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Myocardial oxygenation at high workstates in hearts with left ventricular hypertrophy
R J Bache1, J Zhang, Y Murakami
1Department of Medicine, University of Minnesota Medical School, Minneapolis 55455, USA. bache001@maroon.tc.umn.edu
Insights
Left ventricular hypertrophy (LVH) causes greater depletion of myocardial phosphocreatine (PCr) and inorganic phosphate (Pi) accumulation during high workloads. This is not due to impaired myocyte oxygenation but rather other factors.
Area of Science:
- Cardiology
- Biochemistry
- Physiology
Background:
- High cardiac workloads from catecholamine infusion deplete myocardial phosphocreatine (PCr) and increase inorganic phosphate (Pi).
- These changes are more pronounced in hearts with left ventricular hypertrophy (LVH) compared to normal hearts.
- Ischemia can mimic these metabolic changes, prompting investigation into oxygenation as a cause.
Purpose of the Study:
- To test the hypothesis that exaggerated PCr depletion and Pi accumulation in LVH during high workloads result from impaired myocyte oxygenation.
- To investigate the role of intracellular oxygen availability in the observed metabolic changes in hypertrophied hearts.
Main Methods:
- Utilized 31P- and 1H-NMR spectroscopy to assess myocardial high-energy phosphate levels and myoglobin desaturation.
- Studied eight normal dogs and nine dogs with LVH induced by ascending aortic banding.
- Administered catecholamine infusions (dobutamine, dopamine) to increase cardiac workload and measured metabolic responses.
Main Results:
- LVH hearts showed lower basal PCr/ATP ratios compared to normal hearts.
- Catecholamine infusions induced dose-related decreases in PCr/ATP and increases in Pi, which were more severe in LVH.
- 1H-NMR did not detect deoxymyoglobin even at maximal workloads, indicating adequate oxygenation.
Conclusions:
- Increased cardiac work via catecholamines causes greater PCr decreases and Pi increases in hypertrophied hearts than normal hearts.
- These metabolic abnormalities in LVH are not caused by inadequate intracellular oxygen availability.
- The findings suggest that the observed changes are not due to demand ischemia.
Background:
High cardiac workloads produced by catecholamine infusion result in loss of myocardial phosphocreatine (PCr) and accumulation of inorganic phosphate (Pi) which are more prominent in heart with left ventricular hypertrophy (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:
31P- and 1H-NMR spectroscopy were used to determine myocardial high energy phosphate levels and myoglobin desaturation, respectively, in eight normal dogs and nine dogs with LVH produced by ascending aortic banding. The mean LV weight/body weight ratio was approximately twice normal in the LVH group. Infusion of dobutamine (15 and 30 micrograms/kg/min), and dobutamine + dopamine (each 20 micrograms/kg/min) caused progressive similar increases in the heart rate x systolic LV pressure product to a maximum of 57.4 +/- 3.3 x 10(3) in normal and 63.9 +/- 2.7 x 10(3) in LVH animals, 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, respectively) 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-related decreases in PCr/ATP and appearance of Pi which was more marked in LVH than in normal hearts. 1H-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 catecholamine stimulation resulted in greater decreases of PCr and greater increases of Pi in hypertrophied than in normal hearts. These abnormalities were not the result of inadequate intracellular oxygen availability and consequently cannot be ascribed to demand ischemia.
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