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D J Coltart

Publications and source records attributed to D J Coltart.

At least 19 recordsLinked to original sources
PubMed1992

Effects on coronary artery disease of lipid-lowering diet, or diet plus cholestyramine, in the St Thomas' Atherosclerosis Regression Study (STARS)

To assess the effect of dietary reduction of plasma cholesterol concentrations on coronary atherosclerosis, we set up a randomised, controlled, end-point-blinded trial based on quantitative image analysis of coronary angiograms in patients with angina or past myocardial infarction. Another intervention group received diet and cholestyramine, to determine the effect of a greater reduction in circulating cholesterol concentrations. 90 men with coronary heart disease (CHD), who had a mean (SD) plasma cholesterol of 7.23 (0.77) mmol/l were randomised to receive usual care (U, controls), dietary intervention (D), or diet plus cholestyramine (DC), with angiography at baseline and at 39 (SD 3.5) months. Mean plasma cholesterol during the trial period was 6.93 (U), 6.17 (D), and 5.56 (DC) mmol/l. The proportion of patients who showed overall progression of coronary narrowing was significantly reduced by both interventions (U 46%, D 15%, DC 12%), whereas the proportion who showed an increase in luminal diameter rose significantly (U 4%, D 38%, DC 33%). The mean absolute width of the coronary segments (MAWS) studied decreased by 0.201 mm in controls, increased by 0.003 mm in group D, and increased by 0.103 mm in group DC (p less than 0.05), with improvement also seen in the minimum width of segments, percentage diameter stenosis, and edge-irregularity index in intervention groups. The change in MAWS was independently and significantly correlated with LDL cholesterol concentration and LDL/HDL cholesterol ratio during the trial period. Both interventions significantly reduced the frequency of total cardiovascular events. Dietary change alone retarded overall progression and increased overall regression of coronary artery disease, and diet plus cholestyramine was additionally associated with a net increase in coronary lumen diameter. These findings support the use of a lipid-lowering diet, and if necessary of appropriate drug treatment, in men with CHD who have even mildly raised serum cholesterol concentrations.

Angina Pectoris↗
PubMed1992

Is angiographic ventriculography necessary for the assessment of ischemic patients?

A total of 53 patients with a provisional diagnosis of ischemic heart disease and without any clinical evidence of valvular, congenital, or primary muscle heart disease were studied by echocardiography and biplane left ventricular cineangiography. For angiographic ejection fraction analysis, a program developed in our department for use on an Apple Macintosh computer interfaced to a digitizing tablet was employed. Echocardiographic outlines of systolic and diastolic images were traced with a digitizing system on the screen and ejection fractions were calculated by a program incorporated in the echo machine. Good echo windows allowing ejection fraction calculations were present in 35 patients. There was a good correlation between angiographic and echocardiographic ejection fraction (r = 0.7, SEE = 0.09), and wall motion assessment revealed no significant discrepancies between the two image modalities. The remaining 18 patients had poor echo windows, preventing accurate echocardiographic determination of the ejection fraction. However, limited assessment of left ventricular size and wall motion was possible in all patients and allowed the identification of those who had impaired left ventricular function as judged by angiography (angiographic ejection fraction < 35%). We conclude that even in patients with poor echo windows echocardiographic assessment of left ventricular function provides clinical information similar to angiography which should not be considered mandatory for the investigation of ordinary ischemic patients.

Cardiac Catheterization↗
PubMed1991

Echocardiographic left ventricular wall thickness: a poor predictor of the severity of aortic valve stenosis.

Echocardiographic left ventricular hypertrophy is thought to be helpful in grading the severity of aortic stenosis. This study compared M-mode echocardiographic left ventricular wall dimensions with Gorlin aortic valve area. Good quality echocardiograms were obtained in 294 patients with aortic stenosis who also underwent cardiac catheterization. Patients with grade 3 or 4 aortic regurgitation were excluded. The correlation was calculated between the aortic valve area and the left ventricular wall dimensions. Correlation coefficients were poor; r = 0.13 for the septum, r = 0.15 for the posterior wall, and r = 0.17 for the mean wall dimension. Correlation was not improved significantly if patients with poor left ventricular function or systemic hypertension were excluded. Correlation with other hemodynamic parameters was better, peak left ventricular systolic pressure having r values of 0.36 and 0.30 for posterior wall and septum. Mean and peak aortic valve gradient had r values approaching 0.30 for both dimensions. If the peak gradient was included in multivariate analysis, the wall dimensions then had no predictive power for severity of aortic stenosis. This study demonstrates that the degree of left ventricular wall hypertrophy is not related to the severity of aortic outflow obstruction and therefore cannot be used to grade the severity of aortic stenosis.

