The early natural history of left anterior descending coronary artery (LAD) occlusion and the development of cardiogenic shock was studied in 35 open chest anesthetized dogs observed for 6 hours. Six control dogs underwent LAD isolation without occlusion, 13 underwent isolated LAD occlusion to simulate single vessel disease, and 14 underwent LAD occlusion and a 50% left circumflex coronary artery (LCA) stenosis to stimulate multi-vessel disease. Control dogs undergoing anesthesia showed no significant changes in hemodynamics after 6 hours. All dogs with single vessel disease survived and developed immediate and persistent dyskinesis of the anterior wall, a compensatory hypercontractility of remote muscle (131% of control)*, slight energy and substrate depletion and anaerobic metabolism (increased G6P)* despite maintenance of "normal" blood flow through the LCA. In contrast, early mortality was 57% in simulated multi-vessel disease as intractable ventricular fibrillation and/or cardiogenic shock caused the deaths of 7 of 13 dogs (57%)*. Remote muscle became progressively hypocontractile (61% of control)* and caused progressive reduction in stroke work index (less than or equal to 0.5 g x m/kg)*. Remote muscle showed moderate substrate and energy depletion (greater than or equal to 60% fall of ATP and CP, 37% fall of glutamate)* and more pronounced evidence of anaerobic metabolism (G6P rose 373%)* despite "normal" blood flow. These findings suggest that remote muscle is the principle determinant of mortality after an otherwise non-lethal cardiac event.(ABSTRACT TRUNCATED AT 250 WORDS)
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