Biomedical subjects
Publications and source records attributed to T B Ferguson.
We studied 34 MS patients who were treated experimentally by thymectomy with or without 1 year of azathioprine therapy. After 3 years, there was no evidence of benefit. Relapsing-remitting patients had done as well or better clinically than controls, and the chronic progressive group did less well statistically than controls.
In 50 patients who underwent coronary bypass grafting, the interaction of left- and right-sided filling pressures were prospectively evaluated to determine whether restoration and/or maintainance of a normal central venous pressure/pulmonary capillary wedge pressure (CVP/PCWP) ratio could improve biventricular performance. In 40 patients, the CVP/PCWP ratio was normal (less than 1) and termination of cardiopulmonary bypass was uneventful. In 10 patients, during loading at the termination of extracorporeal circulation, CVP exceeded PCWP and the ratio was reversed (less than 1). Cardiac index and systolic arterial pressure were low. Restoration of normal ratio by emptying the right heart helped in the improvement of systolic arterial pressure and cardiac index. Thus, in the presence of reversed CVP/PCWP ratio at the termination of cardiopulmonary bypass, restoration of the ratio may prevent unnecessary pharmacologic and/or mechanical intervention, such as inotropic agents, balloon pumps, or assist devices.
Those who have had experience with the voluntary system of medical specialty certification will surely prefer it to an imposed bureaucratic type of control. Despite the deficiencies and problems associated with it, as Churchill noted about democracy: "It is the best that exists." Medical science and medical practice are constantly advancing and changing. With those changes it is reasonable to expect change in the specialty credentialing system. However, that change should be thoughtful, cautious, and should be made only in the best interest of the patients for whom we are responsible.
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Paroxysmal supraventricular tachycardia due to atrioventricular nodal reentry is a common arrhythmia that usually responds to medical therapy. When atrioventricular nodal reentry tachycardia is refractory to medical therapy, surgical cryoablation or endocardial catheter ablation of the His bundle has been employed to protect the ventricles from the tachycardia. However, these techniques necessitate implantation of a permanent ventricular pacemaker. The purpose of the present study was to develop a cryosurgical procedure capable of ablating the anatomic-electrophysiological substrate of atrioventricular nodal reentry by modifying, rather than ablating, atrioventricular conduction. Thirty-three adult mongrel dogs underwent either the cryosurgical procedure (n = 23) or a sham operation (n = 10). All animals were restudied immediately postoperatively (acute cryosurgery group [n = 12) and sham group [n = 10]), and 11 animals (chronic cryosurgery group) subjected to cryosurgery were studied 14 weeks postoperatively. Decremental atrial pacing and programmed premature atrial stimulation protocols were utilized to determine atrioventricular nodal conduction time, atrioventricular nodal refractory period, and the Wenckebach point before and after operation in all animals. No electrophysiological alterations were noted in the sham-operated group. In the cryosurgery groups, atrioventricular nodal conduction time, functional refractory period of the atrioventricular node, and the Wenckebach point were all significantly prolonged in the immediate postoperative period, but only atrioventricular nodal conduction time remained prolonged 14 weeks postoperatively. The potential application of the new cryosurgical procedure for the treatment of atrioventricular nodal reentry tachycardia was demonstrated in three animals that exhibited dual atrioventricular nodal conduction preoperatively but had monophasic atrioventricular conduction curves postoperatively. The results in these animals documented that the cryosurgical procedure is capable of ablating the anatomic-electrophysiological substrate necessary for atrioventricular nodal reentry tachycardia.
Studies were performed on lymphocytes from patients with multiple sclerosis before and after thymectomy (group I) and before and after thymectomy and azathioprine therapy (group II), and from matched control patients with multiple sclerosis, control patients with other neurological diseases, and healthy control subjects. Following treatment the percentage of T gamma cells in both group I and group II patients decreased from above the mean normal control levels to below this level; OKT8+ cell numbers in group I became lower than in any of the control groups; the percentage of concanavalin A-induced suppressor activity, which was initially normal, fell in group II and suggestively but not significantly in group I; and total blood lymphocytes in group I decreased from normal to below control levels. Other tests showed no significant changes with therapy. No significant difference in changes in clinical status were observed after one year in the treated patients compared with matched controls.
