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Biomedical subjects

R M Norris

Publications and source records attributed to R M Norris.

At least 109 records · Page 6Linked to original sources
PubMed1979

Bundle branch block after myocardial infarction--a long term follow-up.

Fifty-two patients with myocardial infraction complicated by bundle branch block (27 RBBB and 25 LBBB) survived the hospital period (1967--1972), and were followed up to December 1976. Actuarial survival curves revealed a worse mortality up to five years (P less than 0.05) for LBBB (68%) than for RBBB (33%). All deaths occurred in the first four years. In RBBB, additional hemiblock (seven patients) did not increase the risk of heart block nor worsen the prognosis--one death in seven patients (14%) compared to eight in 20 patients with isolated RBBB (40%). The previous literature on long term survival of BBB was reviewed. Recommended treatment for BBB, a marker of severe myocardial damage, includes antiarrhythmic prophylaxis for anteroseptal infarction with RBBB, aneurysmectomy in selected subsets of patients, and possibly prevention of RBBB or its complications by treatment for reduction of infarct size during the very early phase after onset of infarction.

Arrhythmias, Cardiac↗
PubMed1978

Protective effect of propranolol in threatened myocardial infarction.

Propranolol 0.1 mg/kg intravenously followed by 320 mg orally over 27 h was given to 20 randomly selected patients within 4 h of the onset of suspected myocardial infarction unaccompanied by diagnostic electrocardiographic changes. Patients given propranolol had fewer completed infarcts as assessed by serial electrocardiograms, a lower frequency of serum-creatine-kinase levels above the normal range, and lower peak serum-creatine-kinase levels than 23 control subjects. This evidence suggests that threatened myocardial infarction can in some cases be prevented by early beta-adrenoceptor blockade.

Acute Disease↗
PubMed1978

The effect of glucose-insulin-potassium on experimental myocardial infarction in the dog.

The effect of glucose-insulin-potassium (GIK) infusions was studied in 45 dogs after left anterior descending coronary artery ligation. GIK caused a modest increase in lactate concentration in small veins draining the infarct but did not affect glucose uptake. No effect on creatine kinase activity in the infarct was seen from GIK, although there was a slight increase in blood flow to the centre of the infarct. We concluded that GIK did not reduce infarct size in this experimental model.

Animals↗
PubMed1978

Failure of high doses of propranolol to reduce experimental myocardial ischemic damage.

Myocardial creatine phosphokinase (CPK) activity and myocardial blood flow (MFB, 15 +/- mu microspheres) were measured at 24 hours after ligation of the left anterior descending coronary artery in nine untreated anesthetized dogs, in eight dogs pretreated with intravenous propranolol 5 mg/kg and in eight which had both pretreatment as well as infusion of propranolol (1.25 mg/kg/hour) after occlusion. Loss of CPK activity from the border and center zones of the myocardial infarct was similar in extent in dogs which had pretreatment but no infusion of propranolol as it was in the control group. Loss of CPK from the center zone was greater (P less than 0.005) in dogs receiving pretreatment followed by constant infusion of the drug. Propranolol had no significant effect on collateral blood flow to the border or center zone of the infarct. In separate experiments, there was no important difference in hemodynamic measurements, except a slower heart rate (P less than 0.01), when pretreated dogs were compared with control dogs up to 2 hours after coronary ligation. We conclude that propranolol given in this dose does not influence nyocardial damage, on the basis of regional myocardial blood flow or tissue CPK depletion values at 24 hr after coronary occlusion.

Animals↗
PubMed1978

Reduction of enzyme levels by propranolol after acute myocardial infarction.

