کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2950879 1577361 2009 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Impact of Heterogeneity of Human Peripheral Blood Monocyte Subsets on Myocardial Salvage in Patients With Primary Acute Myocardial Infarction
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی کاردیولوژی و پزشکی قلب و عروق
پیش نمایش صفحه اول مقاله
Impact of Heterogeneity of Human Peripheral Blood Monocyte Subsets on Myocardial Salvage in Patients With Primary Acute Myocardial Infarction
چکیده انگلیسی

ObjectivesWe examined whether distinct monocyte subsets contribute in specific ways to myocardial salvage in patients with acute myocardial infarction (AMI).BackgroundRecent studies have shown that monocytes in human peripheral blood are heterogeneous.MethodsWe studied 36 patients with primary AMI. Peripheral blood sampling was performed 1, 2, 3, 4, 5, 8, and 12 days after AMI onset. Two monocyte subsets (CD14+CD16−and CD14+CD16+) were measured by flow cytometry. The extent of myocardial salvage 7 days after AMI was evaluated by cardiovascular magnetic resonance imaging as the difference between myocardium at risk (T2-weighted hyperintense lesion) and myocardial necrosis (delayed gadolinium enhancement). Cardiovascular magnetic resonance imaging was also performed 6 months after AMI.ResultsCirculating CD14+CD16−and CD14+CD16+monocytes increased in AMI patients, peaking on days 3 and 5 after onset, respectively. Importantly, the peak levels of CD14+CD16−monocytes, but not those of CD14+CD16+monocytes, were significantly negatively associated with the extent of myocardial salvage. We also found that the peak levels of CD14+CD16−monocytes, but not those of CD14+CD16+monocytes, were negatively correlated with recovery of left ventricular ejection fraction 6 months after infarction.ConclusionsThe peak levels of CD14+CD16−monocytes affect both the extent of myocardial salvage and the recovery of left ventricular function after AMI, indicating that the manipulation of monocyte heterogeneity could be a novel therapeutic target for salvaging ischemic damage.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of the American College of Cardiology - Volume 54, Issue 2, 7 July 2009, Pages 130–138
نویسندگان
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