Arrhythmia-Induced Cardiomyopathies: Mechanisms, Recognition, and Management

Abstract

Arrhythmia-induced cardiomyopathy (AIC) is a potentially reversible condition in which left ventricular dysfunction is induced or mediated by atrial or ventricular arrhythmias. Cellular and extracellular changes in response to the culprit arrhythmia have been identified, but specific pathophysiological mechanisms remain unclear. Early recognition of AIC and prompt treatment of the culprit arrhythmia using pharmacological or ablative techniques result in symptom resolution and recovery of ventricular function. Although cardiomyopathy in response to an arrhythmia may take months to years to develop, recurrent arrhythmia can result in rapid decline in ventricular function with development of heart failure, suggesting residual ultrastructural abnormalities. Reports of sudden death in patients with normalized left ventricular ejection fraction cast doubt on the complete reversibility of this condition. Several aspects of AIC, including specific pathophysiological mechanisms, predisposing factors, optimal therapeutic strategies to prevent ultrastructural changes, and long-term risk of sudden death remain unresolved and need further research.

Keywords: atrial fibrillation; atrial flutter; catheter ablation; heart failure; heart rate; tachycardia.

Figure 1. Overview of the Current Understanding of AIC, from Mechanisms to Management and Prognosis

Persistent tachyarrhythmias or frequent ventricular ectopy can lead to dilated cardiomyopathy and decompensated heart failure in patients with or without concomitant structural heart disease. Cellular and extracellular changes in response to the culprit arrhythmia have been identified (see Central Illustration), but specific pathophysiological mechanisms have not been well elucidated. Early recognition of the relationship of a culprit arrhythmia to cardiomyopathy and aggressive arrhythmia control results in improved symptoms, left ventricular (LV) ejection fraction, and functional status and helps establish the diagnosis of arrhythmia-induced cardiomyopathy (AIC). Cellular and extracellular ultrastructural changes can, however, persist and can contribute to a rapid decline in cardiac function with arrhythmia recurrence. Close surveillance is thus crucial to ensure good long-term prognosis. ACE - angiotensin-converting enzyme; MRI - magnetic resonance imaging; PVC - premature ventricular complex.

Central Illustration

In response to rapid pacing in animals, left ventricular (LV) remodeling and heart failure occur in a time-dependent and highly predictable manner, similar to the phenotype of arrhythmia-induced cardiomyopathy. Several cellular and molecular events in response to the initial tachyarrhythmia stimulus take place over a period of approximately 3 to 4 weeks and involve both extracellular matrix (ECM) and myocyte remodeling. Specifically, there is loss of normal extracellular matrix and architecture. This, coupled with alterations in cellular growth and viability, defects in Ca²⁺ handling, and neurohormonal activation, results in LV dilation and severe contractile dysfunction. The natural history of rapid pacing–induced cardiomyopathy progresses from a compensatory phase (approximately >7 days) to an LV dysfunction phase (approximately 1 to 3 weeks) to an LV failure phase (approximately >3 weeks), characterized by progressive LV dilation and dysfunction and increasing neurohormonal activation. ATPase - adenosine triphosphatase; RAAS - renin-angiotensin-aldosterone system.