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H I Palevsky

Publications and source records attributed to H I Palevsky.

At least 19 recordsLinked to original sources

The clinical course of pulmonary embolism.

BACKGROUND: Pulmonary embolism is a potentially fatal disorder. Information about the outcome of clinically recognized pulmonary embolism is sparse, particularly given that new treatments for more seriously ill patients are now available. METHODS: We prospectively followed 399 patients with pulmonary embolism diagnosed by lung scanning and pulmonary angiography, who were enrolled in a multicenter diagnostic trial. We reviewed all hospitalizations, all new investigations of pulmonary embolism, and all deaths among the patients within one year of diagnosis. RESULTS: Of the 399 patients, 375 (94 percent) received treatment for pulmonary embolism, usually conventional anticoagulation. Only 10 patients (2.5 percent) died of pulmonary embolism; 9 of them had clinically suspected recurrent pulmonary embolism. Clinically apparent pulmonary embolism recurred in 33 patients (8.3 percent), of whom 45 percent died during follow-up. Ninety-five patients with pulmonary embolism (23.8 percent) died within one year. The conditions associated with these deaths were cancer (relative risk, 3.8; 95 percent confidence interval, 2.3 to 6.4), left-sided congestive heart failure (relative risk, 2.7; 95 percent confidence interval, 1.5 to 4.6), and chronic lung disease (relative risk, 2.2; 95 percent confidence interval, 1.2 to 4.0). The most frequent causes of death in patients with pulmonary embolism were cancer (in 34.7 percent), infection (22.1 percent), and cardiac disease (16.8 percent). CONCLUSIONS: When properly diagnosed and treated, clinically apparent pulmonary embolism was an uncommon cause of death, and it recurred in only a small minority of patients. Most deaths were due to underlying diseases. Patients with pulmonary embolism who had cancer, congestive heart failure, or chronic lung disease had a higher risk of dying within one year than did other patients with pulmonary embolism.

Adult

Primary pulmonary hypertension in association with human immunodeficiency virus infection. A possible viral etiology for some forms of hypertensive pulmonary arteriopathy.

Recent reports have suggested a possible association between HIV-1 infection and primary pulmonary hypertension (PPH), but most of the patients described to date have either had acquired immunodeficiency syndrome (AIDS) with concurrent lung infections or have administered Factor VIII intravenously for hemophilia. We report three human immunodeficiency virus type 1 (HIV-1)-positive homosexual white males with clinical and hemodynamic diagnoses of PPH. None of the patients had any opportunistic lung infections or other pulmonary pathology, nor were they hemophiliacs. They had no histories of intravenous drug use. Lung tissue from two of the patients revealed hypertensive arteriopathy consistent with PPH and no other pulmonary pathology. Attempts at localizing HIV-1 infection to the vascular endothelium with electron microscopy, immunohistochemistry, DNA in situ hybridization, and polymerase chain reaction techniques did not reveal direct pulmonary artery infection with the virus. These data and the finding of tubuloreticular structures on electron microscopy suggest that HIV-1 may play a role in the pathogenesis of these cases of PPH through mediator release associated with HIV-1 infection rather than by direct endothelial infection.

Acquired Immunodeficiency Syndrome

The management of primary pulmonary hypertension.

Primary pulmonary hypertension is a clinical syndrome characterized by pulmonary hypertension in the absence of sufficient underlying cardiac, parenchymal pulmonary, or systemic disease to account for it. The population of patients with primary pulmonary hypertension is a heterogeneous one, both clinically and histologically. As the etiologic mechanisms are unknown, therapy is directed toward the consequences of the pulmonary vascular process. Oxygen supplementation, the use of digoxin and diuretics for symptomatic heart failure, and anticoagulation all may have a role in treating primary pulmonary hypertension, although vasodilator therapy has been the main area of investigation. Screening for vasodilator responsiveness, defining a favorable vasodilator effect, predicting long-term effectiveness, and deciding who to treat have all been controversial. New approaches, such as use of high-dose calcium channel-blocking agents and continuous intravenous infusion of prostacyclin (an investigational agent), have recently been proposed. When medical therapies are exhausted, heart-lung or lung transplantation has increasingly become an option for selected patients.

