Search PubMed⌕ Search

Biomedical subjects

P Sleight

Publications and source records attributed to P Sleight.

At least 199 records · Page 11Linked to original sources
PubMed1983

Interventions during and after acute myocardial infarction.

There is now evidence that infarct size in man can be reduced by early treatment and that some cases of threatened infarction can be aborted. Beta blockade, given intravenously within about 6-8 hours after the onset of pain can reduce infarct size and abort some infarctions. So far we have no conclusive data on mortality. Beta blockers may act by a number of mechanisms, namely reduction of cardiac contractility, heart rate and blood pressure thus reducing cardiac work and oxygen requirement, prevention of cardiac rupture by the same mechanism, and by an early effect on R on T ectopic beats and hence serious ventricular arrhythmia. Early myocardial revascularization either by coronary graft, percutaneous angioplasty or intracoronary streptokinase are all promising but so far unproven by adequate clinical trial. Randomized trials suggest that intravenous streptokinase may be effective and hyaluronidase appears promising, possibly by promotion of collateral vessel flow. Calcium channel blockade may also be helpful and there are some early studies which support this. Lowering work by sodium nitroprusside also reduces infarct size. Heparin may have a place in the treatment of threatened infarction. After recovery it now appears established that beta 1-blockade will lower mortality. We do not know how long this effect persists. Other agents are less well established perhaps because the trials have been too small. Anticoagulants may have a place but their use is not widespread. Anti-platelet agents are also controversial. Studies of dipyridamole and sulphinpyrazone have been suggestive but not conclusive; the studies of aspirin are moderately encouraging, when all trials are pooled. Anti-arrhythmic therapy after infarction has been disappointing, with the exception of beta blockade. Perhaps more emphasis should also be put upon changes in lifestyle, notably stopping smoking, reduction of fat intake and encouraging regular exercise.

Adrenergic beta-Antagonists↗
PubMed1983

Reduction in infarct size, arrhythmias and chest pain by early intravenous beta blockade in suspected acute myocardial infarction.

Four hundred seventy-seven patients suspected of having had acute myocardial infarction within less than 12 hours were randomized to receive i.v. atenolol followed by oral treatment for 10 days or to a control group. In patients with ECG changes indicative of infarction at entry, i.v. atenolol significantly reduced enzyme release by one-third and enhanced R-wave preservation. In patients without such ECG changes, treatment significantly prevented the development of infarction in a proportion of patients. There was also a significant reduction in R-on-T ectopics, repetitive ventricular arrhythmias and supraventricular arrhythmias. Treated patients had significantly greater pain relief and required fewer opiate analgesics. Significantly fewer atenolol-treated patients died by 10 days (the treatment period), had nonfatal cardiac arrests, developed heart failure, or suffered reinfarction.

Administration, Oral↗
PubMed1982

Ambulatory blood pressure during once-daily randomised double-blind administration of atenolol, metoprolol, pindolol, and slow-release propranolol.

Intra-arterial ambulatory blood pressure was measured over 24 hours, in 34 patients with newly diagnosed hypertension, both before and after double-blind randomisation to treatment with atenolol (n=9), metoprolol (n=9), pindolol (n=9), or propranolol in its slow-release form (n=7). The dosage of each drug was adjusted at monthly clinic visits until satisfactory control of blood pressure was achieved (140/90 mm Hg or less by cuff) or the maximum dose in the study protocol was reached. A second intra-arterial recording was made after these drugs had been taken once daily at 0800 for three to eight months (mean 5.0+/-SD 1.4) and was started four hours after the last dose.At the end of the 24-hour recordings blood pressure was significantly lower with all four drugs. The extent to which the drugs reduced blood pressure, however, differed over the 24 hours. Atenolol lowered mean arterial pressure significantly throughout all 24 recorded hours, metoprolol for 12 hours, pindolol for 15 hours, and slow-release propranolol for 22 hours. Neither metoprolol nor pindolol lowered blood pressure during sleep. A significant reduction in heart rate was observed over 20 hours with atenolol, 20 hours with metoprolol, 10 hours with pindolol, and 24 hours with slow-release propranolol. Atenolol, metoprolol, and slow-release propranolol continued to slow the heart rate 24 hours after the last tablet was taken; this effect on heart rate, however, was not sustained throughout the second morning in those patients taking atenolol. Pindolol, the only drug studied that has intrinsic sympathomimetic activity, increased heart rate and did not lower blood pressure during sleep.Atenolol and slow-release propranolol are effective as antihypertensive agents over 24 hours when taken once daily, whereas metoprolol and pindolol may need to be taken more frequently. At times of low sympathetic tone, however, such as during sleep, beta-blockers with intrinsic sympathomimetic activity may raise heart rate and attenuate the fall in blood pressure with treatment.

Adolescent↗
PubMed1982

Ischemic pain relief in patients with acute myocardial infarction by intravenous atenolol.

Pain relief in acute myocardial infarction (AMI) by the beta-adrenoceptor antagonist, atenolol, was demonstrated by three separate studies. First, 18 patients were randomized to double-blind intravenous atenolol (5 mg) or saline immediately after admission, followed by oral atenolol (50 mg) or placebo 10 minutes later. In patients receiving atenolol, pain relief coincided with reduction in heart rate (HR), systolic blood pressure (SBP), and HR X SBP product (p less than 0.05); however, pain and these parameters were unchanged by placebo. The degree of pain relief was related to the reduction in cardiac work achieved (r = 0.725; p less than 0.001). A second open study involving 22 patients receiving intravenous atenolol (5 to 15 mg) early after AMI showed ischemic pain relief in 17 patients. They achieved a more significant reduction in HR X SBP product than those whose pain remained unchanged (p = 0.004). Finally, a retrospective study of 163 patients randomized to either atenolol or no beta blockade early after AMI revealed that patients receiving atenolol needed less opiate analgesia after admission (p less than 0.001). The safety of this therapy was illustrated by a decreased incidence of left heart failure and atrial fibrillation and no tendency to second- and third-degree heart block.

