Relationship between hypercholesterolemia, lipid-lowering therapy and coronary flow velocity reserve evaluated by stress transesophageal echocardiography in patients with a negative coronary angiogram.
The coronary flow velocity reserve (CFR) depends not only on vascular, extravascular, and rheological factors, but also on metabolic factors, such as the cholesterol level. The aim of the present study was to examine the relationship between hypercholesterolemia, the application or not of 6 months lipid-lowering therapy, and the CFR evaluated by pharmacological stress transesophageal echocardiography (PSTEE) in patients without major coronary artery disease.


METHODS
Sixty-nine patients with a negative coronary angiogram were enrolled in the study. Thirty-two of these patients received lipid-lowering therapy, while 37 did not. The CFR was measured by means of dipyridamole PSTEE in all cases, and was calculated as the ratio of posthyperemic to basal peak diastolic flow velocities.


RESULTS
Of the 32 patients who received lipid-lowering medication, the cholesterol level was normal in 16 cases (CFR 2.47 +/- 0.88), while it remained increased in 16 patients (CFR 2.18 +/- 0.67) at the time of the examination. The 7 patients who did not participate in lipid-lowering therapy and who exhibited an increased cholesterol level were also examined (CFR 2.03 +/- 0.88). In 30 patients with normal cholesterol level, who did not receive any lipid-lowering medication, the CFR was significantly increased compared to cases with an increased level (CFR 2.65 +/- 0.79).


CONCLUSIONS
It may be stated that in the patients who did not receive lipid-lowering medication and who displayed normocholesterolemia, the CFR evaluated by means of PSTEE was significantly higher than in the patients who had an increased cholesterol level.
Nemes
Attila
A
2nd Department of Medicine and Cardiology Center, Albert Szent-Györgyi Medical and Pharmaceutical Center, University of Szeged, Szeged, Hungary. nemes@in2nd.szote.u-szeged.hu
Neu
Klára
K
Forster
Tamás
T
Gruber
Noémi
N
Csanády
Miklós
M
D000328:Adult; D000368:Aged; D000924:Anticholesteremic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001783:Blood Flow Velocity / Q000187:drug effects; D002784:Cholesterol / Q000097:blood; D017023:Coronary Angiography; D003326:Coronary Circulation / Q000187:drug effects*; D003327:Coronary Disease / Q000150:complications / Q000000981:diagnostic imaging / Q000503:physiopathology*; D004176:Dipyridamole / Q000008:administration & dosage; D025401:Echocardiography, Stress; D017548:Echocardiography, Transesophageal; D005229:Fatty Acids, Monounsaturated / Q000494:pharmacology* / Q000627:therapeutic use; D005260:Female; D000077340:Fluvastatin; D006801:Humans; D006937:Hypercholesterolemia / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D007211:Indoles / Q000494:pharmacology* / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D014665:Vasodilator Agents / Q000008:administration & dosage
D000924:Anticholesteremic Agents; D005229:Fatty Acids, Monounsaturated; D007211:Indoles; D014665:Vasodilator Agents; D000077340:Fluvastatin; D004176:Dipyridamole; D002784:Cholesterol