Heart-Lung Transplantation

Diagnosing pulmonary embolism: new facts and strategies.

PURPOSE: To provide a clinical approach to the diagnosis of pulmonary embolism. DATA IDENTIFICATION: An English-language literature search using MEDLINE (1982 to 1990) and bibliographic reviews of textbooks and review articles. STUDY SELECTION: In addition to several reviews, studies that evaluated the diagnostic technology of pulmonary embolism were selected. Preference was given to studies with a prospective design, particularly those done within the past decade. DATA EXTRACTION: Studies were assessed independently by three unblinded observers. Data were chosen to describe the efficacy of diagnostic technology on the basis of disease prevalence, sensitivity and specificity, and predictive value. RESULTS OF DATA ANALYSIS: A normal lung scan or pulmonary angiogram rules out the diagnosis of clinically important pulmonary embolism with at least 95% certainty. Lung scan interpretations indicating high or low probability have approximately a 15% error in diagnosing or ruling out pulmonary embolism. The accuracy of either scan result improves when the clinical suspicion of pulmonary embolism matches the lung scan result. Serial impedance plethysmography of the lower extremities may exclude thromboembolism with 95% certainty in patients without high-probability lung scan results or cardiopulmonary disease. CONCLUSIONS: The combination of clinical suspicion and the results of the lung scan and impedance plethysmography appear to offer acceptable diagnostic accuracy in evaluating many patients suspected of having pulmonary embolism. The usefulness of this approach for patients with cardiopulmonary disease is still unknown.

Decision Trees

The problems of the clinical and laboratory diagnosis of pulmonary embolism.

Suspecting and diagnosing venous thrombosis and pulmonary embolism remain major clinical problems. For a variety of reasons, including the patient's pre-existing cardiac and pulmonary status and the release of humoral mediators, pulmonary emboli evoke varied responses in different patients. Symptoms and signs of pulmonary embolism are not specific; they depend on the size and the hemodynamic and humoral consequences of the embolus. Conversely, they may not be present at all. Chest radiographic and electrocardiographic findings are nonspecific, and may be most helpful in establishing the presence of other conditions that may be confused with pulmonary embolism. Arterial blood gases can only heighten the suspicion of pulmonary embolism; they should never be used to exclude the diagnosis. Clinical and laboratory findings therefore do not diagnose pulmonary embolism; rather, they raise the level of concern and set the stage for the performance of subsequent diagnostic studies.

Blood Gas Analysis

A noninvasive strategy for the management of patients suspected of pulmonary embolism.

As a consequence of recent studies that have (1) established the role for ventilation-perfusion lung scanning in the diagnosis of pulmonary embolism, (2) clarified the contribution of clinical assessment to the diagnostic utility of lung scans, and (3) established a role for the noninvasive assessment of the lower extremities for deep venous thrombosis in patients suspected of having pulmonary embolism, we can now manage clinically stable patients suspected of pulmonary embolism without need for invasive diagnostic procedures. The various studies establishing this approach are reviewed, and an algorithm is presented that allows for the noninvasive workup of clinically stable patients suspected of having pulmonary embolism.

Algorithms

An evaluation of preoperative and postoperative ventilation and perfusion lung scintigraphy in the screening for pulmonary embolism after elective orthopedic surgery.

