Myocardial ischemia in hypertrophic cardiomyopathy.
To investigate the presence, mechanism, and hemodynamic significance of myocardial ischemia in hypertrophic cardiomyopathy, 50 patients underwent a pacing study with measurement of great cardiac vein flow, lactate and oxygen content, and left ventricular filling pressure. Compared to patients without hypertrophic cardiomyopathy, their basal coronary flow, myocardial oxygen consumption, and left ventricular end-diastolic pressure were significantly higher. Further, the 23 patients with basal obstruction to left ventricular outflow had a significantly higher basal great cardiac vein flow and oxygen consumption than the 27 patients without basal obstruction. During pacing to heart rates of 100 and 130 bpm (the anginal threshold for 41 of 50 patients), those with basal obstruction still demonstrated significantly higher coronary flow and oxygen consumption. Most patients, regardless of the presence or absence of obstruction, had metabolic evidence of ischemia, often severe. At a heart rate of 150, most patients with basal obstruction demonstrated an actual decline in coronary flow, which correlated with an increase in left ventricular filling pressures and more severe metabolic evidence of ischemia. In those without obstruction, ischemia occurred at a lower coronary flow, suggesting more impaired coronary flow delivery than those with obstruction. Abnormalities in oxygen extraction were noted in both groups. Thus, obstruction to left ventricular outflow results in higher basal and stress-induced coronary flow and oxygen requirements, related to elevated left ventricular systolic pressures, resulting in rapid exhaustion of coronary flow reserve during stress. Patients without obstruction, with lower left ventricular systolic pressures, may have greater impairment of flow delivery during stress as a cause of myocardial ischemia.
Cardiology Branch, National Heart, Lung and Blood Institute, Bethesda, Maryland.
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Cannon
D000328:Adult; D001696:Biomechanical Phenomena; D002304:Cardiac Pacing, Artificial; D002312:Cardiomyopathy, Hypertrophic / Q000150:complications* / Q000503:physiopathology; D003327:Coronary Disease / Q000209:etiology*; D005260:Female; D006801:Humans; D008297:Male; D012016:Reference Values; D013312:Stress, Physiological / Q000503:physiopathology