C-reactive protein and the severity of atherosclerosis in myocardial infarction patients with stable angina pectoris
M C Tataru1, J Heinrich, R Junker
1Herz- und Gefässklinik, Bad Neustadt/Saale, Germany.
Insights
Elevated C-reactive protein (CRP) levels correlate with the severity of atherosclerosis, including coronary heart disease. This finding supports CRP as a marker for inflammatory processes involved in the development of atherosclerosis.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Pathology
Background:
- Inflammatory processes are increasingly recognized as crucial in atherosclerosis development.
- Elevated C-reactive protein (CRP) levels are observed in patients with various cardiovascular diseases compared to healthy individuals.
Purpose of the Study:
- To investigate the association between plasma CRP concentration and the severity of coronary heart disease and generalized arteriopathy in myocardial infarction survivors.
- To explore the role of inflammation in atherogenesis.
Main Methods:
- Study included 1112 male and 299 female myocardial infarction survivors and a control group.
- Assessed CRP, fibrinogen, D-dimer, lipids, and severity of arteriosclerotic changes in multiple arterial beds.
- Coronary angiography was performed in myocardial infarction patients.
Main Results:
- A significant positive correlation was found between CRP levels and the severity of atherosclerosis, from pre-clinical to clinically manifest stages.
- CRP concentrations increased progressively from controls to patients with increasing atherosclerosis.
- CRP levels were significantly associated with the degree of coronary heart disease detected by angiography.
Conclusions:
- Results support the hypothesis that inflammatory processes in the vessel wall are integral to atherogenesis.
- Findings suggest a causal link between acute phase reactions, indicated by CRP, and the pathogenesis of atherosclerosis in the coronary and peripheral arteries.
Background:
Recent findings provide evidence for the importance of inflammatory processes in the pathogenesis of atherosclerosis. C-reactive protein was elevated in patients with peripheral artery disease, coronary heart disease and myocardial infarction compared to normal subjects.
Methods:
In 1112 male and 299 female survivors of myocardial infarction (mean age +/- SD, men, 50.4 +/- 9.5, women, 56.1 +/- 9.3), we investigated whether plasma C-reactive protein concentration is associated with the severity of coronary heart disease and generalized pre-clinical or clinically manifest arteriopathy. The control group consisted of 326 male and 138 female individuals matched for age without clinical symptoms of coronary disease. The severity of arteriosclerotic changes was determined for the extra-cranial brain-supplying arteries, abdominal aorta, pelvis and leg arteries. In myocardial infarction patients coronary angiography was performed. Laboratory analyses included determination of C-reactive protein, fibrinogen, D-dimer, HDL-cholesterol, LDL-cholesterol and triglycerides.
Results:
The following ranking of C-reactive protein concentrations was found: controls < or = patients after myocardial infarction without atherosclerosis < or = patients with myocardial infarction and pre-clinical atherosclerosis < or = patients with myocardial infarction and clinically manifest atherosclerosis. Additionally, our data showed a significant association between C-reactive protein concentrations and the angiographically detected degree of coronary heart disease.
Conclusions:
As C-reactive protein is a marker of inflammatory processes, our results in patients with clinically manifest and early pre-clinical atherosclerosis support the hypothesis that inflammatory processes in the vessel wall participate in atherogenesis. Moreover, they support the hypothesis of a causal relationship between an acute phase reaction and the pathogenesis of atherosclerosis in coronary arteries and other parts of the arterial vessel system.
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