Alcoholic cardiomyopathy- characterization and outcomes

Abstract

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Alcoholic cardiomyopathy is a severe consequence of chronic alcohol abuse and causes gradual changes in the structure and function of the heart, being a form of dilated cardiomyopathy. Purpose To characterize the population of patients (pts) with alcoholic cardiomyopathy (AC) in terms of baseline characteristics, echocardiographic parameters, alcohol consumption, medication and outcomes. We also intended to evaluate the impact of alcohol reduction/cessation. Methods We performed a retrospective study of the group of pts with the diagnosis of AC, established after exclusion of other aetiologies, followed in the heart failure consultation between 2018 and 2022. We divided the population into patients who maintained (2), reduced (1) (to an average of 2 drinks in men and 1 in women) or discontinued consumption (0). Results A total of 39 pts with a mean age of 68.13 ± 11 years were included. Of these, 35 were males (89.7%). In terms of cardiovascular risk factors, 64.1% had hypertension, 33.3% had diabetes, 53.5% dyslipidaemia, 10.3% had chronic hepatic disease, 30.8% were smokers and 10.3% ex-smokers. The prevalence of atrial fibrillation (AF) was 46.2%, with a median heart rate of 72.50 ± 20.99 bpm. At the beginning of follow-up, this population had a mean left ventricular ejection fraction (LVEF) of 30.46% ± 9.99, a mean indexed LA volume of 58.5 ml/m2 ± 32.63 and a mean indexed LV volume 87.44% ± 27.73. Concerning the alcohol consumption, during the follow-up, 43.6% of the patients stopped drinking alcohol, 10.3% reduced the habits and 20.5% maintained the consumption. Regarding the medication, at the end of follow-up 24.4% were medicated with sacubitril/valsartan, 51.1% with angiotensin-converting enzyme inhibitors, 71.1% with beta blockers, 51.1% with mineralocorticoid receptor antagonists and 35.6% with SGLT2 inhibitors. In a mean follow-up of 26.62± 11.11 months, there was a significant improvement of the ejection fraction (mean of 9.59% ± 12.97, p< 0.001), with a mean LVEF of 40.59% ± 12.78 at the end of follow-up. In fact, in 17.8% of the patients the final LVEF was more than 50%. Regarding indexed LV volume, there was a significant reduction during follow-up (102.250 ± 43.46 ml/m2, p= 0.018). Concerning alcohol consumption, pts who quit drinking had a mean improvement of LVEF of 13,73% ± 15.83 (p= 0.003), pts who reduced alcohol consumption 8.6% ± 5.81 (p=0.03) and pts that kept the consumption 2.67% ± 3.01 (p= 0.82). The variation of LVEF was statistically significant between the groups (p=0.03). These three groups had no statistically significant differences in medical history of hypertension (p=0.37), diabetes (p=0.22), dyslipidaemia (p=0.17), AF (p=0.70) and medication. Conclusion Pts with alcoholic cardiomyopathy had a high prevalence of atrial fibrillation and cardiovascular risk factors. Improvement and even recovery of cardiac function depends on reduction/extinction of alcohol consumption.