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Biomedical subjects

S Goldberg

Publications and source records attributed to S Goldberg.

At least 217 records · Page 12Linked to original sources
PubMed1981

Effect of diuresis on the performance of the failing left ventricle in man.

To determine the effect of diuresis on the performance of the failing left ventricle, we measured cardiac output, pulmonary wedge pressure and M-mode echo left ventricular diastolic dimension before and after diuresis in 13 patients with heart failure. Diuresis increased stroke volume (43 +/- 23 ml to 50 +/- 18 ml (p less than 0.05)) and decreased pulmonary wedge pressure (28 +/- 3 mm Hg to 19 +/- 5 mm Hg (p less than 0.01)), mean blood pressure (100 +/- 14 mm Hg to 88 +/- 10 mm Hg (p less than 0.01)) and systemic vascular resistance (2,059 +/- 622 dynes-sec-cm-5 to 1,783 +/- 556 dynes-sec-cm-5 (p less than 0.05)). Echo left ventricular diastolic dimension was not changed by diuresis (6.0 +/- 0.8 cm to 6.0 +/- 0.8 cm). Percent change in stroke volume correlated with systemic vascular resistance (r = 0.60, p less than 0.05) and with left ventricular diastolic dimension (r = 0.62, p less than 0.05) but not with pulmonary wedge pressure (r = 0.12) or right atrial pressure (r = 0.04). Thus, diuresis improved the performance of the failing ventricle and reduced afterload, but it did not alter left ventricular diastolic dimension, an index of preload. These data suggest that diuresis improves ventricular function by decreasing afterload.

Aged↗
PubMed1981

Effects of respiratory alkalosis on coronary vascular dynamics and myocardial energetics in patients with coronary artery disease.

To determine if respiratory alkalosis produces hemodynamically significant coronary vasoconstriction in coronary artery disease (CAD), we studied the effects of hyperventilation on coronary sinus blood flow (CSBF), myocardial O2 uptake, and lactate extraction in 13 CAD patients. No patient developed chest pain or ischemic ECG changes during hyperventilation. Hyperventilation increased pressure-rate product (myocardial O2 consumption index, MVO2) minimally did not change global CSBF, coronary vascular resistance or lactate extraction. However, hyperventilation increased global myocardial O2 uptake from 14.5 plus or minus 3.2 to 18.7 plus or minus 17.2 ml/min (p less than 0.01) principally due to increased myocardial O2 extraction (65.0 plus or minus 7.4 to 71.6 plus or minus 6.2%, p less than 0.01). The increased pressure-rate product was not sufficient to account for increased myocardial O2 uptake. We conclude that respiratory alkalosis increases myocardial O2 extraction but does not produce hemodynamically significant coronary vasoconstriction in CAD patients.

Adult↗
PubMed1981

Surgical therapy of variant angina associated with nonobstructive coronary disease.

Patients with variant angina refractory to medical therapy pose a difficult management problem. We report two patients with variant angina who had focal spasm in coronary arteries with fixed obstructions of less than 20% of the luminal diameter. Ischemic episodes were accompanied by malignant ventricular arrhythmias and third degree atrioventricular block. Symptoms were refractory to intensive medical management with nitrates and calcium blocking agents in one patient and with nitrates in the other who was treated before calcium blockers were available. Surgery was done; a bypass graft was placed distal to the area of focal spasm and the native artery was ligated proximally. Both patients are asymptomatic 24 and 66 months after surgery and neither takes anginal medication regularly. The surgical procedure outlined should be considered only if therapy to control life threatening ischemic symptoms with nitrates and calcium blocking agents fails.

Angina Pectoris↗
PubMed1981

Principles of neurologic localization.

Organic and nonorganic neurologic conditions can be differentiated by determining whether the symptoms can or cannot be feigned and whether the symptoms make neuroanatomic sense. For localization of organic disease, lower motor neuron signs and dermatome defects suggest peripheral nerves; sensory dissociation points to the spinal cord, and a cranial nerve deficit with a contralateral extremity deficit suggests a brainstem etiology. Higher level, organized dysfunction points to the cerebrum; ataxia during intentional movements indicates cerebellar involvement, and sudden, unintended movements suggest basal ganglia disorders.

