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).