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H I Palevsky

Publications and source records attributed to H I Palevsky.

70 records · Page 4Linked to original sources
PubMed1990

Pulmonary vascular cine MR imaging: a noninvasive approach to dynamic imaging of the pulmonary circulation.

Cine gradient-recalled magnetic resonance (MR) imaging, which has flow sensitivity and high temporal resolution, may potentially yield both morphologic and dynamic flow-related information in the pulmonary vasculature. The authors used this modality to evaluate pulmonary vessels in 12 healthy subjects and in 14 patients with a variety of cardiopulmonary disorders. Normal pulmonary arteries and veins were characterized by distinctive signal intensity and diameter variations as well as motion of the vessels during the cardiac cycle. Patients with pulmonary arterial hypertension demonstrated loss of the normal pulsatile systolic increase and diastolic decline in velocity-related signal intensity and in diameter of the proximal pulmonary arteries. Disorders of pulmonary venous signal and diameter profiles during the cardiac cycle, which show a characteristic biphasic pattern in healthy subjects, were identified in five patients with mitral valvular disease. These initial results indicate that cine MR imaging techniques hold promise in the evaluation of pathophysiologic conditions in the pulmonary circulation.

Adult↗
PubMed1990

Prostacyclin and acetylcholine as screening agents for acute pulmonary vasodilator responsiveness in primary pulmonary hypertension.

Epoprostenol sodium (prostacyclin) administered intravenously is considered the standard for assessing the ability of the pulmonary circulation to vasodilate. At present, epoprostenol sodium is an investigational drug that has limited availability. In contrast, acetylcholine, also a pulmonary vasodilator, is readily available. Therefore, we assessed the feasibility of using acetylcholine as an alternative to prostacyclin in testing for the capacity of the pulmonary vasculature to vasodilate. Twenty-three patients with primary pulmonary hypertension (mean pulmonary arterial pressure, 58.5 +/- 13.4 mm Hg) received incremental infusions of prostacyclin and acetylcholine to predetermined maximal infusion rates as part of a battery of vasodilator agents administered according to standard protocols (mean, 5.4 +/- 1.2 agents/patient; range, 3-8 agents/patient); the administration of the different agents was timed to avoid synergistic effects. Of all the agents tested, prostacyclin and acetylcholine were most consistently effective in evoking acute pulmonary vasodilation, and both seemed to distinguish patients capable of manifesting acute pulmonary vasodilation from those who were not. However, at maximal doses set by protocol, prostacyclin generally elicited a greater vasodilator response than acetylcholine. The difference in magnitude of response may have been due to use of prescribed dosages of acetylcholine that were submaximal. In other respects, the two agents were similar; both were equally well-tolerated, and side effects were mild and resolved rapidly when the vasodilator infusions were stopped. We conclude that in the majority of patients with primary pulmonary hypertension, acetylcholine appears to be an effective and available substitute for prostacyclin in screening for pulmonary vasodilator responsiveness.

Acetylcholine↗
PubMed1990

Pulmonary veno-occlusive disease and its response to vasodilator agents.

Pulmonary veno-occlusive disease (PVOD) is an uncommon form of unexplained (primary) pulmonary hypertension (PPH) rarely diagnosed during life and generally associated with a progressively deteriorating course. We describe three patients with PVOD; in two of them, diagnosis was established by open lung biopsy. All three patients underwent right heart catheterization and acute vasodilator testing, and each responded favorably to at least one test agent. One patient did not receive chronic vasodilator therapy and died seven months after his initial evaluation. The other two patients were treated with chronic vasodilator therapy; one initially improved, but then experienced progressive right heart failure and died 23 months after the start of therapy, the third patient is alive and clinically improved 72 months after beginning vasodilator therapy. Details of the vasodilator studies, and the rationale for treating this uncommon disorder, are provided.

Aged↗
PubMed1989

Two-dimensional and Doppler-echocardiographic and cardiac catheterization correlates of survival in primary pulmonary hypertension.

To determine correlates of survival in primary pulmonary hypertension, we compared 41 echocardiography-Doppler and nine catheterization parameters with outcome in 26 patients. Mean follow-up was 19.7 months in survivors; mean survival was 4.8 months in 16 nonsurvivors. Cox life-table univariate analysis correlated two echocardiographic, three Doppler, and three catheterization variables with poor survival (p less than or equal to 0.05), and chi 2 analysis ensured the best critical values: severity of pericardial effusion, heart rate of more than 87 beats/min, pulmonic flow acceleration time of less than 62 msec, tricuspid early flow deceleration (T-DEC) equal to or less than -300 cm2/sec, mitral early flow-to-atrial flow velocity ratio (M-E/A) equal to or less than 1.0, catheterization cardiac index (CI) equal to or less than 2.3 l/min/m2, mean pulmonary artery pressure of more than 61 mm Hg, and diastolic pulmonary artery pressure of more than 43 mm Hg. Multivariate life-table analysis of noninvasive variables revealed the severity of pericardial effusion to be independently significant (p = 0.006), whereas analysis of catheterization variables revealed cardiac index to be independently significant (p = 0.014). Combined multivariate analysis did not differ from the noninvasive results alone. Categorical modeling of the eight significant variables split at their critical values (present or absent) revealed M-E/A, T-DEC, and CI to be independently significant by multivariate analysis (p = 0.0014). Analysis of the five echocardiography-Doppler variables alone revealed M-E/A, T-DEC, and heart rate to be independently significant (p = 0.0016). In both cases, mortality increased with the number of critical values reached.(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗
PubMed1989

Primary pulmonary hypertension. Vascular structure, morphometry, and responsiveness to vasodilator agents.

