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Biomedical subjects

D Kilpatrick

Publications and source records attributed to D Kilpatrick.

At least 55 records · Page 3Linked to original sources
PubMed1990

Importance of the great vessels in the genesis of the electrocardiogram.

The electrocardiogram is the graphic representation against time of the difference in potential between points of the body caused by the current field of the heart. To examine the origin of this current field, a method of transforming body surface electrocardiographic data to the epicardial surface has been developed. The computed epicardial current density distributions in 219 patients with acute inferior myocardial infarction showed that, in 89% of patients, the current flow out of the heart during the ST segment came from two regions, not only from the infarction region but also from a region over the great vessels. This findings suggests that current flows from the ischemic region, through the low-resistance pathway provided by the intracavity blood, out the great vessels, and back to the epicardium. A similar pathway has been hypothesized when ischemia caused endocardial ST elevation, such as during a stress test or with unstable angina. To test this hypothesis, a group of patients with ST depression on the 12-lead electrocardiogram, not associated with ST elevation, was examined with body surface mapping. Ninety-four percent of patients had epicardial current density distributions that showed a region of current flow out of the heart and over the great vessels that was consistent with this hypothesis. This could explain the poor localization of coronary artery disease by electrocardiographic techniques when there is ST depression on the body surface.

Aorta↗
PubMed1990

The vascular resistance of arterial stenoses in series.

The vascular resistance of stenoses in series has been studied in vitro by use of fiber optic laser Doppler anemometry to measure the cross-sectional areas of the stenoses. Pressure gradients across each of the stenoses were measured while both the severity and the separation of the stenoses were altered. The individual resistances were compared with the combined resistance. Resistance at a stenosis is a nonlinear function of the severity of the stenosis. The resistance is a complex function of the perfusion pressure and the cross-sectional area of the stenosis and cannot be accurately predicted from a single plane angiographic image. With multiple stenoses an approximate assessment of the combined effect can be obtained by summing the value of the resistance for each stenosis but not the degree of the stenoses. The nonlinear relationship of resistance to stenosis severity means that if one stenosis is more severe than the other, the combined effect can be regarded as the same as the effect of the more severe stenosis acting by itself. The distance between the stenoses does not change their combined effect.

Arteries↗
PubMed1989

Prognostic significance of ST potentials determined by body surface mapping in inferior wall acute myocardial infarction.

Electrocardiographic body surface mapping on admission to coronary care has been shown to predict prognosis in a previous study of 100 patients with inferior wall acute myocardial infarction (AMI). A further 98 patients with first inferior wall AMI were now studied by body surface mapping on admission to coronary care to confirm that both the spatial distribution or map pattern of ST-segment potentials and the precise measurement of the maxima and minima are of prognostic significance. Each ST-segment map was compared by correlation coefficient to the average map pattern of the 4 groups derived in a previous study and placed in the group with the highest correlation coefficient. Analysis of these groups against outcome confirmed that the group dominated by a large area of marked anterior ST depression was associated with a high rate of complications and a significantly lower survival free of coronary artery bypass grafting (p less than 0.01). Patients in this group had more extensive and severe coronary artery disease than patients in the other groups. Increasing values of maximal ST depression correlated with mortality and complication rates. The extent by which the magnitude of ST-segment depression exceeded the magnitude of ST-segment elevation correlated with mortality and incidence of left ventricular failure. The results confirm the findings of the original study. Body surface mapping is of prognostic significance in inferior wall AMI.

Adult↗
PubMed1989

Natural history of ST-segment potential distribution determined by body surface mapping in patients with acute inferior infarction.

