Atrial fibrillation is common in heart failure patients (15% to 30%). It carries a variety of adverse hemodynamic consequences impacting prognosis and accelerating the progression of left ventricular systolic dysfunction.
Hemodynamic impact of atrial fibrillation
The mechanisms of hemodynamic deterioration include a chronically fast heart rate and variation in ventricular cycle lengths (R-R intervals), which together significantly depress cardiac output. Added factors are the loss of atrioventricular synchrony (which lowers end-diastolic pressure and volume in both ventricles and may further decrease stroke volume), an increase in mean atrial diastolic pressure, ventricular valvular regurgitation, and shortened passive diastolic filling. Indirectly adverse effects include those caused by the drugs commonly used to control atrial fibrillation: thus, calcium channel blockers may assist rate control, but have negative inotropic effects, while antiarrhythmics, notably the class I agents, can be fatally arrhythmogenic. Yet, despite these adverse consequences, the prognostic implications of atrial fibrillation remain debated.
New York Heart Association classes I and II
Carson et al studied the impact of atrial fibrillation in patients with mild-to-moderate heart failure entered into the Holter substudy of the Vasodilator-Heart Failure Trials (V-HeFT), which compared combination therapy with hydralazine and isosorbide dinitrate to placebo (Ve-HeFT I) and enalapril (Ve-HeFT II). Survival in patients with atrial fibrillation, whether chronic or paroxysmal, did not differ statistically from that in patients in sinus rhythm in either study. Moreover, atrial fibrillation, whether chronic or paroxysmal, was not associated with all-cause mortality or sudden death on either univariate or multivariate analysis.
In a retrospective analysis of the Studies Of Left Ventricular Dysfunction (SOLVD) prevention and treatment trials, Dries et al (1998) assessed the survival impact of ACE inhibition in asymptomatic and symptomatic heart failure (prevention and treatment arms, respectively). In both arms, atrial fibrillation was independently associated with an increased risk of all-cause mortality, largely explained by an increased risk of pump-failure death (Figure 1), and also with the composite end point of death or hospitalization for worsening heart failure. In contrast to previous data, however, atrial fibrillation was not associated with an increased risk of arrhythmic death.
Figure 1. Kaplan-Meier event-free survival curves for the end point of deaths due to progressive pump failure. Patients with atrial fibrillation (n=419; solid line) were more likely to die from progressive pump failure than those in sinus rhythm (n=6098; broken line) (log-rank P<0.001). Data are the numbers of survivors at each 365-day interval per group. Reproduced from: Dries DL, Exner DV, Gersh BJ, Domanski MJ, Waclawiw MA, Stevenson LW. Atrial fibrillation is associated with an increased risk for mortality and heart failure progression in patients with asymptomatic and symptomatic left ventricular systolic dysfunction: a retrospective analysis of the SOLVD trials. Studies of Left Ventricular Dysfunction. J Am Coll Cardiol. 1998;32:695-703. Copyright © 1998, Elsevier Science Ltd. Noninvasive investigations These are of limited use in the risk stratification of the individual patient. ECG monitoring may provide a diagnosis and useful data for arrhythmic risk stratification. It is diagnostic if it provides a correlation between presynco-pal and syncopal symptoms, and reveals bradycardia or tachycardia. Ventricular pauses >3 seconds, phases of second- or third-degree atrioventricular block, and rapid paroxysmal ventricular tachycardia are typical findings.
Echocardiography grades the severity of structural heart disease and its progression over time. Severe aortic stenosis is a structural cause of syncope.
Exercise testing is indicated in syncope occurring during or shortly after exertion. The pathophysiologic basis seems to be exaggerated reflex vasodilatation. The test is diagnostic if it reproduces the hemodynamic abnormalities associated with syncope. A typical finding is Mobitz II second- or third- degree atrioventricular block.
Carotid sinus massage consists of compressing the carotid artery while monitoring the ECG and blood pressure, and is indicated in syncope of unknown etiology. A positive test is asystole >3 seconds and a fall in blood pressure >50 mm Hg.
Tilt testing confirms neurally mediated syncope after other cardiac causes such as arrhythmia have been excluded.
Electrophysiologic testing (EPS)
EPS is indicated if the history, ECG, and/or structural heart disease suggest arrhythmia. It is diagnostic if it reveals any of the following: sinus bradycardia and a very long sinus node recovery time; baseline HV interval >100 ms (debatable); second- and third-degree block induced during incremental atrial pacing; or induced mono/polymorphous ventricular tachyarrhythmias or rapid symptomatic supraventricular arrhythmias.
The sensitivity, specificity, and predictive value of EPS depend on the clinical presentation and underlying structural disease. The induction of sustained ventricular arrhythmia by EPS identifies high-risk coronary patients with syncope. Recent evidence from clinical trials such as the Multicenter Autonomic Defibrillator Implantation Trial II (MADIT II) also suggests that a depressed left ventricular ejection fraction in ischemic cardiomyopathy without criteria for arrhythmia is an independent predictor of arrhythmic sudden death. On the other hand, in patients with nonischemic cardiomyopathy, heart failure, and unexplained syncope, the negative predictive value is low and noninducibility does not signify a low risk of arrhythmic death.
Cardiac catheterization and angiography
If noninvasive assessment suggests acute myocardial ischemia as the trigger to syncope, by triggering ventricular tachycardia or drastically decreasing cardiac output during ischemia, then coronary angiography is required to assess the severity of coronary heart disease with a view to revascularization.
In conditions for which an arrhythmic cause has been excluded, such as neurally mediated reflex syncope and orthostatic hypotension, treatment aims to prevent recurrence and improve quality of life. It is usually sufficient to explain the benign nature of the condition, and give advice on avoiding trigger agents, in particular relating to antihypertensive therapy.
In arrhythmic syncope, treatment is also designed to prevent recurrence and improve quality of life, but in addition to decrease mortality. A pacemaker should be considered for sinus node dysfunction or an atrioventricular conduction disturbance. The treatment of choice for paroxysmal supraventricular arrhythmia causing syncope is transcatheter ablation. Syncope caused by ventricular tachycardia in heart failure is usually treated with an autonomic implantable cardioverter-defibrillator (AICD), although in a few specific forms, namely right ventricular outflow tract tachycardia and bundle branch reentry tachycardia, ablation is the appropriate first-line therapy.
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