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Biomedical subjects

L G Howes

Publications and source records attributed to L G Howes.

At least 55 records · Page 3Linked to original sources
PubMed1995

Atrial fibrillation after coronary artery bypass grafting is associated with sympathetic activation.

BACKGROUND: We prospectively investigated the role of sympathetic activation in the etiology of atrial fibrillation following coronary artery bypass grafting. METHODS: Continuous ambulatory monitoring was performed for 80 hours in 131 patients after coronary artery bypass grafting. Right atrial plasma norepinephrine levels were assessed preoperatively and every 4 hours for 48 hours postoperatively. RESULTS: Of the 131 patients, 50% (65) had development of atrial fibrillation and 36% (47) required treatment. Onset of atrial fibrillation was preceded by a significant increase in sinus rate and atrial ectopic activity. On multivariate logistic regression, elevated mean postoperative norepinephrine levels (5.78 +/- 2.83 versus 3.57 +/- 1.31 nmol/L; p < 0.0001), increased age (68.9 +/- 5.7 versus 63.8 +/- 8.7 years; p = 0.02), and decreased postoperative magnesium levels (0.79 +/- 0.09 versus 0.83 +/- 0.10 mmol/L; p = 0.02) were independently associated with the occurrence of atrial fibrillation. CONCLUSIONS: Elevated norepinephrine levels suggest that sympathetic activation may be important in the pathogenesis of atrial fibrillation after coronary artery bypass grafting, and this underlines the importance of beta-adrenoceptor blockade as prophylaxis.

Aged↗
PubMed1995

The effects of short-term alcohol intake on clinic and ambulatory blood pressure in normotensive 'social' drinkers.

Office blood pressure (OBP), ambulatory blood pressure (ABP), and vascular reactivity were measured in 12 normotensive 'social' drinkers (mean alcohol consumption of 9.7 +/- 3.1 g/day) after 4 days of alcohol consumption (1 g/kg/day) and compared with the effects of an isocaloric substitute (sucrose, 1.75 g/kg/day) or no intervention. Alcohol consumption did not affect OBP or 24-mean ABP but appeared to decrease nocturnal systolic and diastolic blood pressure soon after consumption. Although vascular reactivity did not differ between the groups, the blood pressure rise in response to isometric exercise tended to be lower following alcohol. Thus, short-term alcohol ingestion by normotensive 'social' drinkers does not increase office or ambulatory blood pressure.

Adult↗
PubMed1995

24 hour ambulatory blood pressure profiles in the acute phase of stroke.

1. Twenty-four hour ambulatory blood pressure monitoring (ABPM) was used to evaluate the blood pressure (BP) changes in acute stroke. 2. Stroke was categorized according to the probable underlying vascular mechanism into lacunar infarction (L), thrombotic infarction (T) and intracerebral haemorrhage (ICH). A total of 37 stroke patients were studied (T = 21, L = 9, ICH = 7). Control patients (n = 15) were acute medical admissions not severely ill or in significant pain. ABPM was performed on day 1 and day 7 following admission. 3. Day 1 mean +/- s.d. 24 h systolic BP (SBP) were L (159 +/- 15.8), ICH (151 +/- 33.4), T (147 +/- 15.2) and controls (134 +/- 17.8). Day 7 mean 24 h SBP were L (138 +/- 9.8), ICH (143 +/- 26.9), T (138 +/- 19) and controls (134 +/- 14.8). In each stroke group BP fell to levels similar to control on day 7, while control mean SBP remained unchanged between days 1 and 7. The highest day 1 BP and the greatest subsequent fall on day 7 occurred for lacunar infarction. Diastolic BP showed similar changes to SBP. 4. The acute stress of hospitalization does not appear to explain elevated BP in acute stroke. Lacunar infarction appears to be particularly associated with temporary BP elevation.

Aged↗
PubMed1995

Which drugs affect potassium?

A number of drugs can affect potassium levels by a variety of different mechanisms. Diuretics remain the most important cause of drug-induced alterations. ACE inhibitors may produce hyperkalaemia, particularly in patients with autonomic neuropathy, adrenal insufficiency, renal impairment and when used in combination with nonsteroidal anti-inflammatory drugs (NSAIDs). Cathartic and/or diuretic abuse should be suspected when hypokalaemia occurs in young patients suspected of having an eating disorder. NSAIDs may occasionally produce hyperkalaemia, particularly in patients with renal impairment or when used with ACE inhibitors. Sympathomimetics and theophylline derivatives may lower serum potassium levels, but this is usually only of clinical significance when overdosage occurs.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Critical assessment of ACE inhibitors. Part 1.