Aortic Valve↗
PubMed1990

Association of antibodies against phospholipids with heart valve disease in systemic lupus erythematosus.

A prospective echocardiographic study was carried out on 132 consecutive patients with systemic lupus erythematosus (SLE) derived from three European university medical centres. The prevalence of valvular lesions in patients with SLE was 22.7% compared with 2.9% in a control group of 68 healthy volunteers. 50 SLE patients had antibodies against phospholipids. The prevalence of valve vegetations (8/50 [16%]) and of mitral regurgitation (19/50 [38%]) was significantly higher among the SLE patients with antiphospholipids than among those without (1 and 10/82 [1.2% and 12%], respectively). During follow-up of the patients with valvular lesions, haemodynamically significant clinical valve disease developed in 6 but surgery was required in only 1; 9 had cerebrovascular occlusions; and 7 died, although no death was due directly to the cardiac involvement. Thus, valvular heart disease, particularly affecting the mitral valve, is common in patients with SLE, and the presence of antibodies against phospholipids is associated with a higher prevalence of valvular abnormalities in these patients.

Adolescent↗
PubMed1990

Infective endocarditis, rheumatoid factor, and anticardiolipin antibodies.

Serum samples from 22 patients with infective endocarditis were analysed for the presence of antibodies to cardiolipin, false positive Venereal Disease Research Laboratory (VDRL) test, and rheumatoid factor in order to determine the prevalence of anticardiolipin antibodies, their level, and to ascertain whether there was any correlation with the presence of rheumatoid factor. Although the latex test was positive in 10/22 (45%) patients, anticardiolipin antibodies, usually of a low level, were raised in only four (18%), and the VDRL test was positive in two patients in whom other antibodies were negative. These results show a clear discordance between these three tests, indicating that B cell production of these antibodies is separate and distinct. As with other infections which result in anticardiolipin antibody production, no thrombotic events were encountered.

Autoantibodies↗
PubMed1990

Cardiology.

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Angioplasty, Balloon, Coronary↗
PubMed1989

Acute hemodynamic effects of single-dose nicorandil in coronary artery disease.

Fifteen patients undergoing routine cardiac catheterization for investigation of chest pain were given a single dose of 40 mg of nicorandil either sublingually (8 patients) or orally (7 patients). Fourteen patients had angina (11 effort, 3 atypical) and 1 had palpitations but all had normal left ventricular (LV) function (mean LV end-diastolic pressure 7.4 mm Hg). Hemodynamic evaluations and plasma drug concentrations were performed at baseline and 5, 15, 30, 45 and 60 minutes after dosing. In addition, venous compliance was determined at baseline, 15 and 45 minutes using forearm venous occlusion plethysmography. Significant (p less than 0.05) central and peripheral hemodynamic changes occurred within 15 minutes. A reduction in preload was apparent from a decrease in LV end-diastolic pressure (from 7.4 +/- 1.7 to -2.6 +/- 1.5 mm Hg [p less than 0.05]) and a simultaneous decrease in mean pulmonary artery pressure (from 10.8 +/- 0.7 to 5.1 +/- 0.6 mm Hg [p less than 0.05]) at 60 minutes after dosing. This reduction in preload may reflect the venous vasodilatory activity of the drug as indicated by significant (p less than 0.05) increases in venous capacitance at 15 and 45 minutes. Total peripheral resistance decreased to a maximum of 19% (p less than 0.05) at 30 minutes and then began to return toward baseline. This effect in reducing afterload led to a substantial decrease (p less than 0.05) in systolic and diastolic aortic blood pressures, which was maximal at 45 minutes (34 and 21%, respectively). Transient increases in heart rate (p less than 0.05) and cardiac contractility indexes (p less than 0.05) were also observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1989

Inaccuracies in using aortic valve gradients alone to grade severity of aortic stenosis.

