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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Platelet survival time (autologous labeling with 51chromium) was measured in 63 patients in order to evaluate the role of platelets in the thromboembolic complications of patients with hypoxemia and pulmonary hypertension. Thirty-eight of these patients had chronic obstructive airways disease; 13, primary pulmonary hypertension; seven, recurrent pulmonary embolism; four, the Eisenmenger syndrome; and one, multiple pulmonary arteriovenous fistula. Forty-three patients were hypeakly associated with arterial oxygen tension ( r = 0.50), but not with the arterial carbon dioxide tension or the level of pulmonary artery pressure. Sulfinpyrazone lengthened platelet survival in 12 of 24 (50%) treated patients but this drug did not alter either arterial oxygen tension arterial carbon dioxide tension, or pulmonary artery pressure. Our results suggest that hypoxemia is associated with shortened platelet survival time and that platelets may, therefore, be involved in the thromboembolic complications that develop in patients with hypoxemia.
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PMID:Platelet survival time in patients with hypoxemia and pulmonary hypertension. 83 12

Four years after an HIV infection and without any preceding illness characteristic of AIDS, a 24-year-old woman developed dyspnoea on exertion and peripheral oedema. She had for several years been an intravenous drug addict and contracted hepatitis A and B. There were no symptoms of the HIV infection. Clinical, radiological and echocardiographic examination demonstrated right ventricular failure caused by pulmonary hypertension not due to pulmonary embolism or another known aetiology. The patient died suddenly 9 months after the diagnosis from heart failure. Autopsy established primary pulmonary hypertension with pathognomonic plexogenic pulmonary arterial disease which had led to cor pulmonale with overload myocarditis. Although there had been no clinical signs of renal failure, there was histological evidence of mesangioproliferative glomerulonephritis and non-destructive interstitial nephritis. This case demonstrates that, in addition to the typical AIDS-associated diseases, other rarer syndromes may, in uncertain ways but connected with the HIV infection, decide the prognosis of such patients.
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PMID:[Primary pulmonary hypertension and mesangioproliferative glomerulonephritis in HIV infection]. 158 15

Thromboembolic pulmonary hypertension can occur in two different settings: either acute pulmonary embolism or chronic pulmonary thromboembolism. During acute pulmonary embolism, when the heart and lungs are normal, the mean pulmonary artery pressure never excesses 40 mmHg, this is the maximum pressure the right ventricle can stand. During chronic thromboembolism, the right ventricle can adapt to slowly increasing pulmonary artery pressure. The mean pulmonary artery pressure is usually very elevated and right heart failure is delayed. Diagnosis is difficult when an history of acute pulmonary embolism or phlebitis is lacking. At the beginning, the main differential is psychogenic dyspnea. A clue to the diagnosis is given by the pulmonary function test mainly arterial blood gases at rest and exercise and radionuclide perfusion scan. When the pulmonary hypertension is patent the main differential is primary pulmonary hypertension. No definitive clear cut can be made between multiple distal chronic thromboembolism and primary pulmonary hypertension.
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PMID:[Thromboembolic pulmonary arterial hypertension]. 185 24

A young woman presented with rapidly progressive dyspnea and clinical findings strongly suggestive of primary pulmonary hypertension or possible pulmonary embolism (or both). She died of acute right-sided heart failure. A diagnosis of pulmonary veno-occlusive disease was made at autopsy. Approximately 100 cases of this disease have been reported previously in the literature. We describe a patient with a particularly florid progression of this unusual disease. Death occurred within six weeks of the onset of symptoms.
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PMID:Florid pulmonary veno-occlusive disease. 220 15

Reversible causes of pulmonary hypertension, such as mitral stenosis or pulmonary embolism, should be corrected causally. The therapy of pulmonary hypertension is difficult in those diseases where the causes or mechanisms are not understood or are unknown. In chronic obstructive lung disease, the primary objective is to improve airflow and alveolar ventilation (theophylline, beta-sympathicomimetics). Long-term oxygen (more than 18 hours a day) should be used in patients with paO2 below 55 mm Hg, since a reduction in pulmonary vascular resistance and a prolonged survival has been demonstrated. The role of vasodilator therapy (hydralazine, nitrates, diazoxide, captopril, calcium-blockers and others) in chronic obstructive lung disease remains uncertain. In primary pulmonary hypertension, a pulmonary vasodilator is recommended after demonstrating (for example with an infusion of prostaglandin I2), that the increased pulmonary vascular resistance is still reversible. The initiation of therapy should be performed cautiously under hemodynamic monitoring.
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PMID:Treatment of pulmonary hypertension. 287 21

