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Independent roles of monocyte chemoattractant protein-1, regulated on activation, normal T-cell expressed and secreted and fractalkine in the vulnerability of coronary atherosclerotic plaques.

BACKGROUND
Monocyte chemotactic factors contribute to the formation of atherosclerotic plaques. The present study aimed to elucidate the roles of monocyte chemoattractant protein-1 (MCP-1), Regulated on Activation, Normal T-cell Expressed and Secreted (RANTES) and fractalkine on the vulnerability of atherosclerotic plaques in patients with acute myocardial infarction (AMI) or unstable angina pectoris (UAP).


METHODS AND RESULTS
Sixty patients with AMI, 60 patients with UAP, 60 patients with stable angina pectoris (SAP) and 40 patients without coronary heart disease comprised the study group. Quantitative coronary angiography and intravascular ultrasound (IVUS) were performed. Concentrations and mRNA expression levels of high-sensitivity C-reactive protein, MCP-1, RANTES and fractalkine were measured by ELISA and RT-PCR, respectively. IVUS found that 51.3% of the AMI patients and 47.7% of the UAP patients had soft lipid plaques. Among the SAP patients, 52.4% had fibrous plaques and only 17.1% had soft plaques. AMI and UAP patients had larger plaque burden and vascular remodeling index than did the SAP patients (P<0.01). The averaged number of migrated monocytes was higher in AMI and UAP patients. Concentrations and mRNA expression levels of MCP-1, RANTES and fractalkine were significantly higher in AMI and UAP patients than in SAP patients (P<0.05-0.01). The plaque burden in UAP patients as measured with IVUS correlated well with monocytes chemotaxis (r=0.56, P<0.01).


CONCLUSIONS
MCP-1, RANTES and fractalkine independently participate in the pathogenesis of plaque vulnerability and subsequent plaque rupture.  