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Biomedical subjects

S R Redwood

Publications and source records attributed to S R Redwood.

9 recordsLinked to original sources
PubMed2000

Postinfarction left ventricular remodeling: a pathophysiological and therapeutic review.

Over the last 50 years, studies investigating the pathogenesis of left ventricular dysfunction have resulted in many potential therapeutic targets being identified and novel classes of drugs designed to treat this condition. Despite this, the long-term prognosis of patients with clinical heart failure remains poor with mortality rates equivalent to many terminal malignancies. This article reviews our present understanding of the pathophysiology of post-infarction left ventricular dysfunction and provides a rationale for current drug usage, drugs undergoing clinical trials and compounds still under pre-clinical development. In addition, the complexities involved in deciphering intra-cellular signalling pathways mediating ventricular hypertrophy which may form the basis of future treatments are also discussed.

Animals↗
PubMed1998

Reversible left ventricular dysfunction: does it affect clinical practice and does it matter?

There is substantial evidence that many patients with impaired left ventricular function secondary to coronary artery disease may have hibernating or stunned myocardium. The identification of these patients is important, as revascularisation is associated with an improvement in function, and there is some evidence that revascularisation of these patients will actually improve prognosis. The most useful investigations for the identification of reversible left ventricular dysfunction are dobutamine echocardiography, thallium scanning and, although not available in many centres, PET scanning.

Coronary Disease↗
PubMed1997

Effect of magnesium sulphate in patients with unstable angina. A double blind, randomized, placebo-controlled study.

AIMS: Administration of intravenous magnesium sulphate has been shown to be protective during acute myocardial ischaemia and it may therefore have beneficial effects in unstable angina. The purpose of this study was to assess the effects of a 24-h infusion of magnesium in patients with unstable angina. METHODS AND RESULTS: Patients who presented with unstable angina with electrocardiographic changes were randomized to receive a 24-h intravenous infusion of magnesium or placebo within 12 h of admission. The primary endpoint was myocardial ischaemia, as assessed by 48 h Holter monitoring. Resting 12-lead ECGs, creatine kinase-MB release and urinary catecholamines were also assessed. Patients were followed for 1 month. Thirty-one patients received magnesium sulphate and 31 placebo. Baseline characteristics and extent of coronary disease were similar in both groups. On 48 h Holter monitoring, 14 patients (50%) had transient ST segment shifts in the magnesium group vs 12 patients (46%) in the placebo group. However, there were fewer ischaemic episodes in the magnesium group (51 vs 101, P < 0.001) and there was a trend towards an increase in the total duration of ischaemia in the placebo group compared to the magnesium group in the second 24 h (2176 min vs 719 min respectively, P = 0.08). Regression of T wave changes on the 24 h ECG occurred more frequently in patients who received magnesium compared to those treated with placebo (11 patients vs 0 patients respectively, P < 0.005). Creatine kinase-MB release was significantly less at 6 and 24 h in patients who received magnesium compared to those treated with placebo. Catecholamine excretion was lower in patients treated with magnesium than in those treated with placebo (adrenaline: 1.05 +/- 0.16 vs 1.61 +/- 0.32 ng.mmol-1 creatinine; noradrenaline: 9.99 +/- 1.82 vs 18.48 +/- 2.41 ng.mmol-1 creatinine respectively in the first 12 h sample, P < 0.05). CONCLUSIONS: Intravenous magnesium reduces ischaemic ECG changes, creatine kinase-MB release and urinary catecholamine excretion in the acute phase of unstable angina. Thus, magnesium may be a beneficial additional therapy for these patients. Further studies are required to confirm these finding.

Adult↗
PubMed1997

Selection of dichotomy limits for multifactorial prediction of arrhythmic events and mortality in survivors of acute myocardial infarction.

AIMS: To evaluate the predictive value and optimum dichotomy limits for different combinations of prognostic indicators for the prediction of arrhythmic events and cardiac mortality in post-infarction patients. BACKGROUND: Studies of new interventions based on risk stratification after myocardial infarction have often used a single variable as a predictor of risk. However, whether the dichotomy limits of these single variables, derived from univariate analyses, should be altered when such variables are combined for the prediction of risk after myocardial infarction has not been examined. METHODS: Left ventricular ejection fraction, signal-averaged electrocardiography, heart rate variability index, mean heart rate and ventricular extrasystole frequency were recorded pre-discharge in 439 survivors of their first myocardial infarction. Arrhythmic events and cardiac mortality were recorded during 1 year (range 1-6 years) follow-up. RESULTS: During follow-up for at least 1 year, there were 25 cardiac deaths and 23 arrhythmic events. Different optimum dichotomy limits were obtained for the prediction of cardiac mortality vs arrhythmic events, for different combinations of variables, for different selected levels of sensitivity and for different numbers of variables abnormal before identification of those at risk. The dichotomy limit of the heart rate variability index for the prediction of events appeared to be the least affected by the inclusion of other variables. For example, when predicting arrhythmic events using combinations of left ventricular ejection fraction and/or heart rate variability, the optimum dichotomy limits when each variable was used alone was 32% and 18 units respectively; 43% and 18 units when either left ventricular ejection fraction or heart rate variability are required to be abnormal, and 52% and 19 units when both are required to be abnormal before identification of those at risk of arrhythmic events. CONCLUSIONS: Dichotomy limits derived from univariate analyses do not optimally predict events when used in the multivariate setting. Risk stratification can be improved by using several variables in combination and is further improved by using dichotomy limits of these variables which are different from those used in or derived from univariate analyses.

