Ventricular function in noncardiacs with alcoholic fatty liver: role of ethanol in the production of cardiomyopathy

Abstract

A B S T R A C T Since many patients with cardiomyopathy have a history of chronic ethanolism often associated with malnutrition, we have evaluated left ventricular (LV) function in alcoholics with fatty liver, who had no clinical evidence of cardiac or nutritional disease.During an afterload test of LV function the pressor response to angiotensin evoked a threefold rise of enddiastolic pressure in the alcoholic group which was substantially greater than the 4 mm Hg rise in control subjects. The stroke volume and stroke work response in the noncardiac alcoholic was significantly less than in controls. Diminished LV function was corroborated in the noncardiac alcoholic at rest, using a contractility index.To evaluate the dose-response relationship of ethanol in the production of cardiac malfunction, two groups of noncardiac alcoholic subjects were studied acutely at low and moderate dose levels. After 6 oz, ventricular function, myocardial blood flow, and metabolism were not significantly affected. After 12 oz, there was a progressive rise of end-diastolic pressure and decrease of stroke output at a mean blood alcohol level of 150 mg/ 100 ml, reverting toward control by 4 hr. The coronary effluent transiently evidenced leakage of cell constituents, despite an increase of coronary blood flow, suggesting a direct but reversible cardiac injury. Myocardial extraction of triglyceride was enhanced, whereas FFA uptake was reduced. A possible role of myocardial triglyceride accumulation in heart muscle was considered in pathogenesis.Chronic ingestion of 16 oz of Scotch daily by an alcoholic subject while on a normal diet-produced, after 12 wk, a progressive increase of heart rate and size,

Evidence for Cardiomyopathy in Familial Diabetes Mellitus

“…Nondiabetic patients who have cardiomyopathy without hypertension or myocardial infarction may exhibit similar hemodynamic abnormalities as seen in diabetes. Thus, the response to afterload increments manifested as an abnormal rise of ventricular filling pressure without a stroke volume increase has also been observed in the preclinical phase of alcoholic cardiomyopathy (6), in which the interstitium is also altered (59). After the onset of decompensation the diabetic myocardium presumably exhibits properties similar to other etiologic types.…”

“…The dose of hormone averaged 1.5 ,ug/kg per min over a 15-min period. Although the response in normals was associated with a significant stroke volume increment and a small rise of end-diastolic pressure (6), the diabetics demonstrated a significant rise of filling pressure compared to controls (P < 0.02), without a significant increment of stroke volume (Table IV). These hemo- dynamic data are consistent with the response of a cardiac medications were discontinued.…”

“…The dilution curves, pressures, electrocardiograms (ECG) were recorded on an Electronics for Medicine, Inc., (White Plains, N.Y.) DR-8 recorder. In selected patients, ventricular function was also assessed during afterload increments with angiotensin (6,22 (27).…”

“…In humans, a functional abnormality was also found in noncardiac adult diabetics by the systolic time-interval method (5), similar to the preclinical abnormality of ethanolism (6,7).…”

Myocardial Function and Lipid Metabolism in the Chronic Alcoholic Animal

“…This has provided a relatively sensitive test of cardiac function in normal humans, producing an increment of a few millimeters of mercury in ventricular end-diastolic pressure and a modest stroke work increase, a response which is altered by subclinical disease (29,30). In a study of intact anesthetized dogs these changes were also associated with a moderate enddiastolic volume elevation (31).…”