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Circulating CD 36 and fractalkine levels are associated with vulnerable plaque progression in patients with unstable angina pectoris
Author(s) -
Li Rui Jian,
Yang Ming,
Li Ji Fu,
Xue Li,
Chen Yu Guo,
Chen Wen Qiang
Publication year - 2014
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12302
Subject(s) - medicine , intravascular ultrasound , lesion , lumen (anatomy) , unstable angina , vulnerable plaque , chemokine , cardiology , target lesion , stenosis , stable angina , gastroenterology , inflammation , pathology , percutaneous coronary intervention , coronary artery disease , myocardial infarction
Summary The chemokine, fractalkine, independently enhances the vulnerability of coronary atherosclerotic plaques. The present study investigated the combined effects of CD 36 and fractalkine on coronary plaque progression in patients with unstable angina pectoris. In the present study, 120 unstable angina pectoris patients undergoing coronary angiography and intravascular ultrasound were divided into two groups: an intermediate lesion group (lumen diameter stenosis 50–70%, 80 patients) and a severe lesion group (at least one lesion with lumen diameter stenosis > 70%, 40 patients). The control group consisted of 40 healthy age‐ and sex‐matched subjects. Concentrations of CD 36 and fractalkine were measured by enzyme‐linked immunosorbent assay. Major adverse cardiovascular events were monitored over a 2‐year follow up. Intravascular ultrasound showed that patients with severe lesions had more calcified and mixed plaques, and a larger plaque area and plaque burden than patients with intermediate lesions ( P < 0.05–0.01). More patients with severe lesions underwent stent deployment ( P < 0.05) than those with intermediate lesions. CD 36 and fractalkine concentrations were significantly higher in the severe lesion patients ( P < 0.05), and both had significant positive correlations ( P < 0.05) with the plaque burden of atherosclerotic lesions. Using the matched nested case–control study, we found that CD 36 and fractalkine levels were higher in patients with recurrent major adverse cardiovascular events than controls ( P < 0.05). In conclusion, CD 36 and fractalkine both promote, and might synergistically enhance, the progression of coronary atherosclerotic plaques.