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Biomedical subjects

R M Norris

Publications and source records attributed to R M Norris.

At least 73 records · Page 4Linked to original sources
PubMed1988

Critique of current therapies of noninsulin-dependent diabetes mellitus.

In summary, there are a number of therapeutic modalities, including life-style modifications and pharmacological intervention, available and useful in the treatment of NIDDM patients. Nonetheless, therapeutic success in the management of NIDDM remains highly dependent upon patient motivation, cooperation, and ability to comply on a regular basis with measures that are inconvenient and of modest efficacy in reversing the physiologic abnormalities of the NIDDM state. There remains considerable need for therapeutic tools of greater efficacy and of greater ease of application than the ones we currently have.

Diabetes Mellitus, Type 2↗
PubMed1987

Effect of intravenous streptokinase on left ventricular function and early survival after acute myocardial infarction.

In a double-blind trial of streptokinase for acute myocardial infarction, 219 consecutive patients presenting with infarction within four hours (mean, 3.0 +/- 0.8) of the onset of chest pain were randomly assigned to treatment with streptokinase (1.5 million units) or placebo, given intravenously over 30 minutes. The primary end point of the study was left ventricular function in patients with first infarctions. Patients who could undergo beta-blockade also received intravenous propranolol. Heparin (for 48 hours) and a combination of low-dose aspirin and dipyridamole were administered to both groups until cineangiography was performed at three weeks. In the patients with first infarctions treated with streptokinase, the left ventricular ejection fraction was 6 percentage points higher (streptokinase vs. placebo, 59 +/- 10.5 vs. 53 +/- 13.5 percent; P less than 0.005), with benefit to patients with either anterior infarction (57 +/- 11.9 vs. 49 +/- 15.9 percent; P less than 0.05) or inferior infarction (60 +/- 9.1 vs. 55 +/- 11.3 percent; P less than 0.05). Left ventricular function was improved regardless of whether concomitant propranolol was given. Survival (at 30 days) was improved with streptokinase: 2 deaths occurred among 79 patients who received this drug, as compared with 12 deaths among 93 patients who received placebo (2.5 vs. 12.9 percent, P = 0.012). Rates of reinfarction (streptokinase vs. placebo, 3 vs. 1 percent) and requirements for surgery or angioplasty (7 vs. 5 percent) were similar in the two groups. We conclude that administration of intravenous streptokinase (1.5 million units) to patients with a first myocardial infarction results in improved left ventricular function and short-term survival.

Adrenergic beta-Antagonists↗
PubMed1987

Post-systolic shortening: a marker of potential for early recovery of acutely ischaemic myocardium in the dog.

Regional diastolic wall motion was studied with sonomicrometry in 30 open chest anaesthetised dogs after left anterior descending stenosis or occlusion. Post-systolic shortening and thickening, defined as the magnitude of segment shortening or wall thickening that occurred after end systole, was measured in peripheral and central ischaemic segments. These post-systolic events developed concurrently with impaired systolic shortening or thickening, either immediately after acute coronary occlusion or during progressive stenosis, and persisted with the development of dyskinesis and during reperfusion. The magnitude of these events in dyskinetic segments of 24 dogs was considerable, reaching 50(2)% (mean(SEM)) and 33(3)% of shortening or thickening that was present before coronary occlusion. Post-systolic shortening and thickening were maximum at 100(2) ms after peak negative dP/dt. Significant correlations were found between systolic shortening or thickening before coronary occlusion and post-systolic shortening (r = 0.74, 56 segments) or thickening (r = 0.84, 19 segments) after occlusion, but there was no correlation between post-systolic shortening or thickening and dyskinetic lengthening or thinning. In seven dogs followed for 4 h after coronary occlusion post-systolic shortening fell by 15% in peripheral segments and by 70% in central segments (p less than 0.002). In 17 dogs reperfused after 60 (n = 9) or 90 (n = 8) min of coronary occlusion the maximal recovery of systolic shortening early after reperfusion was significantly related to the magnitude of post-systolic shortening immediately before reperfusion (60 min occlusion r = 0.84, 90 min occlusion r = 0.88). These data show that post-systolic shortening is a marker of potential for early recovery of function of acutely ischaemic myocardium and suggest that it is due, at least in part, to an active process.

