Background ³¹P-MRS during cardiac stress may provide (patho)physiological insights into the high-energy phosphate metabolism of the myocardium. Accordingly, the purpose of the present study was to determine the metabolic response of normal human myocardium to severe atropine-dobutamine (A-D) stress. To corroborate the results from the present in vivo study, a ³¹P-MRS experiment was performed with a moving phantom to simulate respiratory motion.

Methods and Results The phantom experiment showed no relation (P=.371) between the intensity ratio of two separate phosphate peaks and amplitude of phantom excursions. The phosphocreatine (PCr) and ATP signal strength and the PCr/ATP ratio were determined from the left ventricular wall in 20 healthy subjects (posttest likelihood for coronary artery disease was <2.5%) with ³¹P-MRS at rest and during high-dose A-D stress (rate-pressure product increased threefold). Stress-induced changes were −21% for PCr (P<.001) and −9% for ATP (P<.05). The average PCr/ATP value at rest was 1.42±0.18 and decreased by 14% to 1.22±0.20 during stress (P<.001).

Conclusions The phantom experiment shows that the in vivo decrease of myocardial PCr/ATP due to high-dose A-D stress we observed is not a motion artifact. Consequently, this indicates that myocardial high-energy phosphate metabolism of the normal human heart is altered at high workloads.