American physicians consider euthanasia.
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Biomedical subjects
Publications and source records attributed to S M Ayres.
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OBJECTIVE: To characterize mortality in persons diagnosed with primary pulmonary hypertension and to investigate factors associated with survival. DESIGN: Registry with prospective follow-up. SETTING: Thirty-two clinical centers in the United States participating in the Patient Registry for the Characterization of Primary Pulmonary Hypertension supported by the National Heart, Lung, and Blood Institute. PATIENTS: Patients (194) diagnosed at clinical centers between 1 July 1981 and 31 December 1985 and followed through 8 August 1988. MEASUREMENTS: At diagnosis, measurements of hemodynamic variables, pulmonary function, and gas exchange variables were taken in addition to information on demographic variables, medical history, and life-style. Patients were followed for survival at 6-month intervals. MAIN RESULTS: The estimated median survival of these patients was 2.8 years (95% Cl, 1.9 to 3.7 years). Estimated single-year survival rates were as follows: at 1 year, 68% (Cl, 61% to 75%); at 3 years, 48% (Cl, 41% to 55%); and at 5 years, 34% (Cl, 24% to 44%). Variables associated with poor survival included a New York Heart Association (NYHA) functional class of III or IV, presence of Raynaud phenomenon, elevated mean right atrial pressure, elevated mean pulmonary artery pressure, decreased cardiac index, and decreased diffusing capacity for carbon monoxide (DLCO). Drug therapy at entry or discharge was not associated with survival duration. CONCLUSIONS: Mortality was most closely associated with right ventricular hemodynamic function and can be characterized by means of an equation using three variables: mean pulmonary artery pressure, mean right atrial pressure, and cardiac index. Such an equation, once validated prospectively, could be used as an adjunct in planning treatment strategies and allocating medical resources.
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Qualitative and quantitative studies were performed on pulmonary blood vessels in lung tissue obtained by biopsy, pneumonectomy, or autopsy from 58 patients in the Registry of Primary Pulmonary Hypertension sponsored by the Heart, Lung, and Blood Institute of the National Institutes of Health. In 49 patients (84%), the hypertensive vascular disease involved predominantly or exclusively muscular pulmonary arteries and arterioles. In each of these 49 patients, pulmonary artery medial hypertrophy was observed, and in 48 patients, it was also associated with intimal or luminal lesions. On the basis of the predominant histopathologic features, 25 of the 48 patients were classified as having pulmonary arteriopathy with plexiform lesions characterized by a combination of concentric laminar intimal fibrosis, eccentric intimal fibrosis, and plexiform lesions; in nine of these 25, recanalized thrombi were also present. Pulmonary arteriopathy with thrombotic lesions, defined by the presence of both eccentric intimal fibrosis and recanalized thrombi but without plexiform lesions, was observed in 19 patients. Intimal fibrosis, either concentric or eccentric, without plexiform or thrombotic lesions was found in four patients. Among the remaining nine patients in the Registry, pulmonary veno-occlusive disease was present in seven and chronic pulmonary venous hypertension in one. Pulmonary blood vessels were microscopically normal in a lung biopsy specimen from another patient. In general, patients with plexiform lesions and those with veno-occlusive disease had a much poorer prognosis than patients with thrombotic lesions. The present study shows the existence of several distinct histopathologic patterns of pulmonary vascular disease in individuals with primary pulmonary hypertension diagnosed by standardized clinical and laboratory criteria.
