm analysis.

• Rhythm: Irregular
• P wave: Upright & uniform (except early complexes - biphasic)
• PR interval: 0.16 second
• Interpretation: Sinus Bradycardia with PAC's

Lesson #4: Wandering Atrial Pacemaker

Description.

• Rhythms are often named according to the origin of the electrical activity in the heart or the structure where the problem is occurring.
• Wandering Atrial Pacemaker is aptly named due to the electrical impulses causing the atrial activity are moving or wandering.
• These changes in the locus of stimulation affect the morphology of the P waves.
• In Wandering Atrial Pacemaker, you must observe at least three different shaped P waves. No other changes in the tracing may be observed. The rhythm may or may not be regular.
• The PR interval is often affected, but does not have to be.
• The bottom line, is you must observe at least three different shaped P waves.

Practice Strip

• P wave: Changing Shapes (3 or more)
• PR interval: Variable
• Interpretation: Wandering Atrial Pacemaker

Lesson #5: Multifocal Atrial Tachycardia

• Multifocal Atrial Tachycardia is just a faster version of Wandering Atrial Pacemaker. The criteria is the same as Wandering Atrial Pacemaker with the only difference being the heart rate exceeds 100 bpm.
• These changes in the locus of stimulation within the atria affect the morphology of the P waves.
• Remember, you must observe at least three different shaped P waves.
• Due to the presence of irregular R to R intervals coupled with the changing P wave morphology, some people have confused this rhythm with Atrial Fibrillation.

Lesson #6: Atrial Flutter

• Atrial Flutter occurs when there is an obstruction within the atrial electrical conduction system.
• Due to this impediment a series of rapid depolarizations occur.
• These depolarizations may occur two, three, four or more times per QRS complex.
• The AV node functions like a “gatekeeper” blocking the extra impulses until the ventricular conduction system is able to accept the impulse.
• The impulse that is accepted will cause the QRS complex to occur.
• Each flutter wave represents atrial depolarization. This will be noted next to the P wave step in rhythm analysis. Instead of P waves, this tracing has “F” waves. No P waves mean there is no PR interval measurement.
• When the tracing is interpreted, the ratio of F waves to each QRS complex will be documented along with the rhythm i.e. Atrial Flutter 4:1 (indicates 4 “F” waves to each QRS complex). Not all Atrial Flutter will have a regular rhythm. In that case just document and report your observations.
• Compare your answers with the answers on the next slide.

Practice Strip Answers

• Rhythm: Regular
• Rate: Ventricles - 80, Atria - 320
• P wave: "F" waves
• PR interval: absent
• Interpretation: Atrial Flutter 4:1

Lesson #7: Atrial Fibrillation

• Atrial Fibrillation occurs when multiple electrical impulses occur within the atria. This chaotic electrical activity results in a chaotic wave form between the QRS complexes. P waves are absent. They are replaced by lower case "f" waves. No P waves means there is no PR interval measurement.
• This rapid electrical activity overwhelms the AV node causing impulses to enter the ventricular conduction system at irregular points. This results in irregular R to R intervals.
• Not all fibrillatory waves are created equal. The "f" waves can be coarse (majority measure 3 mm or more) or can be fine (majority of waveforms measure less than 3 mm) to almost absent. Regardless always report your observations. Many times when a patient has "new onset" Atrial Fibrillation the patient will report with a heart rate of 160 bpm or more.
• When a patient experiences A-fib, the atria are not contracting as they normally would. They are just quivering. This absence of contraction of the atria can result in a loss of cardiac output anywhere from 15 - 30% due to the absence of "atrial kick". This is why the heart rate is so high. The body is trying to maintain homeostasis.
• It will be impossible to determine the atrial rate. You will only be able to analyze and report the ventricular rate.
• Atrial Fibrillation with a ventricular response in excess of 100 bpm is commonly referred to as Atrial Fibrillation with “rapid ventricular response” or "uncontrolled A-fib".
• Rate: Ventricles - 90, Atria - Unable to determine (UTD)
• P wave: "f" waves
• Interpretation: Atrial Fibrillation

Lesson #8: Quiz: Test Questions - 312

Authors and reviewers.

• ECG heart rhythm modules: Thomas O'Brien.
• ECG monitor simulation developer: Steve Collmann
• 12 Lead Course: Dr. Michael Mazzini, MD .
• Spanish language ECG: Breena R. Taira, MD, MPH
• Medical review: Dr. Jonathan Keroes, MD
• Medical review: Dr. Pedro Azevedo, MD, Cardiology
• Last Update: 11/8/2021
• Electrocardiography for Healthcare Professionals, 6th Edition Kathryn Booth and Thomas O'Brien ISBN10: 1265013470, ISBN13: 9781265013479 McGraw Hill, 2023
• Rapid Interpretation of EKG's, Sixth Edition Dale Dublin Cover Publishing Company
• EKG Reference Guide EKG.Academy
• 12 Lead EKG for Nurses: Simple Steps to Interpret Rhythms, Arrhythmias, Blocks, Hypertrophy, Infarcts, & Cardiac Drugs Aaron Reed Create Space Independent Publishing
• Heart Sounds and Murmurs: A Practical Guide with Audio CD-ROM 3rd Edition Elsevier-Health Sciences Division Barbara A. Erickson, PhD, RN, CCRN
• The Virtual Cardiac Patient: A Multimedia Guide to Heart Sounds, Murmurs, EKG Jonathan Keroes, David Lieberman Publisher: Lippincott Williams & Wilkin) ISBN-10: 0781784425; ISBN-13: 978-0781784429
• Project Semilla, UCLA Emergency Medicine, EKG Training Breena R. Taira, MD, MPH
• ECG Reference Guide PracticalClinicalSkills.com

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Wandering Atrial Pacemaker EKG Interpretation with Rhythm Strip

Ekg features, wandering atrial pacemaker ekg interpretation example.

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Neonatal and Pediatric Arrhythmias: Clinical and Electrocardiographic Aspects

Affiliations.

• 1 Paediatric Cardiology and Cardiac Arrhythmias Unit, Department of Paediatric Cardiology and Cardiac Surgery, Bambino Gesù Children's Hospital and Research Institute, Piazza Sant'Onofrio 4, Rome 00165, Italy. Electronic address: [email protected].
• 2 Paediatric Cardiology and Cardiac Arrhythmias Unit, Department of Paediatric Cardiology and Cardiac Surgery, Bambino Gesù Children's Hospital and Research Institute, Piazza Sant'Onofrio 4, Rome 00165, Italy.
• PMID: 29784491
• DOI: 10.1016/j.ccep.2018.02.008

Arrhythmias have acquired a specific identity in pediatric cardiology, but for pediatric cardiologists it has always been difficult to recognize and treat them. Changes in anatomy and physiology result in electrocardiogram features that differ from the normal adult pattern and vary according to the age of the child. Sinus arrhythmia, ectopic atrial rhythm, "wandering pacemaker," and junctional rhythm can be normal characteristics in children (15%-25% of healthy children can have these rhythms on the electrocardiogram). Tachyarrhythmias and bradyarrhythmias must be treated according to the severity of symptoms, and the patient's age and weight.

Keywords: Arrhythmias; Bradycardia; Children; ECG; Neonates; Pediatric arrhythmias; Tachycardia.

Copyright © 2018 Elsevier Inc. All rights reserved.

Publication types

• Arrhythmias, Cardiac / diagnosis*
• Arrhythmias, Cardiac / physiopathology
• Diagnosis, Differential
• Electrocardiography / methods*
• Heart Rate / physiology*
• Infant, Newborn

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Sunday 13 November 2016

Wandering atrial pacemaker (wap).

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Multifocal Atrial Tachycardia (MAT)

• Ed Burns and Robert Buttner
• Jun 4, 2021

Multifocal Atrial Tachycardia (MAT) Overview

• A rapid, irregular atrial rhythm arising from multiple ectopic foci within the atria.
• Most commonly seen in patients with severe COPD  or congestive heart failure.
• It is typically a transitional rhythm between frequent premature atrial complexes (PACs) and atrial flutter / fibrillation.

AKA “Chaotic atrial tachycardia”

Electrocardiographic Features

• Heart rate > 100 bpm (usually 100-150 bpm; may be as high as 250 bpm).
• Irregularly irregular rhythm with varying PP, PR and RR intervals.
• At least 3 distinct P-wave morphologies in the same lead.
• Isoelectric baseline between P-waves (i.e. no flutter waves).
• Absence of a single dominant atrial pacemaker (i.e. not just sinus rhythm with frequent PACs).
• Some P waves may be nonconducted; others may be aberrantly conducted to the ventricles.

There may be additional electrocardiographic features suggestive of COPD.