Chronic pulmonary embolism is a rare disease which can occur at first with pulmonary hypertension. In these cases it may be difficult to distinguish between primary pulmonary hypertension. We examined nine patients with Chronic Pulmonary Embolism (CPE) (three females and six males, mean age 45 +/- 13 years, range 21-67 years) and ten patients with Primary Pulmonary Hypertension (PPH) (seven females and three males, mean age 35 +/- 13 years, range 10-56 years) who came to our attention during the years 1973-1986 (mean follow up 3 years). All patients had an electrocardiogram, chest x-ray, echocardiogram, cardiac catheterization with pulmonary angiography; seven patients with CPE and eight with PPH had perfusion lung scans. Progressive dyspnoea was the main feature in all the patients; four out of nine with CPE and none of the ones with PPH had a previous history of thrombophlebitis. In all the patients the electrocardiogram, chest x-ray and echocardiogram showed signs of pulmonary hypertension, so that a clear distinction between the two groups was not possible. Cardiac catheterization showed pulmonary pressure values higher in patients with PPH as compared to the ones with CPE (systolic pressure 96 mmHg vs 70 mmHg, diastolic pressure 49 mmHg vs 31 mmHg, mean pressure 65 mmHg vs 45 mmHg). Pulmonary angiography in more than half of the patients with CPE showed a "cut off" of two or more lobar branches of the pulmonary arteries. In the patients with PPH pulmonary angiography showed a dilatation of the main pulmonary artery and a diffuse bilateral hypoperfusion. Perfusion lung scan in all the cases of CPE showed zonal perfusion defects, while in all cases of PPH, with the exception of one, it was largely normal. Venograms in the districts of the inferior vena cava demonstrated thrombosis in two out of six patients with CPE. Negative venograms were found in the five patients with PPH who had this investigation performed. One patient with CPE had a surgical embolectomy, the other eight had anticoagulant oral treatment. During the follow-up period three patients with CPE and five with PPH died within five years and within fifteen months respectively, of the diagnosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Differences in patients with chronic pulmonary embolism and primary pulmonary hypertension]. 338 46

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.
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PMID:Pulmonary arterial hypertension: value of perfusion scintigraphy. 361 69

A 75-year-old man complaining of dyspnea and having sings of postcapillary pulmonary hypertension was diagnosed as pulmonary veno-occlusive disease and confirmed at autopsy. This is the oldest case ever reported. Almost all the small veins 2 mm or less in external diameter were partially or nearly completely occluded by intimal fibrous tissue, and the obstructive changes in the pulmonary arteries were much more limited. Pulmonary veno-occlusive disease is a rare, almost inevitably fatal disease of unknown etiology which has only recently been separated clearly from primary pulmonary hypertension as a distinct entity. Chest roentgenogram finding suggesting postcapillary pulmonary hypertension is a clue to a diagnosis and differentiates this from two other causes of clinical primary pulmonary hypertension, that is, recurrent pulmonary embolism and plexogenic pulmonary arteriopathy.
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PMID:Pulmonary veno-occlusive disease in an elderly man: case report and review of the literature. 623 4

Echocardiographic analysis of right ventricular ejection time (RVET), pre-ejection time (RVPEP), RVPEP/ET and isovolumic relaxation time (RVIRT) was performed in patients with acute or chronic right ventricular pressure overloading. Fifty-five patients undergoing right ventricular cardiac catheterization, were categorized into seven groups; 11 patients with atrial septal defect (ASD) without pulmonary hypertension (PH) (group 1), 12 with ASD with PH (group 2), six with mitral stenosis (MS) without PH (group 3), nine with MS with PH (group 4), seven with primary pulmonary hypertension (PPH) (group 5), seven with acute pulmonary embolism (PE) (group 6), and three patients with convalescence of PE (group 7). Corrected RVIRT (RVIRTc) and RVET (RVETc) were calculated by regression analysis correlating with heart rate in normal subjects. RVIRTc, RVETc, RVPEP and RVPEP/ET in seven groups were significantly correlated with systolic pulmonary artery pressure (SPAP) (r = 0.62, p less than 0.001; r = -0.41, p less than 0.01; r = 0.61, p less than 0.001; r = 0.65, p less than 0.001, respectively), but RVDd did not correlate with SPAP (r = 0.370, p less than 0.05). Comparing acute right ventricular pressure overloading group (group 6) with each of chronic right ventricular pressure overloading groups (groups 2, 4, 5, and 7), RVIRTc and RVDd were significantly increased in the former than the latter, but RVETc, RVPEP and RVPEP/ET were not significantly different in both groups. There was a significant correlation between RVIRTc and RVPEP/ET in chronic pressure overloading, but not in acute pressure overloading. We concluded that early diastolic RV relaxation and systolic performance were both impaired by increased afterload in chronic pressure overloading. In acute pressure overloading, however, early diastolic RV relaxation was more significantly impaired possibly because of acute changes of muscle architectures due to acute right ventricular expansion and anoxia.
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PMID:[Echocardiographic study of right ventricular performance by acute and chronic pressure overloadings]. 653

The acute pulmonary and systemic haemodynamic response to low (0.15 mg/kg) and high (0.30 mg/kg) doses of intravenous hydralazine was evaluated in 26 consecutive patients with severe pulmonary hypertension due to cor pulmonale (nine patients), primary pulmonary hypertension (11 patients), or pulmonary embolism (six patients). Hydralazine did not cause a significant change in pulmonary arterial resistance or pressure in any group but produced a significant reduction in systemic resistance, which correlated with plasma concentration, and a significant increase in pulmonary blood flow index in all groups. Ten patients who experienced a reduction in pulmonary arterial resistance of at least 5 U X m2 after administration of hydralazine had higher initial values for pulmonary arterial resistance and systemic resistance and a lower pulmonary blood flow index than those who did not respond. Maintenance oral hydralazine treatment during nine to 36 months of follow up did not seem to affect symptoms or mortality. These results indicate that hydralazine has limited value in acutely reducing pulmonary arterial pressure or affecting clinical outcome in patients with pulmonary hypertension.
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PMID:Haemodynamic response to intravenous hydralazine in patients with pulmonary hypertension. 665


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