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Biomedical subjects

H S Loeb

Publications and source records attributed to H S Loeb.

At least 73 records · Page 4Linked to original sources
PubMed1981

Progression of coronary artery disease in medically and surgically treated patients 5 years after randomization.

Repeat angiography was performed at 63 +/- 9 months in 26 medically treated patients and at 66 +/- 10 months in 32 surgically treated patients with chronic angina. The native coronary arteries were divided into three major trunk vessels and 15 angiographic segments. Progression of disease was defined as the appearance of new (greater than 50%) obstruction or significant worsening of existing lesions in a segment or vessel. The incidence of progression was similar in medical and surgical patients, comparing individual segments (69 of 312 [22%] and 91 of [23%], respectively) or vessels (49 of 78 [63%] and 60 of 96 [63%], respectively). In both medical and surgical patients, segments initially free of disease showed a 14% incidence of developing new lesions, compared with the 37% progression in segments initially diseased (p less than 0.001). In the surgical patients, progression occurred in 48 of 219 (22%) nongrafted and 43 of 177 (24%) grafted segments (NS). When analyzed by major trunk vessel, progression occurred in 40 of 57 grafted arteries (70%) and 20 of 39 nongrafted arteries (51%) (NS). The incidence of new total occlusions was similar in medical and surgical patients (6% and 8%, respectively); new total occlusions occurred predominantly in diseases segments (15% and 22%, respectively). In patients with stable angina pectoris who have medical or surgical treatment assigned by randomization, progression of coronary disease at 5 years is not influenced by which mode of therapy was received. Vessels initially free of disease are at relatively low risk for development of disease within 5 years. In surgical patients, grafted and nongrafted vessels show similar rates of progression.

Angiography↗
PubMed1980

Comparative effect of intravenous dipyridamole and sublingual nitroglycerin on coronary hemodynamics and myocardial metabolism at rest and during atrial pacing in patients with coronary artery disease.

The effects of intravenous dipyridamole (20 mg) and sublingual nitroglycerin (0.6 mg) were compared at rest and during rapid atrial pacing in patients with significant coronary obstruction. Dipyridamole, which had no significant effect on resting systolic blood pressure, caused a significant increase in coronary sinus flow (CSF) and reduction of coronary vascular resistance (CVR) and arterial-coronary sinus oxygen difference (AO2CSO2 delta), whereas nitroglycerin reduced resting systolic pressure but had no significant effect on CSF, CVR, or AO2-CSO2 delta. Although theses effects of dipyridamole and nitroglycerin on resting systolic pressure, CSF, CVR, and AO2-CSO2 delta were qualitatively similar during rapid atrial pacing, the onset of chest pain and ischemic ECG changes occurred at a lower heart rate following dipyridamole (136 +/- 5 beats/min) than following nitroglycerin (149 +/- 6 beats/min, p less than 0.01). However, maximal double product and myocardial oxygen consumption achieved during pacing were similar following both dipyridamole and nitroglycerin and were less than control pacing values. Coronary dilatation following dipyridamole appears to reduce tolerance to pacing-induced ischemia probably by maldistribution of coronary flow away from ischemic myocardium. Nitroglycerin differs from dipyridamole by improving tolerance to pacing; however, this difference appears to be due to systemic vasodilator effects of nitroglycerin rather than to enhancement of flow to ischemic myocardium.

Aged↗
PubMed1979

Echocardiographic aortic ejection area as a reflection of left ventricular stroke volume.

Systolic cusp separation of normal aortic valves has been shown by echocardiography and by angiography to be related to left ventricular stroke volume. In this study, stroke volume was compared with echocardiographic area between the aortic cusps in systole (aortic ejection area). An excellent correlation was observed (r = 0.93) over a wide range of stroke volumes, even in the presence of mitral regurgitation. Stroke volume appears to correlate more closely with aortic ejection area than with angiographic or echocardiographic measurements of peak systolic cusp separation.

Aortic Valve↗
PubMed1979

Lack of ouabain effect on pacing-induced myocardial ischemia in patients with coronary artery disease.