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In two preliminary trials, thymectomy was performed on 35 multiple sclerosis (MS) patients, with (Group 1) or without (Group II) azathioprine therapy for 1 year. Formal studies of clinical neurologic status were conducted at yearly intervals after operation. Each group was compared with carefully matched control patients. Group I patients showed significant improvement in total functional groups (Kurtzke scale) and pyramidal functions 1 and 2 years following thymectomy. Other individual functions showed no significant difference. There was a statistical improvement in disability status (Kurtzke) for patients with relapsing-remitting MS 1 and 2 years following thymectomy. This subset also had a significant decrease in MS exacerbations. Group II patients showed none of the favorable trends seen in Group I. Functional groups, disability status scale, and exacerbations were similar to those of the control patients. Several studies indicate azathioprine therapy alone is of questionable benefit in MS. In myasthenia gravis (MG), the full immunosuppressive effect of thymectomy may not be realized for several years. Therefore, it is possible that in Group I patients a dual mechanism of immunosuppression--azathioprine and thymectomy--is yielding a favorable response not yet apparent in the Group II patients having thymectomy alone. If our data still appear favorable after a third follow-up year, a formal pilot study will be undertaken.
The present study was designed to test the hypothesis that hyperkalemia can be prevented if the cardioplegic solution returning to the right heart from the coronary sinus is aspirated. In the control group (15 patients without aspiration), the potassium concentration rose from 3.5 +/- 1 (SD) mEq/L to 6.3 +/- 0.4 mEq/L (p less than 0.001) 10 minutes after the administration of cardioplegic solution and was still high before the patient was weaned from cardiopulmonary bypass (5.2 +/- 0.3 mEq/L (p less than 0.001). Electromechanical recovery time was delayed. In the second group (15 patients with aspiration), serum potassium did not change. Our data indicate that scavenging of cardioplegic solution may prevent hyperkalemia in most patients.
Present methods used to assess the status of myocardial preservation during cardioplegic arrest include monitoring the peripheral electrocardiogram (ECG) and ventricular myocardial temperature, and visual inspection of the heart to verify complete mechanical arrest. This study was designed to determine if these parameters are adequate to ensure complete electromechanical arrest after the application of standard cardioplegic techniques. The electrical status of the ventricle in adult mongrel dogs was monitored continuously during elective hyperkalemic hypothermic arrest for the presence of electrical activity in either the atrium or ventricle with 25 intramural electrodes, three epicardial reference electrodes, a His bundle catheter, and three peripheral ECGs. Occurrence of ventricular electrical activity was documented in the arrested heart (determined visually) when the peripheral ECG was quiescent; the activity persisted for a significant period of time before electromechanical activity could be detected by standard monitoring techniques. This electrical activity is believed to originate in the lower atrial septum and to conduct through the AV node to the ventricles at myocardial temperatures previously thought to be safe. Thus, continuous monitoring of intramural electrical activity would appear to be a more reliable technique than those currently used to determine the adequacy of myocardial preservation during elective cardioplegic arrest.
Atrioventricular conduction abnormalities have become more frequent since the reintroduction of cardioplegic techniques for myocardial preservation during cardiac surgery. An animal model was developed to clarify the role of atrial septal hypothermia in the preservation of the primary site of postoperative conduction delay, the AV node. In our study, 10 animals served as the control group. They were subjected to 40 min of cardioplegic arrest during which the heart was protected with multidose cold potassium cardioplegia. Atrial septal temperatures averaged 27.4 degrees +/- 1.2 degrees C during cardioplegic arrest. We treated 10 additional animals (study group) similarly, except that atrial hypothermia was augmented by intracavitary or specialized topical techniques, which resulted in an average atrial septal temperature of 20.8 degrees +/- 3.3 degrees C (p less than .05). Detailed electrophysiologic studies of both groups were performed at 37 degrees C before and after cardioplegic arrest. Significant prolongation of AV nodal, and to a lesser extent His-Purkinje, conduction times was noted in the control group, but no conduction abnormalities occurred in the study group receiving augmented atrial hypothermia. Thus, conduction block in the specialized conduction system after cardioplegic arrest appears to be related to the adequacy of hypothermic preservation of the atrial septum and can be prevented by augmented atrial hypothermia.
