Immediately after balloon dilation of a fresh thrombotic coronary lesion, 5 patients had angina, ST segment elevation, and a striking reduction of blood flow in the dilated artery. A mean (SEM) pressure gradient across the dilated lesion of only 3(1) mm Hg and an average minimum lesion diameter of 1·7 mm indicated that the decline in resting blood flow was not due to obstruction at the site of the original lesion. Neither distal vascular emboli nor side branch occlusions were visible on the angiogram. An increase in distal coronary artery pressure during a subsequent balloon inflation suggested that the site of vasoconstriction was distal to the origin of collateral vessels. The syndrome lasted 48-80 min and was not reversed with nitroglycerin or thrombolytic drugs. Papaverine lessened the syndrome transiently on one occasion. Such microvascular constriction, caused by release of potent vasoconstrictors from the clot, may partly explain the failure of emergency angioplasty to reduce infarct size in acute myocardial infarction.
Bibliographical noteFunding Information:
This work was supported by grants from the National Institutes of Health (ROI-HL39185) and the American Heart Association. The work was done during the tenure of a Clinician Scientist Award (R. F. W.) from the American Heart Association with funds contributed partly by the Minnesota Affiliate.