Sixteen patients with significant two and three vessel coronary artery disease but without clinical congestive heart failure were studied during rapid atrial pacing before and after infusion of 0.015 mg/kg of ouabain. Seven patients with a decreased (less than 50 percent) ejection fraction and nine patients with a normal ejection fraction had a significant (P less than 0.05) increase in resting arterial systolic pressure after the administration of ouabain. However, resting values for coronary sinus flow, coronary vascular resistance, myocardial oxygen consumption and myocardial lactate extraction did not change significantly in either group. During pacing, patients with a decreased ejection fraction demonstrated more ischemia than patients with a normal ejection fraction; however, the administration of ouabain did not significantly alter pacing-related changes in coronary sinus flow, myocardial oxygen consumption, myocardial lactate extraction, ischemic electrocardiographic changes or onset of chest pain in either group. The administration of ouabain has a negligible effect on coronary hemodynamics, myocardial metabolism or clinical signs of ischemia in patients with coronary artery disease with normal or abnormal left ventricular function.

Adult↗
PubMed1979

Improved survival after surgical therapy for chronic angina pectoris: one hospital's experience in a randomized trial.

Between 1972 and 1974, 121 patients with chronic stable angina pectoris and operative coronary artery disease, excluding significant left main coronary obstruction, were randomized to either medical therapy (60 patients) or surgical therapy (61 patients) as part of a larger Veterans Administration Cooperative Study of Surgery for Coronary Arterial Occlusive Disease. At the time of randomization, medical and surgical groups were similar with regard to clinical and hemodynamic features as well as degree of left ventricular impairment and extent of coronary disease. Follow-up to June 1, 1978, reveals significantly improved survival in surgical patients from 3 through 6 years after randomization. Sixteen cross-over patients (13 medical to surgery, and 3 surgical without surgery) do not appear to influence results. Results of this randomized study from a single hospital differ from the preliminary results of the larger cooperative study, primarily because of a higher mortality in the medical group. The medical mortality in our group is in keeping with other reports of the natural history of patients with angina pectoris, and we propose that the population of patients we randomized closely simulates the usual type of patient with chronic angina being considered for surgical treatment. Our good surgical results thus contrast significantly with the survival of medically treated patients, and this separates our study from the body of the Veterans Administration Cooperative Study.

Angina Pectoris↗
PubMed1979

Hemodynamic improvement following a single dose of oral phentolamine. Administration in patients with chronic low output cardiac failure.

Hemodynamic studies were made in 15 patients with chronic low output cardiac failure before and following a single dose of oral phentolamine (150 mg). After two hours significant (P less than .05) reduction occurred in mean pulmonary, wedge and right atrial pressures and increases in cardiac index and heart rate. In ten patients studied at four hours, wedge pressure remained significantly reduced (-18 percent) and cardiac index significantly increased (+19 percent) from control values. Oral phentolamine results in significant hemodynamic improvement in patients with severe heart failure. Duration of effect for at least four hours after a single dose suggests that intermittent oral therapy may be useful in the management of such patients.

Administration, Oral↗
PubMed1979

Use of catecholamines in acute myocardial infarction.

We review the hemodynamic effects and clinical usefulness of five natural and synthetic catecholamines. Their actions are best understood by an appreciation of the relative ability of each catecholamine to activate alpha, beta 1 and beta 2 adrenergic receptors in the myocardium and peripheral vasculature. Epinephrine, the first catecholamine isolated, is shown to have little useful role in the therapy of acute myocardial infarction. L-norepinephrine has powerful alpha and moderate beta 1 effects. It is the catecholamine of choice in the initial treatment of cardiogenic shock associated with acute myocardial infarction. Isproterenol markedly increases myocardial contractility and heart rate by beta 1 stimulation, while simultaneously decreasing peripheral vascular resistance and, therefore, arterial pressure through its action on beta 2 receptors. It increases cardiac output, but its metabolic costs are high in the presence of ischemia. Its role in the therapy of acute myocardial infarction has largely been supplanted by more selective agents. Dopamine causes slightly less vasoconstriction than l-norepinephrine and slightly less myocardial stimulation than isoproterenol. In low doses, it increases renal and mesenteric blood flow by activation of a non-adrenergic receptor. Tachycardia and associated metabolic deterioration render it a second-line drug in the treatment of severe cardiogenic shock. Dobutamine, a new synthetic catecholamine, has primarily beta 1 activity. It increases myocardial contractility with little effect on heart rate or peripheral vascular resistance. It is ineffective in cardiogenic shock, but may eventually be shown to have a role in the treatment of left ventricular failure uncomplicated by severe hypotension.

