How arrhythmias weaken the ventricle: an often underestimated vicious cycle

Area of Science:

• Cardiology
• Electrophysiology
• Heart Failure

Background:

• Arrhythmia-induced cardiomyopathy (AIC) is a form of dilated cardiomyopathy where abnormal heart rhythms cause left ventricular systolic dysfunction (LVSD).
• AIC can occur in individuals with or without pre-existing heart conditions, worsening left ventricular ejection fraction.
• The potential for reversibility of LVSD by eliminating the underlying arrhythmia makes AIC a distinct and treatable condition.

Purpose of the Study:

• To highlight the underestimation of AIC prevalence in clinical practice.
• To elucidate the pathophysiological mechanisms of AIC in animal models and human myocardium.
• To emphasize the curable nature of AIC through arrhythmia elimination.

Main Methods:

• Review of animal models demonstrating the effects of tachycardic pacing on cardiac function.
• Analysis of studies on human ventricular myocardium investigating cellular responses to atrial fibrillation.
• Clinical observation of LVSD reversibility after arrhythmia termination.

Main Results:

• Continuous tachycardic pacing in animal models induces LVSD, increased filling pressures, LV dilatation, and decreased cardiac output.
• These induced pathologies are generally reversible upon termination of tachycardia.
• Human studies show that even normofrequent atrial fibrillation activates cellular mechanisms contributing to the AIC phenotype.

Conclusions:

• AIC is likely underdiagnosed because it is often recognized only after cardiac function recovery.
• Pathophysiological changes in AIC are reversible, making it a treatable condition.
• Understanding cellular mechanisms activated by arrhythmias is crucial for diagnosing and managing AIC.