Tachycardia-induced cardiomyopathy (TCM) has been known for decades as a reversible form of non-ischemic cardiomyopathy. However, its mechanism and characteristics remain poorly understood.

This retrospective study investigated endomyocardial biopsy (EMB) samples from consecutive patients with TCM and compared them with samples from patients with dilated cardiomyopathy (DCM) and inflammatory cardiomyopathy (InCM).

A total of 684 patients (18 TCM, 170 DCM, 496 InCM) with recent-onset heart failure and reduced ejection fraction unrelated to valvular or ischemic heart disease were analyzed.

In the TCM group, 81% were male, the mean age was 60 ± 13 years, and 94% had heart failure symptoms ≥2 New York Heart Association (NYHA) class. At baseline (BL), 78% had atrial fibrillation/flutter and 12% other forms of tachycardia or frequent extrasystole. The ventricular rate was higher compared to DCM and InCM patients (122 ± 25 versus 78 ± 21; p < 0.001). Mean ejection fraction at BL was lower compared to DCM and InCM (27 ± 12% versus 39.0 ± 14.6%; p = 0.001), but improved to a significantly greater extent during follow-up (FU) (20% versus 6%; p < 0.001). At FU, heart rate and presence of sinus rhythm were similar in all groups; 69% of TCM patients underwent cardioversion or ablation. Compared with DCM patients, TCM patients had stronger myocardial expression of major histocompatibility complex (MHC) class II and an equal amount of infiltration with T‑cells/macrophages. Compared with InCM patients, the presence of T‑cells/macrophages was significantly lower in TCM. The marker of apoptosis (caspase 3) was comparably elevated in TCM/InCM patients.

Tachycardia-induced cardiomyopathy is characterized by immunohistological changes comparable to DCM except for caspase 3 levels, which were similar to those in InCM.