ஜர்னல் ஆஃப் ஆல்கஹாலிசம் & போதைப்பொருள் சார்பு
திறந்த அணுகல்

சுருக்கம்

Alcoholic Cardiomyopathy: Old and New Insights

Joaquim Fernandez-Sola, Ramon Estruch Riba

Alcohol cardiomyopathy (ACM) is a chronic dilated heart disease with decreased left ventricular ejection fraction that may be detected in one-fourth of high-dose alcohol consumers. It causes progressive diastolic and systolic dysfunction, supra and ventricular arrhythmias leading to heart failure and increased mortality. The main etiological factor for ACM is ethanol consumption that affects the myocardium in a dose-dependent manner. The mechanisms of ACM are diverse, synchronic and synergistic. Alcohol alters the channel and receptor structure of the cell membrane, decreases intracellular calcium transients, increases oxidative and inflammatory damage, decreases structural protein synthesis and interferes with excitation-contraction coupling mechanisms. Subjects with excessive alcohol consumption may have a subclinical cardiomyopathy with atrial and LV diastolic dysfunction measured by echocardiography or cardiac MR. Subclinical LV dysfunction may progress and later appear clinical features of heart failure. Cardiac myocytes adapt to ethanol aggression by cell and nuclear hypertrophy and dilatation of heart chambers. Progressive myocyte structure disarray and apoptosis produce myocyte loss, hypertrophy of the remaining cells, subendocardial and interstitial fibrosis and low-degree myocyte regeneration. In addition, ethanol also interferes with cardiac repair and adaptation mechanisms. Thus, local cardiomyokines (FGF-21) and growth factors (myostatin, IGF-1, leptin) are modified by ethanol, limiting cardiac remodeling and myocyte regeneration, and leading to abnormal hypertrophy and eccentric ventricle dilatation. This imbalance between aggression and protection mechanisms induces progressive myocyte loss and heart dysfunction. Alcohol abstention is the main goal in ACM, although control drinking (<-60 g/day) may allow recovery of LV function. Monitoring of systemic mediated alcohol-damage, and correction of vitamin and ion deficiencies is needed. Heart failure in ACM should be treated similar to other dilated cardiomyopathies. Heart transplantation is limited to subjects without other organ damage who are able to abstain from alcohol. New preventive and therapeutic strategies are under development to decrease alcohol-mediated myocyte damage and increase heart protective and repair mechanisms.