Vasoreactivity of the culprit lesion in unstable angina.

Abstract

BACKGROUND Although abnormal vasoconstriction may be involved in the pathogenesis of the acute coronary syndromes, the vasoreactivity of the lesion responsible for unstable angina (culprit lesion) has not been directly investigated. It is also unknown if enhanced vasoreactivity is found downstream to this lesion or extends to uninvolved coronary arteries. METHODS AND RESULTS We studied seven unstable angina patients whose condition had sufficiently stabilized to allow ergometric bicycle exercise and a cold pressor test to be performed as provocative stimuli during coronary arteriography. We measured the luminal diameter of the culprit lesion, a normal-appearing distal segment, and the segment of an uninvolved coronary artery using quantitative coronary angiography. Seven stable angina patients served as controls. Antianginal medications were tapered and interrupted. The culprit lesion constricted significantly with exercise and the cold pressor test compared with a stable angina control lesion. The culprit lesion measured 1.41 +/- 0.07 mm at baseline and diminished to 1.09 +/- 0.07 mm with exercise (P = .001). It measured 1.26 +/- 0.07 mm before the cold pressor test and diminished to 1.09 +/- 0.03 mm with this test (P = .015). In contrast, the profile of the stable lesion in the stable angina control group differed significantly (P = .006). Its luminal diameter measured 1.42 +/- 0.17 mm at baseline and 1.48 +/- 0.21 mm with exercise (P = NS). It measured 1.57 +/- 0.18 mm before and 1.55 +/- 0.18 mm with the cold pressor test (P = NS). There were no significant changes to these stimuli in the uninvolved coronary artery segments in unstable angina and in the distal segments in both unstable and stable angina patients. CONCLUSIONS This study demonstrates increased vasoreactivity of the culprit lesion in unstable angina compared with a control lesion in stable angina. The lack of an effect either in the uninvolved coronary artery or downstream to the culprit lesion suggests that systemic neurohumoral or seeding mechanisms are not operative. This abnormal vasoreactivity might predispose to, or be a marker for, the recurrence of acute ischemia at this site.