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(Circulation. 2001;104:1471.)
© 2001 American Heart Association, Inc.

Clinical Investigation and Reports

Unstable Angina and Elevated C-Reactive Protein Levels Predict Enhanced Vasoreactivity of the Culprit Lesion

Fabrizio Tomai, MD; Filippo Crea, MD; Achille Gaspardone, MD; Francesco Versaci, MD; Anna S. Ghini, MD; Luigi Chiariello, MD; Pier A. Gioffrè, MD

From the Cattedra di Cardiochirurgia, Università di Roma Tor Vergata, and the Istituto di Cardiologia (F.C.), Università Cattolica del Sacro Cuore, Rome, Italy.

Correspondence to Dr Fabrizio Tomai, Divisione di Cardiochirurgia, Università di Roma Tor Vergata, European Hospital, via Portuense 700, 00149 Rome, Italy. E-mail f.tomai{at}tiscalinet.it

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 (0.5 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.

Key Words: angina • inflammation • vasoconstriction • vasodilation

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