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G A Pantely

Publications and source records attributed to G A Pantely.

44 records · Page 3Linked to original sources

Academic physicians' opinions on preliminary reporting of echocardiographic data.

Preliminary reporting of echocardiographic data by cardiac sonographers has become a key issue in the echocardiography community. A survey on this issue was sent to 248 academic physicians and 89 (35.8%) were returned. In response to a question in the survey, 76 physicians stated that they had at least a limited amount of knowledge in echocardiography. For the group, 62% wanted a written or verbal preliminary report and 52% concluded that this report should be a part of the cardiac sonographer's position. If cardiac abnormalities are suspected, 65% wanted the results before the cardiologist reviewed the study, but only 42% of the physicians wanted a diagnostic versus a descriptive type of report. About 49% stated that if necessary they would attempt to influence the cardiac sonographer to give them a preliminary report, whereas 67% of the physicians would possibly use this information to medically manage the patient. Fifty percent believed that it was legal for a cardiac sonographer to give a preliminary report. Another 70% said that the cardiac sonographer would NOT be "practicing medicine without a license" and 66% concluded that they would NOT be "aiding and abetting the unauthorized practice of medicine" if given this information. These data have important potential ramifications for both cardiac sonographers as well as for the practice of cardiology regarding the issue of preliminary echocardiographic reports.

Adult↗

The lack of predictive value of preoperative psychologic distress for postoperative medical outcome in heart transplant recipients.

This follow-up study of 58 heart recipients an average of 2 years after transplantation did not show that the Symptom Checklist 90R, a self-report measure of psychologic distress, predicted medical outcome. Mortality and medical morbidity (graft rejection and infection rate) were the outcome variables used. The findings tend to argue against the validity of some aspects of the psychiatric screening of transplant candidates if prediction of patients' ultimate risk of mortality or medical morbidity is the validation standard.

Adult↗

Late infection in cardiac allograft recipients: profiles, incidence, and outcome.

Infection continues to cause substantial morbidity and mortality after heart transplantation. Studies focusing on this problem have concentrated on the early posttransplant period, and it is uncertain to what extent infection continues to add to morbidity later after transplantation. Fifty-four patients surviving at least 1 year after heart transplantation made up the study population in this study, and they were surveyed for infections beyond 1 year. In this group there were 15 infections, an incidence of 0.3 infections per patient or 0.016 infections per patient-months of follow-up. Only nine of these infections necessitated hospitalization; two, however, were fatal. Actuarial risk of all late infections and late infections necessitating hospitalization was 13% and 6%, respectively, at 2 years. As expected, bacterial infections made up the largest group (60%), followed by viral disease (27%). Two patients had pulmonary infections, one with Aspergillus and one with Pneumocystis. These data demonstrate that although rates of infection in heart recipients continue to exceed those in the general population, the rates are considerably lower than those in what is seen early after heart transplantation. Despite this, the more unusual infectious agents associated with immune compromise continue to be present.

Actuarial Analysis↗

Lack of progressive "restrictive" physiology after heart transplantation despite intervening episodes of allograft rejection: comparison of serial rest and exercise hemodynamics one and two years after transplantation.

It has been suggested that the cardiac allograft becomes less compliant either because of repeated episodes of rejection, chronic hypertension, or as a direct consequence of immunosuppression. A corollary to this hypothesis is that this reduction in compliance should be a progressive, rather than a static, change. To test this hypothesis, rest and exercise filling pressures, cardiac outputs, and radionuclide ventriculographic systolic and diastolic indices were measured in 20 patients at 1 and 2 years after heart transplant by means of identical protocols at both study times. Between studies 10 of 20 patients had no rejection, five of 20 had one rejection episode, and five of 20 had more than one rejection episode. There were no significant differences in resting or exercise heart rates, pulmonary wedge pressures, cardiac outputs, left or right ventricular ejection fractions, left ventricular peak filling rates, or time to peak filling between the studies at 1 and 2 years. Only resting right atrial pressure increased between year 1 and year 2 (6 +/- 2 mm Hg vs 8 +/- 4 mm Hg, p = 0.035). These data demonstrate that cardiac allograft function is unchanged between 1 and 2 years after transplantation, despite episodes of intervening rejection and continued immunosuppression. The data further suggest that the previously reported decrease in cardiac allograft compliance does not appear to be caused by a progressive intrinsic abnormality in the allograft, and that other mechanisms for "restrictive" allograft physiology should be sought.

Adolescent↗

Low-dose oral prednisone in the treatment of acute cardiac allograft rejection not associated with hemodynamic compromise.

