Atorvastatin improve left ventricular hypertrophy and endothelial function in clinical research.docVIP
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Atorvastatin improve left ventricular hypertrophy and endothelial function in clinical research
PAGE \* MERGEFORMAT 12
Atorvastatin improve left ventricular hypertrophy and endothelial function in clinical research
Study: Pan Fu Rong, Xie Kejian, Pan Ping, Cai strong army, Sen Tseng
[Abstract] Objective: To investigate the treatment of atorvastatin on left ventricular hypertrophy (LVH) in patients with circulating plasma endothelin (ET) and nitric oxide (NO). Methods: 80 patients with LVH were randomized into atorvastatin the treatment group of 40 patients (atorvastatin 10 mg day 1) and 40 conventional treatment group, compared before and after 6 months of treatment cycles blood ET, NO levels and left ventricular mass index (LVMI). Results: After treatment conventional treatment group and atorvastatin group were significantly lower than ET and LVMI before treatment (P lt;0.05, P lt;0.01), NO was significantly higher than before treatment (P lt;0.05 or P lt;0.01); with the conventional treatment group after treatment , atorvastatin group ET, LVMI was significantly reduced, and NO increased more (P lt;0.05). Conclusion: LVH patients with atorvastatin treatment can further improve vascular endothelial function and left ventricular hypertrophy, suggesting that in the traditional buck drugs based on the use of atorvastatin treatment on LVH in patients with greater benefits.
[Keywords:] atorvastatin; essential hypertension; left ventricular hypertrophy; nitric oxide; ET
Essential hypertension (essential hypertension, EH) patients with varying degrees of endothelial dysfunction, its causes endothelin (endothelin, ET) and nitric oxide (nitric oxide, NO) metabolic imbalance may be involved in the pathophysiology of EH , in particular the formation of LVH much attention [1]. statin drugs are widely used in clinical disorders of lipid metabolism in a class of powerful lipid-lowering drugs. Recent studies show that [2-3], it has more species independent of the cardiovascular protective effects beyond lipid lowering, but the exact mechanism is still not v
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