The maintenance of cellular levels of high-energy phosphates is required for myocardial function and preservation. In animals, severe myocardial ischemia is characterized by the rapid loss of phosphocreatine and a decrease in the ratio of phosphocreatine to ATP.

To determine whether ischemic metabolic changes are detectable in humans, we recorded spatially localized phosphorus-31 nuclear-magnetic-resonance (³¹P NMR) spectra from the anterior myocardium before, during, and after isometric hand-grip exercise.

The mean (±SD) ratio of phosphocreatine to ATP in the left ventricular wall when subjects were at rest was 1.72±0.15 in normal subjects (n = 11) and 1.59±0.31 in patients with nonischemic heart disease (n = 9), and the ratio did not change during hand-grip exercise in either group. However, in patients with coronary heart disease and ischemia due to severe stenosis (≥70 percent) of the left anterior descending or left main coronary arteries (n = 16), the ratio decreased from 1.45±0.31 at rest to 0.91±0.24 during exercise (P<0.001) and recovered to 1.27±0.38 two minutes after exercise. Only three patients with coronary heart disease had clinical symptoms of ischemia during exercise. Repeat exercise testing in five patients after revascularization yielded values of 1.60±0.20 at rest and 1.62±0.18 during exercise (P not significant), as compared with 1.51±0.19 at rest and 1.02±0.26 during exercise before revascularization (P<0.02).

The decrease in the ratio of phosphocreatine to ATP during hand-grip exercise in patients with myocardial ischemia reflects a transient imbalance between oxygen supply and demand in myocardium with compromised blood flow. Exercise testing with ³¹P NMR is a useful method of assessing the effect of ischemia on myocardial metabolism of high-energy phosphates and of monitoring the response to treatment. (N Engl J Med 1990; 323:1593–600.)