One hundred two patients undergoing elective knee or hip arthroplasty were studied with radionuclide ventilation scans (V) and perfusion scans (Q) preoperatively (preop) and postoperatively (postop) to assess their relative value in the diagnosis of asymptomatic pulmonary embolism (PE) after orthopedic surgery. Postop Q were read in combination with preop V and Q and postop V using prospective investigation of pulmonary embolism diagnosis (PIOPED) criteria. Of 25 postop Q interpreted as either high or intermediate probability for PE, preop Q were judged useful in 96%; the postop V were useful in 78%; and the preop V were not helpful in any of the cases. Of 63 postop Q interpreted as low probability, preop Q were useful in 74%; the postop V were useful in only 33%; and the preop V were useful in only one case. When postop Q were read as normal (14 cases), none of the three auxiliary studies were found to be useful. Overall, postop V were more helpful than preop Q in only 2%, and preop V contributed significantly in only 1%. This experience suggests that preop Q alone is the most useful adjunct to the postop Q in the postoperative evaluation for PE. The authors conclude that to screen for asymptomatic PE after elective orthopedic surgery, preop Q should be performed in all cases, preop V are not necessary, and postop V need be performed only if a baseline preop Q is not available.

Aged

Clinical, laboratory, roentgenographic, and electrocardiographic findings in patients with acute pulmonary embolism and no pre-existing cardiac or pulmonary disease.

The history, physical examination, chest radiograph, electrocardiogram and blood gases were evaluated in patients with suspected acute pulmonary embolism (PE) and no history or evidence of pre-existing cardiac or pulmonary disease. The investigation focused upon patients with no previous cardiac or pulmonary disease in order to evaluate the clinical characteristics that were due only to PE. Acute PE was present in 117 patients and PE was excluded in 248 patients. Among the patients with PE, dyspnea or tachypnea (greater than or equal to 20/min) was present in 105 of 117 (90 percent). Dyspnea, hemoptysis, or pleuritic pain was present in 107 of 117 (91 percent). The partial pressure of oxygen in arterial blood on room air was less than 80 mm Hg in 65 of 88 (74 percent). The alveolar-arterial oxygen gradient was greater than 20 mm Hg in 76 of 88 (86 percent). The chest radiograph was abnormal in 98 of 117 (84 percent). Atelectasis and/or pulmonary parenchymal abnormalities were most common, 79 of 117 (68 percent). Nonspecific ST segment or T wave change was the most common electrocardiographic abnormality, in 44 of 89 (49 percent). Dyspnea, tachypnea, or signs of deep venous thrombosis was present in 107 of 117 (91 percent). Dyspnea or tachypnea or pleuritic pain was present in 113 of 117 (97 percent). Dyspnea or tachypnea or pleuritic pain was present in 113 of 117 (97 percent). Dyspnea or tachypnea or pleuritic pain or atelectasis or a parenchymal abnormality on the chest radiograph was present in 115 of 117 (98 percent). In conclusion, among the patients with pulmonary embolism that were identified, only a small percentage did not have these important manifestations or combinations of manifestations. Clinical evaluation, though nonspecific, is of considerable value in the selection of patients in whom there is a need for further diagnostic studies.

Acute Disease

Echo/Doppler and hemodynamic correlates of vasodilator responsiveness in primary pulmonary hypertension.

To determine correlates of acute vasodilator responsiveness in primary pulmonary hypertension, we retrospectively studied 25 patients, comparing 41 resting echo/Doppler and nine resting catheterization variables with the maximal reduction in pulmonary vascular resistance achieved during vasodilator trials. Twelve vasodilators were tested (mean, 5.6 drugs per patient; range, three to eight). Eight patients were vasodilator responsive, as defined by a reduction in pulmonary vascular resistance greater than or equal to 30 percent in response to at least one agent. Univariate and multivariate analyses revealed only Doppler pulmonic peak flow velocity to be an independent correlate of responsiveness (p less than 0.05). Responders differed from nonresponders in having a higher Doppler pulmonic peak flow velocity (PV) (SD 81 +/- 24 vs 64 +/- 15 cm/s; p = 0.05), lower mean right atrial pressure (RAP) (6 +/- 4 vs 13 +/- 7 mm Hg; p = 0.04), and longer median survival (37 vs 5 months; p = 0.03). Seven of eight responders had RAP less than or equal to 10 mm Hg, and all responders had PV greater than 60 cm/s. Seven of ten patients with both RAP less than or equal to 10 and PV greater than 60 and one of the 15 remaining patients were vasodilator responsive (p less than 0.001). Thus, echo/Doppler and invasive hemodynamic parameters correlate with acute vasodilator responsiveness in primary pulmonary hypertension. Patients with low PV and high RAP values were almost never vasodilator responsive. Doppler pulmonic peak velocity and mean RAP may be useful in identifying patients most likely to respond to acute vasodilator trials and those in whom testing is unlikely to yield positive results.