The severity of aortic stenosis is an important determinant of prognosis in patients with symptoms who do not undergo valve replacement. To assess the pitfalls of using valve gradients alone 636 patients with aortic stenosis in whom the aortic valve area had been calculated by the Gorlin formula were studied. The correlation between valve area and aortic gradients was poor. No gradient was found that was both sensitive and specific for aortic stenosis. The maximum predictive accuracy was 81% for a mean gradient of 30 mm Hg and 80% for a peak gradient of 30 mm Hg. A mean gradient of 50 mm Hg or a peak gradient of 60 mm Hg were specific with a 90% or more positive predictive value. It proved difficult, however, to find a lower limit with a 90% negative predictive value. Patients with severe aortic stenosis and low gradients (peak or mean gradient of less than 30 mm Hg) had small ventricles (on both angiographic and echocardiographic data) with good ejection fractions and so were unlikely to be detected subjectively. In comparison patients with mild aortic stenosis and low gradients tended to have more aortic regurgitation but have similar degrees of left ventricular hypertrophy on echocardiographic or electrocardiographic criteria. The aortic valve area should be measured in all patients with the suspicion of severe aortic stenosis with a mean gradient of less than 50 mm Hg (50% of patients in this study) or a peak gradient of less than 60 mm Hg (47% of patients in this study).

Age Factors↗
PubMed1987

Double-blind trial of the long-term effects of acebutolol and propranolol on serum lipoproteins in patients with stable angina pectoris.

In order to evaluate the long-term effects of propranolol and acebutolol on serum lipoprotein lipids, a double-blind clinical trial was carried out. Fifteen patients with stable angina pectoris, aged 32 to 79 years (mean = 53), were randomized to propranolol (80 to 160 mg/day) or acebutolol (400 mg/day) treatment groups, and followed for approximately 1 year (mean = 371 days). Blood was collected on the day treatment was begun, after approximately 5 months (mean = 158 days), and on completion of the trial. Very low-density lipoproteins (VLDL) (alpha less than 1.006), low-density lipoproteins (LDL) (1.006 to 1.063), and high-density lipoproteins (HDL) (1.063 to 1.125 [HDL2] and 1.125 to 1.21 [HDL3]) were isolated by sequential preparative ultracentrifugation, and their cholesterol and triglyceride quantified by enzymic procedures. After 1 year propranolol had raised the mean VLDL triglyceride concentration by 79% (p less than 0.005) and had lowered total HDL cholesterol by 24% (p less than 0.005). As LDL cholesterol was unchanged, the LDL cholesterol/HDL cholesterol ratio was increased by 26% (p less than 0.005). Mean values at 5 months were intermediate between those at baseline and those at 1 year. In contrast to these changes, acebutolol had no significant effect on any measured lipoprotein lipid.

Acebutolol↗
PubMed1985

Effects of intracoronary and intravenous amrinone infusions in patients with cardiac failure and patients with near normal cardiac function.

The effects of intracoronary and intravenous infusions of amrinone were studied to distinguish the drug's direct cardiac actions from its peripheral vascular and neuroendocrine properties. Intracoronary infusions of amrinone were found to have no haemodynamic effect other than producing a slight reduction in the left ventricular ejection fraction and some suggestion of coronary vasodilatation in patients with impaired left ventricular function. They did not improve contractility, cardiac output, or filling pressures and had no significant effect on myocardial metabolism, although therapeutic concentrations of the drug were detected in coronary sinus blood. Intravenously administered amrinone reduced filling pressures and improved the cardiac index in all patients, but haemodynamic improvements were most pronounced in the patients with the worst cardiac function. These changes were accompanied by improvements in the indices of contractility only in patients in whom alterations in concentrations of free fatty acid, glycerol, and glucose suggested peripheral catecholamine release. In the patients with the best basal cardiac function intravenously administered amrinone produced a reduction in myocardial work and evidence of myocardial ischaemia, as a result of excessive reduction of coronary perfusion pressure and increased heart rate, without any appreciable increase in cardiac index. It is concluded that, at the concentrations of the drug that can be achieved in man without adverse effects, amrinone has no direct positive inotropic effect. Haemodynamic changes are predominantly the result of vasodilatation, although catecholamines may be released in some patients.

Adult↗
PubMed1985

The genesis of arrhythmias during myocardial ischemia. Dissociation between changes in cyclic adenosine monophosphate and electrical instability in the rat.