Clinical Relevance

• Usually occurs in seriously ill elderly patients with respiratory failure (e.g. exacerbation of COPD / CHF).
• Tends to resolve following treatment of the underlying disorder.
• The development of MAT during an acute illness is a poor prognostic sign, associated with a 60% in-hospital mortality and mean survival of just over a year. Death occurs due to the underlying illness; not the arrhythmia itself.

Arises due to a combination of factors that are present in hospitalised patients with acute-on-chronic respiratory failure:

• Right atrial dilatation (from cor pulmonale )
• Increased sympathetic drive
• Hypoxia and hypercarbia
• Beta-agonists
• Theophylline
• Electrolyte abnormalities: Hypokalaemia and hypomagnesaemia  (e.g. secondary to diuretics / beta-agonists)

The net result is increased atrial automaticity.

ECG Examples

Multifocal atrial tachycardia:

• Rapid irregular rhythm > 100 bpm.
• At least 3 distinctive P-wave morphologies (arrows).

MAT with additional features of COPD :

• Rapid, irregular rhythm with multiple P-wave morphologies (best seen in the rhythm strip).
• Right axis deviation, dominant R wave in V1 and deep S wave in V6 suggest right ventricular hypertrophy due to cor pulmonale. 

Related Topics

• The ECG in COPD
• Right atrial enlargement (P pulmonale)
• Right ventricular hypertrophy

Advanced Reading

• Wiesbauer F, Kühn P. ECG Mastery: Yellow Belt online course. Understand ECG basics. Medmastery
• Wiesbauer F, Kühn P. ECG Mastery: Blue Belt online course : Become an ECG expert. Medmastery
• Kühn P, Houghton A. ECG Mastery: Black Belt Workshop . Advanced ECG interpretation. Medmastery
• Rawshani A. Clinical ECG Interpretation ECG Waves
• Smith SW. Dr Smith’s ECG blog .
• Zimmerman FH. ECG Core Curriculum . 2023
• Mattu A, Berberian J, Brady WJ. Emergency ECGs: Case-Based Review and Interpretations , 2022
• Straus DG, Schocken DD. Marriott’s Practical Electrocardiography 13e, 2021
• Brady WJ, Lipinski MJ et al. Electrocardiogram in Clinical Medicine . 1e, 2020
• Mattu A, Tabas JA, Brady WJ. Electrocardiography in Emergency, Acute, and Critical Care . 2e, 2019
• Hampton J, Adlam D. The ECG Made Practical 7e, 2019
• Kühn P, Lang C, Wiesbauer F. ECG Mastery: The Simplest Way to Learn the ECG . 2015
• Grauer K. ECG Pocket Brain (Expanded) 6e, 2014
• Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice: Adult and Pediatric 6e, 2008
• Chan TC. ECG in Emergency Medicine and Acute Care 1e, 2004

LITFL Further Reading

• ECG Library Basics – Waves, Intervals, Segments and Clinical Interpretation
• ECG A to Z by diagnosis – ECG interpretation in clinical context
• ECG Exigency and Cardiovascular Curveball – ECG Clinical Cases
• 100 ECG Quiz – Self-assessment tool for examination practice
• ECG Reference SITES and BOOKS – the best of the rest

ECG LIBRARY

Emergency Physician in Prehospital and Retrieval Medicine in Sydney, Australia. He has a passion for ECG interpretation and medical education | ECG Library |

Robert Buttner

MBBS (UWA) CCPU (RCE, Biliary, DVT, E-FAST, AAA) Adult/Paediatric Emergency Medicine Advanced Trainee in Melbourne, Australia. Special interests in diagnostic and procedural ultrasound, medical education, and ECG interpretation. Editor-in-chief of the LITFL ECG Library . Twitter: @rob_buttner

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Article Contents

Introduction, conclusions, supplementary data, declarations, data availability, ethical approval, pre-registered clinical trial number.

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Secondary tricuspid regurgitation: incidence, types, and outcomes in atrial fibrillation vs. sinus rhythm

Matteo Castrichini and Hossam H. Ibrahim contributed equally to the study.

• Article contents
• Figures & tables

Jwan A Naser, Matteo Castrichini, Hossam H Ibrahim, Christopher G Scott, Grace Lin, Eunjung Lee, Rekha Mankad, Konstantinos C Siontis, Mackram F Eleid, Patricia A Pellikka, Hector I Michelena, Sorin V Pislaru, Vuyisile T Nkomo, Secondary tricuspid regurgitation: incidence, types, and outcomes in atrial fibrillation vs. sinus rhythm, European Heart Journal , Volume 45, Issue 31, 14 August 2024, Pages 2878–2890, https://doi.org/10.1093/eurheartj/ehae346

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Incidence and types of secondary tricuspid regurgitation (TR) are not well defined in atrial fibrillation (AFib) and sinus rhythm (SR). Atrial secondary TR (A-STR) is associated with pre-existing AFib; however, close to 50% of patients with A-STR do not have AFib. The aim of this study was to assess incidence, types, and outcomes of ≥ moderate TR in AFib vs. SR.

Adults with and without new-onset AFib without structural heart disease or ≥ moderate TR at baseline were followed for the development of ≥ moderate TR. Tricuspid regurgitation types were pacemaker, left-sided valve disease, left ventricular (LV) dysfunction, pulmonary hypertension (PH), isolated ventricular, and A-STR.

Among 1359 patients with AFib and 20 438 in SR, 109 and 378 patients developed ≥ moderate TR, respectively. The individual types of TR occurred more frequently in AFib related to the higher pacemaker implantation rates (1.12 vs. 0.19 per 100 person-years, P < .001), larger right atrial size (median 78 vs. 53 mL, P < .001), and higher pulmonary pressures (median 30 vs. 28 mmHg, P < .001). The most common TR types irrespective of rhythm were LV dysfunction-TR and A-STR. Among patients in SR, those with A-STR were older, predominantly women with more diastolic abnormalities and higher pulmonary pressures. All types of secondary TR were associated with all-cause mortality, highest in PH-TR and LV dysfunction-TR.

New-onset AFib vs. SR conferred a higher risk of the individual TR types related to sequelae of AFib and higher pacemaker implantation rates, although the distribution of TR types was similar. Secondary TR was universally associated with increased mortality.

Incidence, types, and outcomes of tricuspid regurgitation in atrial fibrillation (AFib) and sinus rhythm (SR). Top panel: Atrial fibrillation, compared with SR, is associated with increased risk of lead-associated tricuspid regurgitation type A due to increased rate of cardiac implantable electronic devices as well as increased risk of subtypes of secondary tricuspid regurgitation (TR) related to increase in right atrial (RA) size and right ventricular systolic pressure (RVSP). Middle panel: The distribution of incident TR subtypes in AFib and SR is shown. Factors associated with atrial secondary TR in SR include older age, female sex, diastolic abnormalities, and elevated RVSP. Bottom panel: all subtypes of secondary TR are associated with increased mortality. The mortality was independent of left ventricular (LV) dysfunction in LV dysfunction-TR.CI, confidence interval; CIED, cardiac implantable electronic device; HR, hazard ratio; LTR, lead-associated tricuspid regurgitation; LV, left ventricular; PH, pulmonary hypertension; RA, right atrial; RVSP, right ventricular systolic pressure; SR, sinus rhythm; TR, tricuspid regurgitation.

See the editorial comment for this article ‘Impact of new-onset atrial fibrillation on the incidence of tricuspid regurgitation: a call to attention’, by D. Muraru and L.P. Badano, https://doi.org/10.1093/eurheartj/ehae382 .

Tricuspid regurgitation (TR) can result from intrinsic abnormalities of the tricuspid valve (i.e. primary TR), remodelling of right heart chambers (i.e. secondary TR), or cardiac implantable electronic devices (CIED). 1 , 2 Secondary TR is heterogeneous and can occur in the setting of tricuspid annular dilation and leaflet tethering due to right ventricular (RV) remodelling [ventricular secondary TR (V-STR)] or right atrial (RA) dilation and tricuspid annular dilation [atrial secondary TR (A-STR)]. 1–3 Atrial fibrillation (AFib) is considered an important risk factor for this latter type of secondary TR due to its established association with RA enlargement 4–9 and has been also associated with incident TR after left-sided valve surgery. 10 , 11 Rhythm control can result in reverse RA remodelling and reduction in TR severity. 12 , 13 The association between AFib and other types of TR, however, has been variable, 14–16 and no previous study assessed how AFib modifies the risk of other specific types of TR such as TR in left ventricular (LV) dysfunction or pulmonary hypertension (PH). Furthermore, whether there is a differential impact for AFib on types of incident TR is unknown.

