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J Clin Invest. 1990 Aug;86(2):575-84.

Evidence for altered epicardial coronary artery autoregulation as a cause of distal coronary vasoconstriction after successful percutaneous transluminal coronary angioplasty.

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Division of Cardiology, Stanford University Medical Center, California 94305.


To determine whether vasoconstriction distal to the site of successful percutaneous transluminal coronary angioplasty (PTCA) is a result of altered autoregulation in a hypoperfused coronary artery, we examined the association of this distal vasoconstriction with lesion severity in 20 patients. Lesion severity was classified as moderate, severe or critical (greater than 1.0, 0.5-1.0, and less than 0.5 mm, respectively). Quantitative coronary measurements were made at 3, 15, and 30 min after PTCA, and then after intracoronary (IC) nitroglycerin, in coronary segments distal to the dilated lesion (distal) and in a nonmanipulated vessel (control). Coronary vasoconstriction in the Distal segment after PTCA correlated with lesion severity, with 14 +/- 4%, 28 +/- 2%, and 41 +/- 5% vasoconstriction (vs. IC nitroglycerin, 30 min after PTCA) in the moderate, severe and critical lesion severity subgroups, respectively (P less than 0.01 for critical or severe vs. moderate). This vasoconstriction was significantly greater than that observed in the corresponding control segment for patients with severe (P less than 0.01), and critical (P less than 0.001) lesions. These findings suggest that hypoperfused human epicardial coronary arteries "reset" their autoregulatory responsiveness and that distal vasoconstriction after PTCA is the result of this altered autoregulation. These findings have clinical implications concerning the etiology, prophylaxis and treatment of coronary spams after PTCA and coronary bypass surgery.

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