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Biomedical subjects

P Sleight

Publications and source records attributed to P Sleight.

At least 217 records · Page 12Linked to original sources

Early intravenous atenolol treatment in suspected acute myocardial infarction. Preliminary report of a randomised trial.

214 patients were studied in a randomised trial to determine whether administraiton of intravenous atenolol within 12 hours of chest pain reduced eventual infarct size, as estimated by cumulative enzyme release and by ECG changes. 135 patients already had ECG evidence of infarction at entry; 72 received atenolol which significantly decreased subsequent enzyme release (atenolol and control means = 121 IU, SE +/- 10 and 177 IU, SE +/- 17; 2p < 0.005) and enhanced R-wave preservation (atenolol and control means = 46% +/- 3 and 36% +/- 3; 2p < 0.02). 79 patients had no evidence of infarction at entry; 44 did not receive atenolol and 27 of these subsequently developed infarction, whereas only 11 of 35 treated patients infarcted during their hospital stay (2p < 0.01). In hospital, fewer atenolol patients died (4 vs 9), had non-fatal cardiac arrests (2 vs 6), or required therapy for heart-failure (36 vs 47). Unlike many previous trials which had negative results, in this trial we gave the drug intravenously and promptly (median of 4 hours from onset of pain to injecton), thereby achieving early beta-blockade.

Acute Disease↗

Heart rate and ectopic prematurity in relation to sustained ventricular arrhythmias.

Forty-four patients with acute myocardial infarction were studied using 24-hour electrocardiographic monitoring. A linear correlation has been shown to exist between heart rate preceding accelerated idioventricular rhythm and ventricular tachycardia and the rates of these. The prematurity index was found to be inversely related to the preceding heart rate and also to the rate of accelerated idioventricular rhythm or ventricular tachycardia. Faster heart rates preceded extrasystoles with shorter prematurity indices and a significant inverse correlation was observed between preceding heart rate and prematurity index. Patients developing ventricular tachycardia had more frequent isolated ventricular extrasystoles and faster heart rates preceding the episode as compared with patients not showing ventricular tachycardia. No association was observed between ventricular tachycardia and accelerated idioventricular rhythm. All four patients developing ventricular fibrillation showed preceding ventricular tachycardia, with three of these patients demonstrating faster rates of ventricular tachycardia (greater than 170/min) and shorter prematurity indices (less than 0.80) than patients without ventricular fibrillation. Heart rate may influence the severity of ventricular arrbythmia; the prematurity of an extrasystole is of importance in patients developing accelered idioventricular rhythm or ventricular tachycardia.

Arrhythmias, Cardiac↗

Adaptation of hypertensives to treatment with cardioselective and non-selective beta-blockers. Absence of correlation between bradycardia and blood pressure control, and reduction in slope of the QT/RR relation.

Thirty mild hypertensives were treated for more than two months with either cardioselective (atenolol or metoprolol) or non-selective (propranolol or pindolol) beta-blockers; the patients were assigned to the drugs in a double-blind manner. A procedure was designed to distinguish between the effects of the drugs themselves while treatment continued, and the development of adaptive changes which would persist when the drugs had been eliminated from the body. Though individual responses to treatment varied in both groups, the mean effect of the cardioselective and non-selective drugs in the control of hypertension was similar. There was no evidence of the development of supersensitivity or "rebound". On the contrary, an adaptive bradycardia (that is a fall of not less than 10% in heart rate persisting 52 hours after stopping treatment) was observed at rest in 17/30 patients, and peak heart rates and blood pressures during exercise were lower in both groups than before treatment. Cardioselective drugs induced a significantly greater bradycardia at rest than non-selective, but on exercise increases in heart rate were reduced more by the non-selective drugs, so that the same peak heart rates were reached on exercise in both groups. Adaptation also affected QT. The results suggest that two factors govern the shortening of QT by increases in heart rate, a "metabolic" effect, determined by sympathetic drive, and a "biophysical" effect determined by heart rate. The adrenergic effect is attenuated by acute beta-blockade, or by adaptation to prolonged blockade, leaving a shallow, rate-determined, slope to the QT/RR regression.

Adaptation, Physiological↗

Effect of atenolol on recovery of the electrocardiographic signs of myocardial infarction.

The most notable changes in the 35-lead precordial electrocardiogram in 22 subjects in the first 6--12 months after acute myocardial infarction were a reduction in the amplitude of Q waves and a significant increase in the amplitude of the R waves. Patients who, in a random trial, had been given 100 mg atenolol daily from admission showed a significantly greater recovery in R-wave amplitude and decrease in Q waves than patients given placebo. It is concluded that atenolol improves the recovery of the electrocardiographic signs of myocardial infarction.

Acute Disease↗

Orthostatic hypertension.

A 40 year old man was found to have marked hypertension when he was in the upright position with normal pressures when he was supine. Investigations disclosed normal catecholamine and renin levels. The baroreceptor reflex was somewhat depressed. The mechanism of this orthostatic hypertension is not known. The condition has not been reported previously.

Adult↗

Arterial distensibility in normal and hypertensive man.