Despite the established association between A-STR and AFib, previous studies demonstrated that up to 50% of patients with A-STR do not have a history of AFib, 5 , 17 , 18 indicating that other factors may predispose to A-STR. The rate of A-STR and its predisposing factors in sinus rhythm (SR) remain to be investigated. Herein, we aimed to (i) compare incidence and types of ≥ moderate TR in patients with and without new-onset AFib without structural heart disease at baseline, (ii) identify potential mechanisms of TR in AFib by assessing RA, RV size, and estimated pulmonary pressures at time of TR, (iii) analyse the characteristics of patients in SR who develop A-STR, and (iv) assess the relationship between types of incident TR and all-cause mortality.

Study population

The institutional review board approved the study. All adults with a new electrocardiographic diagnosis of AFib at any time between 2010 and 2021 at Mayo Clinic sites in the USA (Rochester, Arizona, Florida, the upper Midwest) who had a transthoracic echocardiogram (TTE) performed within one month after AFib diagnosis were identified. The earliest TTE within one month after AFib was the baseline TTE. All patients who had no diagnosis of AFib by electrocardiograms, Holter monitors, or International Classification of Diseases (ICD) codes at any time before or between 2010 and 2021 and had a TTE in that period were identified (SR group); the earliest TTE in the study period was considered the baseline TTE. Patients were excluded if they had previous cardiac surgery/procedure including CIED implantation, cardiomyopathy, regional wall motion abnormalities, primary tricuspid disease, congenital heart disease, rheumatic, carcinoid, or radiation heart disease, ≥moderate TR at baseline, left-sided valve disease [≥moderate aortic stenosis/regurgitation or mitral regurgitation (MR), any mitral stenosis], diastolic dysfunction (DD) or uncertain diastolic function with incomplete data, previous/current ejection fraction (EF) < 50%, diagnosis of heart failure (HF), RV systolic pressure (RVSP) ≥ 50 mmHg, any RV enlargement/dysfunction, or no TTE follow-up ≥6 months. In this study, DD was defined as ≥3/4 abnormal diastolic function parameters including mitral medial e ′<7 cm/s, mitral medial E / e ′>15 during SR or >11 during AFib, left atrial volume index (LAVI) > 34 mL/m 2 , and TR velocity >2.80 m/s. 19 In this context, the presence of two normal and one or two abnormal diastolic function parameters did not meet the definition of DD.

Exclusion of the above disorders allowed the identification of patients with relatively healthy hearts, wherein the impact of new-onset AFib (vs. SR) on incident TR could be relatively isolated. Comorbidities were identified using ICD codes.

Atrial fibrillation was classified as paroxysmal if it terminated spontaneously within seven days of onset or persistent otherwise. A clinical diagnosis of HF with preserved EF (HFpEF) at follow-up was defined as HF diagnosed using ICD codes, hospitalization due to HF, or clinical appointment at the HF subspeciality clinic in the absence of low EF.

Echocardiography

All TTEs were clinically indicated, performed according to the guidelines, 20 and interpreted by level III board-certified echocardiologists. Tricuspid regurgitation severity was classified as no/trivial, mild, moderate, or severe using an integrative approach based on colour flow Doppler (jet area, vena contracta, flow convergence), density of the regurgitant jet, proximal isovelocity surface area (effective regurgitant orifice area and regurgitant volume), inferior vena cava size, and hepatic vein flow pattern. 21 Diastolic function parameter assessment was according to the guidelines. 19 Right ventricular function and size were assessed quantitatively. 22 Measurements of RV end-systolic and end-diastolic areas and RV midventricular diameter from RV-focused apical four-chamber views were performed de novo on the stored echocardiographic images by two readers, and the fractional area change (FAC) was calculated for assessment of RV function. Right atrial size was measured de novo from apical four-chamber views at end-systole using the single-plane summation method. Tricuspid annulus (TA) diameter was measured at end-diastole in the apical four-chamber view. Tricuspid valve tenting height was measured at end-systole as the distance between the TA plane and the atrial aspect of the leaflets. Interobserver agreement for RV, RA, TA, and tricuspid tenting height measurements was assessed using the intraclass correlation coefficient (ICC) in a random 10-patient sample. Right ventricular systolic pressure was estimated using the peak TR jet velocity.

Classification of incident tricuspid regurgitation

Classification of tricuspid regurgitation according to associated cardiac disease.

Patients were followed for the development of ≥ moderate TR using all available follow-up TTEs. When ≥ moderate TR occurred, its type was identified in the hierarchal order described previously (see Supplementary data online , Figure S1 ). 17 , 23 There were no patients with primary TR at the time of follow-up, and all patients had secondary or lead-associated TR (LTR). First, LTR type A was defined in the presence of RV lead thought to be directly causing the TR, irrespective of left-sided valve disease, LV function, pulmonary pressures, or RV function. 24 Second, left-sided valve disease-associated TR was defined as ≥ moderate aortic stenosis/regurgitation, any mitral stenosis, ≥moderate organic MR, or an aortic/mitral prosthesis. Third, LV dysfunction-associated TR was defined in the setting of EF <50%, ischaemic cardiomyopathy resulting in ≥ moderate ischemic MR, or DD. Fourth, PH-TR was defined with RVSP ≥50 mmHg in the absence of the prior conditions. Fifth, isolated V-STR (iV-STR) was defined in the setting of ≥ moderate RV enlargement or RV dysfunction, measured quantitatively at time of the TR, in the absence of the previous conditions. Right ventricular dysfunction was defined as FAC <35%, tricuspid annular plane systolic excursion (TAPSE) < 17 mm, or tricuspid lateral s’ velocity < 9 cm/s, and ≥ moderate RV enlargement as RV end-diastolic or end-systolic area more than 1 SD higher than the upper limit of normal (i.e. RV end-diastolic area >27.5 cm 2 in men and >23 cm 2 in women; RV end-systolic area >18 cm 2 in men and >13 cm 2 in women). 22 We chose these cutoffs for moderate RV enlargement (more than 1 SD from upper limit of normal) given the lack of standardized definition of ≥ moderate RV enlargement. Finally, A-STR was defined if all the previous conditions were absent and in the setting of RA enlargement (≥29 mL/m 2 in women and ≥34 in men) or TA dilation (end-diastolic TA diameter ≥40 mm or ≥22 mm/m 2 in men and ≥35 mm or ≥21 mm/m 2 in women). 25 Atrial secondary TR was still considered in the presence of atrial secondary MR with RVSP <50 mmHg, since the mechanism in both is atrial myopathy.

Notably, many previous studies did not include a separate category for DD; instead, DD was considered part of the PH category. 17 , 26 A limitation of such approach is that underestimation of RVSP with significant TR would mean patients meeting other criteria for DD (elevated E / e ′, reduced e ′, and enlarged LA) would be classified as isolated TR. Other studies, however, included a separate category for DD. 27

In addition to studying incidence of ≥ moderate TR in new-onset AFib and SR, we also studied the incidence of the cardiac diseases/conditions associated with TR. These conditions included CIED implantation, ≥moderate left-sided valve disease, LV dysfunction (EF <50%, ≥ischaemic MR, or DD), PH, and ≥ moderate isolated RV enlargement/dysfunction. Because CIED can be the cause of TR or an incidental finding, other aetiologies of TR were still investigated in patients who had implantation of CIED. These other aetiologies were considered in a hierarchical order, as described above, starting from left-sided valve disease and ending in isolated RV enlargement/dysfunction. Although LV dysfunction and left-sided valve disease can lead to TR due to the resulting PH, PH in the context of this paper was used to refer to PH not due to “evident” left-sided disease.

Classification of tricuspid regurgitation according to mechanism (atrial vs. ventricular)

In a separate analysis, secondary TR was classified solely based on anatomic and functional features suggested by the Tricuspid Valve Academic Research Consortium (TVARC). 24 Features that suggested V-STR (rather than A-STR) were tenting height >9 mm, RV midventricular diameter >38 mm, FAC <35%, TAPSE <17 mm, tricuspid lateral s’ < 9 cm/s, ≥moderate RV enlargement, LVEF <50%, or RVSP ≥50 mmHg, whereas A-STR was classified in the absence of these features and in the setting of RA enlargement or TA dilation.

The primary outcome of the study was incident TR and its subtypes. All-cause death was studied as a secondary outcome and determined based on the electronic medical records.

Statistical analysis

Continuous variables are reported as median [inter-quartile range (IQR)] and categorical variables as number (percentage). The Student’s t -test and the Wilcoxon test were used to compare continuous variables, as appropriate, while the Chi-square test was used to compare categorical variables. Incidence rates were calculated as number of events on follow-up divided by total follow-up time in person-years and expressed per 100 person-years.