Animals↗
PubMed1978

Sinus node dysfunction. An overview with emphasis on autonomic and pharmacologic consideration.

Sinus node dysfunction is a disorder of impulse generation and impulse conduction. Previous works have emphasized that the dysfunction occurs not only within the sinus node but also within the escape pacemaker. Adrenergic and cholinergic mechanisms, as well as pulsations and pressure within the sinus node artery, play an important role in normal sinus node activity. Although perinodal fibers act as a buffer zone for sinoatrial conduction, their role in man is yet to be clarified. During normal sinus node activity, pacemaker shifts from the sinus node to the crista terminalis have been shown to occur. Following sinus node destruction, similar shifts do occur. Clinical methods of determining sinus node function, such as the sinus node recovery time and sinus atrial conduction time, are useful but have limitations. Dynamic electrocardiographic monitoring provides the best clinical method available for detecting sinus node dysfunction. Digitalis appears to improve the parameters of sinus node function by increasing the automaticity of latent atrial pacemakers. The atrial arrhythmia of sinus node dysfunction appears to be related to the characteristics of latent atrial pacemaker and "enhanced" cholinergic tone.

Arrhythmias, Cardiac↗
PubMed1978

Effects of pharmacologically-induced hypertension on myocardial ischemia and coronary hemodynamics in patients with fixed coronary obstruction.

Twenty patients with fixed coronary artery obstruction were studied during rapid atrial pacing and methoxamine infusion. During pacing to heart rates of 142 +/- 4 (mean +/- SEM) beats per minute coronary sinus flow increased from 108 +/- 8 to 187 +/- 15 cc/min and myocardial oxygen consumption increased by + 80 +/- 11%. During methoxamine infusion that raised arterial systolic pressure to 196 +/- 5 mm Hg, similar increases in coronary sinus flow (to 179 +/- 13 cc/min) and myocardial oxygen consumption (+ 77 +/- 12%) occurred. Chest pain and ischemic ST segment changes developed in 17 and 14 patients respectively during atrial pacing, an incidence significantly greater (P less than 0.05) than during infusion of methoxamine (6 and 3 patients). Myocardial lactate extraction which averaged 26 +/- 4% during control was decreased to 10 +/- 8% during pacing and to 24 +/- 7% during methoxamine; the difference between decreases was not significant. The data show that at similar increases in myocardial oxygen consumption stress of increased heart rate results in more myocardial ischemia than stress of increased afterload.

Blood Flow Velocity↗
PubMed1978

Hemodynamic effects of intravenous phentolamine in low output cardiac failu;e. Dose-response relationships.

Nineteen patients with chronic low output cardiac failure were studied before, during and after infusion of phentolamine in doses of 10, 20, 30 and 40 microgram/kg/min. Significant reduction of left- and right-sided pressures and increases in cardiac index and heart rate (HR) were present within 15 minutes of starting phentolamine at the 10 microgram/kg/min dose. Minimal additional effect was observed at 30 minutes. Increased dose from 10 to 20 mu/kg/min resulted in small but significant (P less than 0.05) additional reduction in pressures and increases in HR. No additional significant changes occurred at doses of 30 or 40 microgram/kg/min. Significant hemodynamic changes persisted for at least an hour (53 +/- 3 min) after the phentolamine infusion was discontinued. Near maximal ;emodynamic effects occur within 15 minutes of starting phentolamine infusion and can be achieved at doses of 10 to 20 microgram/kg/min. Increased HR during phentolamine infusion may limit its usefulness in patients with ischemic heart disease.

