کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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1970804 | 1538901 | 2009 | 5 صفحه PDF | دانلود رایگان |

BackgroundCD163 is a scavenger receptor for the uptake of haptoglobin–hemoglobin (Hpt–Hb) complexes. The Hpt–Hb complexes are being formed in the plaque in response to intraplaque hemorrhage, a hallmark of atherosclerotic plaque instability. We therefore investigated whether soluble CD163 (sCD163) was elevated in patients with an acute coronary syndrome.MethodsAll subjects presenting with chest pain suggestive of myocardial ischemia referred to either the emergency department or the coronary care unit were included in a prospective follow-up study. Plasma was collected and frozen at − 80 °C until assayed. sCD163 was measured using a commercially available Elisa assay.ResultsOf 526 included chest pain patients, the final diagnosis was non-cardiac chest pain in 244 (46%) patients, non-STEMI in 67 (13%), and STEMI in 215 (41%). The non-STEMI patients were older, used more medication, had undergone more often coronary interventions, but did not differ with respect to risk factors, except for a higher incidence in dyslipidemia. Unexpectedly, sCD163 did not differentiate between patients with non-STEMI or STEMI and the non-cardiac chest pain patients (2.09 ± 0.76 versus 2.24 ± 0.86).ConclusionAlthough ACS is characterized by intraplaque hemorrhage, the amount of intraplaque Hb release seems not to be substantial enough to result in a measurable difference in sCD163.
Journal: Clinical Biochemistry - Volume 42, Issues 16–17, November 2009, Pages 1662–1666