Acute Disease↗
PubMed1987

Left ventricular end-systolic volume as the major determinant of survival after recovery from myocardial infarction.

Impairment of left ventricular function is the major predictor of mortality after acute myocardial infarction, but it is not known whether this is best described by ejection fraction or by end-systolic or end-diastolic volume. We measured volumes, ejection fractions, and severity of coronary arterial occlusions and stenoses in 605 male patients under 60 years of age at 1 to 2 months after a first (n = 443) or recurrent (n = 162) myocardial infarction and followed these patients for a mean of 78 months for survivors (range 15 to 165 months). There were 101 cardiac deaths, 71 (70%) of which were sudden (instantaneous or found dead). Multivariate analysis with log rank testing and the Cox proportional hazards model showed that end-systolic volume (chi 2 = 82.9) had greater predictive value for survival than end-diastolic volume (chi 2 = 59.0) or ejection fraction (chi 2 = 46.6), whereas stepwise analysis showed that once the relationship between survival and end-systolic volume had been fitted, there was no additional significant predictive information in either end-diastolic volume or ejection fraction. Severity of coronary occlusions and stenoses showed additional prediction of only borderline significance (p = .04 in one analysis), but continued cigarette smoking did remain an independent risk factor after stepwise analysis. For a subset of patients (n = 200) who had taken part in a randomized trial of coronary artery surgery after recovery from infarction, surgical "intention to treat" showed no predictive value.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Volume↗
PubMed1986

Beta blockers and infarct size.

Reduction of myocardial oxygen demand by beta blockers should be beneficial for treatment of the supply-demand imbalance of severe myocardial ischaemia leading to infarction. There is evidence that rate-pressure product, an index of myocardial oxygen demand, is an independent variable for determination of infarct size, and that reduction of rate-pressure product by beta blockers or by other means is beneficial. Although experimental evidence is conflicting, some animal studies have shown protection from beta blockers when a coronary artery is permanently occluded, while a majority of studies show protection when a temporary coronary artery occlusion is followed by reperfusion. Prevention of ventricular fibrillation due to coronary artery occlusion has been shown in animal studies. In patients with developing infarction, rate-pressure product is reduced by approximately 20% when a beta blocker is given intravenously, and cardiac metabolism, assessed by coronary sinus sampling, returns to a more normal "oxidative" pattern. Indirect indices of infarct size, namely serum enzyme release and precordial R wave loss are reduced in patients treated early with intravenous beta blockers compared with control patients. However there is no evidence that left ventricular function is preserved by beta blockers. Very large multicentre trials have shown reduction in mortality among treated patients by about 15% when an intravenous beta blocker is given, suggesting that routine use would save 1 life for every 100-200 patients treated.

Adrenergic beta-Antagonists↗
PubMed1986

Amiodarone-induced torsades de pointes.

Five cases of amiodarone-induced syncope due to torsades de pointes or ventricular fibrillation are described. Amiodarone was used for recurrent supraventricular tachycardia in four cases and frequent ventricular extra systoles complicating congenital QT prolongation in the remaining case. Each was associated with a marked prolongation in the QTc interval following amiodarone. Three cases had had a previous history of life-threatening ventricular arrhythmias secondary to anti-arrhythmic drugs. Hypokalemia may have been a contributory factor in two. The clinical features, predisposing factors, and treatment are discussed.

Adult↗
PubMed1985

Right ventricular infarction, bradyarrhythmias, and cardiogenic shock: importance of atrial or atrioventricular sequential pacing.

We report two patients with inferior myocardial infarction, complicated by bradyarrhythmia, hypotension, and clinical evidence of right ventricular infarction. Conventional therapy of volume expansion and inotropic support was insufficient to maintain an adequate blood pressure. Sequential atrioventricular (AV) pacing for AV block (Case 1) or atrial pacing for junctional bradycardia (Case 2) resulted in immediate and sustained improvement in blood pressure and clinical indices of perfusion. We recommend consideration of these pacing modes in patients with inferior infarction with evidence of right ventricular infarction, bradyarrhythmia, and cardiogenic shock. The likely mechanism of improvement is by restoration of atrial transport with consequent improvement in ventricular function.

