Quantitative Measurements of Cardiac Phosphorus Metabolites in Coronary Artery Disease by 31 P Magnetic Resonance Spectroscopy

Abstract

Background 31 P metabolite measurements in the human heart by magnetic resonance spectroscopy (MRS) have been reported previously. By use of a method in which metabolite content was quantified with reference to a standard located outside the chest, it has become possible to measure the content of phosphocreatine (PCr) and ATP in vivo in the human heart. In this study, PCr and ATP contents were measured by 31 P MRS and compared in human myocardium with reversible ischemia or scar diagnosed by exercise thallium scintigraphy. Methods and Results Forty-one subjects with stenosis of the left anterior descending coronary artery (>50%) and 11 healthy control subjects (C) composed the present study group. Patients were divided into two groups on the basis of exercise 201 Tl scintigraphy: a reversible 201 Tl defect group (RD[+], n=29) who demonstrated redistribution at late image and a fixed 201 Tl defect group (RD[−], n=12). While the subjects lay supine within the magnet, 31 P MR spectra were obtained from the anterior and apical regions of the left ventricle by slice-selected one-dimensional chemical shift imaging. For metabolite quantification, a standard was placed at the center of the surface coil. ANOVA revealed significant differences among the three groups with respect to the mean (±SD) PCr at rest (C, 12.14±4.25 >RD[+], 7.64±3.00 >RD[−], 3.94±2.21 μmol/g wet heart tissue, P <.05) as well as a significant decrease in ATP in the RD(−) group (C, 7.72±2.97; RD[+], 6.35±3.17 >RD[−], 4.35±1.52 μmol/g wet heart tissue, P <.05). Conclusions Compared with healthy control subjects, PCr content decreased significantly in patients with both reversible and fixed 201 Tl defects, and ATP content decreased significantly in subjects with fixed thallium defects. These results suggest that the measurement of ATP content in the human heart by 31 P MRS is a clinically important method for the evaluation of myocardial viability.