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Biomedical subjects

D A McGill

Publications and source records attributed to D A McGill.

7 recordsLinked to original sources
PubMed1994

Abnormal platelet reactivity in men with premature coronary heart disease.

BACKGROUND: Continuous platelet aggregation does not occur in patients with stable coronary heart disease (CHD). However, there may be a latent potential for increased aggregation given appropriate stimuli, since increased in-vitro platelet aggregation appears to be predictive of cardiac events. This study evaluates the relationship between in-vitro platelet aggregation and coronary artery disease (CAD) as defined by angiography. METHODS: In-vitro platelet aggregation was assessed in a case-control study of 53 men with CHD younger than 50 years, and in 48 control subjects without CHD who were matched for age, sex, and socioeconomic status. All major risk factors were evaluated. Semi-quantitative composite scores of the extent of arterial wall involvement and composite scores for the severity of discrete lesions were documented from standard coronary angiography. Measures of platelet aggregation in response to adrenaline, adenosine diphoshate (ADP), and collagen included: (1) the maximum slope of the aggregation curve (rate); (2) lag time to 50% maximum aggregation (LT50%); and (3) the threshold concentration of each agonist to cause maximal aggregation. RESULTS: The CHD patients had larger platelets than patients in the control group (mean platelet volume 9.40 +/- 0.73 versus 8.88 +/- 0.87; P < 0.01). The aggregation rate was significantly faster with adrenaline in the group with CHD than patients in the control group (rate of aggregation 13.9 +/- 8.8 versus 8.6 +/- 4.0 cm/s respectively, mean +/- SD; LT50% for adrenaline 130 +/- 70 versus 230 +/- 10 s respectively, mean +/- SD). Fewer CHD patients had no aggregation response to adrenaline than in the control group (8 versus 31%, P < 0.05). Adrenaline-induced platelet aggregation, as measured by LT50% for adrenaline, weakly but significantly correlated with the number and severity of discrete obstructive coronary lesions (r = -0.28, P < 0.05). This association remained significant after multivariate regression analysis. No association was found between any measure of platelet reactivity and the extent of disease as measured by a semi-quantitative composite score; this measured the extent of disease of the coronary artery walls visible by angiography. CONCLUSIONS: These findings indicate that platelets from men with premature CHD are larger and aggregate more rapidly in response to platelet agonists, particularly adrenaline. An increased rate of aggregability with adrenaline predicted the severity of CAD lesion but not the extent of the disease, and this suggests that platelets play a role in the formation of localized obstructive lesions in coronary arteries, and therefore acute coronary events.

Adenosine Diphosphate↗
PubMed1993

Relationship of blood cholesterol and apoprotein B levels to angiographically defined coronary artery disease in young males.

BACKGROUND: Coronary heart disease is mainly caused by the effects of obstruction to blood flow in the coronary arteries from discrete mural lesions that encroach into the lumen and usually occur in arteries that are involved by atherosclerosis. Even though the level of certain lipoproteins is indisputably related to the degree of this atherosclerotic involvement of the coronary arteries, the question of whether lipoproteins are also associated with the obstructive lesions remains uncertain. METHODS: This study addressed the question in 53 males (age, 44.6 +/- 4.9 y) with premature coronary heart disease and angiographically proven coronary artery disease. The cholesterol, triglyceride, high-density lipoprotein, apoprotein B, and apoprotein A-I levels were compared by linear correlation to semiquantitative angiographic measures of coronary artery disease severity (coronary stenosis score and mean coronary stenosis score), the extent of mural involvement (coronary atheromatous score and mean coronary atheromatous score), and also the number of normal coronary artery segments, an alternative severity score (Jenkins), and left ventricular function score. RESULTS: Age, past and present cholesterol, low-density lipoprotein cholesterol, and apoprotein B levels correlated directly with the extent of disease (r = 0.27, 0.46, 0.29, 0.26, 0.35, respectively, P < 0.05 with coronary atheromatous score; r = 0.29, 0.44, 0.33, 0.30, 0.35, respectively, P < 0.05 with mean coronary atheromatous score). Age and New York Heart Association angina functional class correlated directly with disease severity (r = 0.25, 0.31, respectively, P < 0.05 with coronary stenosis score; r = 0.25, 0.34, respectively, P < 0.05 with mean coronary stenosis score). There was an inverse association between age, past and present cholesterol, low-density lipoprotein cholesterol, and apoprotein B levels with the number of normal segments (r = -0.23, -0.46, -0.38, -0.35, -0.39, respectively, P < 0.05). Multiple regression analysis was undertaken with lipoproteins and age as independent variables and angiographic scores as dependent variables; the apoprotein B level was the most predictive of the extent of coronary artery disease (P < 0.02) and inversely predicted the number of normal segments (P < 0.002). Of those variables entered into the regression model, only age was independently predictive of the severity of angiographic coronary artery disease. CONCLUSION: Apoprotein B levels are not predictive of coronary artery disease severity but do predict independently the extent of involvement of coronary atherosclerosis defined angiographically.

Adult↗
PubMed1985

The acute haemodynamic effects of oral nicardipine.

The haemodynamic effects of oral nicardipine at two different doses were assessed in fifteen patients at rest following diagnostic cardiac catheterisation. Six patients received four doses of 20 mg nicardipine hydrochloride orally every 8 h, and nine patients received four doses of 30 mg orally every 8 h. No side effects were encountered with either dose. At both dose levels, there was a significant fall in systemic vascular resistance, significant increases in heart rate and cardiac output, and no change in stroke volume index. No changes were seen in pulmonary vascular haemodynamics, and there were no significant changes in mean arterial pressure. Plasma levels of nicardipine reached a peak within 1 h. In parallel with the haemodynamic effects, the plasma concentrations achieved after the third and fourth doses were higher than after the first dose. These haemodynamic changes are consistent with a vasodilator effect, which produces a decrease in peripheral vascular resistance. It would appear that the 30 mg dose has a more potent vasodilator action than the 20 mg dose and, in the patients studied, this larger dose was not associated with any side effects.

Administration, Oral↗