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Updated: Aug 16, 2026

Interventional Diagnostic Procedure: A Practical Guide for the Assessment of Coronary Vascular Function
Published on: March 15, 2022
[Disease activities and serum C-reactive protein levels in patients with vasospastic angina pectoris]
Naoyuki Katayama1, Koichi Nakao, Kenji Horiuchi
1Cardiovascular Center, Saiseikai Kumamoto Hospital, Kumamoto, Japan. naoyuki@estate.ocn.ne.jp
Objectives:
To evaluate the relationship between serum C-reactive protein (CRP) levels and disease activities of vasospastic angina pectoris.
Methods:
We reviewed 284 consecutive patients who underwent the coronary artery vasospasm provocation test with intracoronary administration of acetylcholine. No patient had significant organic stenosis in the coronary artery on control angiography. No patient was given nitrates, calcium channel blockers, aspirin or statins before the provocation test. Serum CRP levels were measured on the day before the provocation test.
Results:
Significant transient coronary artery stenoses associated with chest symptoms and ST-T changes in electrocardiogram was found in 132 patients (positive group), but the remaining 152 showed no spasm (negative group). Serum CRP levels were significantly higher in the positive group than in the negative group (0.29 +/- 0.12 vs 0.08 +/- 0.06mg/dl, p < 0.01). Furthermore, high frequency of angina pectoris ( > or = 3 times/week), low dose of acetylcholine required to induce vasospasm, provocation of total occlusion and provocation of multivessel spasm were associated with significantly higher serum CRP levels in the positive group. Multivariate logistic regression analysis showed low dose of acetylcholine required to induce vasospasm as the strongest predictor of elevated levels of serum CRP (p < 0.001, odds ratio 4.52, 95% confidence interval 2.00-10.44).
Conclusions:
Serum CRP levels were related to the inductivity of coronary artery spasm in patients clinically suspected of having vasospastic angina pectoris. Inflammation may be important in the disease activity through the endothelial dysfunction of coronary artery trees.
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