It has been proposed that increases in tissue cyclic adenosine monophosphate during ischemia may be responsible for the induction of arrhythmias that occur during the early minutes of ischemia. We have tested this hypothesis using the isolated perfused rat heart with coronary artery occlusion for 30 minutes. In control hearts, after a transient small rise, cyclic adenosine monophosphate content remained close to its preischemic value (3.0 +/- 0.1 nM/g dry weight) throughout the period of occlusion. Eight percent (1/12) of the hearts fibrillated. Ninety-two percent (11/12) of the hearts exhibited ventricular tachycardia, and the mean total number of premature ventricular complexes was 528 +/- 121. Inclusion of epinephrine (1.0 microM) in the perfusion fluid elevated cyclic adenosine monophosphate prior to coronary occlusion (to 10.7 +/- 0.6 nM/g dry weight) and also throughout the ischemic period. It also increased arrhythmias such that 83% (20/24) of hearts fibrillated, 100% exhibited ventricular tachycardia, and the mean number of premature ventricular complexes increased to 747 +/- 86. Inclusion of forskolin (0.2 microM), which stimulates adenyl cyclase independently of the beta-receptor, increased cyclic adenosine monophosphate content to a greater extent than epinephrine, to 14.1 +/- 0.9 nM/g dry weight before the onset of ischemia and to 8.2 +/- 0.4 nM/g dry weight after 30 minutes of ischemia. Despite the large increase in cyclic adenosine monophosphate, there was no increase in rhythm disturbances which were less than those seen in controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1985

Reperfusion-induced ventricular fibrillation. Modification by pharmacological agents.

We have assessed the ability of several of the main groups of antiarrhythmic agents to modify the incidence of reperfusion-induced ventricular fibrillation in the isolated working rat heart preparation with transient coronary artery occlusion. Hearts were perfused with Krebs-Henseleit medium containing 5 microM epinephrine to provide some level of exogenous catecholamine support. Compounds selected were: the fast sodium channel inhibitors lignocaine (1 and 10 microM) and prenylamine (4 microM) (the latter also possessing slow calcium channel antagonistic actions); the beta-adrenergic blocking agents oxprenolol (1.2 microM), timolol (0.13 microM), metoprolol (1.0 microM), and acebutolol (5.6 microM); and the slow calcium channel antagonist nifedipine (0.05 and 0.5 microM). After 15 min of coronary artery occlusion, over 90% of control hearts fibrillated 30-60 sec after the onset of reperfusion. Drugs reduced this to the following: prenylamine, 0% (p less than 0.001); 1 microM lignocaine, 83%; 10 microM lignocaine, 33% (p less than 0.01); oxprenolol, 92% (NS); timolol, 92% (NS); metoprolol, 42% (p less than 0.01); acebutolol, 67% (p less than 0.05); 0.05 microM nifedipine, 83% (NS); and 0.5 microM nifedipine, 67% (NS). Thus, inhibition of the fast inward sodium channel with agents such as prenylamine and lignocaine, (when begun before coronary-artery occlusion) offers maximal protection against reperfusion-induced ventricular fibrillation, while beta-blockade with timolol and oxprenolol and slow calcium channel inhibition with nifedipine do not offer any significant protection. The beta-blocking agents metoprolol and acebutolol produce a partial reduction that may be due to a membrane-stabilizing action, rather than to beta-blockade.

Adrenergic beta-Antagonists↗
PubMed1979

A computerised dichromatic earpiece densitometer for the measurement of cardiac output.

This study assesses a precalibrated dichromatic earpiece densitometer and microprocessor for the measurement of cardiac output by indocyanine green dye dilution. The measured cardiac output is compared with values of cardiac output simultaneously determined using a cuvette densitometer. The microprocessor computation of cardiac output agreed very closely with the cardiac output determined by manual calculation from the same dye dilution curves (standard deviation +/- 1.47%). The reproducibility of the earpiece densitometer (standard deviation +/- 5.2%) was virtually identical to that of the cuvette densitometer (+/- 5.3%). In a comparison of earpiece and cuvette densitometers for 60 measurements of cardiac output following pulmonary arterial injection of dye and for 50 measurements following femoral venous injection of dye, correlation coefficients were 0.83 and 0.78 and the standard deviations of the differences of simultaneous measurements were 7.2% and 8.3% respectively. The instrument offers an accurate reproducible and relatively noninvasive technique for measuring cardiac output.

Cardiac Output↗