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nicotinic acid/infarkt

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Strana 1 od 63 výsledky

Control of ventricular arrhythmias during myocardial infarction by antilipolytic treatment using a nicotinic-acid analogue.

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The effect of lowering raised plasma-free-fatty acids (F.F.A.) on the incidence of serious ventricular arrhythmias after myocardial infarction was assessed by a double-blind trial in eighty-one patients. A nicotinic-acid analogue (N.A.A.) with very slight haemodynamic effects was given within 12

Effect of a nicotinic-acid analogue on raised plasma-free-fatty-acids after acute myocardial infarction.

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Proceedings: Effect of nicotinic acid analogue on plasma free fatty acids and ventricular arrhythmias after myocardial infarction.

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[On the use of nicotinic acid in myocardial infarct].

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[Arteriosclerosis--nicotinic acid therapy. 1. Risk factors in myocardial infarct].

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Limitation of myocardial infarct size by metabolic interventions that reduce accumulation of fatty acid metabolites in ischemic myocardium.

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The effects on myocardial damage of metabolic interventions by nicotinic acid, oxfenicine, or a combination of the two were assessed in open-chest dogs exposed to coronary artery occlusion for 6 hours. The accumulation of metabolites of free fatty acids (FFAs) was studied in tissue samples of the

Synthesis and biological evaluation of novel hydrogen sulfide releasing nicotinic acid derivatives.

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Twelve novel hybrids of slowly releasing hydrogen sulfide donor ADT-OH combined with nicotinic acid were synthesized. All of their structures had been confirmed by 1H NMR, 13C NMR and MS spectra. The target compounds were evaluated for their neuroprotective effects on hippocampal neuron HT22 cells
In the field of dyslipidemia and metabolic syndrome, four innovative therapies are reviewed: Ezetimibe (Ezétrol) is a selective cholesterol absorption inhibitor. Co-administration of ezetimibe with low dose of statins shows LDL lowering comparable to that of the highest dose of the respective statin

Secondary prevention of myocardial infarction with drugs.

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Clinical trials in the field of secondary prevention of myocardial infarctions are reviewed, with emphasis on those studies that were randomized and included at least 100 patients. Standardized total mortality data, when available, are provided. Five groups of drugs are reviewed: 1) antiarrhythmic

[The structuro-functional state of the ischemic myocardium under the action of a terrilitin-nicotinic acid mixture in animal experiments].

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Histochemical evidence of the activity and distribution of glycolysis redox enzymes, tissue respiration and terminal oxidation pattern (dehydrogenase of lactic, malic, succinic and isocitric acids, NAD-N- and NADPh-N-ase, cytochrome oxidase) as well as the levels of the major carbohydrates
VIP, SS and PP which exist in gastrointestinal tract and CNS might be to play an important role in nervous system as neurotransmitters of neuromediaters. There have been a few of reports about their changes in plasma and CSF in ICVD. The effects of acupuncture, which was used in treatment of ICVD
Carotid bifurcation atherosclerosis was demonstrated in 34 of 108 patients with familial hypercholesterolemia and coronary artery disease by B-scan, continuous-wave Doppler sonography, and intravenous digital subtraction angiography. An intensive combined therapy of diet, colestipol, and nicotinic

Complementary effects of pravastatin and nicotinic acid in the treatment of combined hyperlipidaemia in diabetic and non-diabetic patients.

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BACKGROUND Given that treatment with a single drug is frequently unsuccessful in patients with combined hyperlipidaemia, there is a rationale for the study of regimens using drugs that have complementary therapeutic profiles. We therefore set out to compare the efficacy of a combined pravastatin and

The effects of nicotinic acid treatment on high density lipoprotein particle size subclass levels in hyperlipidaemic subjects.

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Twenty-three consecutive hyperlipidaemic patients were treated with 4 g nicotinic acid daily for 6 weeks. The treatment resulted in the expected reduction of serum very low density (VLDL) and low density lipoproteins (LDL) and in the increase of high density lipoproteins (HDL). The cholesterol
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