Our analysis involved two main starting points: the time of baseline TTE or the time of onset of the cardiac diseases ( Figure 1 ). Time zero was the time of baseline TTE in analysis of (i) incidence of ≥ moderate TR and its different types in new-onset AFib vs. SR and (ii) incidence of each of the cardiac diseases associated with TR (e.g. left-sided valve disease, LV dysfunction, etc.). Then, to evaluate whether the difference in the incidence of TR in AFib vs. SR is related to the rhythm itself or to one group developing more cardiac diseases/conditions that predispose to TR (e.g. LV dysfunction, PH), we also studied prevalence of TR at the time when the incident cardiac disease/condition developed as well as incidence of TR after these diseases developed (time zero was the onset of the cardiac conditions/diseases). Similarly, incidence of TR was also compared between AFib and SR in patients who developed HFpEF at follow-up where time zero was the onset of HFpEF. An overview of the study timeline and analysis plan is shown in Figure 1 .

Overview of study timeline and analysis plan. The starting point and outcome of interest for each analysis are included, represented by arrows for incidence rates or mortality rates and in a circle for prevalence. The wide (blue) arrow represents the timeline of the study. The green arrows (the first consecutive 3 arrows) start at baseline (time zero is baseline transthoracic echocardiogram), whereas the yellow arrows (the second three arrows) start at time of the cardiac conditions (time zero is the cardiac condition). Separate Cox models, one for each cardiac condition, were used for analyses highlighted in yellow arrows

Kaplan–Meier curves were used for survival analysis. Cox regression was used for adjusted survival analysis. All comparisons of incidence rates of TR between AFib vs. SR were adjusted to age, sex, and mild (vs. no) TR at baseline; RVSP was adjusted for based on a priori knowledge of mechanisms of TR (i.e. when pulmonary pressures play a pathophysiologic role in TR). Patients without the event of interest were censored at their last available follow-up. Because baseline differences existed between patients with incident AFib and SR, propensity score matching was additionally performed to compare incidence of ≥ moderate secondary TR between new-onset AFib and SR (time zero was baseline TTE). The propensity score was calculated using logistic regression based on confounders including age, sex, history of transient ischaemic attack, ischaemic stroke, hypertension, diabetes mellitus, sleep apnoea, lung disease, coronary artery disease, mild vs. no TR at baseline, RVSP, medial E / e ′ ratio, and EF at baseline and was used to match patients in the new-onset AFib group to patients in the SR group in a 1:5 ratio. These variables were chosen based on knowledge of the a priori relationships between the variables and incidence of TR in these patients with otherwise relatively healthy hearts. Patients with missing values of any of the matching parameters were excluded from the matching process.

When studying the association of incident TR types with all-cause mortality, we analysed TR as a time-dependent covariate. In the first analysis, time zero was the baseline TTE; in this analysis, the association of incident TR with mortality could not be separated from the associated cardiac disease (e.g. the impact of TR due to LV dysfunction vs. no TR could not be isolated from the impact of LV dysfunction). To overcome this issue, we performed a second analysis where we analysed the association of prevalent/incident ≥ moderate TR in the subset of patients who developed the corresponding cardiac disease (e.g. we assessed the association of prevalent/incident TR with all-cause death in patients with LV dysfunction who developed TR compared with patients with LV dysfunction without TR). In this second analysis, time zero was the time of occurrence of the cardiac condition associated with TR (i.e. LV dysfunction in the example above), and TR was analyzed as a time-dependent covariate ( Figure 1 ). Analysis of all-cause mortality was universally adjusted to confounders including age, sex, rhythm, and comorbidities (i.e. independent of clinical characteristics).

A P -value <.05 was considered statistically significant. All analyses were performed with JMP Pro version 16.2.0 (SAS Institute Inc., Cary, NC, USA) and R version 4.2.2 (R Foundation for Statistical Computing, Vienna, Austria).

Overall, 1359 patients with new-onset AFib and 20 438 patients in SR were included. Patients with AFib were older (median age 67 vs. 60 years), were more frequently male (66% vs. 46%), and had more frequently lung disease and hypertension. They also had lower EF, higher LV mass index, larger LA size, and higher RVSP compared with SR ( Table 1 ). Atrial fibrillation was paroxysmal in 763 (56%) patients. Duration-to-first follow-up echocardiogram was median 2.1 (IQR 1.0–4.3) years. Patients in SR had median 9 (IQR 4–17) ECGs at follow-up, and 3356 patients in SR had a Holter monitor on follow-up without evidence of AFib. By study design, patients in SR had no documented AFib in the study period.

Baseline clinical and echocardiographic characteristics in the overall cohort with new-onset atrial fibrillation and sinus rhythm

Values are presented as median (IQR) or number (percentage).

CAD, coronary artery disease; LVEDD, left ventricular end-diastolic dimension; LVEF, left ventricular ejection fraction; LVESD, left ventricular end-systolic dimension; LVMI, left ventricular mass index; RVSP, right ventricular systolic pressure; TIA, transient ischaemic attacks; TR, tricuspid regurgitation.

a Qualitative assessment at baseline echocardiogram.

Incident ≥ moderate tricuspid regurgitation in new-onset atrial fibrillation vs. sinus rhythm

Over median 3.2 (IQR 1.6–5.3) years, 109 patients with new-onset AFib developed incident ≥ moderate TR [2.11 per 100 person-years]. In comparison, incident ≥ moderate TR occurred in 378 patients in SR over median 3.8 (IQR 1.9–6.7) years {0.41 per 100 person-years; age- and sex-adjusted hazard ratio (HR): 5.40 [95% confidence interval (CI) 4.33–6.74], P < .001}. In patients with AFib, incidence of TR was higher with persistent AFib [age- and sex-adjusted HR: 1.54 (1.05–2.26), P = .03] vs. paroxysmal AFib.

All types of ≥ moderate TR also developed more frequently in the new-onset AFib group vs. SR except for left-sided valve disease TR, which did not achieve statistical significance due to low numbers ( Table 2 ). Number of available follow-up TTEs was similar in AFib [mean 1.9 (SD 1.6)] and SR [mean 1.9 (SD 1.8), P = .93]. The most common types of incident TR in new-onset AFib were LV dysfunction-associated TR [43%, of which 49% cases had DD (overall 21%)], A-STR (19%), and iV-STR (19%) ( Figure 2 ). In contrast, the most common type of incident TR in SR was A-STR (31%) followed by LV dysfunction-associated TR (30%; of which 36% had DD [overall 11%]). Notably, despite a higher proportion of A-STR among TR types in SR, the incidence rate of A-STR in AFib was three times that in SR ( Table 2 ).

Distribution of types of incident ≥ moderate tricuspid regurgitation in atrial fibrillation and sinus rhythm

Incidence of ≥ moderate tricuspid regurgitation and its different types in the overall cohort with new-onset atrial fibrillation and sinus rhythm

Time zero was the baseline echocardiogram. The presented hazard ratios (95% confidence intervals) were derived from separate Cox models.

AFib, atrial fibrillation; A-STR, atrial secondary tricuspid regurgitation; CI, confidence interval; HR, hazard ratio; iV-STR, isolated ventricular secondary tricuspid regurgitation; LTR, lead-associated TR; LV, left ventricle; PH, pulmonary hypertension; SR, sinus rhythm; TR, tricuspid regurgitation.

a Numbers represent incidence rates per 100 person-years.

b Adjusted to age, sex, and presence of no vs. mild TR at baseline.

c Additionally adjusted to RVSP given the role of pulmonary hypertension in TR in these mechanisms.

Similar results were observed in the matched 870 patients with AFib and 4350 patients in SR. Baseline characteristics of these patients are shown in Supplementary data online , Table S1 . Incident secondary TR of all types, except left-sided valve disease TR, occurred more frequently with new-onset AFib vs. SR (see Supplementary data online , Table S2 ).

Atrial secondary tricuspid regurgitation in sinus rhythm

Atrial secondary TR contributed to 31% of TR cases in patients with SR. To understand the potential mechanisms of A-STR in the absence of AFib, we compared echocardiographic characteristics between the two groups at time of A-STR or last follow-up TTE (if patients did not develop TR or the aforementioned cardiac conditions). Patients with A-STR were older, were predominantly female (81% vs. 55%), had smaller LV dimensions, had higher E / e ′ ratio, RVSP, and LAVI, and had more frequently 2/4 abnormal diastolic function parameters ( Table 3 ). Notably, patients who developed ≥3 abnormal diastolic function parameters were included in the LV dysfunction by definition.

Characteristics of patients in sinus rhythm who developed atrial secondary tricuspid regurgitation at time of the tricuspid regurgitation vs. those who did not develop tricuspid regurgitation at time of last follow-up

LVEDD, left ventricular end-diastolic dimension; LVESD, left ventricular end-systolic dimension; RVSP, right ventricular systolic pressure; TR, tricuspid regurgitation.

Incidence of cardiac diseases associated with tricuspid regurgitation in atrial fibrillation and sinus rhythm

Cardiac implantable electronic device lead implantation, LV dysfunction, and isolated RV dysfunction/enlargement occurred more frequently in the AFib group compared with SR (see Supplementary data online , Table S3 ). However, ≥moderate left-sided valve disease and incident PH occurred at similar rates in both groups (see Supplementary data online , Table S3 ).