The authors studied the natural history of the electrocardiographic ST-segment using body surface mapping in 123 patients with acute inferior infarction who were not treated with thrombolytic agents. In 91 patients they compared body surface ST-segment maps recorded at 7.9 +/- 5.4 hours after the onset of acute myocardial infarction with maps recorded at 32.6 +/- 21.6 hours after infarction. In 46% of the patients the ST-segment distribution map pattern was unchanged. Twenty-eight percent of the patients moved to a ST-segment distribution associated with low mortality, and 7% correlated with a normal ST-segment distribution. Patients who started in a group dominated by marked anterior ST-segment depression or who developed this pattern at the time of the late map had a 45% morbidity, compared to 13% for patients who never developed this pattern (p less than 0.005). In a second group of 61 patients they compared maps recorded at 15.0 +/- 15.8 hours after infarction and repeat maps 19.6 +/- 13.0 recorded months later. At follow-up mapping, 44% of the patients correlated with a normal ST-segment distribution, 38% of patients had a low-risk pattern map and in 7% the map pattern was dominated by anterior ST-segment potential depression. The latter patients had a higher morbidity than patients in the other groups, but this did not reach statistical significance. Four of seven patients in this last group had significant angina at the time of follow-up mapping, compared to 2 of 54 patients in the other two groups (p less than 0.001).

Aged↗
PubMed1989

The relationship of ST elevation to eventual QRS loss in acute inferior myocardial infarction.

The electrocardiographic changes of ST-segment elevation in acute myocardial infarction are related to the region of infarction. The authors examined body surface map data in 70 patients with acute inferior infarction to determine the exact relationship of the initial ST elevation to the eventual loss of QRS. The patients had no evidence of previous myocardial infarction and no subsequent infarction and did not receive thrombolytic therapy or other acute interventions, such as surgery. Maps were recorded on admission to the hospital, during the hospital admission and again at follow-up examination 6-48 months after infarction. The region of ST elevation of the initial body surface map was compared to a QRS loss region derived by subtracting the follow-up map, integrated over the 80 msec after the onset of the QRS, from a "QRS loss region" derived from 381 normal patients using the same interval. In 76% of patients there was a direct relationship between the position of the ST elevation and the QRS loss region (mean correlation coefficient, 0.49). In a further 15% of patients there was a general relationship without specific features, and in the remaining 8% the difference maps were not related to the position of ST elevation. The region of ST elevation predicts the eventual QRS loss in the majority of patients and may be useful for monitoring interventions in acute myocardial infarction.

Aged↗
PubMed1989

Derived epicardial potentials differentiate ischemic ST depression from ST depression secondary to ST elevation in acute inferior myocardial infarction in humans.

It was hypothesized that in acute inferior wall myocardial infarction, an additional ischemic area in the subendocardium of the noninfarcting territory would produce a selective current dipole between the infarcting and ischemic regions. A resistance network model to calculate epicardial potentials from body surface electrocardiographic potentials was developed and used to examine the hypothesis in 219 patients with acute inferior myocardial infarction. In the learning set of 110 patients, two characteristic dipole patterns were observed, each associated with a high mortality rate in the ensuing 15 months when compared with that in the remaining patients. In the test set of 109 patients, a double-blind analysis of the patterns showed that the 34 patients with a dipole pattern had a collective mortality rate of 35% at 15 months compared with a 15 month rate of 5% in the remaining patients. In the total group of 219 patients, the magnitude of ST segment elevation and both the magnitude and integral of the area voltage of ST depression on the epicardium were significantly correlated with the mortality rate (p less than 0.0002 for all variables against death at 15 months). This study strongly suggests that ST depression due to ischemia can be differentiated from ST depression secondary to the ST elevation in acute inferior infarction by the examination of epicardial potential distributions.

Aged↗
PubMed1987

The analysis of Yaba monkey tumor virus DNA.

Yaba monkey tumor virus DNA was analyzed by digestion with the restriction enzymes Hind III, Eco R I, Bam H I, Sal I, and Bgl I. The restriction fragments from 0.7% and 1.4% agarose gels were used to determine an average molecular weight of 95.0 X 10(6). The location of the terminal cross-links was determined using formamide denaturation. Bam H I fragments D and K (molecular weight 9.6 X 10(6) and 3.3 X 10(6), respectively) were shown to be cross-linked.

