BACKGROUND: Recent studies suggest that fractalkine (FKN or CX3CL1) and its cognate receptor, CX3CR1, play a role in atherogenesis, so the relationship between coronary plaque rupture, as observed by preintervention optical coherence tomography, and plasma levels of FKN and CX3CR1 was investigated in this study. METHODS AND RESULTS: The study population consisted of 46 patients with unstable angina pectoris (UAP), 30 patients with stable angina pectoris, and 25 healthy controls. The UAP patients underwent a preintervention optical coherence tomography study, which revealed that the number of patients with and without plaque rupture at the culprit site was 27 (rupture group) and 19 (non-rupture group), respectively. Plasma levels of soluble FKN (sFKN) and CX3CR1 were measured by enzyme-linked immunosorbent assay and flow cytometry, respectively. The plasma levels of sFKN were significantly increased in UAP patients with plaque rupture compared with patients in the other groups. Multiple logistic regression analysis showed that CD14(+)CD16(+)CX3CR1(+) monocytes and CD3(+)CX3CR1(+) lymphocytes were independent predictors of the presence of ruptured plaque. CONCLUSIONS: Increases in the FKN level and the number of CX3CR1-expressing mononuclear cells might contribute to coronary plaque rupture.
BACKGROUND: Recent studies suggest that fractalkine (FKN or CX3CL1) and its cognate receptor, CX3CR1, play a role in atherogenesis, so the relationship between coronary plaque rupture, as observed by preintervention optical coherence tomography, and plasma levels of FKN and CX3CR1 was investigated in this study. METHODS AND RESULTS: The study population consisted of 46 patients with unstable angina pectoris (UAP), 30 patients with stable angina pectoris, and 25 healthy controls. The UAP patients underwent a preintervention optical coherence tomography study, which revealed that the number of patients with and without plaque rupture at the culprit site was 27 (rupture group) and 19 (non-rupture group), respectively. Plasma levels of soluble FKN (sFKN) and CX3CR1 were measured by enzyme-linked immunosorbent assay and flow cytometry, respectively. The plasma levels of sFKN were significantly increased in UAP patients with plaque rupture compared with patients in the other groups. Multiple logistic regression analysis showed that CD14(+)CD16(+)CX3CR1(+) monocytes and CD3(+)CX3CR1(+) lymphocytes were independent predictors of the presence of ruptured plaque. CONCLUSIONS: Increases in the FKN level and the number of CX3CR1-expressing mononuclear cells might contribute to coronary plaque rupture.
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