At the time of occurrence of these cardiac diseases, prevalence of ≥ moderate TR was significantly higher in AFib in patients who developed left-sided valve disease, LV dysfunction, PH, and ≥ moderate isolated RV enlargement/dysfunction but not with CIEDs (see Supplementary data online , Table S4 ). Subsequent incident ≥ moderate TR during follow-up occurred more frequently in AFib in patients who developed LV dysfunction, PH, or isolated RV enlargement/dysfunction (see Supplementary data online , Table S5 ).

Over median 2.2 (IQR 1.1–4.5) years, HFpEF was diagnosed in 181 patients with AFib and 1098 patients in SR. Tricuspid regurgitation occurred in 31/181 of these patients in AFib [14.69 per 100 person-years] and 54/1098 patients in SR [2.99 per 100 person-years, age- and sex-adjusted HR 4.98 (95% CI 3.06–8.10), P < .001].

Potential mechanisms behind the increased incidence of tricuspid regurgitation in atrial fibrillation

To analyse the potential mechanisms that contribute to incident TR in patients with AFib, we compared RA volume, RV size/function, and RVSP at time of ≥ moderate TR between AFib and SR ( Table 4 ). Overall, patients with AFib had larger RA volumes, worse RV function, and higher RVSP. There were only 22 patients with left valve-associated TR and available RA/RV measurements, and separate subgroup analysis was not feasible in this subset. In patients with LV dysfunction-associated TR, iV-STR, and A-STR, both RA volume and RVSP were higher in those with AFib ( Table 4 ). Patients with AFib and A-STR also had slightly worse RV FAC. Although there were no significant differences in these parameters in patients with PH-TR, the RA volume was numerically higher in patients with AFib.

Right atrial and ventricular measurements in patients who developed at least moderate tricuspid regurgitation at the time of the tricuspid regurgitation in atrial fibrillation and sinus rhythm

AFib, atrial fibrillation; A-STR, atrial secondary tricuspid regurgitation; FAC, fractional area change; iV-STR, isolated ventricular functional tricuspid regurgitation; LV, left ventricle; PH, pulmonary hypertension; RA, right atrium; RV, right ventricle; RVSP, right ventricular systolic pressure; SR, sinus rhythm; TR, tricuspid regurgitation.

a Values represent median (IQR).

Association of incident tricuspid regurgitation with all-cause death

Over median 6.2 (IQR 3.5–9.1) years, 3213 patients died. Incident TR in general was independently associated with mortality after adjustments for age, sex, AFib, and comorbidities [HR: 4.97 (4.18–5.91), P < .001]. This was also the case for every single type of TR except LTR type A ( Table 5 ). Patients who developed LV dysfunction-associated TR or PH-TR had increased mortality compared with other types of TR. The increased mortality observed in this analysis is related to both TR and the predisposing cardiac disease.

Association of incident ≥ moderate tricuspid regurgitation and its types with all-cause death

Time zero was the baseline echocardiogram. HR presented is in comparison with no TR.

Adjusted HR: HR adjusted to age, sex, rhythm, and comorbidities.

A-STR, atrial secondary tricuspid regurgitation; HR, hazard ratio; iV-STR, isolated ventricular secondary tricuspid regurgitation; LTR, lead-associated TR; LV, left ventricle; PH, pulmonary hypertension; SR, sinus rhythm; TR, tricuspid regurgitation.

a Compared with A-STR.

b Compared with iV-STR.

c Compared with valve TR.

We then analysed the association of prevalent/incident TR with mortality in each of the subgroups with cardiac diseases ( Table 6 ). Tricuspid regurgitation was associated with mortality among patients who developed LV dysfunction (vs. patients with LV dysfunction and no TR) [adjusted HR (95% CI) to age, sex, AFib, and comorbidities was 3.21 (1.39–7.43) and 2.34 (1.73–3.18), respectively].

Association of incident ≥ moderate tricuspid regurgitation with mortality in the subset of patients who developed each of the associated cardiac conditions

Time zero was the onset of the cardiac condition in each of the presented cardiac conditions. Separate Cox models were used for each row. Comorbidities were updated at the new time zero.

HR, hazard ratio; iV-STR, isolated ventricular secondary tricuspid regurgitation; LTR, lead-associated TR; LV, left ventricle; PH, pulmonary hypertension; SR, sinus rhythm; TR, tricuspid regurgitation.

Tricuspid regurgitation classification based on mechanism (atrial vs. ventricular)

When classified based on the TVARC anatomic or functional features, regardless of the associated cardiac disease, incident ≥ moderate V-STR occurred in 77 patients with new-onset AFib (1.49 per 100 person-years) and 237 patients in SR (0.26 per 100 person-years, P < .001), whereas incident ≥ moderate A-STR occurred in 29 patients with new-onset AFib (0.56 per 100 person-years) and in 131 patients in SR (0.14 per 100 person-years, P < .001). Distribution of V-STR and A-STR among TR categories classified based on the associated cardiac condition is presented in Supplementary data online , Table S6 . Notably, around a quarter of TR in the setting of left valve disease or DD met the A-STR morphologic criteria.

Both incident V-STR and A-STR were associated with increased mortality [HR adjusted to age, sex, rhythm, and comorbidities: 6.73 (95% CI 5.55–8.16), P < .001, and 2.43 (1.65–3.58), P < .001, respectively), and mortality was higher with V-STR vs. A-STR [adjusted HR 2.77 (1.81–4.25), P < .001].

Interobserver variability in right ventricular and right atrial measurements

In a 10-patient sample randomly selected for measurement by two observers, ICC showed good reliability (0.77 for RV end-diastolic area; 0.85 for RV end-systolic area; 0.75 for RA volume, 0.70 for TA diameter).

In this study, we evaluated the incidence, types, and outcomes of ≥ moderate TR in patients with new-onset AFib and SR without structural heart disease at baseline ( Structured Graphical Abstract ). We found that patients with new-onset AFib more frequently developed all individual types of ≥ moderate TR compared with SR. In the case of LTR type A, this was simply related to the increased rates of CIED implantation in AFib, but in other types of TR (i.e. ventricular or atrial secondary), this was independently associated with AFib where both pulmonary pressures and RA size were higher, suggesting the presence of mixed mechanisms of TR in AFib. The distribution of TR types was relatively similar between AFib and SR. Patients in SR with A-STR were older and mostly females with frequent LV diastolic function abnormalities and high-normal/high RVSP, indicating potentially occult DD. Finally, the development of all types of secondary TR was associated with mortality, highest in PH-TR and LV dysfunction-associated TR.

Incident tricuspid regurgitation in patients with new-onset atrial fibrillation and sinus rhythm

Atrial fibrillation is known to be associated with RA enlargement and tricuspid annular dilation and is a major risk factor for A-STR, 4–8 whereas rhythm control is associated with reverse RA and RV remodelling and reduction of TR. 12 , 13 In addition to A-STR, AFib has been associated with incident TR after left-sided valve surgery 10 , 11 but not with LTR. 28 However, studies have shown variable results regarding the association between AFib and TR. 4 , 15 , 16 Furthermore, no study assessed the association of AFib with other specific types of TR including TR associated with LV dysfunction, PH, and isolated RV dysfunction, and the incidence rates and types of TR in patients with or without new-onset AFib remained unknown.

In this study, we found that ∼2.1% of patients with new-onset AFib and no structural heart disease develop incident moderate/severe TR every year. This was numerically lower than the incidence estimated in a previous study (∼3.9% of patients every year), 29 likely due to the differences in comorbidities (we excluded patients with HF or any RV enlargement/dysfunction) and duration of follow-up (if TR tends to develop more frequently at longer follow-up). In contrast, only 0.4% of patients with SR and no structural heart disease develop ≥ moderate TR every year with a five-fold increased risk in patients with new-onset AFib, independent of baseline differences. New-onset AFib was associated with higher incidence rates of subtypes of TR due to CIED, LV dysfunction, PH, isolated RV dysfunction, and A-STR. Further analysis showed that the increased incidence of LTR in AFib was simply related to the increased rate of CIED implantation. However, AFib remained associated with TR independently of the associated cardiac disease in patients with LV dysfunction, PH, and isolated RV dysfunction.

To determine whether the association between AFib and TR is related to worse atrial component, ventricular component, or both, we compared right heart parameters in patients with and without AFib at the time of TR. We found that regardless of TR type, AFib was associated with significantly larger RA size and higher RVSP. Even in patients with A-STR, AFib was associated with higher RVSP despite being ‘in the normal range’. The association between AFib and atrial enlargement has been widely studied. 9 , 30 The higher pulmonary pressures can be the result of loss of atrial contraction with or without concomitant occult DD. 14 , 31 , 32 Taken together, our findings indicate that mixed mechanisms predispose to TR in patients with AFib, and the attribution of TR to one hierarchical mechanism is likely oversimplistic.

