title: Impact of heterogeneity of human peripheral blood monocyte subsets on myocardial salvage in patients with primary acute myocardial infarction.
abstract: OBJECTIVE
  We examined whether distinct monocyte subsets contribute in specific ways to myocardial salvage in patients with acute myocardial infarction (AMI).
  
  
  BACKGROUND
  Recent studies have shown that monocytes in human peripheral blood are heterogeneous.
  
  
  METHODS
  We 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.
  
  
  RESULTS
  Circulating 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.
  
  
  CONCLUSIONS
  The 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.
authors: Department of Cardiovascular Medicine, Wakayama Medical University, 811-1 Kimiidera, Wakayama City, Wakayama, Japan.
authors: Hiroto
authors: H
authors: Tsujioka
authors: Toshio
authors: T
authors: Imanishi
authors: Hideyuki
authors: H
authors: Ikejima
authors: Akio
authors: A
authors: Kuroi
authors: Shigeho
authors: S
authors: Takarada
authors: Takashi
authors: T
authors: Tanimoto
authors: Hironori
authors: H
authors: Kitabata
authors: Keishi
authors: K
authors: Okochi
authors: Yu
authors: Y
authors: Arita
authors: Kohei
authors: K
authors: Ishibashi
authors: Kenichi
authors: K
authors: Komukai
authors: Hideaki
authors: H
authors: Kataiwa
authors: Nobuo
authors: N
authors: Nakamura
authors: Kumiko
authors: K
authors: Hirata
authors: Atsuhsi
authors: A
authors: Tanaka
authors: Takashi
authors: T
authors: Akasaka
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015906:Angioplasty, Balloon, Coronary / Q000379:methods*; D017023:Coronary Angiography; D004562:Electrocardiography; D005260:Female; D005434:Flow Cytometry; D005500:Follow-Up Studies; D006801:Humans; D018950:Lipopolysaccharide Receptors / Q000097:blood* / Q000276:immunology; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology*; D009203:Myocardial Infarction / Q000175:diagnosis / Q000276:immunology* / Q000628:therapy; D009206:Myocardium / Q000276:immunology / Q000473:pathology*; D009336:Necrosis / Q000097:blood / Q000276:immunology / Q000473:pathology; D011379:Prognosis; D017452:Receptors, IgG / Q000097:blood* / Q000276:immunology; D013997:Time Factors
chemical_list: D018950:Lipopolysaccharide Receptors; D017452:Receptors, IgG