Alcoholic cardiomyopathy.

Abstract

Since the introduction of the term “alcoholic cardiomyopathy” in 1902, the diagnosis is mainly based on a long-term history of excessive alcohol consumption without abnormal load conditions (hypertension, valve disease), coronary artery disease, drugs or another specific disease. Excessive alcohol use is a frequent cause of dilated cardiomyopathy, responsible for up to 40% of cases of idiopathic dilated cardiomyopathy. Alcohol abuse initially causes asymptomatic left ventricular dysfunction, but when continued it can lead to the the familiar signs and symptoms of congestive heart failure. They usually shown typical signs such as progressive dyspnea, ankle swelling, orthopnea, reduced exercise capacity, arrhythmias, thromboembolic events and sudden cardiac death.
The available medical therapy is no different from that for other etiologies of heart failure, except for including alcohol abstinence as a basis. Survival is bad for those who continue to drink heavily, with 4-year mortality levels close to 50%.
Echocardiographic abnormalities, such as an increase in the size of the left atrium and in the thickness of the left ventricular wall, as well as a decrease in fractional shortening, precede the appearance of clinical symptoms or physical findings in alcoholics.
The worst prognosis is observed in patients with lower ejection fraction or severe diastolic dysfunction, leading to terminal heart failure with subsequent need for implantation of a left ventricular assist device or heart transplant. The implant of internal cardio-defibrillator is of particular interest in alcoholic myocardiopathy, since these patients are at high risk for ventricular arrhythmias.