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Unstable angina and elevated C-reactive protein levels predict enhanced vasoreactivity of the culprit lesion

Tomai, F.; Crea, F.; Gaspardone, A.; Versaci, F.; Ghini, A.S.; Chiariello, L.; Gioffrè, P.A.

Circulation 104(13): 1471-1476

2001


ISSN/ISBN: 0009-7322
PMID: 11571238
DOI: 10.1161/hc3801.096354
Accession: 011614218

Background: Because plaque inflammation may modulate coronary vasomotion, the association between systemic levels of C-reactive protein (CRP) and coronary vasoreactivity was assessed in patients with stable or unstable angina. Methods and Results: In 31 patients with stable angina and 23 patients with unstable angina undergoing coronary angiography, minimal luminal diameter (MLD) of the culprit lesion was measured by quantitative coronary angiography at baseline, during the cold pressor test (CPT), and after intracoronary administration of nitroglycerin (NTG) and expressed as percent change from baseline. MLD of patients with unstable angina exhibited a greater reduction during CPT and a greater increase after NTG than did patients with stable angina (-17+-14% versus -5+-12%, P=0.0013, and 34+-25% versus 8+-20%, P<0.001, respectively). According to preprocedural serum levels of CRP, 36 patients had normal (ltoreq0.5 mg/dL) and 18 patients had elevated CRP levels. MLD of patients with elevated CRP levels exhibited a greater reduction during CPT and a greater increase after NTG than of patients with normal CRP levels (-15+-12% versus -7+-14%, P=0.037, and 31+-23% versus 13+-25%, P=0.011, respectively). Both unstable angina and elevated CRP levels resulted in independent predictors of enhanced vasoreactivity at the multivariate analysis. Conclusions: This study confirms enhanced vasoreactivity of the culprit lesion in patients with unstable angina compared with those with stable angina. More importantly, it demonstrates that inflammatory mechanisms play a key role in modulating the reactivity of coronary atherosclerotic plaques and may partially account for the enhanced vasoreactivity of the unstable plaques.

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