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Biomedical subjects

J Ohar

Publications and source records attributed to J Ohar.

5 recordsLinked to original sources
PubMed1997

Amiodarone pulmonary toxicity: cytopathology, ultrastructure, and immunocytochemistry.

One hundred ninety cardiac patients were prospectively enrolled in an amiodarone protocol. Over a 10-year period, 16 patients developed new or progressive respiratory symptoms while taking amiodarone. These symptoms included dyspnea associated with abnormal chest radiographs or new or worsening abnormalities on pulmonary function testing. Specimens for microscopic examination were obtained by fiberoptic bronchoscopy with transbronchial lung biopsy (TBB), bronchoalveolar lavage (BAL), open lung biopsy (OLB), or autopsy. Large foamy macrophages with characteristic lamellated cytoplasmic inclusions were noted in all specimens, regardless of other evidence of pulmonary toxicity, suggesting that foamy macrophages represent a routine drug effect. Foamy macrophages were not present in BAL specimens from 53 normal controls and were rarely seen in specimens from 27 patients who had other interstitial lung diseases. When present, the foamy macrophages were less prominent than those seen in specimens from patients receiving amiodarone. Fibrosis was noted in 11 of 16 histological specimens, whereas type II-cell-hyperplasia was observed in 7 of the 16 specimens. Four of the 16 patients with respiratory symptoms died, and their autopsy revealed a combination of foamy macrophages with fibrosis and type II cell hyperplasia reflective of amiodarone pulmonary toxicity. Hyperplastic type II cells were not found in the absence of fibrosis. Immunocytochemistry allowed differentiation between foamy macrophages and type II cells and represents a useful tool for future investigations of the pathogenesis of amiodarone-induced pulmonary disease.

Adult↗
PubMed1995

Right ventricular function in patients with severe COPD evaluated for lung transplantation. Lung Transplant Group.

Right ventricular function was measured in ten patients with severe COPD (mean FEV1 = 0.48 +/- 0.2 L/s) as part of an evaluation for single lung transplant (SLT). Right ventricular ejection fraction (RVEF) was determined by two methods: first-pass radionuclide scan by multigated acquisition (MUGA) and by using a fast thermistor tipped RVEF/volumetric pulmonary artery catheter. None of the patients had clinical evidence of active right heart failure, although mild resting pulmonary hypertension (mean pulmonary artery pressure [PAP] = 24 +/- 4 mm Hg) that worsened with minimal exercise (mean PAP = 39 +/- 11 mm Hg) was present. There was a significant difference in RVEF measured by the two methods (mean MUGA RVEF = 57 +/- 10%, mean catheter RVEF = 27 +/- 8%; p < 0.00005). RVEF determined by both methods was correlated with hemodynamic and gas exchange variables obtained during rest and at maximal exercise. There were significant, yet inverse, correlations between RVEF measured by catheter and cardiac index measured during exercise (CIex), as well as with exercise pulmonary vascular resistance index (PVRI). There were no significant correlations found between MUGA RVEF and any gas exchange or hemodynamic variables. Significant correlations were found with the catheter-measured right ventricular end-diastolic volume (RVEDV) and CIex (r = 0.9 p < 0.005), with maximal oxygen consumption during exercise (VO2max) (r = 0.86 p < 0.0025), with exercise stroke volume index (SVI) (r = 0.76 p < 0.01), and exercise central venous pressure (CVP) (r = 0.62 p < 0.05). Echocardiographic studies revealed right ventricular dilatation and mild tricuspid regurgitation (TR) in all patients. The strong correlation between RVEDV, CIex, and VO2max supports the concept that in these patients, as long as there is no clinical evidence of right heart failure (resting CVP still within normal limits), those with the largest RVEDVs use the Frank Starling principle to their best advantage to remain more functional.(ABSTRACT TRUNCATED AT 400 WORDS)

Blood Pressure↗
PubMed1993

Diffusing capacity decreases after heart transplantation.

We evaluated the following spirometric values: forced vital capacity (FVC), first second expiratory volume (FEV1), FEV1/FVC, the lung volumes, total lung capacity (TLC), residual volume (RV), and single breath diffusing capacity for CO in 22 patients, before and after heart transplant. We found abnormal pulmonary function in 21 patients before heart transplantation. Despite postoperative increases in lung volumes in 10 patients, abnormal pulmonary function persisted in 20 patients after heart transplant. Mean values for lung volumes and flow rates did not change but diffusion for CO decreased significantly after heart transplantation. Diffusion failed to correlate with ejection fraction, pulmonary arterial pressure, pulmonary capillary wedge pressure (PCWP), and pulmonary vascular resistance; however, in a subset of patients with improved postoperative lung volumes, preoperative diffusion for CO correlated with preoperative PCWP. We conclude that pulmonary function abnormalities are common among heart transplant recipients. Diffusion abnormalities are not linearly related to indices of cardiac function measured before transplantation and diffusion abnormalities appear to be multifactorial in cause. The posttransplant decrease in diffusion appears to result from the combined effects of decreased postoperative lung volumes in some patients and relief of heart failure induced pulmonary vascular engorgement in others. Improvement in lung volumes and flow rates may occur but cannot be expected after heart transplantation, and diffusion decreases after heart transplantation. The fact that pulmonary function and lung volumes do not improve following heart transplantation implies to underlying lung disease or permanent lung alterations result from chronic heart failure.

Adult↗
PubMed1985

The role of vasodilators in patients with progressive systemic sclerosis. Interstitial lung disease and pulmonary hypertension.

The use of systemic vasodilator drugs in reducing pulmonary artery pressures in patients with pulmonary hypertension is controversial. The effect of hydralazine in four patients with pulmonary hypertension resulting from interstitial lung disease (group 1) and nifedipine in four patients with pulmonary hypertension secondary to progressive systemic sclerosis (group 2) was investigated. Hydralazine blunted exercise induced elevations in pulmonary arterial pressures in individual group 1 patients; nifedipine failed to effect significant salutory hemodynamic changes in any group 2 patients.

Humans↗