title: Reduced coronary flow reserve in hypercholesterolemic patients without overt coronary stenosis.
abstract: BACKGROUND
  Reduced coronary flow reserve (CFR) in hypercholesterolemic patients without evidence of ischemia has been reported. However, it remains uncertain whether this abnormality occurs without overt coronary atherosclerosis. This study aimed to clarify whether CFR is impaired even in anatomically normal coronary arteries in hypercholesterolemic patients and to compare CFR between familial hypercholesterolemic (FH) patients and secondary hypercholesterolemic (SH) patients.
  
  
  RESULTS
  Twenty-two patients with hypercholesterolemia (11 FH, 11 SH) and 11 control subjects were studied. Baseline myocardial blood flow (MBF) and MBF during dipyridamole loading were measured in segments perfused by angiographically normal coronary arteries with the use of positron emission tomography and 13N-ammonia, and CFR was calculated. Baseline MBF (mL/min per 100 g heart wt) in FH (81.3 +/- 31.4) and SH (70.0 +/- 20.7) patients was not different from that in control subjects (75.0 +/- 34.9). However, MBF during dipyridamole loading was significantly lower in FH patients (129 +/- 19.1) than in control subjects (322 +/- 174, P < .01) and SH patients (210 +/- 71.2, P < .01). CFR in FH patients (1.59 +/- 0.41) was also significantly lower compared with both control subjects (4.22 +/- 1.42, P < .01) and SH patients (3.00 +/- 0.96, P < .01). CFR in SH patients was also significantly lower than that in control subjects (P < .05). CFR correlated significantly with both plasma total cholesterol (r = .67, P < .01) and LDL cholesterol concentrations (r = .69, P < .01).
  
  
  CONCLUSIONS
  CFR was decreased even in anatomically normal coronary arteries in hypercholesterolemic patients. This abnormality was more prominent in FH patients.
authors.affiliation: Second Department of Internal Medicine, University of Tokyo, Japan.
authors.forename: I
authors.initials: I
authors.lastname: Yokoyama
authors.forename: T
authors.initials: T
authors.lastname: Ohtake
authors.forename: S
authors.initials: S
authors.lastname: Momomura
authors.forename: J
authors.initials: J
authors.lastname: Nishikawa
authors.forename: Y
authors.initials: Y
authors.lastname: Sasaki
authors.forename: M
authors.initials: M
authors.lastname: Omata
mesh_terms: D001794:Blood Pressure; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D002932:Cineangiography; D017023:Coronary Angiography; D003326:Coronary Circulation / Q000187:drug effects; D003327:Coronary Disease; D003331:Coronary Vessels / Q000187:drug effects / Q000502:physiology / Q000503:physiopathology*; D004176:Dipyridamole / Q000494:pharmacology; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D006937:Hypercholesterolemia / Q000097:blood / Q000503:physiopathology*; D006938:Hyperlipoproteinemia Type II / Q000097:blood / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology / Q000503:physiopathology; D012016:Reference Values; D014055:Tomography, Emission-Computed; D014280:Triglycerides / Q000097:blood
chemical_list: D002784:Cholesterol; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D004176:Dipyridamole; D006442:Glycated Hemoglobin; D014280:Triglycerides