Myocardial oxygenation at high workstates in hearts with left ventricular hypertrophy

Background: High cardiac workloads produced by catecholamine infusion resul t in loss of myocardial phosphocreatine (PCr) and accumulation of inorganic phosphate (Pi) which are more prominent in hearts with left ventricular hy pertrophy (LVH) than in normal hearts. Since ischemia can cause changes in phosphorylated compounds similar to those during catecholamine stimulation, this study tested the hypothesis that the exaggerated depletion of PCr and accumulation of Pi during high workloads in LVH is the result of impaired myocyte oxygenation. Methods and results: P-31- and H-1-NMR spectroscopy we re used to determine myocardial high energy phosphate levels and myoglobin desaturation, respectively, in eight normal dogs and nine dogs with LVH pro duced by ascending aortic banding. The mean LV weight/body weight ratio was approximately twice normal in the LVH group. Infusion of dobutamine (15 an d 30 mu g/kg/min), and dobutamine+dopamine (each 20 mu g/kg/min) caused pro gressive similar increases in the heart rateXsystolic LV pressure product t o a maximum of 57.4+/-3.3.10(3) in normal and 63.9+/-2.7.10(3) in LVH anima ls, while myocardial oxygen consumption increased from 0.09+/-0.01 to 0.24/-0.04 in normals and from 0.10+/-0.02 to 0.25+/-0.03 ml/min/g in LVH. PCr/ ATP ratios during basal conditions were lower in LVH hearts (1.73+/-0.10, 1 .61+/-0.09 and 1.51+/-0.09 in subepicardium, midwall and subendocardium, re spectively) as compared with normals (2.24+/-0.09, 2.01+/-0.08 and 1.89+/-0 .07; each p<0.01 normal vs. LVH). Catecholamine infusions caused dose-relat ed decreases in PCr/ATP and appearance of Pi which was more marked in LVH t han in normal hearts. H-1-NMR spectroscopy did not detect deoxymyoglobin in either normal or LVH hearts even during the highest workloads. In contrast , occlusion of the anterior descending coronary artery resulted in a large deoxymyoglobin signal. Conclusions: Increases of cardiac work produced by c atecholamine stimulation resulted in greater decreases of PCr and greater i ncreases of Pi in hypertrophied than in normal hearts. These abnormalities were not the result of inadequate intracellular oxygen availability and con sequently cannot be ascribed to demand ischemia. (C) 1999 Elsevier Science B.V. All rights reserved.