title: Coronary circulatory function in patients with the metabolic syndrome.
abstract: The metabolic syndrome affects 25% of the U.S. population and greatly increases the risk of diabetes and coronary artery disease (CAD). We tested the hypothesis that the metabolic syndrome is associated with impaired coronary vasodilator function, a marker of atherosclerotic disease activity.
  
  
  METHODS
  Four hundred sixty-two patients at risk for CAD, as defined by a low-density lipoprotein cholesterol ≥ 160 mg/dL with fewer than 2 coronary risk factors, a low-density lipoprotein cholesterol ≥ 130 mg/dL with 2 or more coronary risk factors, or with documented CAD were included. A subset of 234 individuals underwent repeated PET at 1 y. Myocardial blood flow (MBF) and vasodilator reserve were assessed by PET. Modified criteria of the National Cholesterol Education Program, Adult Treatment Panel III were used to characterize the metabolic syndrome.
  
  
  RESULTS
  Adenosine- and cold-stimulated MBF were similar in patients with and without metabolic syndrome, whereas baseline MBF showed a stepwise increase with increasing features of the syndrome. Consequently, patients with metabolic syndrome showed a lower coronary flow reserve (CFR) (2.5 ± 1.0) than those without metabolic syndrome (3.0 ± 0.9, P = 0.004). Differences in CFR were no longer present after correcting rest flows for the rate-pressure product. Change in MBF and CFR at 1 y were not different across groups of patients with increasing features of the metabolic syndrome.
  
  
  CONCLUSIONS
  Patients with metabolic syndrome demonstrate impaired CFR, which is related to the augmentation in resting coronary blood flow caused by hypertension. In high-risk individuals, peak adenosine- and cold-stimulated blood flows are impaired even in the absence of the metabolic syndrome.
authors.affiliation: Departments of Medicine Cardiology and Radiology, and Division of Nuclear Medicine and Molecular Imaging, Brigham and Women's Hospital, Harvard Medical School, Boston Massachusetts, USA. mdicarli@partners.org
authors.forename: Marcelo F
authors.initials: MF
authors.lastname: Di Carli
authors.forename: David
authors.initials: D
authors.lastname: Charytan
authors.forename: Graham T
authors.initials: GT
authors.lastname: McMahon
authors.forename: Peter
authors.initials: P
authors.lastname: Ganz
authors.forename: Sharmila
authors.initials: S
authors.lastname: Dorbala
authors.forename: Heinrich R
authors.initials: HR
authors.lastname: Schelbert
mesh_terms: D000081:Acetamides; D000085:Acetates / Q000627:therapeutic use; D000241:Adenosine; D000293:Adolescent; D000328:Adult; D000368:Aged; D000924:Anticholesteremic Agents / Q000627:therapeutic use; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D015331:Cohort Studies; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging; D003326:Coronary Circulation / Q000502:physiology*; D003627:Data Interpretation, Statistical; D004311:Double-Blind Method; D005260:Female; D053805:Fractional Flow Reserve, Myocardial; D006801:Humans; D008297:Male; D024821:Metabolic Syndrome / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D008875:Middle Aged; D017395:Plasminogen Activator Inhibitor 1 / Q000378:metabolism; D049268:Positron-Emission Tomography; D012307:Risk Factors; D013449:Sulfonamides; D013451:Sulfonic Acids / Q000627:therapeutic use; D014655:Vascular Resistance / Q000502:physiology; D014665:Vasodilator Agents; D055815:Young Adult
chemical_list: D000081:Acetamides; D000085:Acetates; D000924:Anticholesteremic Agents; D017395:Plasminogen Activator Inhibitor 1; D013449:Sulfonamides; D013451:Sulfonic Acids; D014665:Vasodilator Agents; C423185:avasimibe; D002097:C-Reactive Protein; D002784:Cholesterol; D000241:Adenosine