Abstract
Introduction and aims
Coronary occlusions resulting in acute events often occur at the site of non-severe
stenoses. We sought to assess the prognostic value of non-obstructive coronary stenoses
and C-reactive protein (CRP) levels in patients with chronic stable angina (CSA).
Methods
We studied 790 consecutive patients with CSA who underwent routine coronary arteriography.
High sensitivity CRP and coronary angiograms were assessed at study entry. Angiographic
coronary disease severity was graded using a “vessel score” (number of coronary arteries
showing at least 50% reduction in lumen diameter) and extent of disease with an “extension
score” (proportion of the coronary artery tree showing angiographically detectable
atheroma). Patients were followed up for 1 year.
Results
Significant left main stem disease was present in 54 patients (6.8%). 368 patients
(46.6%) underwent revascularization. 71 patients (9%) had at least one of the events
comprised in the combined study end-point (unstable angina, myocardial infarction
(AMI) and cardiac death). Patients who suffered cardiac adverse events had a significantly
higher vessel score (n) (2.0 [2.0–3.0] vs. 2.0 [1.0–2.0], P < 0.001), extension score (%) (23.5 [17–34.5] vs. 16.0 [6.0–27.0], P < 0.001) and CRP levels (mg/L) (3.0 [1.8–7.2] vs. 2.3 [1.1–4.7], P = 0.001) compared to patients without events. Age, previous history of AMI, vessel score,
extension score and CRP levels were significantly associated with the study end-point.
Multivariate analysis showed extension score (OR 5.3 [2.8–10.3] CI 95%; P < 0.001), revascularization (OR 0.26 [0.14–0.48] CI 95%; P < 0.001) and CRP levels (OR 1.9 [1.1–3.2] CI 95%; P = 0.03), but not vessel score (P = 0.1), to be independent predictors of the combined end-point.
Conclusions
In patients with CSA, independently of revascularization, extension score and CRP
levels predict cardiac adverse events, regardless of the presence or absence of flow
limiting coronary lesions.
Keywords
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Article info
Publication history
Published online: September 29, 2008
Accepted:
August 1,
2008
Received in revised form:
July 29,
2008
Received:
March 6,
2008
Identification
Copyright
© 2008 Elsevier Ireland Ltd. Published by Elsevier Inc. All rights reserved.
