title: Inflammation and microvascular dysfunction in cardiac syndrome X patients without conventional risk factors for coronary artery disease.
abstract: OBJECTIVE
  The aim of this study was to ascertain whether coronary microvascular dysfunction (CMD) and inflammation are related in cardiac syndrome X (CSX).
  
  
  BACKGROUND
  CMD can lead to CSX, defined as typical angina and transient myocardial ischemia despite normal coronary arteriograms. Inflammation has been suggested to play a role in the pathogenesis of myocardial ischemia in CSX.
  
  
  METHODS
  We assessed 21 CSX patients (age 52 ± 10 years; 17 women) without traditional cardiovascular risk factors and 21 matched apparently healthy control subjects. Positron emission tomography was used to measure myocardial blood flow (MBF) and coronary flow reserve (CFR) in response to intravenous adenosine, whereas high-sensitivity C-reactive protein (CRP) was measured to assess inflammation. Patients were subdivided a priori into 2 groups according to CRP concentrations at study entry (i.e., ≤3 or >3 mg/l).
  
  
  RESULTS
  There were no differences in resting (1.20 ± 0.23 ml/min/g vs. 1.14 ± 0.20 ml/min/g; p = 0.32) or hyperemic MBF (3.28 ± 1.02 ml/min/g vs. 3.68 ± 0.89 ml/min/g; p = 0.18) between CSX patients and the control group, whereas CFR was mildly reduced in CSX patients compared with the control group (2.77 ± 0.80 vs. 3.38 ± 0.80; p = 0.02). Patients with CRP >3 mg/l had more severe impairment of CFR (2.14 ± 0.33 vs. 3.16 ± 0.76; p = 0.001) and more ischemic electrocardiographic changes during adenosine administration than patients with lower CRP, and a negative correlation between CRP levels and CFR (r = -0.49, p = 0.02) was found in CSX patients.
  
  
  CONCLUSIONS
  CSX patients with elevated CRP levels had a significantly reduced CFR compared with the control group, which is indicative of CMD. Our study thus suggests a role for inflammation in the modulation of coronary microvascular responses in patients with CSX.
authors: Medical Research Council Clinical Sciences Centre and National Heart and Lung Institute, Imperial College School of Medicine, London, United Kingdom.
authors: Alejandro
authors: A
authors: Recio-Mayoral
authors: Ornella E
authors: OE
authors: Rimoldi
authors: Paolo G
authors: PG
authors: Camici
authors: Juan Carlos
authors: JC
authors: Kaski
mesh_terms: D000241:Adenosine; D000328:Adult; D000704:Analysis of Variance; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D016022:Case-Control Studies; D003326:Coronary Circulation; D004562:Electrocardiography; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000150:complications* / Q000276:immunology; D018836:Inflammation Mediators / Q000097:blood; D008297:Male; D008833:Microcirculation; D017566:Microvascular Angina / Q000097:blood / Q000209:etiology* / Q000276:immunology / Q000503:physiopathology; D055806:Microvessels / Q000503:physiopathology*; D008875:Middle Aged; D055414:Myocardial Perfusion Imaging / Q000379:methods; D049268:Positron-Emission Tomography; D012307:Risk Factors; D015854:Up-Regulation; D014665:Vasodilator Agents
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators; D014665:Vasodilator Agents; D002097:C-Reactive Protein; D000241:Adenosine