Effect of tissue fat and water content on nuclear magnetic resonance relaxation times of cardiac and skeletal muscle

Abstract

Understanding tissue determinants that affect the nuclear magnetic resonance (NMR) properties of myocardium would improve noninvasive characterization of myocardial tissue. To determine if NMR relaxation times would reflect changes in tissue fat content, two experimental models were investigated. First, an idealized model using mixtures of beef skeletal muscle and beef fat was studied to investigate the effects of a wide range of tissue fat content. Second, myocardium with varying fat content from hogs raised to have varying degrees of ponderosity was analyzed. Tissue fat and water contents and spin-lattice ( T 1) and spin-spin ( T 2) relaxation times at 20 MHz were measured. The skeletal muscle/fat mixtures ranged in fat content from 35% to 95% with water content variations from 50% to 75%. Water content decreased as fat content increased. A significant inverse linear relationship was found between T 1 and sample fat content ( r = −0.997). Spin-spin relaxation times showed a significant positive curvilinear relationship with fat content ( r 2 = 0.96). In the animal experiments, 18 hogs were studied with samples obtained from both right and left ventricular (LV) free walls, with care taken to avoid epicardial fat. Myocardial fat content ranged from 3% to 25%. A significant correlation was found between LV fat content and corrected LV mass ( r = 0.62), which suggested that the increase in LV mass could be explained, at least in part, by changes in myocardial fat content. Similar to the muscle/fat mixture model, a significant positive curvilinear relationship was found between myocardial T 2 and tissue fat content ( r 2 = 0.67) for all the myocardial samples. These data support the hypothesis that both tissue fat and water content are determinats of NMR relaxation times in muscle. Quantitating tissue components that alter NMR relaxation times should allow a better understanding of observed changes in T 1 and T 2 that occur in diseased states.