Improvement of impaired myocardial vasodilatation due to diffuse coronary atherosclerosis in hypercholesterolemics after lipid-lowering therapy.
BACKGROUND
Diminished myocardial vasodilatation (MVD) in hypercholesterolemics without overt coronary stenosis has been reported. However, whether the diminished MVD of angiographically normal coronary arteries in hypercholesterolemics can be reversed after lipid-lowering therapy is not known.


RESULTS
A total of 27 hypercholesterolemics and 16 age-matched controls were studied. All patients had >1 normal coronary artery, and those segments that were perfused by anatomically normal coronary arteries were studied. Myocardial blood flow (MBF) was measured during dipyridamole loading and at baseline using positron emission tomography and 13N-ammonia, after which MVD was calculated before and after lipid-lowering therapy. Total cholesterol was significantly higher in hypercholesterolemics (263+/-33.8) than in controls (195+/-16.6), and it normalized after lipid-lowering therapy (197+/-19.9). Baseline MBF (ml. min-1. 100 g-1) was comparable among hypercholesterolemics (both before and after therapy) and controls. MBF during dipyridamole loading was significantly lower in hypercholesterolemics before therapy (189+/-75.4) than in controls (299+/-162, P<0.01). However, MBF during dipyridamole loading significantly increased after therapy (226+/-84.7; P<0.01). MVD significantly improved after therapy in hypercholesterolemics (2.77+/-1.35 after treatment [P<0.05] versus 2. 02+/-0.68 before treatment [P<0.01]), but it remained significantly higher in controls (3.69+/-1.13, P<0.01). There was a significant relationship between the percent change of total cholesterol and the percent change of MVD before and after lipid-lowering therapy (r=-0. 61, P<0.05).


CONCLUSIONS
Diminished MVD of anatomically normal coronary arteries in hypercholesterolemics can be reversed after lipid-lowering therapy.
Departments of Cardiovascular Medicine, Metabolic Diseases, Radiology and Gastroenterology, University of Tokyo, Graduate School of Medicine, Tokyo, Japan.
I
I
Yokoyama
S
S
Momomura
T
T
Ohtake
K
K
Yonekura
W
W
Yang
N
N
Kobayakawa
T
T
Aoyagi
S
S
Sugiura
N
N
Yamada
K
K
Ohtomo
Y
Y
Sasaki
M
M
Omata
Y
Y
Yazaki
D000368:Aged; D003324:Coronary Artery Disease / Q000209:etiology* / Q000503:physiopathology*; D003326:Coronary Circulation / Q000187:drug effects / Q000502:physiology; D003331:Coronary Vessels / Q000503:physiopathology*; D003920:Diabetes Mellitus / Q000503:physiopathology; D004176:Dipyridamole / Q000494:pharmacology; D004562:Electrocardiography; D005260:Female; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D006937:Hypercholesterolemia / Q000150:complications* / Q000188:drug therapy*; D006973:Hypertension / Q000503:physiopathology; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D014664:Vasodilation / Q000502:physiology*; D014665:Vasodilator Agents / Q000494:pharmacology
D000960:Hypolipidemic Agents; D014665:Vasodilator Agents; D004176:Dipyridamole