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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 31-year-old woman was admitted to our hospital because of dyspnea on exertion. She had had the same symptom a few years earlier. A chest radiograph revealed ground-glass-like shadows on both sides, and the arterial PaO2 was 54 Torr when the patient was breathing room air. We first suspected hypersensitivity pneumonitis, but the dyspnea and hypoxemia did not resolve during treatment in the hospital, and returned home. She felt no obvious changes in symptoms while at home. We found no antibodies to Tricosporon cutaneum in her serum. Computed tomography of the chest revealed diffuse pan-lobular areas of high density. Bronchoalveolar lavage was done and the total cell count was 9.6 X 10(7). About three quarters (73%) of the recovered cells were lymphocytes. Examination of a transbronchial biopsy specimen showed alveolar thickening with infiltration of small mononuclear cells. No granulomas or Massons bodies were seen, and no antibodies specific to collagen-vascular disease were detected. We therefore excluded the diagnosis of hypersensitivity pneumonitis, idiopathic interstitial pneumonia and collagen-associated pneumonitis. There was no evidence of drug-induced pneumonitis. She was seropositive for HTLV-I. We suspected that this was a case of HTLV-1-associated pneumonitis.
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PMID:[Interstitial pneumonia in an HTLV-I carrier]. 910 56

A 22-year-old first man came to our hospital because of dyspnea on exertion in February 1993, and was admitted in September 1994 because of progression of dyspnea. A chest roentgenogram showed diffuse ground-glass-opacities in the middle and lower lung fields, and an elevated diaphragm. Pulmonary-function testing revealed a low %VC and a low diffusing capacity. Examination of a specimen obtained by thoracoscopic lung biopsy revealed usual interstitial pneumonia. Immunohistochemical examinations showed the expression of intercellular adhesion molecule-1 on vascular endothelial cells and on alveolar epithelial cells. Dust inhalation and collagen vascular disease were ruled out and the diagnosis was idiopathic interstitial pneumonia. This condition develops only rarely in patients under 60 years old.
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PMID:[Juvenile onset of idiopathic interstitial pneumonia]. 916 50

In this article, we describe pulmonary hypertension in two men (31 and 43 years of age) with human immunodeficiency virus (HIV) infection who were examined at Mayo Clinic Rochester. Among 88 reported cases (including the two current ones) of HIV- or acquired immunodeficiency syndrome (AIDS)-associated pulmonary hypertension, 61% were male; the age range was 2 to 56 years (mean, 32). Dyspnea was the usual initial symptom. Of the 74 patients in whom pulmonary artery pressure was recorded or calculated by echocardiography, systolic pressures ranged from 49 to 118 mm Hg (mean, 68). Of the 33 cases in which lung tissue was evaluated microscopically, 28 (85%) were of the plexogenic variant of pulmonary arterial hypertension. Of the other five cases examined histologically, three consisted of thrombotic pulmonary arteriopathy (one was due to recurrent thromboembolism, and the other two were due to in situ thrombosis), and two were of pulmonary venoocclusive disease. No correlation existed between either CD4 counts or a history of pulmonary infections and the development of pulmonary hypertension. In 15 of the 88 patients (17%), confounding factors for hypertensive pulmonary vascular disease were present, including coexisting liver disease in 13 and coagulation abnormalities in 2. In 83% of the patients, the development of pulmonary hypertension seems to have been related primarily to the chronic HIV infection. Pulmonary hypertension was more rapidly progressive in patients with HIV or AIDS than in those with primary pulmonary hypertension; the reported time intervals between onset of symptoms and diagnosis were 6 months and 30 months, respectively. The 1-year survival rate for patients with HIV and pulmonary hypertension was 51%, based on the follow-up data compiled from the 63 patients in whom it was described; this compares with a 1-year survival rate of 68% for patients with primary pulmonary hypertension. Death was considered a direct consequence of pulmonary hypertension in 29 (76%) of the 38 fatal cases.
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PMID:Human immunodeficiency virus infection and pulmonary hypertension: two new cases and a review of 86 reported cases. 944 76

Establishing an underlying cause and treatment plan for patients with pulmonary hypertension presents a significant challenge to practicing physicians. Doppler echocardiography is a simple, cost-effective tool for detecting pulmonary hypertension and evaluating right ventricular function. Nonspecific therapy (use of digoxin and diuretics, anticoagulation) for pulmonary hypertension and right ventricular failure achieves a degree of symptomatic improvement and should be considered in patients with moderate to severe disease. CTEPH should be considered in patients with dyspnea. Because severs forms of pulmonary hypertension usually are not discovered until late in the disease course, a high level of suspicion is required when evaluating symptoms and risk factors consistent with pulmonary vascular disease. Pulmonary hypertension is classified as idiopathic, or primary, when no secondary cause can be identified. Primary pulmonary hypertension is a devastating disease that largely affects young women. Significant advances in treatment have been made and will be discussed in detail in part 2 of this article.
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PMID:How to manage secondary pulmonary hypertension. 1002 12