The effect of propranolol (0.1 mg/kg intravenously followed by 320 mg given over 27 hour orally) on serum levels of creatine kinase enzyme was studied in a randomized trial involving 95 patients seen within 12 hours of onset of symptoms of uncomplicated myocardial infarction. In 15 patients who were treated with propranolol within 4 hours of onset, and who eventually developed pathological Q waves, peak measured enzyme levels were 27% (P less than 0.0125) lower than in 19 control patients who were also seen within 4 hours of the onset but had no specific treatment. Total calculated enzyme appearance was also lower in the treated patients (reduced 25%, P less than 0.05) as was the calculated rate of the appearance (33%, P less than 0.005). No significant difference was found for treated compared with control patients entering the trial more than 4 hours after the onset of chest pain. This evidence suggests that propranolol may reduce the size of uncomplicated infarctions if it is given intravenously within 4 hours of the onset.

Acute Disease↗
PubMed1978

Myocardial damage following infarction.

It is likely that the size of the infarct is the main determinant of survival in acute MI. Infarct size can be judged effectively by using simple bedside techniques coupled with accurate interpretation of the chest radiograph. A more sensitive indicator of the patient's hemodynamic status can be gained by using the Swan-Ganz thermodilution catheter. Much more research is required for the development of methods for accurate measurement of infarct size. At present none of these is entirely satisfactory, although the measurement of metabolic substances released into the bloodstream from the infarct, particulary CK enzyme, appears to be the most promising.

Creatine Kinase↗
PubMed1977

Vitamin A stimulation of parathyroid hormone: interactions with calcium, hydrocortisone, and vitamin E in bovine parathyroid tissues and effects of vitamin A in man.

The effect of vitamin A, a membrane surface-active agent, on parathyroid hormone secretion was studied in vitro, using bovine parathyroid tissue, and in vivo in man. Parathyroid tissues were incubated with vitamin A (retinol), retinoic acid, and calcium, and with hydrocortisone and vitamin E, agents that antagonize the membrane effects of vitamin A. The stimulation of parathyroid hormone release by vitamin A, 10(-6) to 10(-9) mol/1 in vitro, was dose and time dependent. Retinoic acid did not stimulate secretion. High calcium concentration, hydrocortisone, 10(-5) mol/1 and 10(-6) mol/1, and vitamin E, 10(-5) mol/1, antagonized vitamin A-induced parathyroid hormone secretion. Vitamin A increased the lysosomal cathepsin D activity of parathyroid tissues. In human studies, eleven healthy men received two intramuscular injections of vitamin A palmitate, 25 000 units each, within 24 h. In every subject, serum parathyroid hormone increased after vitamin A administration. Our studies indicate that: (1) vitamin A stimulates parathyroid hormone secretion in vitro, possibly through modification of the cell or secretion granule membrane, or through stimulation of lysosomal proteolytic activity, and (2) vitamin A increases serum parathyroid hormone in vivo, and this effect may be important in clinical states of vitamin A excess.

Adult↗
PubMed1977

The effect of verapamil on experimental myocardial ischaemia with a particular reference to regional myocardial blood flow and metabolism.

The effects of verapamil on epicardial ST segment elevation, regional myocardial metabolism and collateral blood flow were studied in open-chest anesthetized dogs following left anterior descending coronary artery occlusion. Collateral blood flow was measured by radioactive microspheres (15 +/- 5 micron diameter) and regional metabolism was studied by measuring lactate concentration in venous blood draining the infarcting myocardium. Verapamil (0-2 mg/kg intravenously) produced a significant reduction (50-60%) in the epicardial ST elevation when it was given before coronary occlusion; when administered 15 minutes after coronary occlusion and infusion continued for two hours, it minimized (30-40%) ST segment elevation, and prevented the fall in cardiac index and rise in systemic resistance found in the untreated animals in which the ST segment remained persistently elevated. Changes in epicardial ST segment occurred without alterations in the QRS duration. Verapamil had no effect on either the total collateral blood flow or the relative distribution of flow to the endocardial and epicardial halves of the ischemic ventricular myocardium. No significant differences were found between the levels of lactate in blood sampled from small epicardial veins at the center of the infarct when the control animals were compared with those treated with verapamil.

