Biomedical subjects
Publications and source records attributed to K M Moser.
A case of digital clubbing in a patient with pulmonary artery sarcoma and severe pulmonary hypertension is presented. The differential diagnosis of clubbing and clinical features of pulmonary artery sarcoma are reviewed with emphasis on the possible association of clubbing with pulmonary artery sarcoma.
UNLABELLED: The finding of a restrictive pulmonary defect may divert clinicians from considering the diagnosis of chronic thromboembolic pulmonary hypertension because lung volumes are usually normal in this disorder. We have, however, encountered a significant number of these patients with reduced lung volumes. Furthermore, we have observed many patients who have developed parenchymal scars and/or pleural thickening. To determine whether such findings are associated with lung volume restriction, we analyzed patients evaluated at our institution for chronic thromboembolic pulmonary hypertension over a 20-month period in whom thoracic high-resolution CT scans and pulmonary function testing had been performed. Patients with obstructive or restrictive lung disease from another cause were excluded. We compared the presence of lung restriction (total lung capacity below 80% of predicted) with the extent of parenchymal scarring, pleural thickening, and pulmonary artery diameter on CT scans. Of 191 patients evaluated, 51 met criteria for entry. Eleven patients (22%) had lung restriction. Parenchymal scarring was highly associated with lung restriction (p = 0.01). Neither pleural thickening (p = 0.08) nor pulmonary artery diameter (p = 0.80) was associated with lung restriction. CONCLUSIONS: A significant number of patients with chronic thromboembolic pulmonary hypertension may have restrictive lung defects. The restriction may be due to parenchymal scarring.
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A reduced diffusing capacity for carbon monoxide (DCO) is common among patients with chronic thromboembolic pulmonary hypertension (CTEPH) and often persists for more than a year following successful pulmonary thromboendarterectomy (PTE). To determine the relative contribution the pulmonary membrane diffusing capacity (DM) and pulmonary capillary blood volume (VC) make to the reduction in DCO, we measured both in 29 patients with CTEPH before and approximately 3 weeks after PTE. Mean preoperative DM was reduced in patients with CTEPH (28 mL min-1 mm Hg-1 vs 43 mL min-1 mm Hg-1 in control subjects; p < 0.001) and dropped significantly following PTE (21 mL min-1 mm Hg-1; p < 0.001). Mean preoperative VC was mildly reduced in the CTEPH group compared with healthy control subjects (57 vs 67 mL; p = 0.044) and did not rise following PTE (57 mL pre-PTE vs 54 mL post-PTE; p > 0.05) despite substantial reduction in mean pulmonary artery pressure and increase in cardiac output after surgery. We conclude that the low DCO observed in patients with CTEPH before and after PTE is principally caused by a reduced DM and to a lesser extent by a low VC. The mechanisms responsible remain speculative but may reflect pathophysiologic changes in the pulmonary microcirculation caused by chronic pulmonary hypertension that did not improve in the postoperative period studied.
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BACKGROUND: Distinguishing chronic major vessel thromboembolic pulmonary hypertension from primary pulmonary hypertension is critical because the treatment options differ markedly. Surgical thromboendarterectomy is potentially curative in the former condition, whereas oxygen, vasodilators, perhaps anticoagulation, and lung transplantation are the options for the latter. The development of large thrombi in the main, right, or left pulmonary arteries has not been previously described in patients with primary pulmonary hypertension. METHODS AND RESULTS: Three pulmonary hypertensive patients with massive thrombi in the central pulmonary arteries are described. The data indicate that the large central thrombi in these three patients were not hemodynamically significant. In none did perfusion lung scans demonstrate segmental or larger defects. CONCLUSIONS: Large central thrombi can develop in patients with primary pulmonary hypertension. Perfusion lung scans that do not demonstrate segmental or larger defects should alert physicians to this possibility. Chest computed tomography and other studies identifying such thrombi are not adequate in distinguishing such a development from operable chronic major vessel thromboembolic hypertension. Careful review of lobar and segmental artery findings and the pulmonary angiogram, angioscopy, and cardiac catheterization data demonstrating the hemodynamic significance (or lack thereof) of these thrombi are essential in making this important distinction. Furthermore, these observations may constitute an additional indication for anticoagulant therapy in primary pulmonary hypertension.
