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Biomedical subjects

J E Muller

Publications and source records attributed to J E Muller.

At least 163 records · Page 9Linked to original sources
PubMed1981

Efforts to limit the size of myocardial infarcts.

Throughout the last decade, multiple interventions have been shown to decrease myocardial ischemic injury and limit infarct size in animal models of acute myocardial infarction. Results of pilot studies have suggested that some of these interventions may also have beneficial effects in humans with evolving myocardial infarction. This review focuses on the rationale for limiting infarct size, efficacy of methods for estimating size of infarcts, and current clinical data on specific intervention therapy. No intervention has yet been proved sufficiently efficacious to warrant its routine clinical use. However, treatment with beta-adrenergic blockers, intravenous nitroglycerin, and hyaluronidase has been shown to affect one or more indexes of infarct size in patients with acute myocardial infarction. Large, randomized clinical trials of these and other promising interventions are underway and will provide data on whether infarct size can be limited in humans and whether residual cardiac function and patient prognosis can thereby be improved.

Adrenergic beta-Antagonists↗
PubMed1980

Calcium channel blocking agents in the treatment of cardiovascular disorders. Part I: Basic and clinical electrophysiologic effects.

Calcium ions play an important role in the cardiovascular system. They are involved in electrophysiologic processes, link excitation to muscular contraction, control energy storage and utilization, and constrict vascular smooth muscle in coronary and systemic arteries. A new group of pharmacologic agents that block the passage of calcium ions across cell membranes has been developed. These agents act during the slow inward current of cellular depolarization. The most extensive clinical experience has been obtained with four of these agents: verapamil, nifedipine, perhexiline, and diltiazem. Verapamil, which has profound electrophysiologic effects on the slow inward current, is emerging as a valuable antiarrhythmic agent. Re-entrant supraventricular arrhythmias, such as paroxysmal supraventricular tachycardia, are particularly amenable to treatment with intravenous verapamil. Preliminary trials of long-term therapy with oral verapamil for control of atrial fibrillation, atrial flutter, and paroxysmal supraventricular tachycardia suggest that this agent is effective for therapy of these arrhythmias.

Action Potentials↗
PubMed1980

Calcium channel blocking agents in the treatment of cardiovascular disorders. Part II: Hemodynamic effects and clinical applications.

The calcium channel blocking agents have multiple hemodynamic effects that make them potentially valuable in treating many cardiovascular disorders. They are potent dilators of coronary and peripheral arteries and in isolated tissue preparations exert potent negative inotropic, chronotropic, and dromotropic effects. In intact animals the peripheral arterial vasodilatation induces reflex-mediated adrenergic activity, which opposes the direct negative inotropic, chronotropic, dromotropic, and hypotensive effects. The individual calcium channel blockers have different relative potencies on various cardiovascular functions. The net hemodynamic and electrophysiologic effect of each agent, therefore, results from a complex interplay of direct and reflex phenomena. The clinical efficacy of these agents in classic angina pectoris relates to their ability to decrease afterload, myocardial contractility, and heart rate and increase coronary blood flow. The agents have been used to prevent coronary spasm in Prinzmetal's variant angina. The negative inotropic effects of verapamil are valuable in improving the symptoms and hemodynamic disturbances of hypertrophic cardiomyopathy. The role of these agents in treating arterial hypertension, unstable angina pectoris, acute myocardial infarction, and ischemia during cardiopulmonary bypass needs to be determined.

Benzazepines↗
PubMed1979

Inappropriate coronary vasoconstriction in patients with coronary artery disease: a role for nifedipine?

Coronary arterial vasoconstriction, well recognized in Prinzmetal's variant angina, may participate in the pathogenesis of classic angina as well. Several recent studies in patients with obstructive coronary artery disease suggest that apparently spontaneous reductions in coronary blood flow can result in myocardial ischemia and even infarction. Evidence supporting the alpha adrenergic nervous system as a cause of such coronary vasoconstriction is reviewed, particularly the results of provocative testing with the cold pressor stimulus. Upon exposure of the skin to cold, patients with coronary artery disease demonstrate an inappropriate coronary vasoconstrictor response, often sufficient to produce angina. Normal patients, by contrast, show no change in coronary vascular resistance. In patients with a diseases coronary circulation, inappropriate vasoconstriction further restricts myocardial perfusion and appears to be little affected by beta adrenergic blocking agents or nitrates in the usual dosages. Nifedipine has proved effective in preventing coronary arterial spasm in patients with Prinzmetal's angina. Studies currently in progress suggest that it is also effective in blocking inappropriate coronary vasoconstriction in patients with typical angina. Nifedipine may thus be a useful addition to the treatment of ischemic heart disease.

