Search PubMed⌕ Search

Biomedical subjects

M F Oliver

Publications and source records attributed to M F Oliver.

At least 109 records · Page 6Linked to original sources
PubMed1985

Lack of impact of prevention on sudden cardiac death.

There are many different and relatively discrete mechanisms leading to ventricular fibrillation. Therefore, any single approach to prevention is likely to be unsuccessful, particularly because the circumstances that finally cause sudden cardiac death may not be present for more than a short time before the onset of ventricular fibrillation. It should not be surprising, therefore, that neither primary nor secondary prevention trials directed at correcting risk factors for coronary heart disease have been associated with a reduction in the incidence of sudden cardiac death. More trials are needed in patients with unstable angina, in whom there is a relatively high incidence of sudden cardiac death within a short period. Methods of modulating catecholamine response, myocardial vulnerability and thrombotic mechanisms require more formal testing. However, because the sensitivity and specificity of prediction of those likely to die suddenly are so poor, it may become necessary to accept that the majority of sudden cardiac deaths is not yet preventable and focus on continuing to improve cardiopulmonary resuscitation services.

Angina Pectoris↗
PubMed1985

A comparison of the nutrient intake of some Scotsmen with dietary recommendations.

During 1980 and 1982, 164 men aged 45-54 in North Edinburgh and West Fife participated in a 7-day individual weighed dietary survey. The mean energy intake was 11.2 MJ (2700 kcal), 38.1 per cent of which came from fat and 6.7 per cent from alcohol. The P:S ratio was 0.30 and the mean daily fibre intake 19.8 g. Saturated fatty acids accounted for 16.3 per cent of the energy and polyunsaturated fatty acid for 4.6 per cent. Oleic acid was the principal dietary fatty acid accounting for 32.4 per cent of fatty acids. The major polyunsaturated fatty acid was linoleic acid and contributed 3.5 per cent of energy. Cereal and cereal products were the principal source (30.8 per cent) of linoleic acid. Though this study was conducted prior to the publication of recent dietary recommendations, a small proportion of the men were achieving some of them but few would have met the recommendations in full.

Animals↗
PubMed1984

Adipose tissue and platelet fatty acids and coronary heart disease in Scottish men.

The relation between coronary heart disease (CHD) and fatty acid composition of adipose tissue and platelets was examined in a random sample of 448 middle-aged Scottish men. The linoleic acid (18:2n6) content in adipose tissue of 28 men with previously unidentified CHD was significantly lower than that in the rest of the group. Platelet linoleic and other fatty acids were not significantly different in men with new CHD. Fatty acid content of adipose tissue reflects long-term dietary intake, and a 7-day weighed dietary record in a random sub-sample of 164 men confirmed that intake of linoleic acid in 10 of the 28 new CHD cases was significantly lower than in the healthy men. In a multiple logistic analysis adipose tissue linoleic acid, age, high density lipoprotein cholesterol, and weight/height index each made an independent contribution to the explanation of new CHD. When all fatty acids were included in a second regression analysis, low concentrations of dihomo-gamma-linolenic (20:3n6) acid in adipose tissue showed a more significant relation with new CHD than did linoleic acid.

Adipose Tissue↗
PubMed1984

Mechanisms of phase 1a and 1b early ventricular arrhythmias during acute myocardial ischemia in the dog.

Two phases of ventricular arrhythmia occur within the first 30 minutes of experimental myocardial ischemia. Possible differences in their mechanisms of pathogenesis were investigated in anesthetized dogs by detailed mapping of patterns of epicardial activation and regional myocardial blood flow during phase 1a and phase 1b early ventricular arrhythmias induced by high ligation of the left anterior descending coronary artery. Data were derived from 80 sites in a 4 by 5 cm area of left ventricular anterior free wall and displayed using computer graphics. Regional myocardial blood flow and the relation of regional flow to epicardial delay did not differ significantly during the 2 phases of arrhythmia in central ischemic or nonischemic areas, although epicardial flow in border region segments was increased during phase 1b. Significantly greater mean epicardial delays and spatial heterogeneity of epicardial delay (assessed by intersite variance within the ischemic area) occurred during phase 1a arrhythmias. Serial studies show striking increases in spatial heterogeneity of delays during phase 1a, but not during phase 1b, relating to temporal dispersion of a phenomenon of transient prolongation of activation delay at individual electrode sites. These data are consistent with the concept that phase 1a and 1b arrhythmias arise through different electrophysiologic mechanisms independent of flow-dependent effects.

Acute Disease↗
PubMed1984

Relationship of neurosympathetic responsiveness to early ventricular arrhythmias in ischaemic myocardium.

Myocardial catecholamine overflow has been measured in open-chest anaesthetised dogs after graded stimulation of the left ansa subclavia before and during left anterior descending coronary artery occlusion and on reperfusion. Sequential 1 min periods of ansa stimulation over 3 h resulted in reproducible, frequency dependent regional myocardial noradrenaline (NA) overflow without tachyphylaxis. In seven dogs, two successive 10 min periods of LAD occlusion did not modify peak myocardial NA overflow from the predominantly ischaemic (I) or non-ischaemic (NI) areas at either low (1 Hz) or high (10 Hz) frequency ansa stimulation. In a second group of nine dogs, myocardial catecholamine overflow was related to changes in ischaemic area epicardial activation delay during repeated ansa stimulation on four occasions during 75 min of ischaemia. Stimulation at the period of peak spontaneous arrhythmias 5 and 17 min after coronary occlusion resulted in NA overflow from I of 2.8 +/- 1.3 and 3.0 +/- 1.6 pmol X ml-1 respectively and a significant increase in mean activation delay in I of 12 +/- 4 ms at 5 min and 9 +/- 4 ms at 17 min (p less than 0.05). In contrast, stimulation 30 and 60 min after coronary occlusion, when spontaneous arrhythmias are rare, was not associated with NA overflow from ischaemic areas (0.3 +/- 0.3 and 0.9 +/- 0.5 pmol X ml-1 respectively) and resulted in a minor reduction in mean activation delay in ischaemic areas of 2 +/- 3 ms at 30 min and 3 +/- 4 ms at 60 min. NA overflow from non-ischaemic areas and increases in blood pressure and myocardial lactate release were similar during each period of ansa stimulation. Coronary reperfusion induced massive overflow of NA (11.4 +/- 2.8 pmol X ml-1) and reduced extraction of adrenaline (A) from ischaemic areas with a time course similar to early reperfusion arrhythmias. Stimulation-evoked release of NA in ischaemic myocardium is thus maintained during the early period of enhanced vulnerability to arrhythmias and during reperfusion but is inhibited after 30 min. This temporal variability may be a factor in the time course of spontaneous arrhythmias in this model.

Animals↗
PubMed1984

Strategy of reducing coronary risk and the use of drugs.

The strategy of primary prevention of coronary heart disease (CHD) needs reconsideration. Recent results of trials of reducing the risk of CHD in those at moderate risk have been inconclusive and disappointing. More may be expected from intervention in those at high risk, and a selective policy is advocated. But, in those at high risk, it is usually necessary to give drugs in order to reduce the risk from hypertension and hypercholesterolaemia. Many currently used and popular drugs have never been submitted to rigourous long-term testing of their safety, although it was only through formal clinical trials that the adverse effects of clofibrate and of thiazides were identified. More, not fewer, clinical trials are needed if we are to avoid new tragedies. A plea is made for the urgent establishment of drug data banks to permit accurate monitoring of changes in the incidence of commonly occurring diseases in relation to the increasing use of drugs for primary prevention of vascular diseases and for social convenience.

Adrenergic beta-Antagonists↗