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The present study describes a surgical method for the permanent prolongation of atrioventricular (AV) conduction. In 22 dogs, a series of nine discrete cryolesions were placed along the perimeter of the triangle of Koch while the His bundle electrogram was being monitored continuously. Ten dogs underwent a sham operation to control for the effects of cardiopulmonary bypass and atriotomy on AV conduction. The conduction time through the AV nodal region was significantly (p less than 0.01) prolonged acutely (3 hours postoperatively) and chronically (14 weeks postoperatively) in the animals subjected to cryosurgery. Thus selective cryosurgery in the AV nodal region produces a permanent alteration in AV conduction. This cryosurgical technique may result in ablation of the electrophysiological substrate required for paroxysmal supraventricular tachycardia resulting from AV nodal reentry.
An ad hoc committee was appointed by The Society of Thoracic Surgeons (STS) in 1977 in order to determine the available manpower and workload of thoracic surgeons in 1976. This committee conducted a survey of the professional activities and geographic location of all known surgeons certified by the American Board of Thoracic Surgery (ABTS) at that time. A summary of this study indicated the available and projected thoracic surgery manpower. The report also determined the present and projected health care needs of the population of the United States through 1993. Because thoracic surgery needs to continue to meet the health care needs of the United States in an appropriate yet economical fashion, the STS and The American Association for Thoracic Surgery (AATS) undertook a joint review to determine again the available manpower and its workload in calendar year 1980. In addition, this study compared its findings with the 1976 report in order to detect changes in the workload and need for thoracic surgical services. A questionnaire was mailed to 3,584 certified thoracic surgeons. There were 2,675 responses. The material was sent to the Academic Computer Services at George Washington University Medical Center for tabulation and data processing. This report summarizes the results of this survey. It also compares these data with those obtained in the 1976 study and, based on this information, attempts to project the thoracic surgery manpower needs in the next decade by using several hypothetical models.
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This report summarizes five years of laboratory investigations and the initial six-month clinical experience with a calcium antagonist, nifedipine, added to a cold hyperkalemic cardioplegic solution for enhancement of myocardial protection. Regional ischemia was created in 112 dogs and global ischemia in 98 dogs, under normothermic and two hyperthermic states. Control solutions, two clinical cardioplegic solutions, and nifedipine solutions were compared. Infusion of nifedipine during regional ischemia and reperfusion intervals resulted in a two-to-threefold reduction in injury volume and maintenance of normal left ventricular function in contrast infusion of nitroprusside. Nifedipine solutions (0.2 microgram/ml) provided superior preservation of left ventricular function in comparison to the two cardioplegic solutions after one hour of global ischemia at 37 degrees C and two hours at 18 C. In a clinical trial of nifedipine in cold potassium cardioplegia, 38 high risk patients with poor ventricular function have been treated; 22 of which were intensively studied serially with radionuclide ventriculography and pyrophosphate scans, myocardial isoenzyme determinations, 24 hour EKG recordings and intra- and postoperative hemodynamic studies. Of the 35 patients admitted to the intensive care unit (ICU), 33 have survived. Stroke work and cardiac indices return promptly to near normal levels after operation. The time-isoenzyme activity curves are low and radionuclide determined ejection fractions show no change for the study group. Death from acute postischemic cardiac failure did not occur in treated patients and the usage of intra-aortic balloon pump (IABP) has decreased threefold in comparison with 40 similar high risk patients treated concurrently with cardioplegic solution alone. It is concluded that nifedipine is a potent adjunct to cold hyperkalemic cardioplegic solution in high risk patients.
Due to their unique structure, lysophosphoglycerides (such as lysophosphatidylcholine, LPC), compounds known to accumulate in ischemic myocardium, form micelles at concentrations exceeding the critical micelle concentration (CMC). In this study, we found that sub-CMC levels of LPC exerted dose-dependent morphological changes on red blood cells and elicited dysrhythmia and contracture while increasing coronary artery resistance in isolated hearts. LPC at supra-CMC concentrations lysed red blood cells, elicited virtually instantaneous contracture in perfused hearts, and constricted isolated coronary arteries. Because bile salts form micelles also, effects of LPC were compared with those induced by selected concentrations of bile salts. At sub-CMC levels, bile salts did not affect red cell morphology appreciably and exerted only negative ino- and chronotropic effects in isolated hearts. However, at supra-CMC concentrations, bile salts lysed red blood cells and caused contracture in the hearts. Thus LPC exerts specific effects at sub-CMC levels independent of nonspecific detergent effects of micelles. These specific effects may contribute to the mechanical and electrical dysfunction associated with myocardial ischemia.