Arrhythmia-Induced Cardiomyopathy

Abstract

Background: Heart failure affects 1–2% of the population and is associated with elevated morbidity and mortality. Cardiac arrhythmias are often a result of heart failure, but they can cause left-ventricular systolic dysfunction (LVSD) as an arrhythmia-induced cardiomyopathy (AIC). This causal relationship should be borne in mind by the physician treating a patient with systolic heart failure in association with cardiac arrhythmia.

Methods: This review is based on pertinent publications retrieved by a selective search in PubMed (1987–2017) and on the recommendations in current guidelines.

Results: The key criterion for the diagnosis of an AIC is the demonstration of a persistent arrhythmia (including pathological tachycardia) together with an LVSD whose origin cannot be explained on any other basis. Nearly any type of tachyarrhythmia or frequent ventricular extrasystoles can lead, if persistent, to a progressively severe LVSD. The underlying pathophysiologic mechanisms are incompletely understood; the increased ventricular rate, asynchronous cardiac contractions, and neurohumoral activation all seem to play a role. The most common precipitating factors are supraventricular tachycardias in children and atrial fibrillation in adults. Recent studies have shown that the causal significance of atrial fibrillation in otherwise unexplained LVSD is underappreciated. The treatment of AIC consists primarily of the treatment of the underlying arrhythmia, generally with drugs such as beta-blockers and amiodarone. Depending on the type of arrhythmia, catheter ablation for long-term treatment should also be considered where appropriate. The diagnosis of AIC is considered to be well established when the LVSD normalizes or improves within a few weeks or months of the start of targeted treatment of the arrhythmia.

Conclusion: An AIC is potentially reversible. The timely recognition of this condition and the appropriate treatment of the underlying arrhythmia can substantially improve patient outcomes.

Figure 1

Schematic representation of the pathophysiology of arrhythmia-induced cardiomyopathy. Persistent tachycardia (due to pacemaker stimulation) reproducibly induces systolic heart failure in various animal models within days to weeks. As part of this, one sees neurohumoral activation typical of heart failure with increased plasma levels of brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP), sympathetic activation, and excessive activity of the renin-angiotensin-aldosterone system. If tachycardia stimulation is stopped, these changes normalize within days to weeks in animal models and within weeks to months in humans (21).

Figure 2

Flow diagram for the diagnosis of arrhythmia-induced cardiomyopathy (AIC). DCM: dilated cardiomyopathy; LV: left ventricular *see Box for triggering arrhythmias

Figure 3

Therapy and clinical treatment of arrhythmia-induced cardiomyopathy * Medication depending on the stage of heart failure as well as the extent of left ventricular systolic dysfunction and in accordance with the guidelines (1, 4). ACE-I, angiotensin-converting enzyme inhibitor ARB, aldosterone receptor blocker ARNI, angiotensin receptor neprilysin inhibitor