on June 15, 2009
Published online before print June 15, 2009, doi: 10.1161/CIRCULATIONAHA.108.806877
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Submitted on July 23, 2008
From the Department of Molecular Medicine and Surgery (A.M.J., K.C.), Karolinska Institutet, Stockholm, Sweden; Department of Clinical Physiology (K.C.) and Cardiology (M.H.), Sahlgrenska University Hospital, Göteborg, Sweden; and AstraZeneca R&D, Mölndal (M.H.), Sweden; Research Institute for Internal Medicine (P.A., T.U., C.S.) and Section of Clinical Immunology and Infectious Diseases (P.A.), Rikshospitalet University Hospital, Oslo, Norway; Faculty Division Akershus University Hospital, University of Oslo, Oslo, Norway; and Department of Medicine (T.O), Akershus University Hospital, Lørenskog, Norway. * To whom correspondence should be addressed. E-mail: kenneth.caidahl{at}ki.se.
Background—CXCL16/SR-PSOX is an interferon- Methods and Results—We assessed the association between circulating CXCL16 levels obtained within 24 hours after admission and time to death in 1351 patients (median age 67 years, 30% female) with a diagnosis of unstable angina, non–ST-segment–elevation myocardial infarction, or ST-segment–elevation myocardial infarction. During a median follow-up time of 81 months, 377 patients died. Increased levels of CXCL16 were prognostically unfavorable; the fourth versus first quartile was associated with higher risk of death (hazard ratio 2.1; 95% CI 1.6 to 2.8; P<0.0001), triple risk of developing heart failure (hazard ratio 3.0; 95% CI 1.8 to 5.1; P<0.0001), and a doubling of the risk of rehospitalization for myocardial infarction (hazard ratio 2.1; 95% CI 1.3 to 3.3; P=0.002). After adjustment for conventional risk markers, logarithmically transformed CXCL16 level remained a strong independent indicator of long-term mortality (hazard ratio 1.21; 95% CI 1.09 to 1.36 per 1 SD increase in CXCL16; P=0.0006) and congestive heart failure development (hazard ratio 1.25; 95% CI 1.05 to 1.48; P=0.01). In a subsample of 714 patients, after further adjustment for troponin T, high-sensitive C-reactive protein, pro–B-type natriuretic peptide, and left ventricular ejection fraction, CXCL16 still provided significant additional prognostic information on mortality (hazard ratio 1.21; 95% CI 1.02 to 1.42 per 1 SD increase in CXCL16; P=0.02). Conclusions—In patients with an acute coronary syndrome, CXCL16 levels obtained within 24 hours of admission are associated with long-term mortality after adjustment for other risk factors.
Accepted on May 6, 2009
Soluble CXCL16 Predicts Long-Term Mortality in Acute Coronary Syndromes
Anna M. Jansson MD,
–regulated chemokine and scavenger receptor for oxidized low-density lipoprotein that is expressed in atherosclerotic lesions. Proteolytic cleavage of membrane-bound CXCL16 releases soluble CXCL16, which may promote migration of effector T cells and augment a proatherogenic inflammatory response. We hypothesized that soluble CXCL16 concentrations are associated with long-term outcome in patients with acute coronary syndromes.
Key words: angina pectoris • peptides, natriuretic B-type • proteins, C-reactive • echocardiography • myocardial infarction • prognosis
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