The early ventricular arrhythmias of acute myocardial ischaemia arise against a background of rapid alterations in regional myocardial blood flow and electrophysiological properties. The relation between patterns of flow and epicardial activation has been examined in eight open chest anaesthetised dogs at time of onset of these arrhythmias following a proximal occlusion of the left anterior descending coronary artery. Data were derived from 80 epicardial and endocardial sites within a 4 X 5 cm area of left ventricular free wall and processed utilising a three-dimensional computer plotting program. Mean flow within the ischaemic zone was reduced to 0.27 and 0.24 cm3 x g-1 x min-1 in epicardium and endocardium respectively. Marked epicardial activation delays and fragmentation of conduction were observed confined to areas of flow less than 0.3 cm3 x g-1 x min-1. 74% of endocardial and 71% of epicardial tissue samples within the ischaemic zone derived from this area and analysis of flow distribution between adjacent samples demonstrated spatial heterogeneity of flow. It is suggested that local spatial variability in flow within the central ischaemic region may be a prerequisite for abnormal fractionation of conduction leading to re-entrant excitation at the time of onset of early ventricular arrhythmias.

Animals↗

PubMed1982

Effect of heparin on plasma free fatty acid concentrations after acute myocardial infarction.

Free fatty acid concentrations in plasma measured after in vivo heparinisation are often overestimated because of ex vivo lipolysis of variable degrees. A new method has been developed using immediate extraction of blood which obviates this and shows that the true rise in plasma free fatty acid concentration after heparin in ambulant ward patients and in patients with acute myocardial infarction is less than previously reported. The small rise in plasma free fatty acid concentration after heparin is unlikely to have adverse metabolic effects in most patients during acute myocardial infarction.

Adult↗

PubMed1982

Dietary survey in 40-year-old Edinburgh men.

One hundred and seven healthy 40-yr-old Edinburgh men were asked to participate in a dietary survey involving a 7-d weighed record. Ninety seven successfully completed the record. The results showed that the total energy was made up of 13 per cent protein, 38 per cent fat, 40 per cent carbohydrate and 9 per cent alcohol. A small proportion of the men had exceptionally high alcohol intakes. The mean intake of fat was high, 121 g, it is nevertheless lower than amounts consumed in other areas of Britain. Of the energy from fat, 16 per cent came from saturated-fatty acid, 15 per cent from monounsaturated-fatty acid and 4 per cent from polyunsaturated-fatty acid. Linoleic acid contributed 3 per cent of the mean energy intake. In some mens' diet this essential fatty acid provided under 2 per cent of their total energy consumption.

Adult↗

PubMed1982

Diet and coronary heart disease.

There is a moderately good correlation between dietary saturated fatty acids and coronary heart disease (CHD) when populations in different parts of the world are compared but not within the same cultural community or for individuals. Total energy, essential fatty acids (EFA), dietary fibre, alcohol and salt also contribute to the relationship of diet to CHD. Saturated fatty acids exert their pathogenic role mostly through altering the homoeostasis of lipoprotein metabolism, leading to an increase in cholesterol-rich low-density lipoproteins, and influencing adversely the balance between the accumulation in and clearance of cholesterol esters from the arterial wall. Polyunsaturated fatty acids (PUFA) alter lipoprotein metabolism directly by decreasing synthesis and increasing catabolism and excretion and indirectly by being substitutes for saturated fatty acids, which are therefore consumed in smaller quantities. PUFA have an important additional role, because of their EFA content. A deficiency of the EFA, linoleic and arachidonic acids, relative to the saturated fatty acid intake, can be correlated with CHD mortality. The pathogenic pathways of a relative EFA deficiency leading to CHD are as likely to be related to intravascular coagulation and myocardial metabolism as to lipoprotein metabolism. EFA requirements may not be met in communities having a high intake of saturated fatty acids if there is also a dietary deficiency of antioxidants particularly vitamin E. Two large primary prevention trials of diets enriched with PUFA showed, under institutional circumstances, that it is possible to reduce serum cholesterol by 10-15 per cent. There was in each a reduction in the total incidence of cardiovascular diseases, and the greatest effect was on the incidence of non-fatal myocardial infarction. In both trials there was an increase in non-cardiovascular mortality. The significance of this finding is evaluated in conjunction with a similar finding derived from the only long-term primary prevention trial using a drug. The possibility that gradual depletion of membrane cholesterol over many years might have an adverse effect on the function of ageing cells cannot be dismissed. In communities where there is a high incidence of CHD, the aim should be to reduce plasma cholesterol concentrations to the region of 210 mg/dl. The evidence that it is necessary, practicable or even desirable to reduce plasma cholesterol to lower levels in order to reduce CHD incidence further is not impressive. To achieve this aim by dietary measures there should be a reduction of energy from fats to a level of 35 per cent or below and reduction of the contributions from saturated fats to about 10 per cent. In addition, there is a sound basis for recommending reduction of total energy intake to that actually needed, an increase in dietary cereal fibre and a reduction in alcohol.

Adult↗

PubMed1982