Animals↗
PubMed1987

Spatial distribution and prognostic significance of ST segment potential determined by body surface mapping in patients with acute inferior myocardial infarction.

We investigated the mechanism and significance of ST segment changes in inferior infarction by studying 100 patients with acute inferior infarction in whom body surface maps were recorded on admission. The magnitude of the maximum ST segment elevation (denoted Vmax) and magnitude of the maximum ST segment depression (denoted Vmin), as well as the ST depression on the standard 12-lead electrocardiogram were analyzed against morbidity and mortality (at a median follow-up time of 14 months). A value obtained by subtracting Vmax from Vmin correlated (p less than .0002) with outcome. Correlations were also found between Vmin and complications, Vmin and mortality, and between increasing levels of ST depression on the 12-lead electrocardiogram and mortality. The maps were also studied by grouping the 100 ST segment map patterns into five groups by cluster analysis techniques. One group showed marked anterior negativity and had 37% mortality compared with an overall 5% mortality for the remaining groups. The limited arteriographic and autopsy data available indicated that the findings of a diseased artery or arteries corresponded with the results of mapping. The mean map patterns of the five groups showed that, in most patients with inferior infarction, the standard chest leads V1 to V6 are over a region of steep voltage gradient. Small changes in the position of the standard chest lead can cause large changes in the displayed potentials. This study indicates that patients at high risk after acute inferior infarction can be identified by surface mapping on admission to the coronary care unit.

Electrocardiography↗
PubMed1987

A validation of derived epicardial potential distributions by prediction of the coronary artery involved in acute myocardial infarction in humans.

We have developed computer algorithms that enable epicardial potential distributions to be calculated from electrocardiographic body surface data. To validate this inverse transformation we obtained body surface maps during the ST segment in 55 patients with acute infarction who subsequently underwent coronary arteriography and we constructed epicardial ST segment potential distributions for each patient. From the unlabeled epicardial maps one of us predicted the coronary artery that would be found to be involved in the infarction. These predictions were compared with the results of coronary arteriography and this showed that the analysis of the epicardial map correctly predicted the coronary artery involved in 40 of 55 patients (72.7%). In another eight patients the anatomy was partially predicted. In the 15 patients in whom the prediction was incorrect or partially correct (27.3%), 11 had critical disease or occlusions of the predicted coronary artery but the infarct-related artery was incorrectly identified. This verifies that sensible epicardial potential maps can be calculated from body surface electrocardiographic data, and that these data are sufficiently accurate to predict the vessel involved in acute infarction.

Adult↗
PubMed1987

Forward and inverse electrocardiographic calculations using resistor network models of the human torso.

An automated method of modelling the electrical properties of the human thorax from horizontal section data such as computerized tomographic scans has been used to develop both forward and inverse transformations between epicardial and body surface potential distributions. Eleven torso models with varying geometry and organ configurations have been studied. For the forward calculations, a standard dipole-like source is placed along the axis of the heart. Inverse calculations are performed using a measured body surface potential distribution and are based on a division of the surface of the heart into 25 source regions, producing epicardial potentials on these regions. A regularization method is used to stabilize the inverse solutions. Both forward and inverse solutions show substantial differences between models. These findings imply that matching models with patient geometry may be necessary in order to use such solutions in a clinical setting.

Electrocardiography↗
PubMed1986

Intravascular blood velocity in simulated coronary artery stenoses.

The profiles of blood velocity within arterial stenoses have been measured using fiber optic laser Doppler anemometry (FOLDA). The arterial stenoses were created in arteries and tubes of similar size to human coronary arteries and were perfused in vitro at pressures and flows typical of those in the human circulation. At very low flow rates, flow and peak velocity are linearly related, and thus peak velocity measurement can predict internal cross-sectional areas accurately. With higher flow rates, the intravascular velocities are not linearly related to flow and cannot be used to measure internal cross-sectional area. This is due to flattening of the velocity profile at both more severe stenoses and higher flow rates.