In both patients with and without new-onset AFib, LV dysfunction-associated TR and A-STR were the most common types of incident TR, constituting >60% of the cases. On the other hand, the proportion of left-sided valve disease-associated TR was low since patients with significant left-sided valve disease at time of baseline exam were excluded. This contrasts with the distribution of TR types studied in unselected populations of patients with varying prevalence of structural heart disease where left valve disease, LV dysfunction, and PH were the most common types of TR. 16 , 17 , 26 , 27 Notably, despite the higher proportion of A-STR among incident TR subtypes in SR compared with AFib, the incidence rate of A-STR was 2–3 times higher in the AFib group. The lower proportion of A-STR in AFib is likely related to the increased incidence of LV systolic dysfunction and DD, which translated into higher proportions of TR related to these diseases. Furthermore, the universal association of AFib with increased RA size in the various subtypes of TR indicates the presence of ‘mixed’ A-STR on top of other contributing mechanisms in all types of secondary TR.

Atrial secondary TR has been described extensively in patients with AFib. In fact, AFib has been considered part of the defining criteria for A-STR in the 2020 American College of Cardiology/American Heart Association valve disease guidelines. 33 However, it is becoming increasingly recognized that A-STR may occur in the absence of AFib when other factors associated with atrial myopathy are present. Indeed, up to 50% of patients with isolated TR did not have AFib in previous studies. 5 , 17 , 18 Harada et al . 34 found that A-STR was a more common mechanism for TR in patients with HFpEF than was V-STR.

In our study, 31% of TR occurring in patients in SR was A-STR although it still occurred infrequently (∼1 in every 1000 patients every year). Compared with SR patients without TR, these patients were older, more likely female (81% vs. 55%), with larger LAVI, smaller left ventricles, higher RVSP, and more frequently abnormal diastolic parameters. It is highly possible that these patients have occult or developing DD. Indeed, the sensitivity of resting echocardiography in identifying elevated pulmonary capillary wedge pressure is known to be modest, missing around 60% of patients. 35 Diastolic dysfunction can be a cause of TR through the elevation in pulmonary pressures (which can be underestimated on TTEs when measuring the RVSP in the setting of significant TR) or a concomitant result along with atrial myopathy that could manifest as atrial enlargement and A-STR. Specifically, DD and atrial myopathy share the same underlying pathophysiologic mechanism where the associated proinflammatory state and the subsequent coronary microvascular dysfunction predispose to ventricular and atrial fibrosis and subsequently to DD and atrial enlargement. 36 The role of elevated LV filling pressures, LA enlargement, and elevated pulmonary pressures in the progression of TR was shown previously. 14 Furthermore, some cases of asymptomatic paroxysmal AFib that remained undiagnosed for the study period might have contributed to A-STR in these patients.

The predisposition of females to atrial secondary regurgitation (tricuspid and mitral) has been demonstrated in multiple studies 1 , 16 and is likely related to the higher prevalence of atrial fibrosis and HFpEF in females, 37 , 38 the different composition and size of the tricuspid and mitral annuli between sexes, 39 , 40 and the different tissue responses to stress modulated by sex hormones. 41

Tricuspid regurgitation has been independently associated with increased risk of mortality, 16 , 42 , 43 with V-STR imposing a higher risk compared with A-STR. 17 , 23 While previous studies focused on cases of prevalent TR, our study shows that ‘incident’ TR of any type was associated with increased all-cause mortality, with an inherent advantage of overcoming a potential prevalence–incidence bias in prevalent cases. This mortality was highest in patients with LV dysfunction-associated TR and PH-TR. At least in part, the increased risk of mortality was related to the development of the associated cardiac condition (e.g. the development of PH in patients with PH-TR). Taking this into account and specifically analysing association of TR with mortality in patients with the corresponding cardiac condition, TR remained independently associated with mortality in patients with LV dysfunction, as shown previously. 28 , 44 , 45 The lack of association between TR and mortality in patients with left-sided valve disease is likely related to the small sample size, but this association is well recognized. 46 , 47 There were a low number of patients who developed LTR type A, and the lack of association with mortality can be due to low power. While previous studies investigated association of TR with mortality after CIED implantation, 28 distinction between LTR type A and B was lacking, and future studies are needed to evaluate this association.

Interestingly, mortality rates were not increased with TR in patients with isolated RV dysfunction or PH (compared with patients with isolated RV dysfunction or PH without TR, respectively). Previous studies have shown conflicting results. Some studies demonstrated an association between TR and mortality despite adjustments to RV dysfunction and RVSP, but these studies included heterogeneous TR and did not analyse TR in the subgroups with RV dysfunction or PH. 42 , 43 Other studies, however, found that once RV function deteriorates or PH develops, the association between TR and mortality is lost. 48 , 49 Future studies with larger number of patients with PH are needed to evaluate the impact of TR on mortality across the different subtypes of PH.

Limitations

This was a retrospective study involving all Mayo Clinic sites; some sites (e.g. Rochester) are considered tertiary centres with propensity towards selection bias. Transthoracic echocardiograms in this study were performed based on a clinical indication. Therefore, it is possible that included patients were more predisposed to TR vs. the general population. Patients with AFib were required to have TTEs within 30 days of the AFib diagnosis to avoid including chronic AFib. While this could have introduced selection bias, obtaining a TTE when AFib is diagnosed is recommended for the evaluation of structural heart disease in clinical guidelines, 50 and the presence of this inclusion criterion satisfies these guidelines. Moreover, time to follow-up TTEs was variable. Most of the echocardiographic assessments were based on 2D rather than 3D echocardiography with the potential of underestimation of chamber size, tricuspid valve abnormalities, and lead impingement. 51 Transthoracic echocardiograms were interpreted by multiple echocardiologists, and interobserver variability is possible. However, echocardiographic grading of TR remained consistent between Mayo Clinic sites in the study period. Furthermore, RA and RV measurements were performed by two readers for this study, with good interobserver reliability. Given that significant TR can result in underestimation of RVSP by echocardiography, it is possible that some of the patients with PH-TR were misclassified as having iV-STR or A-STR. Diastolic dysfunction was defined by ≥3/4 abnormal diastolic function parameters in both AFib and SR, and the presence of two normal and 1–2 abnormal diastolic function parameters was considered negative for DD in this context. This differs from the guidelines, where the presence of only two abnormal diastolic function parameters is considered indeterminate, and also simplifies the assessment of diastolic function in AFib, which is known to be challenging. Both these scenarios require the use of additional parameters. 19 However, these additional parameters were not routinely acquired, and we used the specific cutoffs recommended by the guidelines for AFib (e.g. E / e ′ > 11). Cardiac diseases associated with TR have been classified in a retrospective fashion, and some inaccuracies may exist. However, we used a classification approach that has been used previously in multiple studies. 17 , 26 Finally, some cases of asymptomatic paroxysmal AFib might have remained undiagnosed in patients with SR who developed A-STR.

New-onset AFib was associated with increased risk of the different subtypes of TR. In the case of LTR-A, this was related to the increased rates of CIED implantation in AFib. In A-STR or ventricular TR occurring in the setting of LV dysfunction, PH, and isolated RV enlargement/dysfunction, this was independently associated with AFib and was related to both RA dilation and higher pulmonary pressures. The distribution of subtypes of incident TR was similar in AFib and SR, with the most common types being LV dysfunction-TR and A-STR. Atrial secondary TR in SR was associated with older age, female sex, diastolic function abnormalities, and higher RVSP, indicating a high risk of RA myopathy and DD. All types of incident TR were associated with increased mortality, highest in patients with PH-TR and LV dysfunction-associated TR.

Supplementary data are available at European Heart Journal online.

Disclosure of Interest

Nothing to declare.

Data will be available upon reasonable request from the corresponding author (email: [email protected] ).

The institutional review board approved the study and waived the informed consent requirement.

Not applicable.

