P1478 Evaluation of reversibility of alcoholic cardiomyopathy using doubaimine stress echocardiography

Abstract

Abstract Alcoholic cardiomyopathy (CM) is known as a reversible CM. Appropriate medications with cessation of alcohol may lead to full recovery of chamber size and contractility. But there is not much information about morphologic and hemodynamic changes over the course of treatment, and predictors of reversibility. We experienced the patient with alcoholic CM who was admitted with heart failure and recovered over 1 year and 5 months. He consumed daily 180g alcohol for 6 months before admission. On initial echocardiography, left atrial (LA) dimension, left ventricular (LV) systolic dimension (SD) and diastolic dimension (DD), inferior vena cava (IVC) size, and ejection fraction (EF) were 50 mm, 69 mm, 78 mm, 27 mm and 22%, respectively. Doppler examination revealed a restrictive pattern in tansmitral flow, and a systolic peak velocity/diastolic peak velocity (S/D) ratio of less than 1 in pulmonary vein flow (PVF). Pressure gradient through tricuspid regurgitation was 29 mmHg. Coronary angiogram confirmed no significant stenosis. Within 1 week after medications, LVEF increased mainly by decrease of enlarged LVSD which might be partly caused by volume overload, evidenced by respiratory variation of transmitral flow. On 8th day, we performed dobutamine stress echocardiography (DSE) to evaluate reversibility because LVEF slightly decreased despite decrease of LVDD. During dobutamine infusion, both LVDD and LVSD decreased along with increase of LVEF according to dose escalation. From 1 to 2 months, LVEF slightly increased with decrease of LVDD and LVSD. Afterwards, LVEF was normalized mainly with decrease of LVSD, and LVEF was completely normalized at 1 year and 5 month after initiation of treatment. Initial increase of LVEF might reflect decrease of LVSD by relief of volume overload rather than improving LV contractility. Based on this observation of serial change of chambers and LVEF, we speculate that increased LV wall tension, which is induced by increase of preload as a compensating mechanism for increasing stroke volume, might aggravate LVEF in later stage of heart failure with reduced EF. The sequence of normalization in chamber size was IVC, and then LA, and then LVDD. Transmitral flow as an indicator of diastolic dysfunction changed from restrictive (transiently existed only for 1 week) to abnormal relaxation pattern (no change since that time). PVF pattern showed S/D ratio < 1 until 1 week, and then triphasic pattern at 1 month, finally biphasic pattern at 8 month after initiation of medications. We observed a serial change of echocardiographic findings in patient with alcoholic CM, which might provide an insightful information to understand reverse of LV or LA remodeling associated with hemodynamic parameters, and DSE might be helpful to evaluate reversibility of LV systolic function and convince patients who are reluctant to medications.