Blood Flow Velocity↗
PubMed1986

Extrahepatic metabolism and distribution of aspirin in vascular beds of sheep.

The dispositions of aspirin, its metabolite, salicylic acid, and its subsequent metabolite, salicyluric acid, were studied in eight anesthetized sheep infused with aspirin (61 and 485 microgram X min-1 X kg-1) for 75 min. Plasma samples were withdrawn from the portal vein, hepatic vein, pulmonary artery, left ventricle, left femoral vein, and left femoral artery. Significant extraction of aspirin occurred across the liver and hind leg, with mean availabilities of 0.75, 0.98, and 0.82 observed across the liver, lung, and hind leg, respectively. The extraction of aspirin was not affected by coadministration of sodium salicylate (30-1200 mg equiv salicylic acid). This extraction reflected hydrolysis of aspirin to salicylic acid; the metabolism of aspirin in the hind leg, lung, and liver being confirmed with tissue homogenate studies. The metabolism of aspirin in the extrahepatic tissues is significant in relation to the proposed selective presystemic acetylation of platelet cyclooxygenase by aspirin and the use of low-dose aspirin for thrombotic indications.

Animals↗
PubMed1986

Distribution and metabolism of nitroglycerin and its metabolites in vascular beds of sheep.

The disposition of nitroglycerin (NTG) and its metabolites has been examined in anesthetised sheep after infusion of 0.4, 5.7 and 22.1 micrograms of NTG/min/kg through the right femoral vein. Several blood samples were collected from the left ventricle, pulmonary artery, left femoral artery, left femoral vein, portal vein and hepatic vein. Significant extraction of NTG across all vascular beds was demonstrated. The extraction was shown to be dose-dependent reflecting hemodynamic and metabolic events. Evidence for metabolism of NTG was provided by the formation of the dinitro and mononitrate metabolites. A preliminary study also showed that administration of the dinitroglycerin significantly impaired NTG metabolism across the hind leg without affecting markedly the hemodynamic response associated with the infusion of NTG.

Animals↗
PubMed1984

The morphogenesis of Yaba monkey tumor virus in a cynomolgus monkey kidney cell line.

The morphogenesis of Yaba monkey tumor virus (YMTV) was investigated in a cynomolgus monkey kidney cell line. YMTV has been shown to grow less rapidly in high-passage cells (i.e., 65 passages) than in low-passage cells (i.e., between 30 and 60 passages). This prolonged growth cycle in high-passage cells allows for a more detailed analysis of the events in morphogenesis. Samples of YMTV-infected cells were prepared for analysis at 2, 3, 4, and 5 days postinfection. At least 12 "stages" of virus morphogenesis can be identified.

Animals↗
PubMed1982

The molecular biology of Yaba tumour pox virus: analysis of lipids, proteins and DNA.

Cytopathological studies have shown that Yaba tumour pox virus (Yaba virus) infection leads to the accumulation of large lipid vacuoles. The rate of accumulation of these vacuoles increased as the infection proceeded. These lipid vacuoles were not seen in control cells or in cells infected with monkeypox virus (MPV) but were seen during Yaba virus infection in the presence of cytosine arabinofuranoside (100 microgram/ml). Yaba virus also failed to inhibit host protein synthesis as infection proceeded for prolonged periods. Yaba virus proteins were shown to be substantially different from those of MPV when analysed by two-dimensional electrophoresis. The genome of Yaba virus gave restriction enzyme fragments which differed from those of the MPV genome when cleaved with the enzymes HindIII and XhoI. However, Yaba virus DNA hybridized to the HindIII fragments K, L and M and to the XhoI fragments A, B, C, E and G of MPV DNA.

Animals↗