onalcoholic fatty liver disease (NAFLD) is associated with insulin resistance and is considered the hepatic expression of the metabolic syndrome. Subjects with features of the metabolic syndrome are at risk of developing cardiovascular disease and coronary heart disease (CHD), 1 and recent evidence suggest that this is the case in NAFLD as well. In a prospective study, the 14-year risk of mortality from cardiovascular causes was doubled in patients with biopsy-proven NAFLD compared with a reference population. 2 In the Hoorn Study, 3 raised alanine aminotransferase (ALT) at baseline increased the 10-year risk of CHD events, even after adjustment for the components of the metabolic syndrome. Coronary risk factors tend to cluster in patients with NAFLD, who exhibit more advanced atherosclerosis compared with controls. 4 This observation is not surprising considering that the fatty liver is responsible for the overproduction of many cardiovascular disease risk factors, such as very low density lipoprotein, C-reactive protein, and clotting elements. Thus, conventional wisdom suggests that the hemodynamic or metabolic derangements associated with NAFLD may predispose to CHD and heart failure.
Novel data indicate that type 2 diabetes (T2DM) and obesity per se may increase the risk for cardiac dysfunction and heart failure, independent of coronary disease and hypertension. In the early 19th century, Laennec first proposed the concept of fatty degeneration of the heart, 5 a condition later defined as myocardial steatosis and associated with a greater risk for heart disease. Until recently, the study of myocardial steatosis in humans has been limited by difficulties in quantifying lipid content. Magnetic resonance (MR)