Circulation, Vol 90, 5-11, Copyright © 1994 by American Heart Association
P Bogaty, D Hackett, G Davies and A Maseri
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.
ARTICLES
Vasoreactivity of the culprit lesion in unstable angina
Cardiovascular Research Unit, Royal Postgraduate Medical School, Hammersmith Hospital, London, UK.
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