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Biomedical subjects

M Flather

Publications and source records attributed to M Flather.

43 records · Page 3Linked to original sources
PubMed1993

Maximizing benefits of therapies in acute myocardial infarction.

Major advances in the management of acute myocardial infarction have been achieved by a combination of careful experimental work and development of effective pharmacologic and interventional strategies in conjunction with the conduct of large, reliable randomized trials. Current trials indicate that a combination of thrombolytic therapy, aspirin, and intravenous followed by oral beta blockers reduces mortality. There are a number of additional promising interventions, such as intravenous magnesium, nitrates, and the newer antithrombin agents. However, before these agents are used widely in clinical practice, clear proof of benefit and adequate safety should be available from the ongoing randomized trials. Following discharge from the hospital, long-term therapy with aspirin and beta blockers should be considered in all patients. In patients with heart failure and low ejection fraction, angiotensin-converting enzyme (ACE) inhibitors have been shown to reduce mortality, reinfarction, and the need for further hospitalizations for heart failure. Therefore, these therapies, in conjunction with risk factor modification (cessation of cigarette smoking, treatment of hypercholesterolemia, treatment of hypertension), should be considered in all appropriate patients. A number of new strategies for the prevention of atherosclerosis and its complications are currently being evaluated in prospective randomized trials. These include the natural antioxidant vitamins, estrogen replacement therapy, tamoxifen therapy, and ACE inhibitors in patients without evidence of heart failure or left ventricular dysfunction.

Humans↗
PubMed1993

Hemodynamic effects of captopril and isosorbide mononitrate started early in acute myocardial infarction: a randomized placebo-controlled study.

OBJECTIVES: The aim of this study was to study the hemodynamic effects of orally administered captopril and isosorbide mononitrate in suspected acute myocardial infarction. BACKGROUND: Early treatment with converting enzyme inhibitors and nitrates in acute myocardial infarction may limit infarct expansion and prevent left ventricular dilation. METHODS: In a double-blind study, 81 patients were randomized within 36 h of the onset of symptoms of suspected acute myocardial infarction to 1 month of oral captopril (6.25 mg initial dose, followed 2 h later by 12.5 mg and continuing with 12.5 mg three times daily), isosorbide mononitrate (initial dose 20 mg followed by 20 mg three times daily) or matching placebo. The effects of treatment on changes from baseline in mean arterial blood pressure, heart rate, stroke volume, cardiac output and systemic vascular resistance were assessed noninvasively using Doppler echocardiography 1 h after the first dose, 1 week after infarction and at 6 weeks (that is, 2 weeks after the scheduled end of trial treatment). RESULTS: One hour after the start of treatment, blood pressure was reduced by approximately 10% with both captopril and isosorbide mononitrate, but this difference did not persist at 1 week. Captopril was associated with a significant increase in cardiac output compared with placebo of 13 +/- 3% at 1 h (p < 0.01), 23 +/- 5% at 1 week (p < 0.001) and 22 +/- 6% (p < 0.05) at 6 weeks (2 weeks after the end of trial treatment). This increase in cardiac output with captopril was mainly due to a substantial and sustained increase in stroke volume, although there was also a small increase in heart rate at 1 week. Both captopril and isosorbide mononitrate reduced systemic vascular resistance within 1 h of the start of treatment, but only the effect of captopril was sustained (perhaps because the three-times daily nitrate regimen induced tolerance). Study treatment was well tolerated, and the incidence of withdrawal of study treatment for hypotension was not significantly different from that with placebo. CONCLUSIONS: This study indicates that the hemodynamic effects of both captopril and isosorbide mononitrate are well tolerated in the acute phase of myocardial infarction and that captopril favorably influences cardiac function.

Aged↗
PubMed1993

Effects on ventricular arrhythmias of oral captopril and of oral mononitrate started early in acute myocardial infarction: results of a randomised placebo controlled trial.