Bradycardia↗
PubMed1985

Effect of early treatment with propranolol on left ventricular function four weeks after myocardial infarction.

Left ventricular function and exercise capacity were assessed in 79 patients randomised to receive intravenous and oral propranolol (n = 44) or conventional therapy (n = 35) within four hours of onset of their first myocardial infarction. Cineangiocardiography and exercise testing were performed four weeks after infarction to allow for maximum recovery of myocardial function. Left ventriculography showed no improvement in ejection fraction or preservation of regional contractile function in patients treated with propranolol compared with controls. A trend towards smaller end diastolic volumes was seen in the propranolol group (mean (SD) 151(42) ml) compared with controls (167(42) ml). Exercise duration and frequency of angina were not significantly different in the two groups. It is concluded that limitation of infarct size by propranolol does not lead to a significant improvement in ventricular systolic function, although left ventricular dilatation may be reduced. These findings are consistent with the known effect of early intravenous beta blockade which limits infarct size by preservation of subepicardial myocardium.

Adult↗
PubMed1984

Prevention of ventricular fibrillation during acute myocardial infarction by intravenous propranolol.

A trial of intravenous followed by oral propranolol, started within 4 h of onset of suspected myocardial infarction and continued over 27 h, was carried out in 735 patients; 364 received propranolol, 371 were controls. Ventricular fibrillation during the first 48 h after entry to the trial occurred in 2 treated patients and in 14 controls (p = 0.006). Rates of hospital mortality, complications other than ventricular fibrillation, and progression from threatened to completed infarction did not differ between treated and control patients. Ventricular fibrillation was not apparently prevented by prior beta-blocker treatment, which was not a reason for exclusion from the trial. This intravenous/oral propranolol regimen seems to prevent ventricular fibrillation due to evolving myocardial infarction.

Administration, Oral↗
PubMed1984

Prognosis after myocardial infarction: results of 15 year follow up.

A total of 271 out of 757 patients who had suffered a myocardial infarction during 1966-7 were still alive after six years; these patients were subsequently followed up 15 years after the infarction. Two hundred and sixty eight (99%) of the patients alive at six years and 519 (95%) of the 549 originally discharged from hospital were traced. A coronary prognostic index, which had predicted survival both to three years and from three to six years after recovery from the infarct also predicted survival from six to 15 years after recovery. The major factor affecting survival to 15 years was age at the time of the original infarct. Among patients aged under 60 at the time of infarction women fared better than men (p = 0.027). Factors in the coronary prognostic index that were associated with impairment of left ventricular function at the time of infarction and that had predicted mortality to three years and from three to six years also predicted mortality from six to 15 years. These factors were cardiac enlargement, pulmonary venous congestion, and the presence of infarction before the index infarct. The dominant cause of death remained coronary heart disease and its complications.

Age Factors↗
PubMed1984

Prognosis after recovery from first acute myocardial infarction: determinants of reinfarction and sudden death.

Factors associated with total cardiac mortality, sudden cardiac death and reinfarction were studied in 325 male survivors aged younger than 60 years of age (mean 50) of a first myocardial infarction (MI). All patients had undergone exercise testing and cineangiocardiography 4 weeks after MI, 24% underwent coronary artery surgery and 30% received beta-blocking therapy. Patients were followed 1 to 6 years (mean 3.5). Total cardiac mortality was best predicted by the left ventricular (LV) ejection fraction (EF) and by a coronary prognostic index. In contrast, neither the severity of coronary arterial lesions measured with a scoring system nor the results of the exercise test gave significant prediction of mortality. Of the 2 major late sequelae of MI, reinfarction could not be predicted by any clinical or cineangiocardiographic variable. However, sudden death not associated with reinfarction was significantly more common (p less than 0.001) when EF was less than or equal to 40% than when it was greater than 40%. Comparison of patients with an EF less than or equal to 40% who did or did not die suddenly showed that LV dilation (high volumes at ventriculography) was an added risk factor, but the extent of coronary occlusions and stenoses was not. It is concluded that, at least for groups of patients treated with standard modern methods after MI, the main determinant of medium-term survival is the extent of LV damage. The state of the coronary arteries and the presence of ischemic myocardium during exercise are only of secondary importance for survival.

Adrenergic beta-Antagonists↗