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Published on: July 13, 2018
Unstable angina and elevated c-reactive protein levels predict enhanced vasoreactivity of the culprit lesion
F Tomai1, F Crea, A Gaspardone
1Cattedra di Cardiochirurgia, Università di Roma Tor Vergata, Rome, Italy. f.tomai@tiscalinet.it
Insights
Inflammation, indicated by C-reactive protein (CRP) levels, enhances coronary artery reactivity in patients with unstable angina. This suggests inflammatory mechanisms play a key role in modulating atherosclerotic plaque reactivity.
Area of Science:
- Cardiology
- Vascular Biology
- Inflammation Research
Background:
- Plaque inflammation may influence coronary vasomotion.
- Systemic C-reactive protein (CRP) levels are investigated for their association with coronary vasoreactivity.
Purpose of the Study:
- To assess the relationship between systemic CRP levels and coronary vasoreactivity in patients with stable or unstable angina.
- To determine if inflammation modulates coronary atherosclerotic plaque reactivity.
Main Methods:
- Quantitative coronary angiography was used to measure minimal luminal diameter (MLD) changes.
- Patients underwent a cold pressor test (CPT) and nitroglycerin (NTG) administration.
- Serum CRP levels were measured and categorized as normal or elevated.
Main Results:
- Unstable angina patients showed greater MLD reduction during CPT and increase after NTG compared to stable angina patients.
- Elevated CRP levels correlated with greater MLD reduction during CPT and increase after NTG.
- Multivariate analysis identified unstable angina and elevated CRP as independent predictors of enhanced vasoreactivity.
Conclusions:
- Enhanced vasoreactivity of the culprit lesion is confirmed in unstable angina patients.
- Inflammatory mechanisms, evidenced by CRP, significantly modulate coronary atherosclerotic plaque reactivity.
- Inflammation may partially explain the enhanced vasoreactivity observed in unstable plaques.
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.
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