Hahn   RT . Tricuspid regurgitation . N Engl J Med   2023 ; 388 : 1876 – 91 . https://doi.org/10.1056/NEJMra2216709

Google Scholar

Hahn   RT , Badano   LP , Bartko   PE , Muraru   D , Maisano   F , Zamorano   JL , et al.    Tricuspid regurgitation: recent advances in understanding pathophysiology, severity grading and outcome . Eur Heart J Cardiovasc Imaging   2022 ; 23 : 913 – 29 . https://doi.org/10.1093/ehjci/jeac009

Vahanian   A , Beyersdorf   F , Praz   F , Milojevic   M , Baldus   S , Bauersachs   J , et al.    2021 ESC/EACTS guidelines for the management of valvular heart disease: developed by the Task Force for the management of valvular heart disease of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS) . Rev Esp Cardiol (Engl Ed)   2022 ; 75 : 524 . https://doi.org/10.1016/j.rec.2022.05.006

Ortiz-Leon   XA , Posada-Martinez   EL , Trejo-Paredes   MC , Ivey-Miranda   JB , Pereira   J , Crandall   I , et al.    Tricuspid and mitral remodelling in atrial fibrillation: a three-dimensional echocardiographic study . Eur Heart J Cardiovasc Imaging   2022 ; 23 : 944 – 55 . https://doi.org/10.1093/ehjci/jeac045

Topilsky   Y , Khanna   A , Le Tourneau   T , Park   S , Michelena   H , Suri   R , et al.    Clinical context and mechanism of functional tricuspid regurgitation in patients with and without pulmonary hypertension . Circ Cardiovasc Imaging   2012 ; 5 : 314 – 23 . https://doi.org/10.1161/CIRCIMAGING.111.967919

Utsunomiya   H , Itabashi   Y , Mihara   H , Berdejo   J , Kobayashi   S , Siegel   RJ , et al.    Functional tricuspid regurgitation caused by chronic atrial fibrillation: a real-time 3-dimensional transesophageal echocardiography study . Circ Cardiovasc Imaging   2017 ; 10 : e004897 . https://doi.org/10.1161/CIRCIMAGING.116.004897

Florescu   DR , Muraru   D , Florescu   C , Volpato   V , Caravita   S , Perger   E , et al.    Right heart chambers geometry and function in patients with the atrial and the ventricular phenotypes of functional tricuspid regurgitation . Eur Heart J Cardiovasc Imaging   2022 ; 23 : 930 – 40 . https://doi.org/10.1093/ehjci/jeab211

Kwak   S , Lim   J , Yang   S , Rhee   TM , Choi   YJ , Lee   HJ , et al.    Atrial functional tricuspid regurgitation: importance of atrial fibrillation and right atrial remodeling and prognostic significance . JACC Cardiovasc Imaging   2023 ; 16 : 575 – 87 . https://doi.org/10.1016/j.jcmg.2022.11.014

Guta   AC , Badano   LP , Tomaselli   M , Mihalcea   D , Bartos   D , Parati   G , et al.    The pathophysiological link between right atrial remodeling and functional tricuspid regurgitation in patients with atrial fibrillation: a three-dimensional echocardiography study . J Am Soc Echocardiogr   2021 ; 34 : 585 – 94 . e1. https://doi.org/10.1016/j.echo.2021.01.004

Kwak   JJ , Kim   YJ , Kim   MK , Kim   HK , Park   JS , Kim   KH , et al.    Development of tricuspid regurgitation late after left-sided valve surgery: a single-center experience with long-term echocardiographic examinations . Am Heart J   2008 ; 155 : 732 – 7 . https://doi.org/10.1016/j.ahj.2007.11.010

Wang   G , Sun   Z , Xia   J , Deng   Y , Chen   J , Su   G , et al.    Predictors of secondary tricuspid regurgitation after left-sided valve replacement . Surg Today   2008 ; 38 : 778 – 83 . https://doi.org/10.1007/s00595-007-3721-3

Soulat-Dufour   L , Lang   S , Addetia   K , Ederhy   S , Adavane-Scheuble   S , Chauvet-Droit   M , et al.    Restoring sinus rhythm reverses cardiac remodeling and reduces valvular regurgitation in patients with atrial fibrillation . J Am Coll Cardiol   2022 ; 79 : 951 – 61 . https://doi.org/10.1016/j.jacc.2021.12.029

Itakura   K , Hidaka   T , Nakano   Y , Utsunomiya   H , Kinoshita   M , Susawa   H , et al.    Successful catheter ablation of persistent atrial fibrillation is associated with improvement in functional tricuspid regurgitation and right heart reverse remodeling . Heart Vessels   2020 ; 35 : 842 – 51 . https://doi.org/10.1007/s00380-019-01546-3

Mutlak   D , Khalil   J , Lessick   J , Kehat   I , Agmon   Y , Aronson   D . Risk factors for the development of functional tricuspid regurgitation and their population-attributable fractions . JACC Cardiovasc Imaging   2020 ; 13 : 1643 – 51 . https://doi.org/10.1016/j.jcmg.2020.01.015

Shiran   A , Najjar   R , Adawi   S , Aronson   D . Risk factors for progression of functional tricuspid regurgitation . Am J Cardiol   2014 ; 113 : 995 – 1000 . https://doi.org/10.1016/j.amjcard.2013.11.055

Prihadi   EA , van der Bijl   P , Gursoy   E , Abou   R , Mara Vollema   E , Hahn   RT , et al.    Development of significant tricuspid regurgitation over time and prognostic implications: new insights into natural history . Eur Heart J   2018 ; 39 : 3574 – 81 . https://doi.org/10.1093/eurheartj/ehy352

Topilsky   Y , Maltais   S , Medina Inojosa   J , Oguz   D , Michelena   H , Maalouf   J , et al.    Burden of tricuspid regurgitation in patients diagnosed in the community setting . JACC Cardiovasc Imaging   2019 ; 12 : 433 – 42 . https://doi.org/10.1016/j.jcmg.2018.06.014

Fender   EA , Petrescu   I , Ionescu   F , Zack   CJ , Pislaru   SV , Nkomo   VT , et al.    Prognostic importance and predictors of survival in isolated tricuspid regurgitation: a growing problem . Mayo Clin Proc   2019 ; 94 : 2032 – 9 . https://doi.org/10.1016/j.mayocp.2019.04.036

Nagueh   SF , Smiseth   OA , Appleton   CP , Byrd   BF  III , Dokainish   H , Edvardsen   T , et al.    Recommendations for the evaluation of left ventricular diastolic function by echocardiography: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging . J Am Soc Echocardiogr   2016 ; 29 : 277 – 314 . https://doi.org/10.1016/j.echo.2016.01.011

Mitchell   C , Rahko   PS , Blauwet   LA , Canaday   B , Finstuen   JA , Foster   MC , et al.    Guidelines for performing a comprehensive transthoracic echocardiographic examination in adults: recommendations from the American Society of Echocardiography . J Am Soc Echocardiogr   2019 ; 32 : 1 – 64 . https://doi.org/10.1016/j.echo.2018.06.004

Zoghbi   WA , Adams   D , Bonow   RO , Enriquez-Sarano   M , Foster   E , Grayburn   PA , et al.    Recommendations for noninvasive evaluation of native valvular regurgitation: a report from the American Society of Echocardiography developed in collaboration with the society for cardiovascular magnetic resonance . J Am Soc Echocardiogr   2017 ; 30 : 303 – 71 . https://doi.org/10.1016/j.echo.2017.01.007

Lang   RM , Badano   LP , Mor-Avi   V , Afilalo   J , Armstrong   A , Ernande   L , et al.    Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging . J Am Soc Echocardiogr   2015 ; 28 : 1 – 39 . e14. https://doi.org/10.1016/j.echo.2014.10.003

Galloo   X , Dietz   MF , Fortuni   F , Prihadi   EA , Cosyns   B , Delgado   V , et al.    Prognostic implications of atrial vs. ventricular functional tricuspid regurgitation . Eur Heart J Cardiovasc Imaging   2023 ; 24 : 733 – 41 . https://doi.org/10.1093/ehjci/jead016

Hahn   RT , Lawlor   MK , Davidson   CJ , Badhwar   V , Sannino   A , Spitzer   E , et al.    Tricuspid valve academic research consortium definitions for tricuspid regurgitation and trial endpoints . Eur Heart J   2023 ; 44 : 4508 – 32 . https://doi.org/10.1093/eurheartj/ehad653

Muraru   D , Badano   LP , Hahn   RT , Lang   RM , Delgado   V , Wunderlich   NC , et al.    Atrial secondary tricuspid regurgitation: pathophysiology, definition, diagnosis, and treatment . Eur Heart J   2024 ; 45 : 895 – 911 . https://doi.org/10.1093/eurheartj/ehae088

Dietz   MF , Prihadi   EA , van der Bijl   P , Fortuni   F , Marques   AI , Ajmone Marsan   N , et al.    Sex-specific differences in etiology and prognosis in patients with significant tricuspid regurgitation . Am J Cardiol   2021 ; 147 : 109 – 15 . https://doi.org/10.1016/j.amjcard.2021.02.016

Vieitez   JM , Monteagudo   JM , Mahia   P , Perez   L , Lopez   T , Marco   I , et al.    New insights of tricuspid regurgitation: a large-scale prospective cohort study . Eur Heart J Cardiovasc Imaging   2021 ; 22 : 196 – 202 . https://doi.org/10.1093/ehjci/jeaa205

