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ventricular fibrillation/triglyceride
Linkki tallennetaan leikepöydälle
Sivu 1 alkaen 21 tuloksia
Dietary flaxseed protects against ventricular fibrillation induced by ischemia-reperfusion in normal and hypercholesterolemic Rabbits.
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Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), the (n-3) PUFA found in fish oils, exert antiarrhythmic effects during ischemia. Flaxseed is the richest plant source of another (n-3) PUFA, alpha-linolenic acid (ALA), yet its effects remain largely unknown. Our objective was to determine
Alimentary lipemia enhances procoagulatory effects of inflammation in patients with a history of acute myocardial infarction complicated by ventricular fibrillation.
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BACKGROUND
Acute myocardial infarction, often occurring postprandially, can be complicated by ventricular fibrillation. The role of acute alimentary lipemia and inflammation in the occurrence of ventricular arrhythmias in acute myocardial infarction has not been described yet.
RESULTS
Before and 2 h
Ventricular fibrillation by hypothermia in spinal fusion surgery: A case report.
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A 63-year-old man was scheduled for T12-S1 posterolateral spinal fusion surgery. The patient's vital signs were stable and there were no specific laboratory findings except for high triglycerides. In addition, echocardiography showed mild left ventricular hypertrophy, but normal left ventricular
Omega-3 fatty acids and atorvastatin suppress ventricular fibrillation inducibility in hypertriglyceridemic rat hearts: implication of intracellular coupling protein, connexin-43.
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Omega-3 fatty acids (omega-3 FA) and statins exhibit besides lipid-lowering effects the antiarrhythmic ability in clinic, while definite mechanisms are not yet elucidated. Our goal was to examine whether these compounds can modulate inducibility of hypertriglyceridemic (HTG) rat heart to ventricular
Protective effect of fenofibrate against ischemia-/reperfusion-induced cardiac arrhythmias in isolated rat hearts.
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Fenofibrate is a peroxisome proliferator-activated receptor (PPAR)-α activator that lowers triglycerides and influences cytochrome P-450 (CYP-450) epoxygenase-dependent arachidonic acid (AA) metabolism. CYP-450 epoxygenase metabolizes AA to epoxyeicosatrienoic acids (EETs). EETs have coronary
Absence of coronary or aortic atherosclerosis in rats having dietary lipid modified vulnerability to cardiac arrhythmias.
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Laboratory studies have shown that saturated fats in the diet increase vulnerability to ventricular fibrillation and other cardiac arrhythmias while polyunsaturates, especially the n-3 fatty acids of fish oils, are antiarrhythmic. Similarly, dietary saturated fat has been implicated in the
Sotalol: a new class III antiarrhythmic agent.
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The chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage of sotalol hydrochloride are reviewed. The chemical name of sotalol hydrochloride is 4'-[1-hydroxy-2-(isopropylamino)ethyl]methanesulfonanilide monohydrochloride. Sotalol is a class III antiarrhythmic that
Glucose stabilization and coronary infarction with artificial pancreas in heart-lung preparation.
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In the performance of heart-lung preparations, after 4-8 hours, it is an usual feature to have multiple microinfarctions, and, finally, heart failure and ventricular fibrillation. We have studied glucose, triglycerides and conjugated fructose consumption by the heart-lung preparation and found a
Exploring newer cardioprotective strategies: ω-3 fatty acids in perspective.
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In the 1980s, observational retrospective studies showed an inverse relation between coronary heart disease (CHD) and consumption of fish containing fatty acids that belong to the omega (ω)-3 family. Large case-control studies and prospective intervention trials consistently showed that ω-3 fatty
Effect of voluntary breathing exercises on stable coronary artery disease in heart rate variability and rate-pressure product: a study protocol for a single-blind, prospective, randomized controlled trial
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Background: At present, China has more than 11 million patients with stable coronary heart disease and this is becoming a major public health problem. The pathological changes of coronary heart disease can lead to dysfunction of the
Arrhythmia susceptibility and myocardial composition in diabetes. Influence of physical conditioning.
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Abnormal myocardial composition in diabetes mellitus has been described, but the effects on ventricular vulnerability have not been defined. We have assessed the susceptibility to arrhythmias in a canine model after 1 yr of mild diabetes induced by alloxan. Since physical conditioning can affect
Formation of prostacyclin-sensitive platelet aggregates in human whole blood in vitro. Part II. The occurrence of the phenomenon in males suffering from acute myocardial infarction.
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The de-aggregatory effect of prostacyclin (PGI2) and the rate of spontaneous platelet aggregation (SPA) were studied in vitro in whole blood of 24 males with acute myocardial infarction (MI) and 18 males, patient controls (PC). The de-aggregatory effect of PGI2 and the rate of SPA (measured as a
Hematologic and chemical changes observed during and after cardiac arrest in a canine model--a pilot study.
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OBJECTIVE
To evaluate the effect of cardiac arrest and cardiopulmonary resuscitation (CPR) on blood chemistry in a canine model.
METHODS
Evaluative canine animal study.
METHODS
Animal laboratory accredited by the Association for Assessment and Accreditation of Laboratory Animals.
METHODS
Twenty-six
Raised plasma non-esterified fatty acids (NEFA) during ischaemia: implications for arrhythmias.
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Raised plasma non-esterified fatty acids (NEFA) have been directly implicated in the development of serious ventricular arrhythmias and death during acute myocardial infarction. Since this was first proposed by Oliver and Kurien in 1970, clinical and experimental evidence has been conflicting, but
41-month follow-up of risk factors correlated with new coronary events in 708 elderly patients.
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A prospective study correlated coronary risk factors with new coronary events in 192 elderly men and 516 elderly women, mean age 82 +/- 8 years. Follow-up was 41 +/- 6 months (range 24-44). Coronary events (myocardial infarction, primary ventricular fibrillation, and sudden cardiac death) occurred
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