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Circulation, Vol 63, 817-825, Copyright © 1981 by American Heart Association
D Opherk, H Zebe, E Weihe, G Mall, C Durr, B Gravert, HC Mehmel, F Schwarz and W Kubler
Hemodynamic and metabolic studies were performed in 15 patients without
heart disease (controls, group A), in 21 patients with typical stress-
induced anginal pain but normal coronary and left ventricular angiograms
(angina pectoris with normal arteriogram, group B), and in 10 patients with
angiographically proved coronary artery disease (CAD, group C). Coronary
dilatory capacity, determined by measuring total myocardial blood flow at
rest and during maximal coronary vasodilatation (dipyridamole, 0.5 mg/kg
i.v.), was markedly reduced in group B and C patients. In group B patients,
left ventricular catheter biopsy specimens revealed no evidence of
small-vessel disease, but did show histologic alterations of mitochondria.
During atrial pacing, the control subjects showed no changes in myocardial
lactate uptake, whereas in group B patients, myocardial lactate production
occurred. In contrast to controls, patients in group B showed a significant
decline in ejection fraction and circumferential fiber shortening during
isometric exercise. These findings suggest that myocardial ischemia is the
cause of angina pectoris in patients who have angina but normal coronary
arteriograms.
ARTICLES
Reduced coronary dilatory capacity and ultrastructural changes of the myocardium in patients with angina pectoris but normal coronary arteriograms
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