OBJECTIVE: To assess the effects of oral vasodilator treatment on ventricular arrhythmias in acute myocardial infarction. SETTING: Coronary care units at the John Radcliffe Hospital, Oxford, and the Royal Infirmary, Edinburgh. PATIENTS: 100 patients with suspected acute myocardial infarction entered the study at a mean of 13 hours from symptom onset. DESIGN OF INTERVENTION: Double blind randomisation to 4 weeks treatment with captopril (12.5 mg three times a day after a 6.25 mg test dose (n = 32)) or isosorbide mononitrate (20 mg three times a day (n = 31)) or placebo control (n = 37). OUTCOME MEASURES: Ventricular arrhythmic events assessed by 48 hours of Holter monitoring starting at the time of randomisation. RESULTS: The number of ventricular extrasystoles/hour for captopril, mononitrate, and placebo was respectively (median and range) 6 (0-162), 4 (0-38), and 10 (0-932) (2p < 0.02 mononitrate v placebo). The number of episodes of multiple extrasystoles/hour was 0.2 (0-22), 0.3 (0-4), and 0.5 (0-19); (2p < 0.02 mononitrate v placebo). Episodes of ventricular tachycardia showed a non-significant decrease in the captopril and mononitrate groups (mean (SEM) 3.2 (0.8), 2.4 (0.7), and 4.7 (1.3) for the 48 hour period). The incidence of idioventricular rhythm was also reduced in both active treatment groups (28%, 19%, and 46% (2p < 0.05 mononitrate v placebo)). CONCLUSIONS: Oral mononitrate (and perhaps also captopril) seems to reduce the incidence of ventricular arrhythmias in the early phase of acute myocardial infarction. The effects on life-threatening arrhythmias, such as ventricular fibrillation, and on death can only be assessed in a much larger trial.

Administration, Oral↗
PubMed1992

Early and late changes in left ventricular filling after acute myocardial infarction and the effect of infarct size.

To characterize the early (1 week) and late (6 weeks) changes in left ventricular (LV) filling pattern associated with acute myocardial infarction (AMI) 45 patients (mean age 65 +/- 2 years) were studied by Doppler echocardiography. Based on clinical criteria, patients were divided into those with large (group L; n = 12) and those with small (group S; n = 33) infarcts and then compared with 16 age-matched control subjects. The following parameters were calculated from the mitral velocity waveform: (1) peak early and peak atrial velocities and their integrals; (2) peak early to atrial velocity ratio and velocity integral ratio; and (3) the pressure half-time of the early wave. One week after AMI, group L showed a decreased atrial and increased early velocity, velocity ratio and integral ratio, whereas the pressure half-time of the early wave was shorter than that in group S and in control subjects. At 6 weeks group L showed a reduction in early velocity, early to atrial velocity ratio and integral ratio, whereas pressure half-time increased. When groups S and L were combined there was a good inverse correlation between pressure half-time and infarct size as measured by peak enzyme release (r = -0.64, p < 0.001). These data suggest that, depending on infarct size, patients exhibit a "restrictive" filling pattern early after the acute event. This is manifested by the greater proportion of filling occurring in early diastole, reflecting an overall increase in chamber stiffness. At 6 weeks, this pattern is less pronounced presumably due to the remodeling process.

Aged↗
PubMed1988

Early diagnosis of myocardial infarction by timed sequential enzyme measurements.

Serum samples from patients admitted to a coronary care unit with a history of acute chest pain suggestive of myocardial infarction in the previous 12 h were obtained on admission and at 6 and 12 h, thereafter. Creatine kinase (CK), CK-MB isoenzyme, CK-MM sub-bands, myoglobin, and lactate dehydrogenase (LD) isoenzymes were examined. Changes were evaluated in relation to the diagnosis obtained from clinical examination, serial electrocardiography and 'routine' cardiac enzymes (CK, aspartate transaminase and alpha-hydroxy butyrate dehydrogenase daily for 3 days following admission). The slope of the logarithms of CK, CK-MB activity and CK-MB concentration in the early post infarct period fully distinguished between infarct and non-infarct patients. Measurement of myoglobin and lactate dehydrogenase isoenzymes was less sensitive. Serial estimation of CK-MM sub-band patterns allowed the time from infarction to be estimated. Serial estimation of CK in the 12 h following admission can be substituted for conventional daily enzyme estimations for the diagnosis of acute myocardial infarction in patients with onset of chest pain within the previous 12 h. This could reduce laboratory and in-patient costs.

Adult↗