Critical assessment of ACE inhibitors is an independent review of an important group of drugs widely used in the management of hypertension and heart failure. The paper is presented in two parts: Part 1 contains an overview of their action and their use in the treatment of hypertension. Part 2 focuses on the use of ACE inhibitors in heart failure and in pregnant women and in children.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Critical assessment of ACE inhibitors. Part 2.

Angiotensin converting enzyme (ACE) inhibitors are now widely used for the treatment of hypertension and heart failure. They are of particular value in treating hypertensive patients with left ventricular dysfunction, and in diabetics where they have been shown to delay the progression of diabetic nephropathy. Differences in the metabolism, pharmacokinetics, and pharmacodynamics between the various ACE inhibitors generally do not translate into significant clinical differences in the majority of patients. However, fosinopril may be the preferred ACE inhibitor in patients with significant renal dysfunction because of a reduced requirement for dosage reduction. The duration of action of ACE inhibitors is determined by two properties, the plasma half-life and the affinity of binding to tissue ACE. All of the ACE inhibitors (with the possible exception of captopril) can provide satisfactory 24-hour blood pressure control in the majority of patients with mild to moderate hypertension when given once daily. Lisinopril provides consistently better 24-hour control of blood pressure than either captopril or enalapril. Evidence for superior 24-hour blood pressure control over enalapril has not been as well established for the other ACE inhibitors. Captopril may be preferred for initiating therapy in patients with severe heart failure who are at risk of first dose hypertension because of its rapid onset of action and relatively short duration of action. There is evidence, however, that perindopril may have a low risk of first dose hypertension in heart failure because of its gradual onset of action. Long-acting ACE inhibitors may be preferable for chronic therapy of heart failure. All of the ACE inhibitors have a low incidence of adverse effects in both young and elderly patients, and there is no convincing evidence of differences in tolerability between the drugs.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1994

A single-dose comparison of the bioavailability of aluminium from two formulations of sucralphate in normal volunteers.

The oral bioavailability of aluminium was compared after administration of 1 g sucralphate as either a tablet or a suspension (1 g/5 ml) in a crossover study in 16 healthy volunteers. Aluminium levels were detectable in all subjects pre-dose (21.4 +/- 8.8 micrograms l-1 before tablet; 21.4 +/- 7.4 micrograms l-1 before suspension) and there was a measurable increase in the plasma concentrations of aluminium in all subjects after administration of the suspension, and in 14 of the subjects after administration of the tablet formulation, with Cmax reached within the first 8 h in most subjects. Plasma levels were still elevated 72 h after dosing. The variability in plasma levels of aluminium was significantly higher after administration of the suspension (CV 39-53%) than after administration of the tablet (CV 29-44%), reflecting greater absorption of aluminium from the suspension formulation in three subjects. Similarly, the variance of the Cmax, AUC(0-72 h), and AUC(0-infinity) (for both the raw data and the baseline adjusted data) were all higher for the suspension than for the tablet. A point estimate of the difference of the pharmacokinetic parameters (determined from the median of the arithmetic Walsh averages) indicated little or no difference in Cmax, Tmax, or AUC(0-infinity) in the two formulations. In summary, the performance of the suspension formulation of sucralphate is more variable than the tablet formulation in vivo and some patients may therefore have higher circulating levels of aluminium on therapy with the suspension formulation.

Administration, Oral↗
PubMed1994

Efficacy of drug intervention for lipids in the prevention of coronary artery disease.

Meta-analysis of the benefit of drug intervention in hypercholesterolaemia has produced conflicting conclusions, dependent upon which studies were included or which outcomes were considered. We have approached this question by considering coronary artery disease (CAD) outcomes, fatal and non-fatal, in studies considered to be pivotal--those of sufficient size and duration and those achieving sufficient cholesterol reduction to be likely to have a statistically significant outcome. In parallel, we have reviewed all the published angiographic trials of adequate design (randomised and controlled). In four pivotal primary prevention studies, CAD morbidity was reduced in the range 19-45%. CAD mortality was reduced significantly in one of these studies. Women were included in only one study and they did not exhibit the favourable outcome observed in men. In four pivotal secondary prevention studies, CAD morbidity was reduced in the range 5-36%. CAD mortality was significantly reduced in two studies. In eight angiographic intervention studies, lipid intervention was associated with consistently more evidence of regression or stable coronary disease. These studies also yielded suggestive evidence of improved clinical outcome. We conclude that drug intervention to lower cholesterol levels effectively reduces CAD morbidity and mortality in men already suffering from CAD (and may do so in women). Treatment is similarly effective in men with hypercholesterolaemia having no prior history of CAD. We lack evidence of the value of treatment in the elderly or in women having no prior CAD.

