Clinical Features of Tachyarrhythmia-Induced Cardiomyopathy

By Michael H. Crawford, MD, Editor

SYNOPSIS: A prospective observational study of patients with left ventricular dysfunction without known cause and tachyarrhythmias has shown that restoration of sinus rhythm significantly improves left ventricular function in more than 80% of such patients by six months and, initially, normal left ventricular size can be predictive of this response.

SOURCE: Schach C, Körtl T, Zeman F, et al. Clinical characterization of arrhythmia-induced cardiomyopathy in patients with tachyarrhythmia and idiopathic heart failure. JACC Clin Electrophysiol 2024; Feb 28. doi: 10.1016/j.jacep.2024.102332. [Online ahead of print].

Although tachyarrhythmia-induced cardiomyopathy (TAC) is well known, its frequency, time to recovery post-rhythm correction, and early diagnostic markers are not. To elucidate these issues, a prospective, multicenter, observational study was conducted in Germany. Patients with atrial fibrillation (AF) or flutter and heart rate > 100 beats/minute with newly diagnosed left ventricular (LV) ejection fraction (EF) < 50% were screened. Those with alternative causes of cardiomyopathy, such as valvular disease, myocarditis, or relevant coronary artery disease, were excluded.

All patients underwent a rhythm control strategy and were followed periodically for six months. Also, those with recurrent tachyarrhythmias were excluded. Patients whose LVEF increased by ≥ 15% or by ≥ 10% with an LVEF ≥ 50% were categorized as TAC. The primary endpoints were the frequency of TAC and the time to restoration of LV systolic function by the criteria mentioned earlier. Secondary endpoints were echocardiographic structural/functional measures, biomarkers, cardiovascular magnetic resonance (CMR) late gadolinium enhancement (LGE) and New York Heart Association (NYHA) functional class.

Between 2018 and 2020, 95 patients were screened, and 68 patients met inclusion criteria. During the course of the study, 18 patients were excluded, the majority (12) for recurrent arrhythmias, leaving a final population of 50 patients (mean age 68 years; 66% men). Initial treatment consisted of cardioversion in 32 patients, ablation in 15 patients, and amiodarone infusion in one patient. Two patients converted spontaneously. Criteria for TAC were met in 58% of patients by two months, 68% of patients at four months, and 82% of patients at six months.

In the TAC patients, LVEF increased from 35% to 57% (P < 0.0001) compared to non-TAC patients (37% to 44%, P = 0.003) at six months. Most (79%) of the recovery in LVEF in the TAC patients occurred in the first two months. After two months, the TAC group showed a small further increase in LVEF (about 5%) compared to < 1% in the non-TAC group. Additionally, by six months, 90% of TAC patients had an LVEF > 50%, and none of the patients had an EF of < 35%.

On multivariate analysis, only LV end-diastolic diameter at baseline (53 mm TAC vs. 60 mm non-TAC, P = 0.01) was predictive of TAC, with an odds ratio of 0.71 (95% confidence interval, 0.48-0.95; P = 0.04) and an area under the curve of 0.82 (P = 0.002). Biomarkers, CMR LGE, and NYHA class were not predictive. The authors concluded that TAC is frequent, with most patients recovering quickly, and that LV diastolic diameter seemed predictive of TAC.

COMMENTARY

Tachyarrhythmias can result in LV dysfunction and heart failure, but heart failure from other causes also can increase heart rate and cause tachyarrhythmias. Thus, it is hard to separate out the patients for whom rhythm restoration could improve LV function and those for whom it will not. Previous studies of LV functional recovery after AF ablation are not comparable because the patient populations were not purged of those with existing LV disease.

In the Schach et al study, coronary angiography and echocardiography were done in all their patients and CMR was done in 78% of their patients. These studies informed the recruitment of patients with no known heart disease. In this group, the incidence of TAC was high at 82% in six months, with most patients with TAC diagnosed by two months.

Also, after restoration of normal rhythm, the recovery rate of LV function was fastest in the first two months but continued for six months. This is consistent with animal studies that exhibited LV dysfunction within days of tachypacing, heart failure within a month, and full recovery of LV function in two weeks after cessation of pacing. In addition, LV end-diastolic diameter was the only clinical predictor of TAC, with the cut point at ≤ 57 mm.

There are several limitations to the Schach study. It is an observational study, so it could be subject to biases. For example, patients with recurrent arrhythmias were excluded because it would have been unclear in which group to put them and, if included, there would be a persistent trigger for LV dysfunction. Also, occult cardiomyopathy or genetic predisposition to cardiomyopathy cannot be excluded. In addition, subclinical arrhythmias could have occurred.

However, two-thirds of the patients had electrocardiogram monitoring after rhythm restoration. CMR was not found to be useful to predict TAC, but only 78% of the patients had CMR as the result of renal issues and claustrophobia. Finally, the number of patients without TAC was small (18%), weakening any comparisons to the TAC group.

In summary, this small, carefully done observational study suggests that in patients with tachyarrhythmias and LV dysfunction, if no other cause of cardiomyopathy is discovered, the tachyarrhythmia is highly likely to be the cause and that efforts to rid the patient of the arrhythmia are worthwhile, especially if LV end-diastolic diameter on echocardiography is ≤ 57 mm.