Background:
Arrhythmia induced cardiomyopathy (AiCM) is defined as a reversible impairment of cardiac function caused by arrhythmias. However, the diagnosis of AiCM can only be made after the arrhythmia has ceased. Based on current knowledge, it cannot be reliably predicted whether the arrhythmia represents a comorbidity of cardiomyopathy or is its trigger.
The aim of the study is to evaluate the predictive value of clinical, laboratory, ECG and echocardiographic (echo) parameters for the identification of AiCM and predict a clinically relevant improvement of LVEF after arrhythmia treatment.
Methods:
This study included pts with heart failure (HF), reduced LVEF (≤ 50%) and accompanying arrhythmias, such as atrial fibrillation (Afib), atrial flutter (Afla), and premature ventricular contractions (PVC). Pts were referred for treatment of the arrhythmias. Baseline clinical, laboratory, ECG and echo parameter were collected. Follow-up (FU) was performed after 3 months. The LVEF improvement of ≥10% was classified as significant (responder).
Results:
A total of 77 pts was included. Mean age was 70±10 years; 45 pts (58%) were male. Mean baseline LVEF was 38±11 %, BMI was 28±4 kg/m², and median baseline BNP was 2454 ng/L (IQR 1439-4189). Baseline echo showed a LASr of 8±4% and LV strain of -9±4%. 56 pts (73%) had hypertension, 20 (26%) had diabetes mellitus, and 18 (23%) had coronary artery disease. All pts received optimal medical HF therapy. Atrial arrythmias were present in 72 pts. Afib only n=55 (71%), Afib/atypical AFla n=5, typical Afla only n=12. In 5 pts the AiCM was suspected due to frequent PVCs. Pts with atrial arrythmias (n=72) underwent catheter ablation in 14 cases (18%), electrical cardioversion in 30 (39%), and rate control therapy in 23 (30%). LAA thrombi were detected in 20 pts (26%). Among pts with PVCs (n=5), 3 underwent catheter ablation and 2 received antiarrhythmic drug therapy.
Overall 51 pts (66%) were responders and showed an improvement in LVEF of ≥10%. A low baseline LVEF is significantly associated with an improvement in LVEF of ≥10% and the only independent predictor (p<0.05). FU LVEF was 50±12%.
Although baseline LASr was not associated with LVEF improvement (p=0.178), LV strain showed a trend towards association with LVEF improvement (p=0.053). In the univariate analysis, treatment with SGLT2 inhibitors (p=0.015) showed a significant association with an improvement in LVEF. The type of therapy of the arrhythmias itself does not play a significant role in LVEF improvement in a FU of 3 months. Furthermore, responders had a baseline median heart rate 115 bpm (IQR 43) that was significantly higher compared to non-responders 100 bpm (IQR 43) (p=0.014). Age, sex, BMI, comorbidities as well as baseline BNP and FU BNP 866 ng/L (IQR 243-1876) showed no statistically significant association with LVEF improvement.
Discussion: Two out of three pts with suspected AiCM showed a clinically relevant improvement in LVEF within 3 months. Lower baseline LVEF and higher baseline hear rate were associated with greater recovery of LV function. Treatment with SGLT2 inhibitors showed a significant association with an improvement in LVEF. The type of therapy of the arrhythmias itself does not play a significant role in LVEF improvement. A larger patient cohort is needed to confirm these findings.
