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Biomedical subjects

J E Muller

Publications and source records attributed to J E Muller.

At least 145 records · Page 8Linked to original sources
PubMed1983

Electrocardiographic and clinical criteria for recognition of acute myocardial infarction based on analysis of 3,697 patients.

Over a 34.5-month period, all admissions to 5 university hospital coronary care units were screened for eligibility for the Multicenter Investigation of the Limitation of Infarct Size (MILIS), an ongoing study of the effects of hyaluronidase, propranolol and placebo on myocardial infarct (MI) size. Of 3,697 patients with greater than or equal to 30 minutes of discomfort that was thought to reflect myocardial ischemia who were assessed for the presence or absence of certain electrocardiographic abnormalities at the time of hospital admission, the electrocardiogram was considered predictive of acute MI if greater than or equal to 1 of the following abnormalities was present: new or presumably new Q waves (greater than or equal to 30 ms wide and 0.20 mV deep) in at least 2 of the 3 diaphragmatic leads (II, III, aVF), or in at least 2 of the 6 precordial leads (V1 to V6), or in I and aVL; new or presumably new ST-segment elevation or depression of greater than or equal to 0.10 mV in 1 of the same lead combinations; or complete left bundle branch block. In the screened population, the diagnostic sensitivity of the electrocardiographic criteria was 81%, whereas the overall infarct rate in the total population screened was 49%. The diagnostic specificity of these entry criteria was 69% and the predictive value 72%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Enzymatic estimation of myocardial infarct size when early creatine kinase values are not available.

Estimates of myocardial infarct (MI) size based on plasma creatine kinase (CK) are used widely for prognosis and in the assessment of therapy designed to salvage ischemic myocardium. However, if the initial plasma CK activity is elevated, MI size will be underestimated. To determine the impact of loss of early CK values on estimates of MI size and to develop a procedure to compensate for it, estimates of MI size based on complete and incomplete MB and total CK time-activity curves from 120 patients (experimental group) were compared. Estimates of MI size based on data inclusion intervals beginning at 24, 12, 8, and 4 hours before peak CK were 11, 14, 23, and 47% smaller than values based on complete CK curves, but the correlation was good between complete and incomplete estimates of MI size at any given interval, with r values ranging from 0.91 to 0.98. The derived correction factors were then prospectively applied to a new population (n = 25) with complete CK curves to compensate for purposely omitted early CK values. The corrected estimates of MI size were within 7% of those based on the complete CK curves. Similar results were obtained for transmural and nontransmural and anterior or inferior MI. Thus, if peak plasma CK is known, underestimation of MI size can be compensated for despite the unavailability of early CK values. Since greater than 90% of patients present before plasma CK has reached its peak (24 hours), MI size can be obtained in nearly all patients. Thus, being able to correct for unavailable early CK values makes MI size a more widely applicable endpoint for use in clinical trials and patient management.

Aged↗
PubMed1983

Role of beta-adrenergic blockade in the therapy of patients with myocardial infarction.

Beta-adrenergic blockade appears to have beneficial effects on ischemic myocardium, both in experimental animals and in patients. There is substantial evidence that beta blockade, when induced promptly after coronary occlusion, is capable of limiting the size of experimentally produced infarcts. Although many mechanisms of action have been proposed, the bulk of available evidence suggests that beta blockade reduces the severity of myocardial ischemia by reducing myocardial oxygen demands. Intravenous and oral therapy with beta-blockers is safe when patients are carefully selected and observed. Invasive hemodynamic monitoring is not usually necessary for safe use of these drugs. Preliminary reports based on studies with several beta-blockers indicate that early intervention might limit infarct size or even prevent its occurrence, particularly in patients with evidence of increased sympathetic activity. However, before early beta blockade can be recommended as standard therapy for uncomplicated myocardial infarction, these findings should be confirmed in rigorously controlled clinical trials utilizing several techniques for assessment of infarct size. The most significant finding with beta-blockers in patients with myocardial infarction has been that these drugs can improve survival when administered to patients on a long-term basis after infarction. Although the mechanism of this protective effect is not yet understood, the results are clear enough to warrant the routine administration of a beta-blocker to patients who have had infarction and who have no contraindications to such therapy.

Adrenergic beta-Antagonists↗
PubMed1983

Prevention by nifedipine of cold pressor-induced decrease in left ventricular ejection fraction.

