Copyright © 2004 by the European Society of Cardiology.
Clinical research
Impaired myocardial vasodilatation during hyperaemic stress is improved by simvastatin but not by pravastatin in patients with hypercholesterolaemia
a Department of Cardiovascular Medicine, Sanno Hospital, International University of Health and Welfare, 8-10-16 Akasaka, Minato-ku, Tokyo 107-0052, Japan
b Department of Cardiovascular Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan
c Department of Radiology, Institute of Medical Science, University of Tokyo, Tokyo, Japan
d Department of Clinical Engineering, Faculty of Medical Engineering, Suzuka University of Medical Science, Suzuka, Japan
e Department of Radiology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan
Received September 1, 2003;
revised February 1, 2004;
accepted February 18, 2004
* Corresponding author. Tel.: +81-3-3402-3151; fax: +81-3-3404-3652
E-mail address: yokochan-tky{at}umin.ac.jp
Aims Impaired myocardial vasodilatation during hyperaemic stress with dipyridamole has been documented in hypercholesterolaemics without evidence of ischaemia. This study investigated whether two commonly used hydroxymethylglutaryl coenzyme A reductase inhibitors, simvastatin and pravastatin, are equally effective in restoring myocardial vasodilatation.
Methods and results Forty-four hypercholesterolaemics with a low probability of coronary artery disease and 22 controls were studied. Before and after lipid-lowering therapy with simvastatin (
) or pravastatin (), myocardial blood flow at rest and during dipyridamole loading was measured using positron emission tomography with [13N]ammonia, and myocardial vasodilatation was assessed. Treatments with simvastatin and pravastatin similarly reduced plasma total cholesterol and plasma low-density lipoprotein cholesterol. Resting myocardial blood flow was comparable in the controls, simvastatin group, and pravastatin group and unchanged after therapy. Myocardial blood flow during dipyridamole loading and myocardial vasodilatation was lower in the two therapy groups before treatment than in the controls. These parameters improved significantly after therapy with simvastatin, whereas no improvement was observed after pravastatin therapy. The per cent change in myocardial vasodilatation after simvastatin therapy was significantly and inversely correlated with per cent changes in plasma lipid fractions.
Conclusion Diminished myocardial vasodilatation in hypercholesterolaemics is improved by simvastatin but not by pravastatin, suggesting differences in vascular effects among statins.
Key Words: Hypercholesterolaemia • Simvastatin • Pravastatin • Coronary circulation • Positron emission tomography
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