Relation between serum-free-fatty-acids and arrhythmias and death after acute myocardial infarction
TL;DR: Serum-F.F.A.A.) levels measured in 200 patients during the first forty-eight hours after an acute myocardial infarction have been related to the prevalence of arrhythmias detected by continuous monitoring of the electrocardiogram, to the clinical state of the patients, and to serum-enzyme and blood-glucose levels.
About: This article is published in The Lancet.The article was published on 1968-04-06. It has received 496 citations till now. The article focuses on the topics: Myocardial infarction & Cardiogenic shock.
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TL;DR: Insulin-glucose infusion followed by a multidose insulin regimen improved long-term prognosis in diabetic patients with acute myocardial infarction.
1,529 citations
TL;DR: In this large, international randomized trial, high-dose GIK infusion had a neutral effect on mortality, cardiac arrest, and cardiogenic shock in patients with acute STEMI.
Abstract: Context Glucose-insulin-potassium (GIK) infusion is a widely applicable, low-cost therapy that has been postulated to improve mortality in patients with acute ST-segment elevation myocardial infarction (STEMI). Given the potential global importance of GIK infusion, a large, adequately powered randomized trial is required to determine the effect of GIK on mortality in patients with STEMI. Objective To determine the effect of high-dose GIK infusion on mortality in patients with STEMI. Design, setting, and participants Randomized controlled trial conducted in 470 centers worldwide among 20,201 patients with STEMI who presented within 12 hours of symptom onset. The mean age of patients was 58.6 years, and evidence-based therapies were commonly used. Intervention Patients were randomly assigned to receive GIK intravenous infusion for 24 hours plus usual care (n = 10,091) or to receive usual care alone (controls; n = 10,110). Main outcome measures Mortality, cardiac arrest, cardiogenic shock, and reinfarction at 30 days after randomization. Results At 30 days, 976 control patients (9.7%) and 1004 GIK infusion patients (10.0%) died (hazard ratio [HR], 1.03; 95% confidence interval [CI], 0.95-1.13; P = .45). There were no significant differences in the rates of cardiac arrest (1.5% [151/10 107] in control and 1.4% [139/10,088] in GIK infusion; HR, 0.93; 95% CI, 0.74-1.17; P = .51), cardiogenic shock (6.3% [640/10 107] vs 6.6% [667/10 088]; HR, 1.05; 95% CI, 0.94-1.17; P = .38), or reinfarction (2.4% [246/10,107] vs 2.3% [236/10,088]; HR, 0.98; 95% CI, 0.82-1.17; P = .81). The rates of heart failure at 7 days after randomization were also similar between the groups (16.9% [1711/10,107] vs 17.1% [1721/10,088]; HR, 1.01; 95% CI, 0.95-1.08; P = .72). The lack of benefit of GIK infusion on mortality was consistent in prespecified subgroups, including in those with and without diabetes, in those presenting with and without heart failure, in those presenting early and later after symptom onset, and in those receiving and not receiving reperfusion therapy (thrombolysis or primary percutaneous coronary intervention). Conclusion In this large, international randomized trial, high-dose GIK infusion had a neutral effect on mortality, cardiac arrest, and cardiogenic shock in patients with acute STEMI.
624 citations
TL;DR: Accumulation of 5′-AMP during ischemia results in an activation of AMP-activated protein kinase, which phosphorylates and inactivates ACC during reperfusion, and the subsequent decrease in malonyl-CoA levels will result in accelerated fatty acid oxidation rates during reperFusion of ischemic hearts.
606 citations
TL;DR: Endogenous triacylglycerol as a source of fatty acids and Carnitine palmitoyltransferase 1 activity and Acetyl-CoA carboxylase regulation of fatty acid oxidation.
550 citations
TL;DR: In chronic angina patients, ranolazine monotherapy was well tolerated and increased exercise performance throughout its dosing interval at all doses studied without clinically meaningful hemodynamic effects.
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TL;DR: The method described here, although not more sensitive than the methods based on the colorimetric estimation of creatine, makes it possible to measure enzymic activities in tissue homogenates and extracts diluted 2000 to 20 000 times, and to follow continuously the time course of the reaction in a total volume of about 4 ml.
Abstract: where ATP = adenosine triphosphate and ADP= adenosine diphosphate. The substances most commonly determined have been creatine or creatine phosphate; e.g. Banga (1943), Askonas (1951), Narayanaswami (1952), Ennor & Rosenberg (1954), Kuby, Noda & Lardy (1954) and Chappell & Perry (1954). These methods may not always be convenient for the determination of creatine phosphokinase activity in tissue homogenates, since the amount of tissue used in reaction mixtures makes the introduction of significant amounts of endogenous substances a distinct possibility. Themethod described here, although not more sensitive than the methods based on the colorimetric estimation of creatine, makes it possible to measure enzymic activities in tissue homogenates and extracts diluted 2000 to 20 000 times, and to follow continuously the time course of the reaction in a total volume of about 4 ml. Under these conditions effects due to endogenous substances are negligible. The method is based on Kornberg's assay procedure for ATP (Kornberg, 1950), whereby the formation of ATP from ADP and creatine phosphate is linked to the reduction of triphosphopyridine nucleotide (TPN). When the rate-limiting step in the reaction sequence is that catalysed by creatine phosphokinase, spectrophotometric measurement of the rate of reduction ofTPN gives the rate ofATP formation, and thus the activity of the enzyme. The method has also been applied to the determination of myokinase activity by measuring the rate of formation ofATP from ADP. The methods for the assay of myokinase due to Kalckar (1943, 1947) are laborious. The most sensitive method is probably that based on the firefly luminescence system for the estimation of ATP (Strehler & Totter, 1952), but is not convenient for general use. The coupled activities of myokinase and creatine phosphokinase have been used by Chappell & Perry (1954) to assay myokinase. The present method has the advantage of convenience over most of the older methods. The reactions are followed continuously in the spectrophotometer, and the rates catalysed by small amounts of tissue can be measured with ease. An outline of the method has been given elsewhere (Oliver, 1954). Complete experimental details are included here.
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TL;DR: The present study was undertaken to determine further the role of fatty acids in myo-cardial metabolism and the methods used have been described in detail in previous studies from this laboratory.
Abstract: The myocardium is able to utilize both carbohydrates and noncarbohydrates for the performance of its work (1). Extraction of an individual substrate is usually determined by its arterial level. Thus, after a carbohydrate meal the heart derives much of its energy from the metabolism of carbohydrates; however, in the fasting state myocardial energy production is dependent upon noncarbohydrates, primarily fatty acids (1). Recent studies (2, 3) have shown that the principal lipid fraction of plasma concerned with the transport and metabolism of fatty acids is the plasma nonesterified or free fatty acid (FFA) fraction. Previous studies have already demonstrated that the heart uses a considerable amount of FFA (3). The present study was undertaken to determine further the role of fatty acids in myo-cardial metabolism. Most of the methods used in this investigation have been described in detail in previous studies from this laboratory. Coronary sinus blood was obtained from a catheter placed in the coronary sinus, and blood samples from metabolic studies were simultaneously obtained from arterial and coronary sinus blood (1). The coronary blood flow was determined with the nitrous oxide desaturation method (4). Blood glucose was determined by the method of Hagedorn and Jensen (5) using Somogyi's method to prepare the blood filtrate (6).
263 citations