Anticholesteremic Agents↗
PubMed1994

Rapidly developing pseudohypertension after renal transplantation diagnosed by non-auscultated blood pressure measurement.

Pseudohypertension has been reported in elderly, diabetic and uraemic patients. A variety of diagnostic methods have been used, generally with poor results with the exception of arterial catheterisation. We report a case of pseudohypertension that developed in the year following a renal transplant and was diagnosed by the use of oscillometric and photoplethysmographic blood pressure measurement.

Auscultation↗
PubMed1994

Short term effects of pravastatin on blood pressure in hypercholesterolaemic hypertensive patients.

In this study, which was primarily designed to determine the lipid-lowering efficacy of pravastatin in the setting of background antihypertensive therapy with ACE inhibitors and calcium antagonists, we took the opportunity to examine whether pravastatin interacts with antihypertensive therapy to produce additional falls in blood pressure. This may help clarify the mechanism of action of pravastatin's rapid beneficial effects on cardiovascular morbidity. We treated 25 hypertensive hypercholesterolaemic patients with 12 weeks of either pravastatin or placebo in this double blind, placebo controlled parallel group study. Placebo treatment did not alter plasma lipids, whereas 12 weeks' treatment with pravastatin reduced total cholesterol by 27% (from 7.1 +/- 0.27 to 5.2 +/- 0.18, p < 0.001 compared with placebo) and low density lipoprotein cholesterol by 35% (from 4.9 +/- 0.36 to 3.2 +/- 0.17, p < 0.001). There were no changes in systolic or diastolic blood pressure either following 12 weeks' treatment or 3 weeks' withdrawal of pravastatin. Thus, pravastatin remains efficacious as a lipid lowering agent in the presence of antihypertensive therapy but does not enhance the blood pressure lowering action of these drugs. Therefore it is unlikely that blood pressure reduction is the mechanism by which pravastatin mediates its reported short term effects on cardiovascular morbidity.

Blood Pressure↗
PubMed1993

The effects of dietary lipid modification on blood pressure, cardiovascular reactivity and sympathetic activity in man.

OBJECTIVES: To examine the effect of dietary lipid modification on 24-h ambulatory blood pressure, cardiovascular reactivity and sympathetic activity in man. DESIGN: Twenty-four normal volunteers consumed either a high-fat or a low-fat diet for 2 weeks in an open, randomized, crossover study of duration 6 weeks. Diets were isocaloric and balanced for sodium and potassium content. METHODS: Cardiovascular reactivity was assessed by measurement of blood pressure responses to incremental infusions of angiotensin II and noradrenaline, and to sympathetic reflex testing. Plasma noradrenaline spillover and clearance rates were estimated using [3H]-noradrenaline infusion. RESULTS: Total plasma cholesterol and low-density lipoprotein-cholesterol levels both fell significantly on the low-fat compared with the high-fat diet, as did heart rate and mean arterial pressure (recorded by 24-h ambulatory monitoring). These changes were accompanied by reductions in blood pressure responses to cold pressor testing and to noradrenaline infusion on the low-fat diet. Plasma noradrenaline spillover and clearance rates did not change. Post hoc analysis showed an association between oral contraceptive use and increased noradrenaline sensitivity on the high-fat diet among the females tested. CONCLUSION: Dietary fat intake alters heart rate, blood pressure and cardiovascular reactivity to noradrenaline in man without changes in basal noradrenaline metabolism.

Adult↗
PubMed1992

Pharmacokinetic comparison of a slow-release clonidine with a conventional formulation after acute and chronic administration in hypertensives.

The pharmacokinetic characteristics of a slow-release formulation of clonidine (150 micrograms) were compared with those of a conventional formulation (75 micrograms) after acute and chronic (2 week) administration to 12 hypertensive subjects. The Tmax of the slow-release formulation was significantly later than for the conventional formulation after both acute (8.3 +/- 6 hr vs. 2.1 +/- 2 hr) and chronic administration (4.0 +/- 3 hr vs. 2.5 +/- 2 hr). Although the Tmax did not change significantly with acute and chronic administration of the conventional preparation, it was significantly shorter after chronic administration of the slow-release formulation when acute and chronic administration were compared. The Cmax was approximately 60% lower for the slow-release formulation (1 x 150 micrograms; 0.42 +/- 0.09 ng/mL) compared with the conventional formulation (2 x 75 micrograms; 0.70 +/- 0.12 ng/mL) after acute administration, whereas in the steady state, in which the dose of the conventional preparation was halved (75 micrograms), the Cmax values were comparable: 1 x 150 micrograms-0.99 +/- 0.27 ng/mL, 1 x 75 micrograms-0.84 +/- 0.20 ng/mL and the dose-normalized interdose AUC were identical for the conventional (16.2 +/- 4.3 ng/mL.hr) and slow release (16.6 +/- 5.3 ng/mL.hr) products. T1/2 values for the conventional formulation of clonidine exceeded 20 hours in all but one subject and were considerably longer than those in previous reports, including those of the authors, in which a less sensitive assay was used.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

A study of the alpha-1 adrenoceptor blocker prazosin in the prophylactic management of autonomic dysreflexia in high spinal cord injury patients.