Animals↗
PubMed1976

Regional differences in lactate concentration in experimental myocardial infarction.

Lacate concentrations were measured in blood from (a) coronary veins within ischaemic myocardium and (b) veins nearer to the coronary vein, for periods of up to 2 1/2 hours after ligation of the left anterior descending artery in dogs. Concentrations at (a) were three to four times higher than at (b), while blood sampled simultaneously from two veins at (a) yielded similar concentrations of lactate. At 2 1/2 hours after ligation the veno-arterial difference of lactate concentration in blood from (a) was about one half of the difference at 15 minutes. Lactate concentration at (a) was approximately twice as great when the area of ischaemic myocardium drained by the vein was large (18 not equal to 1% of heart weight) than when it was small (6 not equal to 1% of heart weight). No close correlation was apparent between the height of epicardial ST-segment elevation and the level of lactate release. These experiments extend previous observations that changes in lactate concentration at a given site may reflect changes in venous dilution, rather than in the rate of production of lactate, and emphasize that caution is necessary in interpretation of changes in concentrations of metabolites in coronary sinus blood after acute myocardial infarction in man.

Animals↗
PubMed1976

Failure of ST segment elevation to predict severity of acute myocardial infarction.

Praecordial ST segment elevation was measured at 35 electrode positions in each of 40 patients admitted to a coronary care unit after acute transmural anterior myocardial infarction. Serial praecordial electrocardiographic maps were recorded to determine (a) the time course as well as reproducibility of measurements of ST segment alterations, and (b) the degree of correlation between the magnitude of ST segment elevation and the severity of infarction, as assessed clinically or by sequential estimations of serum creatine kinase activity. Large variations in ST segment elevation were found in different patients with a comparable degree of myocardial damage, and at intervals of as little as four hours in the same patient. These variations were greater than could be explained by technical factors, and were not related to apparent changes in the patients' clinical status. The patterns of release of myocardial creatine kinase showed that the time course of ST segment elevation was longer than the period of myocardial necrosis. No correlation was found between the myocardial infarct size as determined by enzyme release and the highest levels of ST segment elevation recorded. The findings suggest that ST segment elevation as measured by praecordial electrocardiographic mapping does not constitute a reliable index of the size or severity of myocardial infarcts in man.

Adult↗
PubMed1976

Prognosis in unstable angina.

A retrospective study was made of 158 patients with unstable angina admitted to a coronary care unit over a 4-year period. Twenty patients (13 per cent) had myocardial infarcts while in hospital, and of these 3 died; three others died without preceding evidence of myocardial infarction. There was thus an acute mortality rate of 4 per cent. Patients with persisting angina after the first 24 hours and those without a previous history of myocardial ischaemia were more likely to develop a myocardial infarct or to die in hospital. Follow-up information, ranging from 3 to 7 years, was available in 144 of 152 hospital survivors. Patients older than 60 years (P less than 0-05), with cardiomegaly (P less than 0-01) and with pulmonary venous congestion (P less than 0-05) were found to have significantly increased long-term mortality. Long-term mortality was also found to rise with increasing coronary prognostic index. The average mortality rate for the whole group of hospital survivors was about 5 per cent per annum. Of the 111 patients who were alive at follow-up, 19 (17%) had had a myocardial infarct after leaving hospital, and a similar number had moderate or severe angina.

Age Factors↗
PubMed1976

Relationship between epicardial ST-segment elevation and myocardial ischemic damage after experimental coronary artery occlusion in dogs.