PURPOSE: An increased occurrence of thrombotic events has been described in patients exhibiting a lupus anticoagulant (LA). In patients with chronic, major vessel thromboembolic pulmonary hypertension, not only has there been a relatively high frequency of the LA, but also an unexpected association with heparin-related thrombocytopenia. This retrospective report emphasizes the frequency of this association. PATIENTS AND METHODS: We retrospectively reviewed the medical records of 216 patients admitted to the University of California, San Diego, Medical Center who were being considered for surgical correction of their chronic thromboembolic pulmonary hypertension. For each patient, the following information was sought: presence of an LA, variation in platelet numbers during the preoperative evaluation, and determination of whether an observed thrombocytopenia was related to heparin use. RESULTS: An LA was found in 23 of the 216 patients (10.6%). Of the remaining patients, sufficient platelet data for comparison were available for 68 patients. These 68 patients constituted the control group. Within the LA group, platelet counts during the preoperative evaluation declined to 51.6% +/- 16.7% of baseline counts, a highly significant difference (P < 0.0001) compared with the non-LA control group, who underwent a comparable evaluation with similar heparin exposure. In addition, heparin-associated thrombocytopenia developed in 13 of the 23 LA patients (56.5%) and in none of the control patients. Heparin-induced arterial thrombosis was implicated as the cause of a myocardial infarction in 1 of the patients with heparin-associated thrombocytopenia. CONCLUSIONS: In patients with chronic thromboembolic pulmonary hypertension, a high incidence of the LA and an accompanying association with heparin-related thrombocytopenia have been observed. Although further prospective studies of this relationship are needed, physicians should be alert to the possibility of thrombocytopenia when using heparin for patients exhibiting an LA.
Chronic obstruction of pulmonary arteries can be due to a variety of disease processes, including chronic thromboembolic disease, fibrosing mediastinitis, or neoplasia. Large vessel arteritis is another unusual cause of pulmonary artery obstruction and can be difficult to distinguish from the above-listed etiologies. We present four patients referred to our institution with the provisional diagnosis of chronic thromboembolic pulmonary hypertension who were subsequently diagnosed with Takayasu's arteritis involving the pulmonary arteries. We review the historical, physical examination, and radiologic characteristics that help distinguish Takayasu's arteritis from chronic thromboembolic disease.
Bleomycin-induced lung injury is an established murine model of human pulmonary fibrosis. Although procoagulant molecules (e.g., tissue factor [TF]) and fibrinolytic components (e.g., urokinase [u-PA] and type 1 plasminogen activator inhibitor [PAI-1]) have been detected in alveolar fluid from injured lungs, the origin of these molecules remains unknown. We therefore examined the expression of procoagulant and fibrinolytic components in relation to the distribution of parenchymal fibrin in bleomycin-injured lungs. Extravascular fibrin localized to the alveolar and extracellular matrix in injured lung tissue. Injured lung tissue extracts contained elevated levels of PAI-1 activity and decreased levels of u-PA activity. Whole lung PAI-1 and TF mRNAs were dramatically induced by lung injury. In situ hybridization of injured lungs revealed that PAI-1, u-PA, and TF mRNAs were induced within the fibrin-rich fibroproliferative lesions, primarily in fibroblast-like and macrophagelike cells, respectively, while TF mRNA was also induced in perilesional alveolar cells. Taken together, these observations suggest that the induction of PAI-1 and TF gene expression plays and important role in the formation and persistence of extracellular fibrin in bleomycin injured murine lungs.