The use of pharmacologic agents in the treatment of pulmonary hypertension has not proved to be uniformly successful or predictable. One possible reason for the vagaries in response is that the pulmonary vascular lesions are not consistent. We examined the relation between the structure of the pulmonary resistance vessels in unexplained (primary) pulmonary hypertension and the response to pulmonary vasodilators. Our study involved 19 patients with clinically unexplained pulmonary hypertension (mean pressure, 59 +/- 14 mm Hg). After characterizing them clinically and performing control hemodynamic measurements, we determined the acute effects of a series of vasodilator agents that have different mechanisms of action. In 16 patients, lung biopsy material was related to the hemodynamic studies; in nine patients, including six who had undergone open lung biopsy, the hemodynamic studies were related to the pathologic changes found at autopsy. Histologic specimens from all 19 patients were evaluated qualitatively and sorted into three subsets of hypertensive pulmonary arteriopathy: medial hypertrophy (with minimal intimal proliferation), arteriopathy with plexiform lesions (associated predominantly with concentric laminar intimal proliferation and fibrosis), and arteriopathy with microthrombotic lesions (associated predominantly with eccentric intimal proliferation and fibrosis). The 16 lung biopsies were also quantitated by morphometric techniques. Using a decrease in calculated pulmonary vascular resistance of more than 30% accompanied by a decrease in mean pulmonary arterial pressure of at least 10% to define vasodilation, only four patients were responders. The patients varied considerably in their responses to different vasodilator agents. Patients with similar clinical and hemodynamic profiles differed considerably with respect to the nature of their pulmonary vascular obstructive lesions and their responses to vasodilator agents. Qualitative histologic examination of lung tissue did not provide a basis for predicting how individual patients would respond to vasodilator agents. However, quantitative morphologic analysis of the initial open lung biopsy specimens did prove helpful in predicting acute responsiveness to vasodilator agents and the subsequent clinical course of these patients with unexplained (primary) pulmonary hypertension. An intimal area of more than 18% of the vascular cross-sectional area had an 85% predictive value for identifying the patients who did poorly during the first 36 months of follow-up.

Adolescent↗
PubMed1989

Pulmonary hypertension and thromboembolic disease in women.

This chapter provides a review of several major disorders affecting the pulmonary circulation. These disorders may result in the development of significant symptoms, particularly during exertion, as well as substantial long-term morbidity and even mortality. All of these conditions are complicated by difficulties in diagnosis and the lack of universally successful therapeutic options. Although these conditions may be found in patients of all demographic characteristics, this discussion has focused on those aspects that are of particular relevance to women. It is hoped that with a heightened awareness of these conditions will come earlier diagnosis, thereby allowing for the institution of therapies at a time when the prospect for successful intervention is greater.

Female↗
PubMed1988

Pulmonary hypertension complicating portal hypertension: findings on chest radiographs.

Pulmonary hypertension is a rare but well-established complication of portal hypertension with a prevalence of 0.73% in one large autopsy series. In this report, we review the findings on chest radiographs in eight patients with this complication. Portal hypertension in these patients was evidenced by the presence of esophageal varices and/or ascites. The causes of portal hypertension were liver cirrhosis in seven patients and portal venous thrombosis in one patient. Pulmonary hypertension was established by right heart catheterization and pressure measurement. Qualitative assessment of the radiographs showed that four patients had the classic findings of pulmonary hypertension including prominent central pulmonary arteries and right ventricular enlargement, three had subtle abnormalities, and one had only cardiomegaly. Measurements of the width of the right descending pulmonary artery and the pulmonary lobar diameter/transverse thoracic diameter ratio were made in five of the patients in whom postero-anterior radiographs were available. The results confirmed our qualitative analysis, although they did not establish the diagnosis in borderline cases. We also observed that pulmonary vascular redistribution to the upper lobes was present in four patients, a finding that has been reported in patients with other causes of pulmonary hypertension. We conclude that the possibility of pulmonary hypertension should be raised in patients with portal hypertension, even when only subtle chest radiographic findings are present to suggest that diagnosis.

Adolescent↗
PubMed1987

Pulmonary arterial hypertension: value of perfusion scintigraphy.