The relationship between early and late epicardial electrocardiographic changes as well as those in regional myocardial blood flow (MBF) and the severity of myocardial damage was determined in 12 anesthetized dogs with left anterior descending coronary artery ligation. Radioactive microspheres (15 mum) were used to measure regional MBF at 15 min (early) and 24 h (late) after coronary occlusion. Severity of myocardial damage was assessed by the extent of myocardial creatine phosphokinase depletion 24 h after coronary ligation. There was a close linear correlation between myocardial creatine phosphokinase activity and regional MBF both early (r=0.93, 2P less than 0.001) and late (r=0.88, 2P less than 0.001). An inverse but less precise relationship existed between acute epicardial ST-segment elevation and early (r=-0.41, 2P less than 0.001), or late (r=0.35, 2P less than 0.05) regional MBF. Similarly, a weak correlation was found between myocardial creatine phosphokinase (IU/mg protein) at 24 h and early epicardial ST (millivolt) elevation (r=-0.36, 2P less than 0.02). In the center zones of the infarct with MBF 1/10 of normal, about 35% of the areas with normal QRS width had no epicardial ST-segment elevation 15 min after coronary occlusion. About 44% of the areas which developed pathological Q-waves in the electrocardiogram at 24 h had no ST elevation 15 min after coronary ligation. Late evolution of abnormal Q-waves occurred almost invariably in areas in which the early MBF was reduced to less than 50% of normal and in areas which subsequently had myocardial creatine phosphokinase levels reduced to less than 60% of normal. After coronary occlusion, the severity of the ultimate myocardial damage, which was directly proportional to the degree of reduction in MBF, was therefore not reliably predicted by the early epicardial ST-segment elevation. The data obtained in these studies suggest the need for caution in the use of acute ST-segment elevation as a predictive index of the extent or severity of myocardial ischemic damage.

Animals↗
PubMed1976

Enzyme release after myocardial infarction: comparison of serial serum alpha-hydroxybutyrate dehydrogenase with creatine phosphokinase levels.

Serial measurements on serum creatine phosphokinase (CPK) and alpha-hydroxybutyrate dehydrogenase (HBD) activity were made in 17 patients with acute myocardial infarction. Activities of both enzymes were measured 4-hourly from less than 12 h after the onset of chest pain until CPK activity had returned to near-normal levels. Blood was then sampled twice daily for a further 4--6 days in order to follow the decline in HBD activity. Degradation rates (KD) were calculated for both enzymes, and individual figures for KD were used in order to estimate the total cumulative release of each enzyme. We found a significant correlation between the duration (r = 0.66, P less than 0.01) and magnitude (r = 0.67, P less than 0.01) of release of the 2 enzymes, comparing different patients with one another. Duration od HBD release was 11 h greater than the duration of CPK release in 9 of the 17 patients who were suffering from cardiac failure (t = 0.01, P less than 0.02). Degradation rate (KD) for HBD was on average about one quarter of that for CPK, but there was no significant correlation between KD for the 2 enzymes. KD did not appear to be reduced in patients with cardiac failure. We conclude that the release patterns of CPK and HBD after myocardial infarction are similar, and this strengthens the case for acceptance of total enzyme release as a valid index of myocardial infarct size.

Adult↗
PubMed1975

Effects of intravenous verapamil on cardiac arrhythmias and on the electrocardiogram.

The effects of intravenous verapamil on the electrocardiogram in 15 patients with heart disease in sinus rhythm and in 44 patients with supraventricular and ventricular tachyarrhythmias were evaluated. Verapamil prolonged the P-R interval without effect on the QRS duration or the Q-Tc interval. In patients with atrial flutter and fibrillation, A-V block was increased, with slowing of the ventricular rate, in almost all cases but sinus rhythm was restored in only 1 of 12 patients in atrial fibrillation and in 2 of the 11 patients with flutter. Verapamil had no effect in 3 patients with atrial fibrillation complicating WPW syndrome; in 1 of 5 patients with ventricular tachycardia it caused reversion to sinus rhythm. Sinus rhythm was restored promptly by verapamil in 13 of 17 patients with paroxysmal supraventricular tachycardias; in 2 others, sinus rhythm became established 1 to 2 hours after administration of the drug. Transient hypotension, not requiring treatment, was the only side effect noted but not in the patients with supraventricular tachycardias, in whom blood pressure generally increased after reversion to sinus rhythm by verapamil.

Adolescent↗