cerivastatin has been researched along with Cardiomyopathy--Dilated* in 2 studies
1 trial(s) available for cerivastatin and Cardiomyopathy--Dilated
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Beneficial effects of statins in patients with non-ischemic heart failure.
HMG CoA reductase inhibitors (statins) may exert a wide array of cholesterol independent effects including antihypertrophic effects on the heart. Their role in the treatment of heart failure has not been studied.. 15 patients with heart failure NYHA II-III based on non-ischemic dilated cardiomyopathy were randomized in a double-blind study to 0.4 mg cerivastatin or placebo for an average treatment period of 20 weeks. Quality of life and exercise capacity increased significantly in the statin treatment but not in the placebo group (Minnesota Living with Heart Failure Questionnaire, 6 min walking test). Concomitantly, there was a trend towards increased left ventricular ejection fraction (radionuclear ventriculography) and improved endothelial function (forearm blood flow). Statins decreased plasma concentrations of troponine T, high sensitive C-reactive protein (hsCRP), plasminogen activator inhibitor-1 (PAI-1) and tumor necrosis factor alpha (TNFalpha).. Statins induce beneficial effects in patients with non-ischemic cardiomyopathy leading to improvement of quality of life and exercise capacity disclosing a promising novel treatment strategy for patients with heart failure. Topics: Anticholesteremic Agents; Cardiomyopathy, Dilated; Double-Blind Method; Exercise Test; Female; Heart Failure; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Inflammation Mediators; Male; Middle Aged; Prospective Studies; Pyridines; Quality of Life; Stroke Volume; Treatment Outcome | 2004 |
1 other study(ies) available for cerivastatin and Cardiomyopathy--Dilated
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[TPM1 gene mutation is associated with dilated cardiomyopathy in Kazaks in Xinjiang].
Detect the relationship between TPM1 gene mutations and dilated cardiomyopathy (DCM) of Kazaks and Hans in Xinjiang.. TPM1 gene was screened from 31 family members in a Kazak family with familiar DCM (FDCM), 100 patients with idiopathic DCM (IDCM, 50 Kazaks and 50 Hans), and in 100 healthy controls (50 Kazaks and 50 Hans). All the samples were the inpatients or outpatients of First Affiliated Hospital of Xinjiang University from 2012 to 2014. PCR was used to amplify 9 exons and nearby introns of the TPM1 gene. The amplified products were sequenced and compared with the standard sequence with CHROMAS software and BLAST software in Pubmed to identify mutation sites. The relationship between TPM1 gene mutations in the Kazak IDCM and healthy volunteers, between Han and Kazak IDCM and healthy volunteers was analyzed. Tropomyosin was qualitatively and quantitatively detected by ELISA in all subjects.. A novel variant (c.524 G > T) was identified in two FDCM patients at exon 3, this mutation caused an amino acid substitution, Gln111His. The FDCM, IDCM from Kazak and Han, healthy volunteers from Kazak and Han were founded a rs1071646 (c.644C > A, Ala151Ala). There was a significant difference in the genotype distribution (χ(2) = 13.36, P = 0.001) and allele frequency (χ(2) = 10.25, P = 0.001) between Kazaks with IDCM and Kazak controls of rs1071646, while these parameters were similar between Han IDCM patients and Han controls (all P > 0.05). The tropomyosin content of Kazak and Han IDCM patients were significantly lower than Kazak and Han controls ((1 764.2 ± 350.9) ng/L vs. (2 369.7 ± 345.9) ng/L, P = 0.001).. TPM1 gene of rs1071646 polymorphism is a possible independent risk factor for IDCM in Kazaks but not Han Chinese. Topics: Cardiomyopathy, Dilated; Exons; Gene Frequency; Genotype; Humans; Mutation; Polymorphism, Genetic; Pyridines; Risk Factors; Tropomyosin | 2015 |