Key result
Acute ischemic heart failure induced by coronary flow reduction in dogs did not depress total myocardial ATP stores (6.66 vs 6.65 μmoles/g), despite a fall in creatine phosphate stores.
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Preserved ATP despite CP loss in canine ischemic HF challenges energy depletion as primary driver; leaves open relevance to human HF.
The effects of acutely induced ischemic heart failure on myocardial high energy phosphate stores were studied in dogs following an abrupt reduction (avg. 40%) of left main coronary arterial flow. Left ventricular biopsies were obtained before and during the onset of heart failure. Myocardial ATP stores were unchanged (control, 6.65 μmoles/g; ischemia, 6.66 μmoles/g) at a time when left ventricular end-diastolic pressure had risen from 3.9 to 11.3 mm Hg and left ventricular stroke work had fallen from 7.9 to 4.9 g-m. The average myocardial creatine phosphate (CP) stores fell from 13.2 μmoles/g to 7.9 μmoles/g. These results indicate that acute ischemic heart failure is not initiated by a detectable depression in total myocardial ATP stores.
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Covell et al. (1967) studied Acutely induced ischemic heart failure. Abrupt reduction of left main coronary arterial flow vs. Baseline (before onset of heart failure) was evaluated on Myocardial ATP stores. Acute ischemic heart failure induced by coronary flow reduction in dogs did not depress total myocardial ATP stores (6.66 vs 6.65 μmoles/g), despite a fall in creatine phosphate stores.
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