Aged↗
PubMed1996

Effect of magnesium on the monophasic action potential during early ischemia in the in vivo human heart.

OBJECTIVES: This study sought to examine the effects of magnesium on epicardial action potential duration in patients during early myocardial ischemia. BACKGROUND: Magnesium has been shown to reduce arrhythmias in experimental models of myocardial ischemia. Experimental and clinical observations suggest an effect on repolarization. METHODS: Patients undergoing elective coronary artery bypass surgery were randomized (double blind) to receive intravenous magnesium (n = 10) or placebo (n = 10). Patients were placed on cardiopulmonary bypass and paced at 600 ms, and stable monophasic action potentials were obtained. Ischemia was achieved by aortic cross-clamping for 2 min while normothermia was maintained. RESULTS: Serum magnesium levels increased from 0.60 +/- 0.03 to 1.69 +/- 0.07 mmol/liter (mean +/- SEM) in the magnesium group, with no change in the placebo group. Epicardial temperature was identical in the two groups and did not alter during ischemia. At 90% repolarization, initial action potential prolongation was observed in the placebo group over the first minute of ischemia (282.0 +/- 6.0 to 294.0 +/- 4.8 ms) but not in the magnesium group (278.3 +/- 5.9 to 274.5 +/- 7.4 ms). At 2 min of ischemia, action potential duration was shorter in the magnesium group than in the placebo group (258.1 +/- 5.5 vs. 281.3 +/- 5.9 ms, respectively, p < 0.05). CONCLUSIONS: Intravenous magnesium infusion altered the epicardial action potential response to ischemia in patients. These findings may have important implications in the pathogenesis of arrhythmias in ischemic myocardium.

Action Potentials↗
PubMed1996

Esmolol aids extubation in intensive care patient with ischaemic pulmonary oedema.

A 49-year-old man with a history of ischaemic heart disease failed successful tracheal extubation on four consecutive occasions following emergency surgery because of the development of acute pulmonary oedema. Attenuation of the cardiovascular responses to tracheal tube removal by pretreatment with an intravenous infusion of esmolol hydrochloride allowed successful extubation of the patient to be achieved.

Adrenergic beta-Antagonists↗
PubMed1995

Autoimmunity to alpha myosin in a subset of patients with idiopathic dilated cardiomyopathy.

OBJECTIVE: To use an enzyme linked immunoassay (ELISA) technique to assess frequency and disease specificity of anti-alpha-myosin antibodies in patients with dilated cardiomyopathy and their relatives. METHODS: Evaluation was performed on sera (dilution 1/320) from 123 consecutive patients with dilated cardiomyopathy (WHO criteria) (age 42 (SD 14) years), 252 of their relatives (35 (17) years), 203 healthy controls (45 (16) years), and 92 patients with ischaemic heart disease (63 (11) years). RESULTS: Abnormal antibody levels were commoner in patients with dilated cardiomyopathy (25, 20%) than in ischaemic heart disease (4, 4%), or normal controls (4, 2%, P = 0.001). Forty one (16%) of the relatives had abnormal results compared to the controls (4, 2%, P < 0.001) and antibodies were detected in 20 (38%) of pedigrees. Relatives from non-familial kindreds had higher antibody levels than those with familial disease (P << 0.001), and higher antibody levels were identified in 53 relatives of probands who had abnormal results compared to 116 relatives for whom the proband had a normal result (0.37 (SEM 0.02) v 0.22 (0.01); P < 0.001). CONCLUSIONS: The finding of anti-alpha-myosin antibodies in 20% of patients with dilated cardiomyopathy, in 16% of their asymptomatic relatives, and in 38% of families (particularly those with non-familial disease and where proband also had an abnormal result) provides additional evidence for autoimmunity against alpha myosin in a subset of patients.

Adult↗