Angina Pectoris, Variant↗
PubMed1978

Insulin therapy for depressed myocardial contractility after prolonged ischemia.

Insulin was administered to two patients whose diminished myocardial contractility made it difficult to terminate cardiopulmonary bypass. In both instances, bypass was successfully terminated shortly after the insulin injection. These clinical observations led to experiments under the controlled conditions provided by the isolated, working rat heart preparation. The recovery of contractility after 30 minutes of severe ischemia was assessed in all 11 control and 11 insulin-treated hearts. Myocardial performance, as judged by the product of heart rate and peak systolic blood pressure, was significantly greater in the insulin-treated hearts. These clinical observations and experimental findings suggest the need for more extensive study of the potential value of insulin in treating depressed contractility after prolonged myocardial ischemia.

Animals↗
PubMed1978

Nifedipine therapy for Prinzmetal's angina.

A case is described in which nifedipine, a new coronary vasodilator, was effective in relieving attacks of Prinzmetal's angina unresponsive to conventional therapy. The extreme frequency of the anginal attacks provided evidence that lower doses of nifedipine lost their effectiveness approximately 4 hours after administration. A month after initiation of nifedipine, nitrates were withdrawn since they had been ineffective in controlling the attacks. A myocardial infarction occurred immediately, presumably due to coronary spasm.

Adult↗
PubMed1977

Favorable effects of hyaluronidase on electrocardiographic evidence of necrosis in patients with acute myocardial infarction.

To evaluate hyaluronidase's effect in reducing post-infarction myocardial necrosis, we randomized 91 patients with anterior infarction to control (45) or to hyaluronidase-treatment (46) groups. A 35-lead precordial electrocardiogram was recorded on admission and seven days later. Hyaluronidase was administered intravenously after the first electrocardiogram and every six hours for 48 hours. QRS-complex changes were analyzed to assess the drug's effect. Precordial sites with ST-segment elevation (larger than or equal to 0.15 mV) on the initial electrocardiogram that retained an R wave were considered vulnerable for the development of electrocardiographic signs of necrosis. The sum of R-wave voltages of vulnerable sites fell more in the control group than in the hyaluronidase group (70.9 +/- 3.6 per cent [+/- 1 S.E.M.] vs 54.2 +/- 5.0 per cent P less than 0.01). Q waves appeared in 59.3 +/- 4.9 per cent of the vulnerable sites in control versus 46.4 +/- 4.9 per cent in hyaluronidase-treated patients (P less than 0.05). Thus, hyaluronidase reduced the frequency of electrocardiographic signs of myocardial necrosis.

Acute Disease↗
PubMed1977

Diagnosis of myocardial infarction: historical notes from the Soviet Union and the United States.

Soviet physicians attribute the first description of the clinical presentation of a nonfatal myocardial infarction to V.P. Obraztsov and N.D. Strazhesko; American physicians attribute the same achievement to James B. Herrick. Investigation of the origins of the conflicting claims reveals that the Russian physicians published an accurate account of the syndrome in 1910. Herrick, in his article published in 1912, cites a German translation of the Russian article. Herrick's major contribution consisted of informing American physicians of the symptoms of infarction, and stimulating development of the electrocardiogram as a diagnostic aid.

History, 19th Century↗
PubMed1977

Cholecystokinin and its COOH-terminal octapeptide in the pig brain.

Two components--one resembling intact cholecystokinin in size and charge and immunologic specificity, and the other resembling the COOH-terminal octapeptide of cholecystokinin--have been found in extracts of the pig cerebral cortex. The relative concentrations of the two peptides in the extracts were dependent on the extractant, boiling 0.1 M HCl being more effective than boiling water for the extraction of intact cholecystokinin but less effective for the extraction of the octapeptide. The physiologic role of these peptides in the brain has yet to be elucidated.