The hemodynamic responses to acute vasodilator administration were evaluated in 163 patients who were entered into the National Institutes of Health Registry on Primary Pulmonary Hypertension (PPH) between 1981 and 1985. Of a total of 491 drug administrations in these patients, 135 administrations in 104 patients were performed in a manner acceptable to the Registry. A single vasodilator was tried in 79 patients and more than one vasodilator in 25 patients. Two-thirds of the patients were in New York Heart Association Functional Classes III or IV. When the effects of all vasodilators were grouped together, there were significant decreases from baseline in mean pulmonary artery pressure (60 +/- 2 to 57 +/- 2 mm Hg, p less than 0.05) and total pulmonary resistance index (32.5 +/- 1.7 to 25.1 +/- 1.4 mm Hg/L/min/m2, p less than 0.0001), and increases in cardiac index (2.1 +/- 0.1 to 2.7 +/- 0.1 L/min/m2, p less than 0.0001). Mean systemic blood pressure fell (88 +/- 1 to 79 +/- 1 mm Hg, p less than 0.0001), whereas PaO2 was unchanged (70 +/- 3 to 71 +/- 3 mm Hg, p = NS). A fall in total pulmonary resistance greater than 20% was observed in 55% of the adequate drug trials. Adverse effects occurred in 32 of the total 491 patient-drug trials and were generally minor. Hypotension requiring treatment developed in six patients. There were two deaths attributable to vasodilator administration. Patients who died or had hypotension requiring treatment had higher right atrial pressures than did other treated patients (15 +/- 2 versus 9 +/- 1 mm Hg, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
This study investigated the effects of emissions from the internal combustion engine on pulmonary function and respiratory symptoms in men collecting tolls and directing traffic in areas with high levels of air pollution. Bridge and tunnel officers (BTOs) were administered pulmonary function tests and respiratory questionnaires for up to 11 consecutive years (n = 944). Carboxyhemoglobin levels were also measured. Regression coefficients on year tested were calculated on 466 individuals (49% of all BTOs) tested at least 3 years. The tunnel workers had significantly lower FEV1S (forced expiratory volume at one second) and FVCs (forced vital capacity), respiratory symptoms, and higher carboxyhemoglobin levels than the bridge workers. BTOs working over 20 years had the lowest mean pulmonary function values, the steepest slopes, and the most respiratory symptoms. We believe that the data show an association between working as a bridge and tunnel officer and decreased pulmonary function and increased respiratory symptoms, but it was not readily evident whether the effects were of clinical importance.
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Waste oil contaminated with 2,3,7,8-TCDD was sprayed at various sites in the state of Missouri. Eighty-two individuals who reported living or working in TCDD-contaminated areas and 40 individuals with little or no exposure to TCDD were selected for study; 85% elected to participate in the study. Data were obtained from medical histories, general physicals, neurological and dermatological examinations, and laboratory tests. There were no cases of chloracne reported. The only hematologic comparison that was significant was a higher mean platelet count in the exposed group. This study did not produce any firm indication of increased disease prevalence related to environmental TCDD exposures. Since this was a pilot study, it is important that we continue to limit human exposure to dioxin to the lowest levels technologically feasible until definitive answers to the health consequences of exposure are determined.
A national registry was begun in 1981 to collect data from 32 centers on patients diagnosed by uniform criteria as having primary pulmonary hypertension. Entered into the registry were 187 patients with a mean age (+/- SD) of 36 +/- 15 years (range, 1 to 81), and a female-to-male ratio of 1.7:1 overall. The mean interval from onset of symptoms to diagnosis was 2 years. The most frequent presenting symptoms included dyspnea (60%), fatigue (19%), and syncope (or near syncope) (13%). Raynaud phenomenon was present in 10% (95% of whom were female) and a positive antinuclear antibody test, in 29% (69% female). Pulmonary function studies showed mild restriction (forced vital capacity [FVC], 82% of predicted) with a reduced diffusing capacity for carbon monoxide (DLCO), and hypoxemia with hypocapnia. The mean (+/- SD) right atrial pressure was 9.7 +/- 6 mm Hg; mean pulmonary artery pressure, 60 +/- 18 mm Hg; cardiac index, 2.3 +/- 0.9 L/min X m2; and pulmonary vascular resistance index, 26 +/- 14 mm Hg/L/min X m2 for the group. Although no deaths or sustained morbid events occurred during the diagnostic evaluation of the patients, the typically long interval from initial symptoms to diagnosis emphasizes the need to develop strategies to make the diagnosis earlier.
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2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) has suddenly become the focal point of controversy over the relationship of chemical waste to human health. Specific concern exists regarding its potential association with human malignancy. Subcellular, cellular, and whole-animal experiments suggest that TCDD exerts much of its activity by inducing enzymes that protect the intact organism from the assault of environmental contamination. TCDD is a potent inducer of aryl hydrocarbon hydroxylase, although wide variations between species do exist. Conventional tests for mutagenicity have produced conflicting results. Animal experiments have shown the development of tumors following chronic low level ingestion of TCDD. The human evidence regarding the potential carcinogenicity of TCDD comes from occupational, military and environmental exposures. Several studies have come out of Sweden suggesting an association between sarcoma and exposure to herbicides. Although there is little solid evidence that 2,3,7,8-TCDD produces substantial chronic disability or premature death in man, a significant body of experimental evidence for its carcinogenicity makes it likely that a small number of human malignancies may be due to its action. Since 2,3,7,8-TCDD is an unwanted contaminant it could be eliminated with little measurable consequence.
The function of the human heart relies on the complex interplay of preload, afterload, and contractility. Alterations of all three variables occur in disease states. New developments in monitoring allow assessment of cardiac function at the bedside and contribute to patient care.
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