Zhang   XX , Wei   M , Xiang   R , Lu   YM , Zhang   L , Li   YD , et al.    Incidence, risk factors, and prognosis of tricuspid regurgitation after cardiac implantable electronic device implantation: a systematic review and meta-analysis . J Cardiothorac Vasc Anesth   2022 ; 36 : 1741 – 55 . https://doi.org/10.1053/j.jvca.2021.06.025

Patlolla   SH , Schaff   HV , Nishimura   RA , Stulak   JM , Chamberlain   AM , Pislaru   SV , et al.    Incidence and burden of tricuspid regurgitation in patients with atrial fibrillation . J Am Coll Cardiol   2022 ; 80 : 2289 – 98 . https://doi.org/10.1016/j.jacc.2022.09.045

Muraru   D , Addetia   K , Guta   AC , Ochoa-Jimenez   RC , Genovese   D , Veronesi   F , et al.    Right atrial volume is a major determinant of tricuspid annulus area in functional tricuspid regurgitation: a three-dimensional echocardiographic study . Eur Heart J Cardiovasc Imaging   2021 ; 22 : 660 – 9 . https://doi.org/10.1093/ehjci/jeaa286

Topilsky   Y , Nkomo   VT , Vatury   O , Michelena   HI , Letourneau   T , Suri   RM , et al.    Clinical outcome of isolated tricuspid regurgitation . JACC Cardiovasc Imaging   2014 ; 7 : 1185 – 94 . https://doi.org/10.1016/j.jcmg.2014.07.018

Clark   DM , Plumb   VJ , Epstein   AE , Kay   GN . Hemodynamic effects of an irregular sequence of ventricular cycle lengths during atrial fibrillation . J Am Coll Cardiol   1997 ; 30 : 1039 – 45 . https://doi.org/10.1016/S0735-1097(97)00254-4

Otto   CM , Nishimura   RA , Bonow   RO , Carabello   BA , Erwin   JP  III , Gentile   F , et al.    2020 ACC/AHA guideline for the management of patients with valvular heart disease: executive summary: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines . Circulation   2021 ; 143 : e35 – 71 . https://doi.org/10.1161/CIR.0000000000000932

Harada   T , Obokata   M , Omote   K , Iwano   H , Ikoma   T , Okada   K , et al.    Functional tricuspid regurgitation and right atrial remodeling in heart failure with preserved ejection fraction . Am J Cardiol   2022 ; 162 : 129 – 35 . https://doi.org/10.1016/j.amjcard.2021.09.021

Obokata   M , Kane   GC , Reddy   YN , Olson   TP , Melenovsky   V , Borlaug   BA . Role of diastolic stress testing in the evaluation for heart failure with preserved ejection fraction: a simultaneous invasive-echocardiographic study . Circulation   2017 ; 135 : 825 – 38 . https://doi.org/10.1161/CIRCULATIONAHA.116.024822

Mohammed   SF , Hussain   S , Mirzoyev   SA , Edwards   WD , Maleszewski   JJ , Redfield   MM . Coronary microvascular rarefaction and myocardial fibrosis in heart failure with preserved ejection fraction . Circulation   2015 ; 131 : 550 – 9 . https://doi.org/10.1161/CIRCULATIONAHA.114.009625

Cochet   H , Mouries   A , Nivet   H , Sacher   F , Derval   N , Denis   A , et al.    Age, atrial fibrillation, and structural heart disease are the main determinants of left atrial fibrosis detected by delayed-enhanced magnetic resonance imaging in a general cardiology population . J Cardiovasc Electrophysiol   2015 ; 26 : 484 – 92 . https://doi.org/10.1111/jce.12651

Beale   AL , Nanayakkara   S , Segan   L , Mariani   JA , Maeder   MT , van Empel   V , et al.    Sex differences in heart failure with preserved ejection fraction pathophysiology: a detailed invasive hemodynamic and echocardiographic analysis . JACC Heart Fail   2019 ; 7 : 239 – 49 . https://doi.org/10.1016/j.jchf.2019.01.004

El-Busaid   H , Hassan   S , Odula   P , Ogeng'o   J , Ndung'u   B . Sex variations in the structure of human atrioventricular annuli . Folia Morphol (Warsz)   2012 ; 71 : 23 – 7 .

Addetia   K , Muraru   D , Veronesi   F , Jenei   C , Cavalli   G , Besser   SA , et al.    3-Dimensional echocardiographic analysis of the tricuspid annulus provides new insights into tricuspid valve geometry and dynamics . JACC Cardiovasc Imaging   2019 ; 12 : 401 – 12 . https://doi.org/10.1016/j.jcmg.2017.08.022

Dworatzek   E , Mahmoodzadeh   S , Schriever   C , Kusumoto   K , Kramer   L , Santos   G , et al.    Sex-specific regulation of collagen I and III expression by 17beta-estradiol in cardiac fibroblasts: role of estrogen receptors . Cardiovasc Res   2019 ; 115 : 315 – 27 . https://doi.org/10.1093/cvr/cvy185

Nath   J , Foster   E , Heidenreich   PA . Impact of tricuspid regurgitation on long-term survival . J Am Coll Cardiol   2004 ; 43 : 405 – 9 . https://doi.org/10.1016/j.jacc.2003.09.036

Wang   N , Fulcher   J , Abeysuriya   N , McGrady   M , Wilcox   I , Celermajer   D , et al.    Tricuspid regurgitation is associated with increased mortality independent of pulmonary pressures and right heart failure: a systematic review and meta-analysis . Eur Heart J   2019 ; 40 : 476 – 84 . https://doi.org/10.1093/eurheartj/ehy641

Benfari   G , Antoine   C , Miller   WL , Thapa   P , Topilsky   Y , Rossi   A , et al.    Excess mortality associated with functional tricuspid regurgitation complicating heart failure with reduced ejection fraction . Circulation   2019 ; 140 : 196 – 206 . https://doi.org/10.1161/CIRCULATIONAHA.118.038946

Messika-Zeitoun   D , Verta   P , Gregson   J , Pocock   SJ , Boero   I , Feldman   TE , et al.    Impact of tricuspid regurgitation on survival in patients with heart failure: a large electronic health record patient-level database analysis . Eur J Heart Fail   2020 ; 22 : 1803 – 13 . https://doi.org/10.1002/ejhf.1830

Genereux   P , Pibarot   P , Redfors   B , Bax   JJ , Zhao   Y , Makkar   RR , et al.    Evolution and prognostic impact of cardiac damage after aortic valve replacement . J Am Coll Cardiol   2022 ; 80 : 783 – 800 . https://doi.org/10.1016/j.jacc.2022.05.006

Essayagh   B , Antoine   C , Benfari   G , Maalouf   J , Michelena   HI , Crestanello   JA , et al.    Functional tricuspid regurgitation of degenerative mitral valve disease: a crucial determinant of survival . Eur Heart J   2020 ; 41 : 1918 – 29 . https://doi.org/10.1093/eurheartj/ehaa192

Itelman   E , Vatury   O , Kuperstein   R , Ben-Zekry   S , Hay   I , Fefer   P , et al.    The association of severe tricuspid regurgitation with poor survival is modified by right ventricular pressure and function: insights from SHEBAHEART big data . J Am Soc Echocardiogr   2022 ; 35 : 1028 – 36 . https://doi.org/10.1016/j.echo.2022.06.012

Medvedofsky   D , Aronson   D , Gomberg-Maitland   M , Thomeas   V , Rich   S , Spencer   K , et al.    Tricuspid regurgitation progression and regression in pulmonary arterial hypertension: implications for right ventricular and tricuspid valve apparatus geometry and patients outcome . Eur Heart J Cardiovasc Imaging   2017 ; 18 : 86 – 94 . https://doi.org/10.1093/ehjci/jew010

Joglar   JA , Chung   MK , Armbruster   AL , Benjamin   EJ , Chyou   JY , Cronin   EM , et al.    2023 ACC/AHA/ACCP/HRS guideline for the diagnosis and management of atrial fibrillation: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines . Circulation   2024 ; 149 : e1 – 156 . https://doi.org/10.1161/CIR.0000000000001193

Muraru   D , Guta   AC , Ochoa-Jimenez   RC , Bartos   D , Aruta   P , Mihaila   S , et al.    Functional regurgitation of atrioventricular valves and atrial fibrillation: an elusive pathophysiological link deserving further attention . J Am Soc Echocardiogr   2020 ; 33 : 42 – 53 . https://doi.org/10.1016/j.echo.2019.08.016

Author notes

• atrial fibrillation
• tricuspid valve insufficiency
• pulmonary hypertension
• heart ventricle
• sinus rhythm

Supplementary data

Email alerts, companion article.

• Impact of new-onset atrial fibrillation on the incidence of tricuspid regurgitation: a call to attention

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