title: Coronary microvascular dysfunction is associated with higher frequency of thin-cap fibroatheroma.
abstract: OBJECTIVE
  Both coronary microvascular dysfunction and epicardial plaque vulnerability have been associated with adverse cardiovascular outcomes. However, whether microvascular dysfunction is a predictor of plaque vulnerability is not known. We hypothesized that microvascular dysfunction is associated with greater systemic inflammation and is a predictor of virtual histology-intravascular ultrasound (VH-IVUS)-defined coronary thin-cap fibroatheromas.
  
  
  METHODS
  Invasive physiologic assessment and VH-IVUS were performed and serum high-sensitivity C-reactive protein (hs-CRP) was measured in 51 patients with non-obstructive CAD [fractional flow reserve (FFR)≥0.75]. Microvascular dysfunction was defined as coronary flow velocity reserve (CFVR)<2.0. Lumen area and plaque burden and composition were assessed in each VH-IVUS frame. Frequency of thin-cap fibroatheroma (TCFA) in each artery was defined as the percentage of VH-IVUS frames with plaque burden≥40% and confluent necrotic core≥10% in contact with lumen for at least 3 consecutive frames.
  
  
  RESULTS
  Mean age was 57±12 years and 25% of patients presented with acute coronary syndrome. Despite similar amount of epicardial disease, characterized by lumen area (8.9±3.0 vs. 10.1±3.3mm(2), p=0.3) and FFR (0.90±0.08 vs. 0.92±0.07, p=0.2), patients with microvascular dysfunction had greater hs-CRP (4.2 [2.3, 7.6] vs. 1.0 [0.4, 4.2]ng/ml, p=0.006), greater plaque burden (47±10 vs. 36±13%, p=0.004), and higher frequency of TCFA (17±25 vs. 6±9%, p=0.02). After adjustment for cardiovascular risk factors, hs-CRP, and plaque burden, coronary microvascular dysfunction was an independent predictor of frequency of TCFA (β=+0.42, p=0.033).
  
  
  CONCLUSIONS
  In patients with non-obstructive CAD, coronary microvascular dysfunction is associated with higher serum hs-CRP and is an independent predictor of more TCFAs, a marker for increased epicardial plaque vulnerability.
authors: Division of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA, United States.
authors: Saurabh S
authors: SS
authors: Dhawan
authors: Michel T
authors: MT
authors: Corban
authors: Ravi A
authors: RA
authors: Nanjundappa
authors: Parham
authors: P
authors: Eshtehardi
authors: Michael C
authors: MC
authors: McDaniel
authors: Collins A
authors: CA
authors: Kwarteng
authors: Habib
authors: H
authors: Samady
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D001783:Blood Flow Velocity; D002097:C-Reactive Protein / Q000032:analysis; D003324:Coronary Artery Disease / Q000097:blood / Q000000981:diagnostic imaging / Q000473:pathology* / Q000503:physiopathology; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000000981:diagnostic imaging / Q000473:pathology* / Q000503:physiopathology; D003430:Cross-Sectional Studies; D005260:Female; D005355:Fibrosis; D053805:Fractional Flow Reserve, Myocardial; D005845:Georgia; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D008297:Male; D055806:Microvessels / Q000000981:diagnostic imaging / Q000473:pathology* / Q000503:physiopathology; D008875:Middle Aged; D015999:Multivariate Analysis; D009336:Necrosis; D058226:Plaque, Atherosclerotic; D011379:Prognosis; D018570:Risk Assessment; D012307:Risk Factors; D012720:Severity of Illness Index; D018084:Ultrasonography, Interventional; D015854:Up-Regulation
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators; D002097:C-Reactive Protein