Animals↗
PubMed1976

Use of changes in the epicardial QRS complex to assess interventions which modify the extent of myocardial necrosis following coronary artery occlusion.

The goal of this study was to determine if changes in the epicardial QRS complex after coronary artery occlusion (CAO) can be used to evaluate the efficacy of interventions designed to limit infarct size. Forty-one open-chest dogs with CAO were studied: 15 were controls, 18 received hyaluronidase and eight received propranolol starting 20 minutes after CAO. Epicardial ECGs were recorded at specific time intervals to analyze ST-segment elevation and changes in Q and R waves. Transmural specimens were obtained 24 hours after CAO from the same sites at which ECGs were recorded. Q wave development (deltaQ), R wave fall (deltaR), and their combination (deltaR + deltaQ) at 24 hours correlated with the extent of necrosis, as determined by myocardial creatine phosphokinase activity depression and histologic appearance. In the control group ST-segment elevation 15 minutes after CAO (ST15M) predicted changes in Q and R waves 24 hours later; in the treated groups, the same ST15M prior to drug administration resulted in significantly less QRS changes. Thus, 1) Q wave development and R wave fall 24 hours after CAO accurately reflect myocardial necrosis. 2) ST15M predicts subsequent changes in Q and R waves. 3) The efficacy of hyaluronidase and propranolol, agents previously shown to reduce myocardial necrosis, can be detected by less Q wave development and a smaller fall in R wave voltage.

Animals↗
PubMed1975

Evaluation of precordial electrocardiographic mapping as a means of assessing changes in myocardial ischemic injury.

Precordial electrocardiographic mapping has been proposed as a method for evaluating the extent of myocardial injury in patients with acute myocardial infarction. To assess the relationship between direct measures of myocardial cell damage and findings obtained by precordial mapping, the left anterior descending coronary artery (LAD) was occluded in dogs instrumented for simultaneous recording of epicardial and precordial electrocardiograms. The sum in millivolts of ST-segment elevation recorded from 30 electrodes placed in a Silastic grid sutured to the epicardium (EPIsigmaST) was compared to that recorded from 30 precordial electrodes (PresigmaST). While ischemic injury was: 1) maintained constant with a fixed occlusion; 2) reduced by partial reperfusion; 3) increased by addition of a second occlusion; or 4) increased repeatedly by intermittent infusions of isoproterenol, EPIsigmaST and PresigmaST were always closely correlated in each of the 16 dogs studied: r equal 0.92 plus or minus 0.01 (SEM). In seven control dogs, 30 minutes after coronary occlusion, PresigmaST had fallen to 77.4 plus or minus 6.6% of its value 15 minutes postocclusion. In seven experimental dogs, two branches of the LAD were occluded. Fifteen minutes after double occlusion, one occlusion was released; 30 min after the initial occlusion PresigmaST had fallen significantly more than control, to 43.1 plus or minus 13.1% of its value 15 minutes postocclusion. Simultaneously, epicardial sites in the reperfused area also showed normalization of ST segments and 24 hours later exhibited normal myocardial creatine phosphokinase activity and normal histologic appearance. During the same experiment, the mean precordial R wave voltage of sites with ST-segment elevations exceeding 0.15 mV 15 minutes following occlusion fell significantly (P less than 0.05) more in the control group (from 1.14 plus or minus 0.15 to 0.75 plus or minus 0.06 mV) than in the reperfused group (from 1.06 plus or minus 0.09 to 0.96 plus or minus 0.17 mV) during the ensuing 45 minutes. Thus, more rapid normalization of PresigmaST or preservation of precordial R wave voltage reflected the actual prevention of myocardial necrosis by reperfusion. These findings demonstrate the usefulness of precordial electrocardiographic mapping for evaluation changes in myocardial ischemic injury. Sites at which appearance of epicardial ST segment is not a reliable index of ischemic injury were associated with the development of intraventricular conduction blocks with Q to intrinsic deflection intervals exceeding 40 mesc or QRS durations exceeding 65 msec; these changes were associated with precordial RSR' configurations. Such sites, whether recorded from precordial or epicardial leads, should be excluded from ST-segment measurements used in the assessment of myocardial ischemia.

Acute Disease↗