To examine the effects of nifedipine on changes in ventricular function produced by cold, the cold pressor test was administered to eight patients with angiographically documented coronary artery disease. Radionuclide ventriculograms were obtained at baseline and during the cold pressor stimulus both before and after administration of nifedipine, 10 mg buccally; thus, four serial radionuclide ventriculograms were obtained per patient. The cold pressor stimulus did not produce any significant difference in the mean (+/- standard deviation) peak rate-pressure product during the control or nifedipine test (10,900 +/- 3,390 versus 10,600 +/- 3,700). However, the increase in systolic blood pressure (p = 0.05) and the peak systolic blood pressure achieved (p less than 0.001) were greater during the control (134 +/- 19 to 160 +/- 25 mm Hg) than during the nifedipine (125 +/- 18 to 145 +/- 21 mm Hg) cold pressor test. The mean global left ventricular ejection fraction decreased during the control cold pressor test from a baseline value of 0.60 +/- 0.08 to 0.52 +/- 0.08 (p = 0.004). After nifedipine, this variable did not change during the repeat cold pressor test (0.63 +/- 0.09) compared with the repeat baseline value (0.63 +/- 0.11). Therefore, the difference in left ventricular ejection fraction response during control versus nifedipine cold pressor testing was highly significant (p less than 0.0001). In patients with obstructive coronary artery disease, nifedipine abolished the decrease in left ventricular ejection fraction observed during the control cold pressor test and may be of value to protect patients from cold-induced left ventricular dysfunction. The mechanism may be a combination of coronary artery vasodilation and systolic unloading of the left ventricle.

Adult↗
PubMed1983

Coronary artery thrombosis: historical aspects.

There is intense scientific interest in the possibility that the acute administration of a fibrinolytic agent might be of benefit to patients with acute myocardial infarction. This hypothesis, which will soon be tested in a major trial by the National Heart, Lung, and Blood Institute, has emerged from a confluence of advances in three areas: increased knowledge about the role of thrombosis in myocardial infarction, the development of fibrinolytic agents and the recognition that ischemic myocardial tissue might be salvaged from necrosis by timely reperfusion. Examination of the manner in which these areas of knowledge developed and interacted not only illuminates our path to this specific therapeutic possibility, but also demonstrates the indirect and stuttering manner in which important new ideas often evolve.

Anticoagulants↗
PubMed1983

Nifedipine therapy for coronary vasospasm.

In conclusion, we observed first that nifedipine is highly efficacious in preventing the coronary vasospasm of Prinzmetal's variant angina. Secondly, nifedipine appears to be efficacious in preventing episodes of recurrent rest angina following an acute myocardial infarction. Although coronary vasospasm has not been clearly documented in patients with recurrent rest angina after infarction, a primary decrease in coronary blood flow is the most likely cause of this syndrome since the ischemia occurs at rest, at a time when myocardial oxygen demands are not elevated. In this highly unstable group of patients with coronary disease nifedipine may eliminate the need for bypass surgery or may provide clinical stability prior to more elective cardiac catheterization and surgery.

Angina Pectoris↗
PubMed1982

Nifedipine therapy for recurrent ischemic pain following myocardial infarction.

The efficacy of nifedipine in relieving recurrent ischemic episodes following acute myocardial infarction was studied in 11 patients a mean of 9.2 days post infarction (range 2-42 days). Prior to infarction, all of the patients had a history of exertional angina only, yet following the infarction, episodes of recurrent ischemia occurred at rest in spite of maximal medical management with beta-blockers and/or nitrate preparations, which lowered the heart rate to a mean of 65 beats/min, and the blood pressure to a mean of 109/70 mmHg. Ischemic episodes were associated with ST-segment elevation in 7 patients and ST-segment depression or T-wave inversion in 4 patients. Coronary angiography was performed in 8 patients, and demonstrated multivessel coronary disease in 7. The episodes of rest ischemia were prevented in all but one patient by the addition of nifedipine (mean daily dose 60 mg, range 40-120 mg) without causing a change in heart rate or blood pressure. Two patients continued to have myocardial ischemia with minimal exertion, although rest pains were abolished, and they underwent coronary bypass surgery for relief of exertional pain. Only one patient continued to have episodes of ischemia at rest, although the frequency of ischemic episodes was decreased, and bypass surgery was necessary for pain relief. The other 8 patients have been managed medically for a mean of 5.4 months (range 1-12 months) and have remained pain free on combined regimens of nifedipine, beta blockers, and/or nitrate preparations. We conclude that nifedipine may be efficacious for the relief of recurrent myocardial ischemia at rest following acute infarction. In some patients nifedipine may eliminate the need for coronary artery bypass surgery and in others it may provide clinical stability prior to operation.

