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[C-reactive protein in coronary plaques -- prevalence with acute coronary syndrome]
1Medizinische Klinik und Poliklinik II, Universitätsklinikum Bonn, Sigmund-Freud-Str. 25, 53105 Bonn, Germany.
Insights
C-reactive protein (CRP) is frequently found in human coronary artery plaques, especially in acute coronary syndromes (ACS). Statin therapy significantly reduces intimal CRP levels in ACS patients, potentially explaining their cardiovascular benefits.
Area of Science:
- Cardiovascular Science
- Immunology
- Pathology
Context:
- Atherosclerosis is driven by inflammatory mechanisms.
- C-reactive protein (CRP) is a serum marker predicting cardiovascular events.
- Intimal CRP expression in coronary lesions, particularly in acute coronary syndromes (ACS), remains largely uncharacterized.
Purpose:
- To investigate the presence and localization of CRP within coronary atheromas.
- To compare intimal CRP expression in patients with ACS versus stable angina (SA).
- To assess the impact of chronic statin medication on intimal CRP levels.
Summary:
- Immunohistochemical analysis of 90 coronary atherectomy specimens revealed CRP in 44% of lesions, primarily within macrophages/foam cells.
- Intimal CRP presence and expression were significantly higher in ACS (69%) compared to SA (28%).
- Statin therapy was associated with significantly reduced intimal CRP (29%) compared to non-statin users (61%), particularly in ACS patients.
Impact:
- This study demonstrates frequent intimal CRP in coronary stenoses, with higher prevalence in ACS.
- Findings suggest intimal CRP localization in macrophages/foam cells.
- Reduced intimal CRP with statin therapy in ACS patients may explain the anti-inflammatory and plaque-stabilizing effects observed systemically.
Abstract:
Inflammatory mechanisms are central in human atherosclerosis. Although C-reactive protein (CRP) as a serum marker is highly predictive for cardiovascular events, the intimal expression of CRP in clinically relevant coronary lesions is unknown, in particular in acute coronary syndromes (ACS). Shown by reduced CRP serum values, statins have antiinflammatory and plaque-stabilizing effects. In the present study, the presence of CRP in coronary atheromas with ACS versus stable angina (SA) as well as its possible modification by chronic statin medication was assessed. Coronary atherectomy probes from 90 primary stenoses were immunohistochemically analyzed with regard to the presence and the localization of CRP. Intimal results of patients with ACS (n=36), categorized according to the Braunwald classification, were compared with those of patients with SA (n=54). In 40 of 90 lesions (44%), immunoreaction specific for CRP was observed demonstrating a mean CRP expression of 1.7%. CRP was focally localized in a maximum of 69% of all plaque cells, the most in macrophages/foam cells, infrequently in smooth muscle cells. CRP-positive plaques showed more thrombus than plaques without CRP (63% vs 41%). Intact non-atherosclerotic control tissue revealed no signaling. As a central finding, intimal presence and expression were higher (each p<0.001) with ACS (69% and 3.1%, respectively) compared to SA (28% and 0.8%, respective). Subgroup analysis of target lesions associated with ACS according to the clinical Braunwald classification showed an increase of intimal CRP with classes I-III. In the presence of statin medication, intimal CRP was significantly lower than that without statin therapy (29 and 1.3%, vs 61 and 2.6%, respectively; p<0.01), in particular in the subgroup of ACS patients. Intimal CRP is frequently found in coronary primary stenoses, very often with macrophages/foam cells, and shows a highly significant prevalence with ACS. In this subgroup of patients, statin therapy is associated with significantly reduced intimal CRP. Our in situ findings as shown might explain the well-known serum constellations with statin therapy.