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Biomedical subjects

D N Sharpe

Publications and source records attributed to D N Sharpe.

At least 37 records · Page 2Linked to original sources
PubMed1984

Prevention of ventricular fibrillation during acute myocardial infarction by intravenous propranolol.

A trial of intravenous followed by oral propranolol, started within 4 h of onset of suspected myocardial infarction and continued over 27 h, was carried out in 735 patients; 364 received propranolol, 371 were controls. Ventricular fibrillation during the first 48 h after entry to the trial occurred in 2 treated patients and in 14 controls (p = 0.006). Rates of hospital mortality, complications other than ventricular fibrillation, and progression from threatened to completed infarction did not differ between treated and control patients. Ventricular fibrillation was not apparently prevented by prior beta-blocker treatment, which was not a reason for exclusion from the trial. This intravenous/oral propranolol regimen seems to prevent ventricular fibrillation due to evolving myocardial infarction.

Administration, Oral↗
PubMed1984

Trends in survival after myocardial infarction in New Zealand, 1974-81.

Coronary heart disease mortality in New Zealand has declined by 20% in the 13 years since 1968. One possible explanation for this decline is lower case-fatality rates resulting from improvements in the management of myocardial infarction. This paper tests this hypothesis by examining trends in 1-year survival following a definite myocardial infarction for the population aged 35-69 in Auckland. The data were obtained from two methodologically identical population-based registers of myocardial infarction compiled in 1974 and 1981 in Auckland. In both periods the 1-year crude case-fatality rate was 30% and the pattern of survival over 1 year was similar. These data suggest that factors other than the improved care of myocardial infarction patients are responsible for the decline in coronary heart disease mortality rates in New Zealand.

Adrenergic beta-Antagonists↗
PubMed1984

Enalapril in patients with chronic heart failure: a placebo-controlled, randomized, double-blind study.

A number of studies have shown short-term hemodynamic and symptomatic improvement in patients with congestive heart failure treated with angiotensin converting-enzyme inhibitors. The long-term efficacy of the oral long-acting converting-enzyme inhibitor enalapril remains to be established in controlled studies. We evaluated this drug in 36 patients with New York Heart Association functional class II to III heart failure who were clinically stable on digoxin and diuretic therapy. After baseline assessment of symptoms, exercise capacity, and results of echocardiographic examination and right heart catheterization, patients were randomly assigned to treatment with 5 mg enalapril twice daily (n = 18) or placebo (n = 18) in a double-blind fashion. The two groups had similar clinical, echocardiographic, and hemodynamic characteristics before treatment. After 3 months of treatment, the enalapril group showed a significant improvement as judged by subjective patient impression, functional class, and exercise duration (9.3 +/- 5.7 vs 17.6 +/- 5.6 min; p less than .001). Diuretic dosage was reduced in six patients and increased in one patient, one patient had died and another had been withdrawn from the study. In the placebo group there was no significant change with respect to patient impression, functional class, or exercise duration; diuretic dosage was increased in seven patients and four patients had died. Echocardiographic left ventricular dimensions were significantly reduced and left ventricular shortening fraction significantly increased in the enalapril group but were unchanged in the placebo group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Newer inotropic agents.

Impairment of myocardial contractility results in reduction of cardiac output and activation of various compensatory mechanisms which eventually work to disadvantage. Drug treatment is directed towards improving myocardial contractility with inotropic agents and relieving congestion and vasoconstriction with diuretics and vasodilators. Digitalis is a relatively modest inotropic agent with considerable toxic potential and there is a need for alternative inotropic agents which are potent, active orally, effective long term and have minimal adverse effects. A number of beta agonists have been evaluated but their application appears limited to some extent by the development of tolerance, probably due to downregulation of myocardial beta receptors. Of the non-adrenergic inotropic agents currently under evaluation, amrinone appears most promising although its mechanism of action is not known.

Aminopyridines↗
PubMed1983

Digitalis.

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Digoxin↗
PubMed1983

Prenalterol, an oral beta-1 adrenoceptor agonist, in the treatment of chronic heart failure.

The haemodynamic effects of prenalterol, a new beta-1 agonist, were studied in 10 patients with chronic heart failure. Following intravenous prenalterol infusions of 1 mg, 2.5 mg and 5 mg at 15 min intervals, oral slow release prenalterol 20 mg, 30 mg and 50 mg was given at 2 h intervals and then 50-100 mg bid for one month. There were no significant changes in heart rate or blood pressure. Cardiac output increased significantly from control of 4.4 +/- 0.91/min to a maximum of 5.8 +/- 1.81/min (p less than 0.01) following the 5 mg prenalterol infusion and this increase was maintained following oral prenalterol on Days 1 and 2 and at 1 month. Significant increases in stroke volume and stroke work indices and reduction in systemic vascular resistance were also observed. Maximum increases in cardiac output and stroke work index following intravenous prenalterol correlated significantly with maximum increases observed following oral prenalterol on Day 2. Non-invasive evaluation showed no change in echocardiographic left ventricular end-diastolic dimension but a significant reduction in left ventricular end-systolic dimension on Day 30. PEP/LVET was significantly reduced from control of 0.56 +/- 0.15 to 0.47 +/- 0.12 (p less than 0.05) on Day 2 and 0.49 +/- 0.09 (p less than 0.05) at 1 month. Treadmill exercise duration was significantly improved for the group at 1 month and no adverse effects were noted. Oral slow release prenalterol is a potentially useful new drug for patients with chronic heart failure.