Basal Ganglia Diseases↗
PubMed1981

Provocation of esophageal pain by ergonovine or edrophonium.

Ten patients with anginal symptoms and ergonovine-induced chest pain without coronary artery spasm had esophageal manometry with provocative pharmacologic testing. Increased amplitude of esophageal contractions on baseline manometry (68.2 +/- 10.3 mmHg) was the only characteristic discriminating these patients from normals (40.9 +/- 6.3 mmHg) and from patients with esophageal motility disorders (39.6 +/- 7.5 mmHg). The administration of ergonovine or edrophonium provoked typical chest pain in association with high amplitude, long duration, and repetitive esophageal contractions in all 10 patients. Patients with esophageal motor disorders showed a similar, but less marked esophageal response with pain infrequently produced. Normals showed no response to ergonovine, and a minimal response to edrophonium, but without chest pain. Clinical features of patients with ergonovine-induced chest pain could not distinguish them from patients with coronary artery disease; esophageal symptoms were infrequent and mild. These studies suggest that certain patients with chest pain of esophageal origin may be identified only by provocative testing during esophageal manometry. However, these provocative drugs may also induce coronary artery spasm and should not be used during routine clinical manometry.

Adult↗
PubMed1980

Nifedipine therapy for coronary-artery spasm. Experience in 127 patients.

We report clinical experience with the coronary vasodilator nifedipine in 127 patients with symptoms of myocardial ischemia associated with electrocardiographic or angiographic evidence, or both, of coronary-artery spasm. In the majority of patients conventional antianginal therapy including nitrates and beta-adrenergic blockers failed, and in one third of the patients at least one episode of ventricular tachycardia developed during an attack of angina. Nifedipine (40 to 160 mg every 24 hours) significantly reduced the mean weekly rate of anginal attacks from 16 to two (P less than 0.001). Similar marked reductions in the nitroglycerin requirement were noted. In 63 per cent of the patients complete control of anginal attacks was achieved, and in 87 per cent the frequency of angina was reduced by at least 50 per cent. Nifedipine was generally well tolerated, with only 5 per cent of the patients requiring termination of the drug because of intolerable side effects. This experience with nifedipine suggests that it is a highly effective drug for the treatment of coronary-artery spasm and variant angina.

Adult↗
PubMed1980

Refractory ergonovine-induced coronary vasospasm: importance of intracoronary nitroglycerin.

Recent experience has suggested that the ergonovine maleate test is a safe procedure for the diagnosis of variant angina pectoris, because ergonovine-induced coronary vasospasm has generally been reversible by sublingual nitroglycerin. This report describes five cases of ergonovine-induced coronary vasospasm that were refractory to sublingual nitroglycerin. Four of these patients had cardiac arrest. In two patients the vasospasm was responsive to intracoronary nitroglycerin administration. Three patients died as a reuslt of the test. The two survivors differed from the nonsurvivors in the total dose or ergonovine given (0.1 and 0.15 mg versus 0.17, 0.3 and 0.3 mg, respectively) and in the method of administration of ergonovine. The survivors were given serial doses of 0.05 mg each whereas the three nonsurvivors received either larger initial doses (0.1 followed by 0.07 mg) or progressive incremental doses (0.05, 0.1 and 0.15 mg serially). Sublingual nitroglycerin, given to all five patients, and intravenous nitroglycerin, given to three of the five, were ineffective in reversing vasospasm. Intracoronary nitroglycerin favorably altered the course of the survivors. Thus, the ergonovine maleate test is not benign and may cause severe coronary vasospasm that is unresponsive to sublingual and intravenous nitroglycerin, but may be reversed by intracoronary nitroglycerin.

Administration, Oral↗
PubMed1980

Superficial accessory pathway in the Wolff-Parkinson-White syndrome--electrophysiological, surgical and histologic demonstration.

