Improving Arterial Wall Characteristics in Patients After Myocardial Infarction with a Very Low Dose of Fluvastatin and Valsartan: A Proof-of-Concept Study.

BACKGROUND We tested the concept of improving arterial wall characteristics by treatment with a very low-dose combination of fluvastatin and valsartan (low-flu/val) in stable, post-myocardial infarction (MI) patients. MATERIAL AND METHODS We enrolled 36 post-MI middle-aged males in the treatment (n=20) or control (n=16) group receiving low-flu/val (10 mg/20 mg) or placebo, respectively. The parameters of endothelial function (flow-mediated dilatation (FMD), reactive hyperemia index), and arterial stiffness (carotid-femoral pulse wave velocity (cf-PWV), local carotid PWV, and beta stiffness coefficient) were measured before and after 30 days of therapy, and 10 weeks later. RESULTS Treatment with low-flu/val improved FMD from 3.1±1.3% to 4.8±1.5% (p<0.001; by 54.8%) and cf-PWV from 7.8±1.1 to 6.7±1.5 m/s (p<0.01; by 14.1%) without affecting either lipids or blood pressure. In the treatment group, FMD and/or cf-PWV significantly improved in 17 patients, but the improvements did not correlate. The benefits obtained were still detectable 10 weeks after complete treatment cessation. No changes were obtained in the control group. No other vascular parameters changed. CONCLUSIONS Low-flu/val added "on top of" optimal therapy substantially improves endothelial function and arterial stiffness in post-MI patients. Since these improved parameters are well-known predictors of future coronary events, such treatment could decrease cardiovascular risk. Further studies are therefore warranted.

A Combination of Low Doses of Fluvastatin and Valsartan Decreases Arterial Stiffness in Patients After Myocardial Infarction: A Pilot Study.

BACKGROUND: Despite optimum treatment, patients who experience myocardial infarction are still at high risk for future events. OBJECTIVE: We evaluated the effect of 30 days of treatment with combination of low, subtherapeutic doses of fluvastatin and valsartan on arterial stiffness in patients after myocardial infarction, a therapy that has not been used yet. METHODS: Fourteen male patients with a history of myocardial infarction were enrolled into a pilot double-blind randomized controlled study. They were allocated to receive 10 mg fluvastatin and 20 mg valsartan or placebo for 30 days in addition to their regular pharmacotherapy. Carotid-femoral pulse wave velocity was measured on inclusion, after 30 days, and after 3 months. RESULTS: Mean (SD) carotid-femoral pulse wave velocity decreased significantly in the treatment group after 30 days and persisted at lower values after 3 months (from 8.4 [1.5] m/sec to 7.3 [1.1] m/sec to 7.2 [0.8] m/sec; P < 0.05). The 95% CI for decrease after 30 days in the treatment group was 0.5-1.6. Only nonsignificant changes were observed in the control group. Serum lipid levels and arterial blood pressure did not change significantly in any group. CONCLUSIONS: The treatment resulted in a significant and sustained improvement of arterial stiffness in male patients with a history of myocardial infarction, which highlights the need for further study of this new approach.