Administration, Oral↗
PubMed1982

Hemodynamic effects of captropril in chronic heart failure: efficacy of low-dose treatment and comparison with prazosin.

The acute hemodynamic effects and long-term therapeutic actions of low doses of the oral angiotensin-converting enzyme (ACE) inhibitor captopril (CPT) were evaluated in 18 patients with severe chronic congestive heart failure (CHF). Increasing doses of 1, 2.5, 6.25, 12.5, and 25 mg of CPT were given at 2-hour intervals. Increased stroke volume index (SVI) and reduced mean pulmonary capillary wedge (PCW) pressure occurred at 1 hour (p less than 0.05) with an associated decline of blood pressure. Maximal hemodynamic improvement for the group was seen at 6 and 7 hours following the 6.25 and 12.5 mg doses when SVI was elevated 35% and mean PCW pressure decreased 40% from control. CPT in doses of 12.5 to 50 mg every 8 hours was continued long term in these 18 CHF patients. Four patients died, and one was noncompliant; drug therapy was withdrawn in two patients with symptomatic hypertension and in one patient who experienced an alteration in taste. The remaining 10 patients showed significant improvement in symptoms and treadmill exercise duration at 3 months after CPT therapy was started. Moreover, repeat hemodynamic measurements were similar to optimal measurements obtained during the initial study. In a further study, the acute hemodynamic and hormonal effect of sequentially randomized 5 mg prazosin and 25 mg CPT were compared in 10 CHF patients. While both drugs reduced PCW pressure and vascular resistance, CPT effects were greater. Further, CPT alone effected a small rise in cardiac index and minor decline in heart rate, and CPT diminished aldosterone levels and increased plasma renin activity while prazosin did not.

Aldosterone↗
PubMed1982

Clinical and haemodynamic effects of low dose captopril in severe chronic heart failure.

1 The clinical and haemodynamic effects of low doses of the oral converting-enzyme inhibitor captopril were studied in 18 patients with severe chronic heart failure. Increasing doses of 1 mg, 2.5 mg, 6.25 mg, 12.5 mg, and 25 mg captopril were given at two hour intervals with haemodynamic monitoring. Graded haemodynamic improvement (increased stroke volume index and reduced mean pulmonary capillary wedge pressure) occurred from one hour with reduction of blood pressure closely associated. 2 Maximal haemodynamic improvement for the group was seen at six and seven hours after the 6.25 mg and 12.5 mg doses, when stroke volume index was increased by 35% and mean pulmonary capillary wedge pressure reduced by 40% from control. Captopril 12.5 mg-50 mg eight hourly was continued long-term but withdrawn in two patients with symptomatic hypotension and one patient with altered taste. 3 Four patients died and one was non-compliant with therapy. At three months 10 patients showed significant improvement in symptoms, treadmill exercise duration, and echocardiographic indices of left ventricular size and function. The results of repeat haemodynamic measurements were similar to optimal measurements obtained during the initial study. 4 At two years six patients remained alive, five having maintained their symptomatic improvement. Thus small doses of captopril produce haemodynamic improvement in heart failure with a closely associated reduction of blood pressure. Symptomatic and haemodynamic benefit is maintained with long-term treatment.

Adult↗
PubMed1982

Prazosin and captopril in chronic heart failure: comparison of acute haemodynamic and hormonal effects.

Ten patients with severe chronic heart failure were given prazosin 5 mg and captopril 25 mg in random order on consecutive days. Small increases in cardiac index and reductions in heart rate were effected by both drugs, but these alterations and the accompanying increases in stroke volume index were significant only following captopril. Both drugs significantly reduced mean pulmonary capillary wedge pressure and mean right atrial pressure and also systemic vascular resistance and blood pressure, the effect of captopril being greater than that of prazosin. Following captopril, plasma aldosterone levels were significantly reduced and plasma renin activity increased from control values, whereas prazosin did not alter these hormone indices.

Aged↗
PubMed1981

Trends in coronary heart disease mortality and associated risk factors in New Zealand.

Coronary heart disease mortality declined by 17 percent and 14 percent for New Zealand European men and women respectively between 1968 and 1978. The fall occurred in all age groups and in Maoris and cannot be attributed to change in diagnostic fashions. The decline has been associated with a decrease in the consumption of diary products and more recently with a levelling off of cigarette smoking, an increased awareness of the importance of treating hypertension, and an apparent increase in habitual physical activity in the community. There have also been improvements in the medical management of patients with coronary heart disease which may be contributing to the continuing decline in mortality rates. A programme to monitor trends in CHD incidence and case fatality and the level of risk factors in the community is required to elucidate the reasons for the decline in CHD mortality.

Adult↗
PubMed1981

The effect of captopril on plasma histamine and histamine release in vitro.