Records of 34 patients with established causes of pulmonary arterial hypertension were retrospectively reviewed. The ventilation-perfusion scans were blindly classified according to standardized criteria as normal or high, low, or intermediate probability of pulmonary embolism as the cause of pulmonary arterial hypertension. Twelve of 13 patients with primary pulmonary hypertension had normal or low-probability scans, but the perfusion pattern was not helpful in distinguishing between histologic subtypes. All eight patients with large-vessel thromboembolic hypertension had high-probability scans; however, three of 13 patients with nonembolic secondary pulmonary hypertension also had high-probability scans. While a normal or low-probability scan excluded proximal pulmonary emboli as a cause of pulmonary hypertension, a high-probability scan may be associated with a variety of other nonembolic causes of secondary pulmonary hypertension.

Adult↗
PubMed1986

The effect of antigen-induced bronchoconstriction on phrenic nerve activity.

The effects of acute bronchoconstriction, produced by inhalation of Ascaris suum antigen, on both the amplitude and timing of phrenic nerve activity were studied in anesthetized dogs. Blood gas tensions and inspiratory air flow were maintained constant. Bronchoconstriction resulted in a significant increase in the magnitude and rate of rise of the phrenic neurogram during both normal respiratory cycles and cycles when lung inflation was prevented. The increase in the slope of the phrenic neurogram that results from lung inflation was further increased during bronchoconstriction. In addition, in half the animals, there was a significant increase in the tonic phrenic activity measured during expiration. All of these changes were abolished by bilateral cervical vagotomy. Antigen administration did not affect the timing of the different phases of the cycle equally; inspiratory duration was reduced by 51.8% and expiratory duration by 67.6%. Postinspiratory activity of the phrenic (PIIA) was reduced by only 34.7%; thus, during bronchoconstriction PIIA occupied a proportionally greater fraction of the expiratory phase. Vagotomy abolished the changes in respiratory timing and eliminated all PIIA.

Animals↗
PubMedDate not supplied

A detailed evaluation of patients with acute pulmonary embolism and low- or very-low-probability lung scan interpretations.

BACKGROUND: To determine the clinical characteristics of patients with pulmonary embolism (PE) and low- or very-low-probability ventilation-perfusion lung scan interpretations. METHODS: A retrospective analysis of the data obtained during the Prospective Investigation of Pulmonary Embolism Diagnosis study was performed. The clinical characteristics of patients with acute PE and low- or very-low-probability lung scan interpretation (false-negative interpretations) were compared with patients who had low- or very-low-probability lung scan interpretations and no evidence of acute PE (true-negative interpretations). RESULTS: Of the 1493 patients who gave consent to participate in the Prospective Investigation of Pulmonary Embolism Diagnosis study, 399 patients had angiographic or autopsy evidence of acute PE. Pulmonary embolism was excluded in 960 patients. Patients with false-negative lung scan interpretations more commonly had a history of immobilization (P < .0001), trauma to the lower extremities (P < .003), recent surgery (P < .002), or central venous instrumentation (P < .04) compared with patients with true-negative lung scan interpretations. In patients with low- or very-low-probability lung scan interpretations and none of the above-mentioned risk factors, the prevalence of PE was only 4.5%. In contrast, for patients with low- or very-low-probability lung scan interpretations and two or more of the above-mentioned risk factors, the prevalence of PE was 21%. CONCLUSIONS: Patients with a history of immobilization, trauma to the lower extremities, recent surgery, or central venous instrumentation were more likely to have false-negative lung scan interpretations. Therefore, this population warrants special attention when deciding on the need for peripheral venous studies or angiography in patients with low- or very-low-probability lung scan interpretation.

Acute Disease↗
PubMedDate not supplied

Pulmonary MR angiography utilizing phased-array surface coils.

Magnetic resonance angiography of the pulmonary vasculature was evaluated in 12 subjects using breath-hold gradient echo scans and surface coils at 1.5 T. Flow-compensated GRASS, spoiled GRASS (SPGR), and WARP-SPGR sequences were utilized. Comparisons were made among flip angles of 10-60 degrees, slice thicknesses of 3-10 mm, and body coil as well as Helmholtz pair and phased-array multiple coils. With 30-40 contiguous slices encompassing the lung, intrathoracic vasculature was segmented using a UNIX/X-windows based package dubbed VIDA. Three-dimensional anatomy was visualized by a brightest voxel projection algorithm, following reduction of chest wall pixel intensities by an operator-interactive module. Both SPGR (30 degrees flip angle, 4 mm slice thickness) and WARPSPGR (15 degrees flip angle, 5 mm slice thickness) in combination with phased-array multiple coils provided the most satisfactory images, based upon observations by three radiologists and signal-to-noise ratio measurements. The MR angiograms visualized vessels as distal as sixth to seventh order branches. The technique was successfully applied to three patients with pulmonary embolism. The results of this study demonstrate that the pulmonary vascular tree can be imaged by MR angiography combining a high resolution technique utilizing phased-array multiple coils, fast gradient echo sequences with breath-holding, and postprocessing of the volumetric image data. The technique is attractive since it is noninvasive and provides a full three-dimensional portrayal of the pulmonary vasculature.

Humans↗