BACKGROUND: The decreased morbidity and rapid recovery after thoracoscopic lung biopsy compared with open lung biopsy by thoracotomy is increasingly recognized, as is the ability to obtain satisfactory diagnostic material thoracoscopically. To our knowledge, however, there has been no systematic comparison of specimen quality using different thoracoscopic biopsy techniques. The purpose of this study was to compare histologic features of lung parenchyma obtained by videothoracoscopic forceps and wedge biopsy techniques. METHODS: Five adult swine were anesthetized, intubated, and ventilated. Sequential left and right videothoracoscopies were performed to obtain biopsy specimens of lung parenchyma using 5-mm endoscopic cupped forceps. Specimens were obtained from fully inflated lung and from partially atelectatic (deflated) lung. Electrosurgery was applied during forceps biopsy for airleak closure. Limited wedge biopsy specimens were obtained using an endoscopic stapler. One hundred thirteen forceps biopsy specimens (55 inflated, 58 deflated) and 24 sections from 8 wedge biopsy specimens were examined. Specimens were assessed for overall histologic quality and ease of microscopic interpretation. Specific histologic features were then evaluated including presence of artifact, congestion and hemorrhage, degree of alveolar inflation, and number of bronchioles and vessels per cross-sectional area. Whole lungs from two animals were examined for extent and depth of lung injury at the areas of biopsy. RESULTS: No major differences in overall microscopic specimen quality were detected among the different techniques nor were significant differences noted between lung inflated and lung deflated forceps biopsy technique. Wedge sections contained more vessels per unit area (p < 0.001), perhaps reflecting the more peripheral nature of forceps biopsy. Small amounts of thermal or crush artifact were noted on the surface of forceps biopsy specimens, but did not affect overall specimen quality. CONCLUSIONS: Multiple 5-mm forceps biopsy specimens were of comparable quality to single wedge biopsy specimens obtained by endoscopic stapling. Although greater numbers of vessels were present in endoscopic stapled wedge biopsy specimens, multiple forceps biopsy specimens in fact, contain amply sufficient vessels for histologic analysis.
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Chronic, major-vessel thromboembolic disease represents a potentially correctable form of pulmonary hypertension. A thorough understanding of the unique problems associated with each aspect of care in these patients is essential to ensure a minimal perioperative mortality and satisfactory long-term outcome. This article reviews the cause, natural history, evaluation, surgical management, and postoperative course of patients with chronic thromboembolic pulmonary hypertension undergoing thromboendarterectomy.
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OBJECTIVE: To determine the frequency of pulmonary embolism in patients admitted for treatment of deep venous thrombosis. DESIGN: An open, multicenter, dose-ranging study to assess the safety and pharmacokinetic characteristics of tissue-type plasminogen activator in deep venous thrombosis and pulmonary embolism. Perfusion and ventilation lung scans, chest roentgenograms, and venograms (in deep venous thrombosis) or pulmonary angiograms (in pulmonary embolism) were obtained before and 24 hours after inception of therapy. Heparin therapy was then administered. SETTINGS: Five tertiary-care hospitals. PATIENTS: All patients with suspected deep venous thrombosis or pulmonary embolism seen from August 1987 through November 1988 entered the study if they met inclusion criteria and if the diagnosis was confirmed by venogram (deep venous thrombosis) or pulmonary angiogram (pulmonary embolism). INTERVENTIONS: All patients received tissue-type plasminogen activator followed by intravenous heparin therapy. MAIN OUTCOME MEASURES: The primary measure was the frequency of pulmonary embolism in patients with deep venous thrombosis who had no symptoms of pulmonary embolism. This was not the original purpose of the study but emerged as an important finding as the data were analyzed. RESULTS: Nearly 40% of patients with deep venous thrombosis who had no symptoms of pulmonary embolism had evidence of pulmonary embolism based on ventilation-perfusion scan and chest roentgenogram findings. CONCLUSIONS: Because all of those considered to have embolism had so-called high-probability scan results, the frequency of embolism reported likely represents the minimum incidence of pulmonary embolism in patients with deep venous thrombosis who have no embolic symptoms. These data emphasize that venous thromboembolism is one disorder.
PURPOSE: To study the relationship of regional hypoperfusion and areas of decreased lung attenuation on computed tomographic (CT) scans of patients with chronic pulmonary thromboembolism. MATERIALS AND METHODS: Preoperative CT scans of five patients (four men and one woman, aged 29-72 years) with chronic pulmonary thromboembolism were reviewed and compared with axial single photon emission CT (SPECT) perfusion scans obtained at similar levels. Regions of varying attenuation and perfusion were scored on a three-point scale. RESULTS: In the five patients, 198 regions were identified. Of 176 abnormal regions at SPECT, 133 were abnormal at CT (sensitivity, 75.6%). Eleven of 22 regions interpreted as normal at SPECT were judged to have normal attenuation at CT (specificity, 50%). The overall accuracy of CT for detecting areas of hypoperfusion was 72.7% (P = .011). CONCLUSION: A mosaic pattern of lung attenuation at CT is a sign of variable regional perfusion and may suggest chronic pulmonary thromboembolism as a cause for pulmonary hypertension.