Key result
Atorvastatin 20 mg/day significantly improved exercise VO2 tau and flow-mediated dilatation, and reduced CRP levels compared to placebo in post-myocardial infarction patients.
Why the study?
Does atorvastatin improve exercise oxygen uptake kinetics in normocholesterolaemic post-myocardial infarction patients?
RCT (n=18)
Double-blind
crossover
Does atorvastatin improve exercise oxygen uptake kinetics in normocholesterolaemic post-myocardial infarction patients?
Atorvastatin therapy improves exercise oxygen uptake kinetics and endothelial function in normocholesterolemic patients shortly after an uncomplicated myocardial infarction.
Answers are grounded in this paper and cite their sources.
Supports atorvastatin post-MI irrespective of lipid levels; extends RCT evidence for pleiotropic benefits on endothelial function and exercise kinetics.
BACKGROUND: Statins represent a modern mainstay of the drug treatment of coronary artery disease and acute coronary syndromes. Reduced aerobic work performance and slowed VO(2) kinetics are established features of the clinical picture of post-myocardial infarction (MI) patients. We tested the hypothesis that statin therapy improves VO(2) exercise performance in normocholesterolaemic post-MI patients. MATERIALS AND METHODS: According to a double-blinded, randomized, crossover and placebo-controlled study design, in 18 patients with uncomplicated recent (3 days) MI we investigated the effects of atorvastatin (20 mg day(-1)) on gas exchange kinetics by calculating VO(2) effective time constant (tau) during a 50-watt constant workload exercise, brachial artery flow-mediated dilatation (FMD) as an index of endothelial function, left ventricular function (echocardiography) and C-reactive protein (CRP, as an index of inflammation). Atorvastatin or placebo was given for 3 months each. RESULTS: Atorvastatin therapy significantly improved exercise VO(2) tau and FMD, and reduced CRP levels. We did not observe changes in cardiac contractile function and relaxation properties during all study periods in either group. CONCLUSIONS: In post-MI patients exercise performance is a potential additional target of benefits related to statin therapy. Endothelial function improvement is very likely implicated in this newly described therapeutic property.
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Guazzi et al. (2007) conducted an RCT in post-myocardial infarction (n=18). Atorvastatin vs. Placebo was evaluated on VO(2) effective time constant (tau) during a 50-watt constant workload exercise, brachial artery flow-mediated dilatation (FMD), left ventricular function, and C-reactive protein (CRP). Atorvastatin 20 mg/day significantly improved exercise VO2 tau and flow-mediated dilatation, and reduced CRP levels compared to placebo in post-myocardial infarction patients.
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