Adrenergic beta-Antagonists↗
PubMed1981

Cuff and ambulatory blood pressure in subjects with essential hypertension.

Clinic cuff blood-pressure measurements, obtained on at least three occasions, were compared with mean arterial pressures in 59 patients with borderline or essential hypertension who underwent direct ambulatory monitoring of blood pressure. In 22 patients (group I) mean cuff and ambulatory pressures were similar (+/- 10 mm Hg) while in 32 subjects (group II) cuff pressures were more than 10 mm Hg higher. Groups I and II could not be distinguished on the basis of clinical examination, indices of sympathetic nerve activity, or blood-pressure variability, or by the magnitude of pressure rise during physical or mental exercise. Group II had less cardiovascular target organ damage and better baroreflex sensitivity but there was considerable overlap. There was no reliable way of telling which subjects would have lower ambulatory than cuff pressures. 20 out of 59 subjects classified as hypertensive by cuff measurements had awake ambulatory pressures or less than 140/90 mm Hg.

Adolescent↗
PubMed1981

Variability of electrocardiographic and enzyme evolution of myocardial infarction in man.

We have studied the time course of development of ST segment elevation, R wave loss, and Q wave development in 41 patients using 35 lead praecordial mapping or 12 lead electrocardiograms in those with anterior and inferior infarcts, respectively. The first recording was at a mean time of six hours after the onset of pain; subsequent records were taken every eight hours for 24 hours, every 12 hours for the second day, and every day thereafter. Serial CK MB estimates were obtained at every four hours for the first 72 hours. There was good agreement in the time course between the electrocardiogram and enzyme evolution. Forty-one per cent of patients showed rapid infarction with R wave and Q wave evolution complete within 12 hours of pain and accompanied by a short duration of enzyme release (mean = 19.30 hours). Fifty-nine per cent of patients showed more prolonged infarction with longer R wave and Q wave evolution and enzyme release (mean = 30 hours). Four patients also showed delayed reinfarction. ST segment elevation was maximal at six hours in the whole group and was significantly lower thereafter. Patients with rapid infarction showed high initial ST segment elevation which decreased promptly compared with those with prolonged infarction, who showed moderate but more persistent ST segment elevation. This study shows the variability in the time course of the electrocardiogram and enzyme evolution after myocardial infarction in man.

Aged↗
PubMed1981

Prophylactic antibiotics for cardiac pacemaker implantation. A prospective trail.

A prospective trial was conducted to assess the value of prophylactic antibiotic treatment in preventing postoperative infection of permanent transvenous pacemaker systems. Four hundred and thirty-one patients were randomly allocated to treatment (234) or no-treatment (197) groups. Treated patients received systemic benzylpenicillin and flucloxacillin just before operation and one and six hours afterwards. Nine primary generator pocket infections occurred without evidence of wound dehiscence or skin erosion. Seven infections were in untreated patients and two in treated patients. Antibiotic prophylaxis diminishes the risk of infection after pacemaker implantations.

Adult↗
PubMed1981

Clinical use of beta blockers in hypertension.

Recent work on the use of beta blockade in the treatment of mild hypertension is reviewed. It is clear from these studies that this form of antihypertensive therapy can exercise a protective influence on cerebrovascular events and on fatal and nonfatal myocardial infarction. In particular, there is evidence of reduced rate of reinfarction when beta-blocking agents are started soon after the first event. The comparative efficacy and side effects profile of the various clinically available beta blockers are discussed, as differences between these are now becoming more apparent. In particular, the degree of water or lipid solubility may determine which will penetrate into brain tissue with resultant central effect; the more water soluble, the less likely this is to occur. It is also important that those which are not metabolised by the liver can be more easily titrated as they do not require large changes in dosage; some may be given once daily. The use of beta blockade in the presence of airway resistance is strongly contraindicated but, if it has to be used, this should be started in hospital with a cardioselective agent.

Adrenergic beta-Antagonists↗
PubMed1980

The role of serum myoglobin in the detection and measurement of myocardial infarction.

The use of serum myoglobin determinations in the diagnosis and quantitation of acute myocardial infarction was studied in 53 patients. Serial blood samples collected for the first 72 h after pain were analysed for serum myoglobin using a radioimmunoassay procedure. Samples were also assayed for serum creatine kinase (CK) and its myocardial isoenzyme CK-MB, aspartate aminotransferase (AST) and alpha-hydroxybutyrate dehydrogenase (alpha HBDH). Analysis of first and second samples obtained at mean times of 7.6 and 10.7 h respectively after pain produced the following detection rate: serum myoglobin 85% and 98%; serum CK 71% and 85%; serum AST 58% and 81%; serum CK-MB 29% and 60%; serum alpha HBDH 23% and 33% respectively. Total CK-MB and myoglobin release from damaged myocardium were calculated using the method of Norris et al. [16]. A significant correlation was obtained between infarct size calculated from CK-MB and myoglobin in the whole group (n = 29, r = 0.71, p < 0.001). The correlation was even more significant for smaller infarcts with CK-MB release < 220 U/l (n = 13, r = 0.92, p < 0.001).

Adult↗