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Pàgina 1 des de 911 resultats
HMG-CoA reductase inhibitors inhibit endothelial exocytosis and decrease myocardial infarct size.
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Three-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors protect the vasculature from inflammation and atherosclerosis by cholesterol dependent and cholesterol independent mechanisms. We hypothesized that HMG-CoA reductase inhibitors decrease exocytosis of Weibel-Palade bodies,
Improvement of left ventricular remodeling and function by hydroxymethylglutaryl coenzyme a reductase inhibition with cerivastatin in rats with heart failure after myocardial infarction.
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BACKGROUND
Hydroxymethylglutaryl coenzyme A reductase inhibitors (statins) attenuate angiotensin II-induced cellular signaling. Because angiotensin II is involved in left ventricular (LV) remodeling after myocardial infarction (MI), we examined the effects of statin treatment in an experimental
Mesenteric venous thrombosis with bowel infarction and hyperhomocysteinemia due to homozygous methylenetetrahydrofolate reductase C677T genotype.
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The case of a 30-year-old man with bowel infarction due to mesenteric venous thrombosis and multiple risk factors, including mild hyperhomocysteinemia due to methylenetetrahydrofolate reductase C677T polymorphism and recent abdominal surgery, is reported. His clinical manifestation consisted of
Recurrent Myocardial Infarction Despite Normal C-reactive Protein in a Patient with Behcet's Disease and Compound Heterozygous Methylenetetrahydrofolate Reductase (MTHFR) Mutations (C677T and A1298C).
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A 39-year-old diabetic female with Behcet's disease presented with acute inferior wall myocardial infarction and underwent successful angioplasty of the occluded circumflex artery with a bare-metal stent (balancing increased the bleeding risk with Behcet's). Other coronary vessels were free of
Levels of glutathione reductase and glutathione peroxidase of human platelets in unstable angina and myocardial infarction.
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Levels of glutathione peroxidase and glutathione reductase were measured in the platelets of 30 patients, 10 of them affected by unstable angina, 10 of them reperfused after myocardial infarction and 10 matched healthy controls. The specific activities of both the enzymes were lowered in both group
The rs1801133 polymorphism of methylenetetrahydrofolate reductase gene- the association with 5-year survival in patients with ST-elevation myocardial infarction.
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OBJECTIVE
Methylenetetrahydrofolate reductase (MTHFR) is an enzyme involved in endothelial nitric oxide synthase (eNOS) coupling and homocysteine metabolism. The rs1801133 polymorphism of the MTHFR gene affects risk of coronary artery disease. We assessed its influence on 5-year survival of patients
HMG-CoA reductase inhibition prior reperfusion improves reparative fibrosis post-myocardial infarction in a preclinical experimental model.
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BACKGROUND
Studies in patients support a beneficial effect of statin treatment early after acute coronary syndrome and/or prior percutaneous coronary intervention. However, statin effect during total occlusion remains unknown.
OBJECTIVE
To investigate whether infusion of activated simvastatin during
Cost-effectiveness of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor therapy in older patients with myocardial infarction.
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BACKGROUND
3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) therapy has proven efficacy in reducing the rate of coronary and cerebrovascular events in patients 75 years of age or younger with a history of myocardial infarction. However, in patients older than 75 years of age, the
Methionine Sulfoxide Reductase-B3 Risk Allele Implicated in Alzheimer's Disease Associates with Increased Odds for Brain Infarcts.
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Genome-wide association studies identified a single nucleotide polymorphism (SNP) in the MSRB3 gene encoding Methionine Sulfoxide Reductase-B3 (MsrB3) to be associated with the risk for low hippocampal volume and late onset Alzheimer's disease (AD). Subsequently, we identified AD-associated abnormal
Methylenetetrahydrofolate reductase polymorphism, plasma folate, homocysteine, and risk of myocardial infarction in US physicians.
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BACKGROUND
Hyperhomocysteinemia appears to be an independent risk factor for coronary disease. Elevated levels of plasma total homocysteine (tHCY) can result from genetic or nutrient-related disturbances in the transsulfuration or remethylation pathways for homocysteine metabolism. The enzyme
Genetic analysis of thermolabile methylenetetrahydrofolate reductase as a risk factor for myocardial infarction.
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Hyperhomocyst(e)inemia is associated with an increased risk of coronary artery disease and myocardial infarction. Both genetic and environmental factors influence the plasma level of homocysteine. One of the metabolic pathways for homocysteine involves the enzyme methylenetetrahydrofolate reductase
Hydroxymethylglutaryl-CoA reductase inhibitors in older persons with acute myocardial infarction: evidence for an age-statin interaction.
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OBJECTIVE
To characterize the relationship between hydroxymethylglutaryl-CoA reductase inhibitors (statins) and outcomes in older persons with acute myocardial infarction (AMI).
METHODS
Observational study.
METHODS
Acute care hospitals in the United States from April 1998 to June
Fluvastatin, a 3-hydroxy-3-methylglutaryl coenzyme a reductase inhibitor, attenuates left ventricular remodeling and failure after experimental myocardial infarction.
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BACKGROUND
Short-term administration of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, statins, has been shown to attenuate ischemia-reperfusion injury. However, the effects of long-term administration of statins on left ventricular (LV) remodeling and failure after myocardial
Impact of hydroxymethylglutaryl coenzyme A reductase inhibition on left ventricular remodeling in patients with acute anterior myocardial infarction after primary coronary angioplasty.
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Hydroxymethyglutaryl coenzyme A reductase inhibition (statin) therapy has been shown to reduce cardiac hypertrophy in vitro and in vivo. We assessed the influence of short-term statin therapy on left ventricular (LV) remodeling after acute myocardial in-farction. Thirty-five patients with first
Genetic polymorphism of methylenetetrahydrofolate reductase and myocardial infarction. A case-control study.
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BACKGROUND
Elevated total plasma homocyst(e)ine (tHcy; the composite of homocysteine-derived moieties in their oxidized and reduced forms) levels are a risk factor for coronary heart disease, stroke, and venous thrombosis. tHcy plasma levels are influenced by folate, vitamins B6 and B12, as well as
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