1. The pulse-wave velocity along the brachial radial artery was measured in 38 subjects and volume distensibility values were calculated. 2. Measurements made at each subject's resting blood pressure showed that those with high blood pressure had higher pulse-wave velocity values and hence less distensible arteries. 3. An acute rise in arterial distending pressure was accompanied by a rise in pulse-wave velocity. 4. When pulse-wave velocity was remeasured in all subjects at identical arterial distengin pressures, no difference was found between hypertensive and normal subjects. 5. It appears that poor distensibility of large arteries in hypertensive subjects is a consequence of the elevated distending pressures and not due to irreversible structural changes in the arterial wall.

Adult↗

Baroreflex control of blood pressure and plasma noradrenaline during exercise in essential hypertension.

1. Twelve subjects (mean age 46.3 +/- 12.5 years) with mild to moderate hypertension were studied before, during and after bicycle ergometer exercise. 2. Baroreflex sensitivity was determined by the Oxford phenylephrine method; sensitivity at rest was inversely related to intra-arterial pressure and age. Age and resting arterial pressure were not related. 3. Exercise for 5 min at 50 W and 5 min at 75 W raised the mean arterial pressure from 116.4 +/- 18.0 to 150.0 +/- 25.4 mmHg, the heart rate from 73.2 to 126.7 beats/min and the plasma noradrenaline from 541 +/- 142.7 to 1309.8 +/- 543.5 pg/ml (P less than 0.001). 4. The increase in noradrenaline during exercise and the maximum mean pressure achieved were inversely related to resting baroreflex sensitivity (r = -0.68 and -0.77 respectively). Resting values of noradrenaline were not related to baroreflex sensitivity, age, or resting blood pressure. 5. It is possible that the rise in both plasma noradrenaline and arterial blood pressure produced by exercise is controlled by the baroreceptor reflexes; these are less effective in hypertensive subjects and thus the increases in noradrenaline and arterial pressure during exercise are greater in subjects with raised blood pressure.

Adult↗

Assessment of the antihypertensive effect of atenolol with 24 h ambulatory monitoring of blood pressure.

1. Twenty-four hour intra-arterial blood pressure measurements and electrocardiograms were obtained from 12 subjects with untreated essential hypertension. 2. The patients kept records of their activity, paying particular attention to times of retiring to bed, and times of waking in the morning. 3. All subjects were treated with a single daily dose of atenolol (50 to 200 mg) for between 2 and 9 months, and then underwent a second 24 h blood pressure study. 4. Arterial blood pressure was lowered significantly throughout the 24 h period with a single daily dose of atenolol.

Adult↗

Value of electrocardiogram in predicting and estimating infarct size in man.

The value of the electrocardiogram in assessing infarct size was studied using serial estimates of the MB isomer of creatine kinase (CK MB) in plasma, serial 35 lead praecordial maps in 28 patients with anterior myocardial infarction, and serial 12 lead electrocardiograms in 17 patients with inferior myocardial infarction. In patients with anterior infarcts, sigma ST, sigma R, sigma Q, sigma R/(Q+S), and the number of sites with ST elevation more than 2 mm or with QS waves, were obtained from each map. Correlation between both maximum sigma Q and maximum sigma ST with cumulative CK MB was highly significant. There was also a significant correlation between sigma R and sigma R/(Q+S) with cumulative CK MB. There was no significant correlation between maximum number of sites with ST elevation or with Q or QS waves and cumulative CK MB. Maximum sigma ST and number of sites with ST elevation predicted maximum sigma Q and number of sites with QS or Q waves at a time when infarction was not complete. In patients with inferior infarcts, there was a significant correlation between maximum sigma Q and maximum sigma ST in leads II, III, and a VF, and cumulative CK MB. This study shows that all the waves in the electrocardiogram are useful in assessing infarct size. The fact that maximum sigma ST predicts final sigma Q may be used to assess the efficacy of interventions designed to salvage ischaemic myocardium.

Aged↗

Histology and ultrastructure of the carotid sinus in experimental hypertension.

Histological studies including electron microscopy were performed on the carotid sinuses of dogs with renal hypertension of 17 to 82 days duration or hypertension of two years secondary to aortic coarctation. Physiological abnormalities in the baroreceptors including resetting had been demonstrated before death. Histologically there were no qualitative or quantitative differences in the intrasinus nerve fibers of the hypertensive animals compared tp controls with normal blood pressures, and there was no evidence that baroreceptor degeneration occurred as a consequence of the hypertension. Structural lesions confined to the intima were evident in the sinus walls of some of the renal hypertensive animals whereas the dogs with coarctation showed more advanced sinus wall changes including medial calcification and enlargement of the vascular lumen.

Animals↗

The effect of mental arithmetic on blood pressure variability and baroreflex sensitivity in man.

1. Baroreflex sensitivity was tested in three normal, three borderline and one hypertensive subject before and during mental arithmetic, the prolongation of pulse interval caused by a provoked rise in blood pressure being used as a measure of baroreflex sensitivity. 2. Baroreflex sensitivity was significantly decreased during mental arithmetic. 3. During mental arithmetic the arterial pressure fluctuated markedly. 4. These findings suggest that in man, as well as animals, the defence of alerting reaction depresses baroreflex control and thus contributes to the rise in blood pressure seen at this time.

Blood Pressure↗