title: Improvement in coronary flow reserve determined by positron emission tomography after 6 months of cholesterol-lowering therapy in patients with early stages of coronary atherosclerosis.
abstract: BACKGROUND
  Early stages of coronary atherosclerosis are characterized by a mainly functional impairment of coronary vasodilator capacity under the impact of such risk factors as hypercholesterolemia. The goal of this study was to determine whether 6-month cholesterol-lowering therapy improves coronary flow reserve in patients with angina, reduced flow reserve despite minimally diseased coronary vessels or even normal angiogram, and mild to moderately elevated LDL levels on average.
  
  
  RESULTS
  We noninvasively investigated 23 consecutive patients (18 men, 5 women; mean age, 56+/-7.6 years) with a mean LDL level of 165+/-34 mg/dL at baseline by PET for myocardial blood flow measurement with [13N]ammonia at rest and under dipyridamole stress (0.56 mg/kg) before and after lipid-lowering therapy with simvastatin for 6 months. Between baseline and the 6-month follow-up, total cholesterol concentration fell from 241+/-44 to 168+/-34 mg/dL, and the LDL level decreased from 165+/-34 to 95+/-26 mg/dL (P<0.001). Overall, coronary flow reserve increased from 2.2+/-0.6 to 2.64+/-0.6 (P<0.01). Maximal coronary flow increased significantly from 182+/-36 to 238+/-58 mL/minx100 g (P<0.001) at follow-up. Minimum coronary resistance declined significantly from 0. 51+/-0.12 to 0.40+/-0.14 mm Hg. mL-1. minx100 g (P<0.001). Concomitantly, a regression of anginal symptoms was observed in most patients.
  
  
  CONCLUSIONS
  Our results suggest that cholesterol-lowering therapy with simvastatin may improve overall coronary vasodilator capacity assessed noninvasively by PET in patients with mild to moderate hypercholesterolemia. Consequently, intensive lipid-lowering therapy is considered a vasoprotective treatment for selected patients in very early stages of coronary atherosclerosis with the potential of preventing further disease progression.
authors.affiliation: Department of Cardiology, Heart Center Northrhine-Westphalia, Ruhr-University Bochum, Bad Oeynhausen, Germany.
authors.forename: D
authors.initials: D
authors.lastname: Baller
authors.forename: G
authors.initials: G
authors.lastname: Notohamiprodjo
authors.forename: U
authors.initials: U
authors.lastname: Gleichmann
authors.forename: J
authors.initials: J
authors.lastname: Holzinger
authors.forename: R
authors.initials: R
authors.lastname: Weise
authors.forename: J
authors.initials: J
authors.lastname: Lehmann
mesh_terms: D000328:Adult; D000368:Aged; D000787:Angina Pectoris / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000503:physiopathology; D000924:Anticholesteremic Agents / Q000627:therapeutic use*; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology*; D003326:Coronary Circulation / Q000187:drug effects / Q000502:physiology*; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D019821:Simvastatin / Q000627:therapeutic use*; D013997:Time Factors; D014055:Tomography, Emission-Computed; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology
chemical_list: D000924:Anticholesteremic Agents; D008055:Lipids; D019821:Simvastatin