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- CI, confidence interval
- IVUS, intravascular ultrasound
- LPS, lipopolysaccharide
- MI, myocardial infarction
- OR, odds ratio
- PBMC, peripheral blood mononuclear cells
- TNFα, tumour necrosis factor α
Recent studies have rekindled interest in the possibility that infection, particularly by Gram negative bacteria, may contribute to the inflammatory component of atherosclerosis, and that the activation of monocytes/macrophages may contribute to acute myocardial infarction (MI).1 Recently, several groups have studied the association between the (-260)T allele in the gene encoding the CD14 lipopolysaccharide receptor (CD14) and MI, with differing results.2–5 In the present study we examined the association between the CD14 C(-260)T gene polymorphism and the risk of MI with regard to the severity of the coronary artery stenosis at the culprit lesion site. We revealed one possible mechanism by which CD14 polymorphism could affect the degree of activation of peripheral blood mononuclear cells (PBMC) with small amounts of lipopolysaccharide (LPS).
Study patients were recruited from 333 patients who underwent heart catheterisation (MI patients, 139; non-MI patients, 194) at Nagoya University Hospital and at Nagoya First Red Cross Hospital in Aichi Prefecture, Japan from January 2000 to August 2000. Non-MI patients included those with arrhythmia, valvar disease or congenital heart disease. MI patients were treated by mutant tissue plasminogen activator before coronary angiography. Coronary artery stenosis was defined as significant when the narrowing of the luminal diameter was > 50% after glyceryl trinitrate administration. Of the total of 139 MI patients, 67 had mild coronary artery stenosis of less than 50% of the adjacent …