Adult

Chronic cor pulmonale. Etiology and management.

Cor pulmonale is right ventricular enlargement secondary to pulmonary hypertension. Although most often caused by parenchymal lung disease, derangements of the ventilatory drive, the respiratory pumping mechanism, or the pulmonary vascular bed may also result in right ventricular hypertrophy and dilatation. Arterial hypoxemia (and resultant polycythemia), hypercapnia, and respiratory acidosis all contribute to the increased afterload on the right ventricle. Diagnosis is often difficult, since pulmonary vascular disease, pulmonary hypertension, and cor pulmonale have few specific manifestations, especially early in their evolution. Treatment is primarily directed at the underlying pulmonary or ventilatory disorder, rather than at the right ventricular failure per se. Supplemental oxygen is essential to avoid hypoxia; corticosteroids, anticoagulants, vasodilators, and other specific therapies are used as indicated to treat the underlying pulmonary disorders. When medical therapies fail, lung or heart-lung transplantation has become a possibility for selected patients.

Chronic Disease

Detection of thrombophlebitis with 111In-labeled anti-fibrin antibody: preliminary results.

Deep venous thrombosis remains a major medical problem, affecting a large segment of the population and resulting in significant mortality and morbidity. Current techniques available for detecting deep venous thrombosis present limitations that may mitigate their potential benefit to the patient. Invasive techniques, such as ascending contrast venography, carry risks to the patient with regard to complications such as an allergic reaction to an iodine dye, adverse effects to renal functions, and clot formation in a normal vein. Noninvasive techniques, such as Doppler ultrasound and impedance plethysmography, evaluate only a limited segment of the venous bed. The need remains for a diagnostic technique that is safe, accurate, and widely accessible. A readily available noninvasive scintigraphic technique utilizing radiolabeled monoclonal anti-fibrin antibody may overcome some of these shortcomings. This imaging examination is quite effective in detecting clots in the lower extremities. Compared to contrast venography, 111In-labeled anti-fibrin antibody imaging appears to be as sensitive in identifying acute venous thrombosis. In addition, the preliminary data indicate that anticoagulation with heparin may interfere with adequate visualization of the clots with this technique.

Adult

Radiolabeled antifibrin antibody in the detection of venous thrombosis: preliminary results.

The recent development of monoclonal antibodies against components of coagulated blood may provide new approaches to the diagnosis of venous thrombosis. Scanning with an indium-111-labeled Fab fragment of a murine monoclonal antifibrin antibody (59D8) and ascending contrast venography were performed in 33 patients. Images of the calves, popliteal fossae, thighs, and pelvis were obtained immediately, 4-6 hours, and 24 hours after injection of 2 mCi (74 MBq) of the antibody. All images were read in a blinded manner. Findings in both studies were positive in 28 patients and negative in three. In 19 patients not undergoing heparin therapy, 19 specific anatomic sites were positive on venograms and 29 were positive on antibody images (19 sites matched). In 14 patients undergoing heparin therapy, 34 sites were positive on venograms and 27 were positive on antibody images (22 sites matched). In most patients, positive results were noted within 1 hour of antibody injection. No adverse effects were noted with the antibody preparation. Preliminary data suggest that antifibrin antibody imaging is sensitive in detecting clots, is safe to use, and may have a role in diagnosing and managing venous thrombosis.

Adult

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