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- CAD, coronary artery disease
- CRP, C reactive protein
- GFR, glomerular filtration rate
- hsCRP, high sensitive C reactive protein
- IL6, interleukin 6
- LDL, low density lipoprotein
- LVEF, left ventricular ejection fraction
- NT-proBNP, N-terminal pro-B type natriuretic peptide
- NYHA, New York Heart Association
- sTNFr, soluble tumour necrosis factor receptors
Inflammation plays an important part in the pathophysiology of coronary artery disease (CAD).1 High sensitive C reactive protein (hsCRP) reflects activation of the inflammatory system and independently predicts risk of first coronary events at all levels of low density lipoprotein (LDL)-cholesterol and a full spectrum of Framingham risk categories.2 Recent trials indicate that statins reduce inflammation.3,4 This leads to a better clinical outcome and reduces the rate of atherosclerosis progression independently of the reduction in cholesterol levels. The reasons why patients with raised levels of C reactive protein (CRP) have a worse outcome are, however, not clear.
The inflammatory biomarkers interleukin 6 (IL6), soluble tumour necrosis factor receptors (sTNFr) 1 and 2 have proinflammatory and procoagulant properties. Our first aim was to evaluate whether high levels of hsCRP in patients with stable CAD receiving standard statin treatment are associated with activation of these biomarkers. Our second aim was to evaluate whether hsCRP and cytokine levels are determined by LDL-cholesterol or by neurohumoral activation measured by levels of N-terminal pro-B type natriuretic peptide (NT-proBNP).
We analysed a subgroup of an ongoing prospective study comprising 153 statin treated patients with stable CAD. They were evaluated >6 months from myocardial infarction or cardiac revascularisation, and were free from infection, inflammatory diseases, malignancy and anti-inflammatory treatment. …