Introduction
Long-standing tachycardia is a well-recognized cause of heart failure and left ventricular dysfunction and has led to the nomenclature, tachycardia-induced cardiomyopathy (TCM) [1]. TCM is generally partially or entirely reversible with adequate treatment of the underlying arrhythmia. Therapeutic options include drug therapy, cardioversion, or interventional/surgical ablation [1].
The diagnosis is usually made retrospectively after normalization of heart rate and recovery of left ventricular function (LVEF). The first documented case was described in 1913 in a young patient with atrial fibrillation and symptoms of heart failure [2]. However, the knowledge of the underlying pathophysiological mechanisms and histopathological changes is still limited.
Various animal studies have described the molecular pathophysiological features of TCM [3,4]. Induction of cardiomyopathy through rapid pacing in various animal models has provided insight into the changes that occur within the myocyte as well as the surrounding extracellular matrix [3,4]. In particular, sustained tachycardia causes changes in calcium homeostasis, matrix remodeling, and fibrosis, as well as neurohormonal activation parameters [5,6,7]. A study by Mueller et al. showed changes in cardiomyocyte and mitochondrial morphology accompanied by macrophage-dominated inflammation in TCM [8].
This study aimed to analyze endomyocardial biopsy samples from patients with TCM and compared them with samples from patients with dilated cardiomyopathy (DCM) and inflammatory cardiomyopathy (ICM).