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Detecting vulnerable plaque using peripheral blood: inflammatory and cellular markers
Robert S Schwartz1, Antonio Bayes-Genis, John R Lesser
1Minnesota Cardiovascular Research Institute, Minneapolis Heart Institute Foundation, Minneapolis, MN 55407, USA. rss@rsschwartz.com
Insights
High-sensitivity C-reactive protein (hs-CRP) is a key marker for arterial inflammation and future cardiovascular events. Measuring hs-CRP, along with other inflammatory markers, improves risk assessment for vulnerable patients.
Area of Science:
- Cardiology
- Vascular Biology
- Inflammation Research
Background:
- Coronary atherosclerosis presents as two distinct syndromes: stable and unstable.
- Unstable acute coronary syndromes stem from vascular inflammatory processes, distinct from stable syndromes caused by fixed stenoses.
- Identifying vulnerable patients and plaques remains a diagnostic challenge due to low prevalence and current test limitations.
Purpose of the Study:
- To highlight the role of inflammatory markers in identifying patients at risk for cardiovascular events.
- To underscore the diagnostic challenges in detecting vulnerable plaques.
- To emphasize the need for improved risk assessment strategies in cardiology.
Main Methods:
- Review of current understanding of coronary atherosclerosis pathophysiology.
- Analysis of the correlative strength of high-sensitivity C-reactive protein (hs-CRP) for clinical events.
- Evaluation of hs-CRP, IL-6, and ICAM-1 in conjunction with lipid levels for risk assessment.
Main Results:
- hs-CRP is the strongest correlative factor for future clinical events related to arterial inflammation.
- CRP plasma levels provide the best risk assessment in various cardiac conditions, including stable/unstable angina and post-myocardial infarction.
- Combining CRP, IL-6, and ICAM-1 with lipid levels significantly improves cardiovascular risk assessment over lipids alone.
Conclusions:
- hs-CRP is a crucial biomarker for arterial inflammation and predicting cardiovascular events.
- Enhanced risk assessment can be achieved by incorporating inflammatory markers into diagnostic panels.
- Further development of sensitive and specific risk marker panels is essential for accurately identifying vulnerable plaques.
Abstract:
The concept of the vulnerable patient has arrived. Enhanced diagnostic methods will eventually permit accurately finding and treating these patients and their disease. Clinical Cardiologists now recognize that coronary atherosclerosis is two pathophysiologically distinct syndromes: stable and unstable. Stable coronary syndromes result from fixed, severe stenoses limiting blood flow and causing secondary myocardial ischemia. The unstable acute coronary syndromes are frequently catastrophic and are pathophysiologically distinct. They result from different cell subsets causing vascular inflammatory syndromes rather than gradual lumen constriction by plaque. Though pathophysiologically distinct, they may show common pathophysiology when a ruptured plaque heals and progressively becomes a critical stenosis. For the present hs-CRP measurement is the strongest correlative factor for future clinical events due to arterial inflammation: myocardial infarction, unstable angina, stroke, and peripheral vascular disease in both diseased and apparently healthy, asymptomatic patients. The CRP plasma level also is the best risk assessment in patients with either stable or unstable angina, long term after myocardial infarction, and in patients undergoing revascularization therapies. One study showed the only independent cardiovascular risk indicators using multivariate, age adjusted and traditional risk analysis were CRP and Total/HDL cholesterol ratio. If CRP, IL-6, and ICAM-1 levels are added to lipid levels, risk assessment can be improved over lipids alone. The prevalence of high-risk subjects in the general population is low, amplifying diagnostic problems for vulnerable plaque. Since no test yet has high sensitivity or specificity, diagnostic errors are high, with many false positives and negatives. Sensitivity or specificity must be increased by developing a risk marker panel, or by simultaneously finding other markers that themselves are highly sensitive and specific for vulnerable plaque.