linoleic acid/infarction

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Low dietary intake of linoleic acid predisposes to myocardial infarction.

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Thirty-two men who had recently had a myocardial infarction were matched individually for age with controls who had no evidence of heart disease. The patients had a significantly lower proportion of linoleic acid and a higher proportion of palmitic acid in their plasma triglyceride fatty acids.

Co-treatment with conjugated linoleic acid and nitrite protects against myocardial infarction.

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According to the CDC, the most common type of heart disease is coronary artery disease, which commonly leads to myocardial infarction (MI). Therapeutic approaches to lessen the resulting cardiovascular injury associated with MI are limited. Recently, MicroRNAs (miRNAs) have been shown to act as

Conjugated linoleic acid in adipose tissue and risk of myocardial infarction.

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BACKGROUND Despite the high saturated fat content of dairy products, no clear association between dairy product intake and risk of myocardial infarction (MI) has been observed. Dairy products are the main source of conjugated linoleic acid (CLA; 18:2n-7t), which is produced by the ruminal

Circulating n-3 fatty acids and linoleic acid as indicators of dietary fatty acid intake in post-myocardial infarction patients.

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Population-based studies often use plasma fatty acids (FAs) as objective indicators of FA intake, especially for n-3 FA and linoleic acid (LA). The relation between dietary and circulating FA in cardiometabolic patients is largely unknown. We examined whether dietary n-3 FA and LA were

Plasma and Dietary Linoleic Acid and 3-Year Risk of Type 2 Diabetes After Myocardial Infarction: A Prospective Analysis in the Alpha Omega Cohort.

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To study plasma and dietary linoleic acid (LA) in relation to type 2 diabetes risk in postmyocardial infarction (MI) patients.

RESEARCH DESIGN AND METHODS

We included 3,257 patients aged 60-80 years (80% male) with a median time since MI of 3.5 years

[Linoleic acid and heart infarct].

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A re-analysis of the Sydney Diet Heart Study (Ramsden et al., BMJ 2013) suggested that a diet high in linoleic acid increased the risk of coronary heart disease. The authors ascribe this to a lack of the omega-3 fatty acid, alpha-linolenic acid, in the oils and fats consumed. This argument has some

Experimental myocardial infarction: effects of a lipid peroxide, 13-hydroperoxy linoleic acid on coronary circulation in rats.

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Effects of 13-hydroperoxy linoleic acid on coronary circulation and vasculature were investigated using an electrocardiographic (ECG) and scanning electron microscopic (SEM) techniques. After the intra left ventricular injection of 13-hydroperoxy linoleic acid to rats the ischemic ECG changes, i.e.,

[Linoleic acid, thrombosis diathesis and heart infarct].

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Linoleic acid, platelet aggregation and myocardial infarction.

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Does low dietary intake of linoleic acid predispose to myocardial infarction?

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Does low dietary and serum linoleic acid predispose to myocardial infarction?

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Does low dietary intake of linoleic acid predispose to myocardial infarction?

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

Platelet function and conjugated diene concentrations in diabetic and non-diabetic survivors of acute myocardial infarction.

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OBJECTIVE The aim was to compare platelet function in diabetic and non-diabetic survivors of acute myocardial infarction and to relate it to an index of free radical activity in these patients. METHODS In vivo and in vitro indices of platelet function and diene conjugate molar ratios were measured

Linoleic acid and coronary heart disease.

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Low tissue concentrations of the essential fatty acid, linoleic acid, occur in communities with high rates of coronary disease and in patients with angina and myocardial infarction. This relationship is independent of lipids and blood pressure, but in smokers linoleic acid is particularly low

Myocardial uptake of labeled oleic and linoleic acids.

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Oleic acid labeled with 14C, (14C-OA) or 131I (131I-OA) and 131I-labeled linoleic acid (131I-LOA) were administered intravenously to rats and tissue distribution studies completed at various time intervals from 5 to 60 min. Tissue distribution of 131-I-labeled oleic acid or linoleic acid was also

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