The ability of the alpha-1 adrenoceptor antagonist, prazosin, to reduce the severity and duration of episodes of autonomic dysreflexia was studied in cervical and high thoracic spinal cord injury patients with documented episodes of autonomic dysreflexia. Sixteen patients participated in a double blind parallel group study comparing prazosin 3 mg b.d. with placebo given for 2 weeks. Both groups were matched for age, sex and baseline severity of autonomic dysreflexia episodes. Prazosin was well tolerated and did not produce a significant lowering of resting blood pressure. Compared to baseline measurements, patients allocated to prazosin therapy were found to have fewer severe episodes of autonomic dysreflexia and during these episodes to have significant reductions in average rise in systolic and diastolic blood pressure, symptom duration and requirement for acute antihypertensive medication. The severity of headache during individual autonomic dysreflexia episodes was also diminished with prazosin therapy. No symptom parameter was significantly altered by placebo therapy. It is concluded that prazosin is superior to placebo in the prophylactic management of autonomic dysreflexia and that these findings are consistent with suggestions that alpha-1 adrenoceptors play an important role in the pathogenesis of this syndrome.

Adolescent↗
PubMed1992

Cardiovascular and vasoactive hormone responses to bladder distension in spinal and normal man.

Many patients with high spinal cord injury experience exaggerated blood pressure rises in response to bladder distension. To examine the humoral mechanisms associated with these responses, ECG heart rate, blood pressure and vasoactive hormone levels were measured at baseline and during bladder distension following slow bladder filling in 23 subjects: 9 high spinal lesion patients, 7 low spinal lesion patients and 7 normal control subjects. Systolic blood pressure rose significantly during bladder distension in the high spinal lesion group by an average of 56 mm Hg (48%) and diastolic blood pressure rose by 22 mm Hg (47%), while heart rate fell by a mean of 7.4 beats per minute (15%). By contrast, neither systolic or diastolic blood pressure nor heart rate changed significantly during bladder distension in the low spinal lesion or normal control group. There were no significant changes in plasma levels of noradrenaline, renin, aldosterone, vasopressin, arginine, or atrial natriuretic peptide during bladder distension to account for the blood pressure rise in the high spinal lesion group. These findings suggest that humoral mechanisms are unlikely to play a major role in the mediation of pressor responses to bladder distension in high spinal lesion patients.

Blood Pressure↗
PubMed1992

Risk factors for cardiovascular disease in chronic spinal cord injury patients.

To establish whether the reported increased cardiovascular (CV) morbidity in spinal cord injury (SCI) patients is due to increased levels of established CV risk factors, we assessed overall CV risk in 102 consecutive patients aged 25-64 by calculation of a 'risk factor score' (RFS) derived from the MRFIT study (age, diastolic blood pressure (DBP), total cholesterol (TC) level, cigarettes/day, sex), obtaining a percentile position amongst an age and sex matched peer group from the 1983 Australian Risk Factor Prevalence Study. Chronic SCI patients had a very low overall percentile position of risk of 26.03 + 15.06 (mean +/- S.D.) and those patients with SCI for greater than 10 years had only a slightly higher risk position of 33.16 +/- 29.66. The low relative risk in SCI patients was due mainly to significantly lower DBP levels (67 +/- 13 mm hg), as TC levels (5.38 +/- 1.60 mmol/L) and cigarette consumption (31% smokers, mode 11-20/day) were similar to the control population (83 +/- 12 mmHg, 5.68 +/- 1.2 mmol/L, 28% smokers, mode 11-20/day, respectively). As other known risk factors such as lipoprotein cholesterol fractions were not included in the RFS index, these were measured in 327 consecutive SCI patients. HDL cholesterol levels, which are negatively correlated with CV risk, were significantly lower in SCI patients (1.12 +/- 0.30 mmol/L) compared to controls (1.35 +/- 0.35 mmol/L) and those patients more than 10 years post SCI had still lower levels (1.02 +/- 0.40). These data suggest that the reported increased incidence of CV disease in SCI patients is unexplained by increases in BP, TC or smoking. However, low HDL levels may contribute to CV risk and the role of other risk factors such as increased vascular reactivity remain to be established.

Adult↗