The standard therapy for acute cardiac allograft rejection is intravenous methylprednisolone, usually in doses of about 3 gm per treatment. Treatment is undertaken in most cases solely on the basis of a histologic diagnosis of rejection, irrespective of hemodynamic status. To reduce total corticosteroid dose and administer therapy in an outpatient environment, low-dose oral prednisone protocols were developed for the treatment of acute rejection in the absence of important hemodynamic compromise. A high-dose oral prednisone pulse (2 gm total for the average 75 kg male patient) was used in the first month. Thereafter a series of low-dose oral prednisone pulses were used (range, 0.5 to 1.0 gm total for the average 75 kg male patient). Of 85 transplant recipients at risk, 188 rejection episodes were treated over a 1477 total patient-months of follow-up. The high-dose oral pulse resulted in successful therapy (no subsequent therapy required) in 34 of 65 treatments (52%). The low-dose oral pulse was successful in treating 80 of 123 treatments (65%). This approach to acute rejection did not appear to adversely affect patient or graft outcome based on progression of stable to unstable hemodynamics, survival (84% and 82%, 1- and 2-year actuarial survival, respectively), or left ventricular ejection fraction (0.56 +/- 0.09 and 0.54 +/- 0.08, at 1 and 2 years, respectively). There did not appear to be discriminating factors that determined the therapeutic outcome, other than the higher failure rate within 1 month of transplant. We conclude that acute allograft rejection in the absence of important hemodynamic compromise responds to lower-than-conventional doses of corticosteroids in the majority of cases.

Administration, Oral↗

OKT3-induced hypotension in heart allograft recipients treated for steroid-resistant rejection.

OKT3 (a murine antihuman mature T cell antibody) has become an important therapeutic agent for the treatment of acute allograft rejection unresponsive to corticosteroid therapy. Seven heart allograft recipients received eight 10-day courses (one retreatment) of OKT3 for steroid-resistant rejection. All patients underwent hourly monitoring of vital signs, and one of the patients underwent hemodynamic monitoring during therapy. Age- and sex-matched kidney allograft recipients (including one retreated patient) undergoing the identical OKT3 antirejection protocol served as control patients. All patients had a measured decrease in arterial pressure during OKT3 therapy. The time from first dose to peak hypotensive response was identical in both heart and kidney allograft recipients (31 +/- 11 versus 32 +/- 11 hours, respectively, p = not significant [NS]) and did not coincide with the peak febrile response (22 +/- 12 versus 27 +/- 13 hours, respectively, p = NS). The decrease in mean arterial pressure was significantly greater in the heart allograft patients compared with the kidney allograft recipients (39 +/- 17 versus 22 +/- 10 mm Hg, respectively, p less than 0.03), despite a slightly greater positive fluid balance in the heart allograft recipients (1333 +/- 1991 versus 715 +/- 1224 ml, p = NS). The change in heart rate associated with the hypotension was only slightly and not significantly greater in the kidney allograft recipients. In the one heart allograft recipient undergoing hemodynamic monitoring, the decrease in mean arterial pressure was initially paralleled by a decline in systemic vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex Hormones↗

Relation between recipient: donor body size match and hemodynamics three months after heart transplantation.

Cardiac allograft hemodynamics were compared with respect to donor and recipient body weights to determine whether recipient: donor body size match played a significant role in subsequent recipient hemodynamics. Thirty-four stable outpatients underwent resting right-sided cardiac catheterizations 3 months after heart transplantation. As expected, resting cardiac output correlated positively with recipient body weight (r = 0.50, p = 0.002), and mean cardiac index (2.7 +/- 0.6 L/min/m2) was normal. There was, however, only a weak and statistically insignificant correlation between recipient body weight and stroke volume (r = 0.31, p = 0.072). There was a statistically significant negative correlation between donor: recipient body weight ratio and right arterial pressure (r = 0.41, p = 0.017), pulmonary wedge pressure (r = 0.38, p = 0.027), and heart rate (r = 0.39, p = 0.024). These data demonstrate that although cardiac output is maintained at levels appropriate for recipient size after heart transplantation, patients who receive small hearts rely on an increased heart rate and elevated filling pressures to achieve this end. These data suggest that the cardiac allograft may not adapt to recipient body size by 3 months after transplantation.

Body Constitution↗

Heart transplantation for cardiac amyloidosis: successful one-year outcome despite recurrence of the disease.

Systemic amyloidosis has been considered a theoretical contraindication for heart transplantation because of the concern that amyloidosis is a systemic disease that could potentially recur in the allograft. To date, no patients have been reported to have undergone heart transplantation. One year ago a patient with amyloidosis had a transplantation at the Oregon Health Sciences University, Portland. Results of kidney, rectal, and bone marrow biopsies were normal; however, endomyocardial and gingival biopsies showed positive results for amyloidosis. Recurrence of amyloidosis was detected by electron microscopy 14 weeks after transplantation; however, light microscopy has not shown any amyloidosis at 1 year. No other organ involvement has been documented. The patient is New York Heart Association functional class I, with normal resting hemodynamic parameters 1 year after transplantation. Amyloid heart disease does not necessarily portend a poor early outcome.

Amyloidosis↗