Myocardial ischemia in patients with hypertrophic cardiomyopathy: Contribution of inadequate vasodilator reserve and elevated left ventricular filling pressures

R. O. Cannon, D. R. Rosing, B. J. Maron, M. B. Leon, R. O. Bonow, R. M. Watson, S. E. Epstein

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389 Scopus citations


To study the mechanism and hemodynamic significance of myocardial ischemia in hypertrophic cardiomyopathy, 20 patients (nine with resting left ventricular outflow tract obstruction ≥ 30 mm Hg) with a history of angina pectoris and angiographically normal coronary arteries underwent a pacing study with measurement of great cardiac vein flow, lactate and oxygen content, and left ventricular filling pressure. Compared with 28 control subjects without hypertrophic cardiomyopathy, their resting coronary blood flow was higher (91 ± 27 vs 66 ± 17 ml/min; p < .001) and their coronary resistance was lower (1.13 ± 0.38 vs 1.55 ± 0.45 mm Hg/ml/min; p < .001). Left ventricular end-diastolic pressure (16 ± 6 vs 11 ± 3 mm Hg; p < .001) and pulmonary arterial wedge pressure (13 ± 5 vs 7 ± 3 mm Hg; p < .001) were significantly higher in patients with hypertrophic cardiomyopathy. During pacing, coronary flow rose in both groups, although coronary and myocardial hemodynamics differed greatly. In contrast to the linear increase in flow in control subjects up to a heart rate of 150 beats/min (66 ± 17 to 125 ± 28 ml/min), patients with hypertrophic cardiomyopathy demonstrated an initial rise in flow to 133 ± 31 ml/min at an intermediate heart rate of 130 beats/min. At this point, 12 of 20 patients developed their typical chest pain. With continued pacing to a heart rate of 150 beats/min, mean coronary flow fell to 114 ± 29 ml/min (p < .002), with 18 of 20 patients experiencing their typical chest pain and metabolic evidence of myocardial ischemia. This fall in coronary flow was associated with a substantial rise in left ventricular end-diastolic pressure (30 ± 9 mm Hg immediately after peak pacing). In the 14 patients whose coronary flow actually fell from intermediate to peak pacing, the rise in left ventricular end-diastolic pressure in the same interval was greater than that of the six patients whose flow remained unchanged or increased (11 ± 8 vs 2 ± 2 mm Hg; p < .01). In addition, despite metabolic and hemodynamic evidence of myocardial ischemia, the arteriovenous O2 difference actually narrowed at peak pacing. Thus most patients with hypertrophic cardiomyopathy achieved maximum coronary vasodilation and flow at modest increases in heart rate. Elevation in left ventricular filling pressure, probably related to ischemia-induced changes in ventricular compliance, was associated with a decline in coronary flow. A paradoxic narrowing of the arteriovenous O2 difference, despite apparent limitation of coronary flow, may also be of pathogenetic importance to myocardial ischemia in hypertrophic cardiomyopathy.

Original languageEnglish (US)
Pages (from-to)234-243
Number of pages10
Issue number2
StatePublished - 1985

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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