Cardiac Output↗
PubMed1978

The role of myocardial ischemia in pacing-induced elevation of arterial pressure.

One hundred sixteen patients with suspected or proven coronary arterial disease underwent rapid atrial pacing until the occurrence of pain in the chest or a heart rate of at least 160 beats per minute. Significant elevation of arterial systolic pressure of 25 percent or more above control was observed in 17 patients. Each of these patients had significant coronary arterial disease shown by coronary arteriographic studies. During rapid atrial pacing, each of these 17 patients had pain in the chest and ST-segment changes suggesting ischemia, and 15 had abnormal (less than 10 percent) extraction of myocardial lactate. In the 99 patients who did not have increased arterial systolic pressure during rapid atrial pacing, the frequencies of coronary arterial disease, ischemic ST-segment changes, and abnormal extraction of lactate during rapid atrial pacing were significantly (P less than 0.05) less. Increased arterial systolic pressure during rapid atrial pacing appears to be highly indicative of coronary arterial disease and myocardial ischemia. We suggest that myocardial ischemia may, under certain circumstances, be responsible for short-term increases in arterial pressure.

Adult↗
PubMed1978

Echocardiographic interpretation of pericardial effusion.

Echocardiography has proved to be quite useful in the detection of pericardial effusion. As little as 15 ml of fluid within the pericardial space can be detected. Specific signs of pericardial effusion, such as electrical alternans and paradoxical pulse, have become better understood by echocardiographic study. Yet, with all the benefits of echocardiography, the detection of pericardial effusion still may be quite difficult if careful attention is not given to technique. False-positive diagnosis of anterior pericardial effusion can be seen with epicardial fat pad, pericardial cyst, or foramen of Morgagni hernia. False-positive posterior pericardial effusion can be seen in large left pleural effusion, calcified mitral anulus, or excessively medial transducer angulation. New "switched-gain" circuits have helped detection of pericardial effusion by enhancement of pericardial echoes.

Echocardiography↗
PubMed1977

Treatment of cardiogenic shock in myocardial infarction by intraaortic balloon counterpulsation surgery.

Thirty-seven patients in cardiogenic shock due to acute myocardial infarction were treated with intraaortic balloon counterpulsation and/or surgery. Eighteen of these patients were treated with counterpulsation alone; eight survived and five were in functional class I or II at the time of follow-up; two were in functional class III, and one was in functional class IV. Nineteen patients were treated surgically, eight survived and seven were in functional class I or II at the time of follow-up; one was in functional class III. Good functional recovery with counterpulsation alone is most common with inferior infarction. With surgery, functional recovery depends not only on the extent of the infarction and the coronary anatomy, but also on the ability to perform surgery within 12 hours of infarction or to support the patient with mechanical means for 10 to 14 days after the infarction and then perform surgery.

Adult↗
PubMed1977

Superiority of dobutamine over dopamine for augmentation of cardiac output in patients with chronic low output cardiac failure.

Dobutamine is a newly developed catecholamine reported to have minimal direct vascular effects relative to its inotropic activity and to have less chronotropic and arrhythmogenic properties than other catecholamines used in the treatment of low output states. In this study, the acute hemodynamic effects of dobutamine were compared to those of dopamine in 13 patients with chronic low output cardiac failure. At dosages adjusted to achieve similar increments in cardiac output, dobutamine reduced left ventricular filling pressure (LVEP) from 24 +/- 2 mm Hg (SEM) to 17+/- 2 mm Hg, while dopamine increased LVEP to 30 +/- 3 mm Hg and in six patients caused arterial O2 saturation to fall below 90%. This poor response to dopamine was probably the result of its vasoconstrictive effects and illustrates the potential advantages of using a cardioselective agent such as dobutamine when the desired goal of therapy is to improve ventricular function by direct inotropic stimulation.

Aged↗