Imaging of the Heart: Potential Application to Alcohol-Induced Heart Disease

In addition to its effects on the brain and other organs, chronic heavy alcohol use can lead to cardiovascular diseases including hypertension. Another consequence of heavy drinking is alcohol-induced heart muscle disease, which leads to a diminished pump function of the heart. Several mechanisms related to alcohol and its metabolism in the body can contribute to alcohol-induced heart muscle disease by interfering with the heart's metabolism and energy production and thereby impairing heart muscle function. Noninvasive imaging techniques can help researchers and clinicians to monitor alcohol's effects on the heart and its metabolism. For example, one study found that increasing amounts of alcohol reduced the uptake of fatty acids--the primary fuel used by the heart muscle--into the heart. Other investigators have demonstrated that the heart's metabolism of fatty acids is impaired in patients with alcoholinduced heart muscle disease. Although the potential of imaging techniques for studying alcohol-induced heart muscle disease has not yet been fully explored, these approaches are likely to play an increasingly important role in the future. KEY WORDS: diagnostic imaging; heart function; muscle; metabolism; fatty acids; alcoholic cardiomyopathy; myocardium; single photon emission computed tomography; positron emission tomography; magnetic resonance imaging Athough liver disease is by far the most prevalent physiological consequence of alcohol abuse and dependence, 1 percent to 2 percent of all chronic alcohol abusers also develop overt heart disease, such as a thickened heart resulting from alcohol-induced high blood pressure or heart failure (i.e., the heart's inability to pump sufficient blood to meet the body's needs) (Bing 1982; Lieber 1995; Preedy and Richardson 1994; UrbanoMarquez et al. 1989). Alcohol-induced heart disease afflicts more than 200,000 Americans and accounts for approximately 3 percent of all hospital admissions for heart problems in the United States (Bing 1982; Lieber 1995; Preedy and Richardson 1994). Even alcohol-abusing patients without overt signs of heart failure often may experience signs of depressed cardiac function during increased activity (e.g., shortness of breath when climbing stairs). Alcohol can have many effects on the heart and the cardiovascular system: It can depress the heart's pumping ability, induce irregular heartbeats, increase blood pressure, and alter the fat content and metabolism of the heart muscle. The exact mechanism(s) by which alcohol induces these effects, however, remains unclear. This lack of knowledge is due, in part, to the scarcity of available research methods that allow researchers to explore the heart's structure and function without surgery (i.e., noninvasively). New, noninvasive imaging techniques developed during the past decade promise to be immensely important in evaluating changes in the heart's blood flow and metabolism that are induced by alcohol consumption and other conditions. Although imaging techniques have not yet been applied extensively to the study of alcohol-induced diseases of the heart and other organs, in the future this technology should provide insight into factors that underlie alcohol-induced disease. These techniques also may help elucidate how alcohol-induced changes in heart function respond to abstinence and other therapeutic interventions. This article examines the relationship between alcohol and heart disease and reviews some of the structural and functional imaging techniques being used to study disorders of the heart and cardiovascular system. The results of studies using imaging technology to investigate the abnormalities underlying cardiac dysfunction in alcoholics also are presented. THE RELATIONSHIP BETWEEN ALCOHOL AND HEART DISEASE Many studies have demonstrated that modest alcohol consumption (i.e., one to two drinks1 per day) may help protect the heart from coronary artery2 disease by altering the levels of lipoproteins= in the blood, enhancing the dissolution of dangerous blood clots, and reducing the aggregation of certain blood cells (Bing 1982; Lieber 1995; Preedy and Richardson 1994). …