How arrhythmias weaken the ventricle: an often underestimated vicious cycle.

Arrhythmia-induced cardiomyopathy (AIC) is classified as a form of dilated cardiomyopathy in which left ventricular systolic dysfunction (LVSD) is triggered by tachycardic or arrhythmic heart rates. On the one hand AIC can develop in patients without cardiac disease and on the other hand it can appear in patients with pre-existing LVSD, leading to a further reduction in left ventricular (LV) ejection fraction. A special aspect of AIC is the potential termination or partial reversibility of LVSD; thus, AIC is curatively treatable by the elimination of the underlying arrhythmia. Since arrhythmias are often seen merely as a consequence than as an underlying cause of LVSD, and due to the fact that the diagnosis of AIC can be made only after recovery of LV function, the prevalence of AIC is probably underestimated in clinical practice. Pathophysiologically, animal models have shown that continuous tachycardic pacing induces consecutive changes such as the occurrence of LVSD, increased filling pressures, LV dilatation, and decreased cardiac output. After termination of tachycardia, reversibility of the described pathologies can usually be observed. Studies in human ventricular myocardium have recently demonstrated that various cellular structural and functional mechanisms are activated even by normofrequent atrial fibrillation, which may help to explain the clinical AIC phenotype.