Plasma histamine and the release of histamine from blood in vitro has been determined in patients being treated for hypertension or heart failure with captopril. This drug does not alter plasma histamine levels in either group of patients or release histamine from human basophils, rat peritoneal mast cells or guinea pig lung slices upon challenge in vitro. We conclude that histamine release does not contribute to the cardiovascular or side effects of captopril.

Adult↗
PubMed1980

Low-dose captopril in chronic heart failure: acute haemodynamic effects and long-term treatment.

The acute haemodynamic effects of low doses of the oral converting-enzyme inhibitor, captopril, were studied in 18 patients with severe chronic heart failure. The effects of long-term therapy were also evaluated. Increasing doses (1 mg, 2.5 mg, 6.25 mg, 12.5 mg, and 25 mg) of captopril were given at 2 h intervals with haemodynamic monitoring. Graded haemodynamic improvement (increased stroke-volume index and reduced mean pulmonary capillary wedge pressure) was noted from 1 hand was closely associated with reduction of blood pressure. Maximal haemodynamic improvement for the group was seen at 6 h and 7 h after the 6.25 mg and 12.5 mg doses, when stroke-volume index had risen 35% and mean pulmonary capillary wedge pressure had fallen 40% from control. Captopril 12.5-50 mg every 8 h was continued long term but was withdrawn in 2 patients with symptomatic hypotension and 1 patient with altered taste. 4 patients died and 1 was noncompliant with therapy. At 3 months, 10 patients showed significant improvement in symptoms, treadmill-exercise duration, and echocardiographic indices of left-ventricular size and function. Repeat haemodynamic measurements were similar to optimum measurements obtained during the initial study.

Adult↗
PubMed1980

Captopril in the treatment of refractory high-renin hypertension.

Two cases of high-renin renovascular hypertension, one due to Takayasu's arteritis and the other to a hypersensitivity vasculitis, are described. Both were resistant to maximal standard therapy but responded to treatment with captopril, the orally active angiotensin-converting enzyme inhibitor.

Adult↗
PubMed1980

Arterial connective tissue changes and distribution of 125I-labelled low density lipoprotein in hypertensive pigs.

Young pigs with hypertension of 10 weeks duration, resulting from cellophane perinephritis, were injected with 125I-labelled low-density lipoprotein ([125I]LDL) before being killed 24 h or 48 h later. Intimal thickening and increased acid mucopolysaccharide were demonstrated in the aortas and major arteries of the hypertensive animals. Increased accumulation of [125I]LDL was observed in the inner media beneath areas of intimal thickening. It is suggested that the primary effect of hypertension in atherosclerosis is to produce structural changes in arterial connective tissue which allow increased accumulation of LDL by altering the permeability and binding properties of the arterial wall.

Animals↗
PubMed1979

Lack of correlation between echocardiographic pulmonary valve morphology and simultaneous pulmonary arterial pressure.

Pulmonary valve echograms recorded simultaneously with right heart pressures were correlated with mean and end-diastolic pulmonary arterial pressures and the peak magnitude of the right atrial a wave in an attempt to predict noninvasively levels and changes in pulmonary arterial pressure. Satisfactory pulmonary valve echograms were obtained in 16 of 23 patients studied. No significant correlation was found between hemodynamic measurements and the echographic pulmonary valve a wave amplitude, diastolic E-F slope or the systolic opening B-C slope. Changes in hemodynamic measurements observed in serial observations were not associated with predictable changes in configuration of the pulmonary valve echogram. The combination of mid systolic pulmonary valve notching and an absent a wave was observed in more advanced degrees of pulmonary hypertension and was specific, but not sensitive, for that condition.

Adult↗
PubMed1978

The clinical estimation of acute myocardial infarct size with 99mTechnetium pyrophosphate scintigraphy.

We evaluated scintigraphic techniques in estimating infarct size. In 26 patients with acute transmural myocardial infarction, 99mTechnetium pyrophosphate (TcPYP) infarct scintigraphy, gated cardiac blood pool scintigraphy and 201-Thallium (201-Tl) perfusion scintigraphy were performed. Invasive hemodynamic measurements were obtained and serial venous blood specimens taken for measurement of total and MB creatine phosphokinase (CPK). In farct size was estimated from the area of abnormal TcPYP uptake, the extent of reduced 201-Tl uptake, the percentage of abnormally contracting segments, and serial enzyme measurements. Left ventricular ejection fraction (LVEF) and stroke work index (LVSWI) were calculated. TcPYP infarct area was associated with the extent of reduced 201-Tl uptake (r = 0.66), the percentage of abnormally contracting segments (r = 0.64), and with both LVSWI (r = 0.73) and LVEF (r = 0.58). TcPYP infarct area did not correlate with cumulative total or MB-CPK release or the integrated total CPK-time curve, nor did the enzyme estimates of infarct size correlate with LVSWI or LVEF. Variable perfusion of infarcts of different sizes may explain the lack of correlation between TcPYP infarct area and enzyme estimates of infarct size. A combination of anatomic and functional indices derived from scintigraphic and hemodynamic measurements may provide the best assessment of infarct size.

Acute Disease↗