Aged↗
PubMed1982

The serum kinetics of bovine testicular hyaluronidase in dogs, rats and humans.

There is experimental and clinical evidence that i.v. injection of bovine testicular hyaluronidase (BTH) reduces the extent of necrosis during myocardial infarction. The fate of i.v. administered BTH has not been described. In this study, serum kinetics of BTH enzyme activity in dogs, rats and humans were determined. Tissue distribution of BTH was determined with an 125I-labeled preparation of purified BTH. Serum BTH activity initially decreased exponentially with half-life 2.0 +/- 0.1 min in dogs with coronary artery occlusion (n = 8; 500 U of BTH/kg); 3.2 min in humans with acute myocardial infarction (n = 2; 500 U of BTH/kg); and 3.2 +/- 0.3 min in rats (n = 5; 5,000 U of BTH/kg). In dogs BTH disappearance showed two distinct phases. After injection of high dose BTH (5,000 U of BTH/kg), during the first 7 min serum half-life of BTH was 2.1 +/- 0.2 min (n = 8), but increased to 9.4 min in later serum samples. After the injection of 125I-labeled BTH into the rat, protein-bound 125I disappeared from serum with a half-life (3.4 min) that is similar to the serum half-life of BTH enzyme activity (3.2 min). Twenty minutes after injection of 125I-labeled BTH, 30% of the label was recovered in the liver. It is concluded that BTH activity has a short serum half-life of less than 10 min in dogs, rats and humans. In the rat model, the disappearance of serum BTH activity results from physical removal of circulating BTH molecules rather than serum inhibition or inactivation of BTH enzymatic activity.

Animals↗
PubMed1981

Therapy of coronary vasoconstriction in patients with coronary artery disease.

Patients with obstructive coronary artery disease and stable, exertional angina respond to the alpha adrenergic stimulus of the cold pressor test with an inappropriate increase in coronary vascular resistance. The clinical significance of this abnormal response and its possible role in the pathogenesis of ischemic heart disease are discussed. Comparison of the anti-anginal agents currently in use of undergoing investigation suggests that the calcium antagonists may be the most effective therapy for coronary vasoconstriction. Nifedipine, 10 mg buccally, successfully prevented the increase in coronary vascular resistance during the cold pressor test in 10 of 10 patients, whereas the response in placebo-treated patients was unaltered. This dose of nifedipine was without effect on systemic hemodynamics or myocardial oxygen consumption, suggesting a selective antivasoconstrictor effect on the coronary vasculature.

Angina Pectoris↗
PubMed1981

Prevention of nifedipine of abnormal coronary vasoconstriction in patients with coronary artery disease.

The hemodynamic and myocardial metabolic responses to the cold pressor test were studied in 15 patients with coronary artery disease and stable exertional angina. Every patient had abnormal coronary vasoconstriction during a control cold pressor test, even though 14 were receiving propranolol and 12 were receiving long acting nitrates. Mean coronary vascular resistance for the group increased 18 +/- 6% (SD) (from 0.80 +/- 0.12 to 0.94 +/- 0.20 mm Hg/ml/min, p less than 0.05); coronary sinus blood was unchanged, and the arterial-coronary sinus oxygen difference widened significantly (from 11.5 +/- 1.2 to 12.3 +/- 1.2 ml/100 ml, p less than 0.05). Four patients developed angina, accompanied in each instance by a negative arterial-coronary sinus lactate difference. After the administration of nifedipine (10 mg buccally) in 10 patients, the coronary vascular responses to a repeat cold pressor test were normal in each patient. Mean coronary sinus blood flow increased 27 +/- 12% (from 122 +/- 32 to 153 +/- 35 ml/min, p less than 0.05), coronary vascular resistance decreased 10 +/- 6% (from 0.85 +/- 0.16 to 0.76 +/- 0.16 mm Hg/ml/min, p less than 0.05), and the arterial-coronary sinus oxygen difference was unchanged. No patient experienced angina. The hemodynamic and coronary vascular responses to a repeat cold pressor test in five patients given placebo were unaltered from control responses. The protective effects of nifedipine were unaccompanied by any change in mean arterial pressure, left ventricular filling pressure or myocardial oxygen consumption either at rest or in response to the cold pressor test. Nifedipine appears to exert a selective antivasoconstrictor effect on the coronary vasculature.

Adult↗