A superficial accessory pathway was demonstrated by electrophysiologic techniques and surgical histopathology in 30-year-old male with Wolff-Parkinson-White syndrome, severe mitral valve disease and medically uncontrollable arrhythmias. In this patient, electrode catheter studies in the cardiac catheterization laboratory revealed antegrade and retrograde function of an accessory pathway between the anterior right atrium and the right ventricle. During surgery, electrophysiologic mapping confirmed the anterior location of this pathway. Blunt dissection in the fat pad of the A-V groove between the right atrium and ventricle revealed the accessory pathway which consisted of tissue strands superficial to the A-V ring. These were removed and on histological examination were composed of ordinary myocardial cells. Concomitant replacement of the patient's calcified stenotic and regurgitant mitral valve was carried out. Postoperatively, there was complete regression of the preexcitation and arrhythmias.

Adult↗
PubMed1979

Nifedipine in the treatment of Prinzmetal's (variant) angina.

The clinical response to therapy with the calcium-blocking agent nifedipine was assessed in 12 patients with variant angina pectoris who were 44 to 67 years old. Five patients had vasospasm of the left anterior descending coronary artery, and seven had spasm of a dominant right coronary artery. Before nifedipine therapy, the frequency of anginal attacks per 24 hour period ranged from 1 to 12, with ventricular tachycardia accompanying ischemic episodes in 7 of 12 patients and high grade atrioventricular block occurring in 2 patients. After therapy with nifedipine, 11 of 12 patients had initial relief of symptoms, and 7 of the 11 had long-term relief. Withdrawal of nifedipine led to recurrence of angina on six occasions in four patients. Provocative testing in the cardiac catheterization laboratory by means of the cold pressor test in one patient and ergonovine maleate in another before and after nifedipine administration showed that this agent can block both alpha adrenergic- and regonovine-induced vasospasm. Nifedipine may have a significant role in the therapy of angina caused by coronary spasm.

Adult↗
PubMed1979

[The value of thoracoscopic sympathectomy in the treatment of Raynaud's syndrome].

On the basis of a follow-up period lasting at least 6 years concerning 23 patients, in whom on account of a Raynaud-syndrome a thoracoscopic sympathicotomy in the region Th 2-5 was carried out in most cases bilaterally in two sessions, in comparison with the sympathicectomy performed in major surgery can be established:no mortality, no serious complications, duration of stay in hospital 5-7 days, no absolute healing. In a follow-up period of the same length in an approach of major surgery absolute healings are possible, but only in 35%. This gain is loaded by a longer stay in hospital of at least 10 days and a mortality of 4.3% as well as by a complication rate of 6-41%, to which in 8-13% of the cases a Horner-syndrome comes. Therefore, before an approach in major surgery a thoracoscopic intervention is to be tried. The thoracoscopic operators should strive for a sympathectomy with destroy of the ganglia Th 2 and 3 instead for a sympathicotomy.

Humans↗
PubMed1979

The guidance of optic axons in the developing and adult mouse retina.

Previous studies in chick embryos (Goldberg, '77) indicated that unidirectional guidance of retinal axons toward the optic nerve is restricted to the vitread portion of the ganglion cell fiber layer (GCFL) of the retina; random fiber growth was noted after deflection of the optic axons sclerad to the GCFL. The present study on mice confirms these observations. Silver-stained flat mounts of retinal colobomas were examined. Many optic axons in colobomas do not exit normally from the eye, but travel randomly when deflected sclerad to the GCFL. Newborn mouse axons grew around retinal lesions in a highly directed manner. Such axons were always situated in the vitread portion of the GCFL. The unidirectional guidance found in newborn mice was absent in adults. Deflected adult axons traveled randomly regardless of their level within the GCFL. We propose that defective guidance largely accounts for failure of axonal regeneration in the adult mouse retina. The inability of the adult axons to fasciculate (adhere to one another and form fiber bundles) suggests that impaired cellular adhesivity may be part of the mechanism of regenerative failure.

Animals↗