Ischemic cerebrovascular diseases are commonly induced by atherosclerosis and cardiogenic embolization but rarely they occur in association with Takayasu's arteritis and aortic lesion such as aortic dissection and aneurysm. Here we experienced two cases of acute aortic disease complicated by ischemic cerebrovascular disease (CVD). Patient 1 was a 77-year-old male. He complained of dyspnea and left hemiparesis. He was brought to our hospital by ambulance. Left hemiparesis and dyspnea improved soon. The patient only complained of left lower extremity pain and physical examination revealed hypotension. Brain CT showed no abnormality but chest CT revealed aortic dissection. The resection of the intimal tear and replacement of ascending aorta and aortic arch with 28 mm Hemashield graft were performed under hypothermia and selective cerebral perfusion. The postoperative course was uneventful and he has been doing well. Patient 2 was a 67-year-old female. She was found lying unconscious and brought to our hospital by ambulance. Physical examination revealed right hemiparesis and hypotension. Brain CT demonstrated low density area in the left corona radiata and ruptured aortic aneurysm was seen in abdominal CT. Just after the examination, the patient suddenly complained of severe back pain and died despite cardiopulmonary resuscitation. Aortic lesions can manifest ischemic symptom involving multiple organs following their vascular disorder. Aortic dissection rarely occurs in association with ischemic CVD and in that case it is likely to be seen by neurologists. Aortic dissection and aneurysm deteriorate so suddenly that immediate diagnosis and proper treatment are needed.
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PMID:[Two cases of acute aortic disease complicated by ischemic cerebrovascular disease]. 1076 48

A 53-year-old woman was admitted to our hospital in May 1999, because of progressive dyspnea and liver dysfunction. She had been receiving the replacement therapy of thyroid hormone for thirteen years and suffering from Raynaud's phenomenon for 9 years. She experienced exertional dyspnea and sicca symptom for 3 years, and had an episode of syncope 4 months before admission. An echocardiogram showed dilation of the right ventricle, tricuspid regurgitation and the estimated mean pressure of the pulmonary artery was higher than 120 mmHg. She was diagnosed as having severe pulmonary hypertension (PH) complicated with primary Sjogren's syndrome and primary biliary cirrhosis without portal hypertension She was treated with anticoagulant (warfarin) and oral prostagrandin I2 (prostacyclin). However, right heart failure and jaundice gradually progressed and she suddenly died in December 1999. At autopsy, the heart was enlarged with right ventricular hypertrophy. Small arteries and arterioles in the lung showed concentric intimal proliferation and severe plexogenic vascular disease. Deposition of immunoglobulin was not observed in the pulmonary arteries. Since the prognosis of PH is poor, it is important to analyze the etiology of the disease for the development of the treatment.
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PMID:[Pulmonary hypertension in a patient with primary Sjogren's syndrome, Hashimoto's disease, and primary biliary cirrhosis]. 1115 16

A 67-year-old man with a four-year history of mixed connective tissue disease (MCTD) associated with interstitial pneumonia was admitted to our hospital with a complaint of dyspnea and moist cough. Because the interstitial pneumonia was exacerbated, he was given high-dose steroid treatment (pulse therapy and sequential oral treatment of PSL 50 mg/day). After treatment his general condition showed some improvement, but then he suddenly died of acute respiratory failure. Autopsy disclosed fat emboli in the lungs, kidneys, liver and myocardium. The fat embolism may have been a consequence of the steroid treatment. Fat embolism should be taken into account as one of the causes of the acute respiratory failure in collagen vascular disease patients receiving steroid treatment.
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PMID:[A case of systemic fat embolism in mixed connective tissue disease associated with interstitial pneumonia during steroid treatment]. 1157 27

Diagnostic criteria based on pulmonary function testing for pulmonary vascular disease and CHF are imprecise. Although these tests constitute a necessary part of the work-up of a patient with dyspnea, additional studies are required to obtain a final diagnosis in the setting of cardiopulmonary vascular disease. In contrast, specific pulmonary function tests may offer an objective means of assessing severity of dysfunction resulting from pulmonary hypertension or CHE Serial measurements of pulmonary function offer insight into general and specific patterns of cardiopulmonary vascular disease and are useful in evaluating response to treatment.
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PMID:Pulmonary function test abnormalities in pulmonary vascular disease and chronic heart failure. 1178 62

The cardiopulmonary exercise test (CPET) is frequently used for the quantitative evaluation of exercise tolerance and for the qualitative assessment of the origin of dyspnea. Although reasonably safe, CPET is contraindicated in acute clinical situations and relatively contraindicated in severe pulmonary hypertension. Pulmonary emboli are usually present during the acute onset of pulmonary hypertension; however, in situations where pulmonary vascular disease is more unsuspected, CPET may help with the diagnosis. We present a report of a 47-year-old Caucasian female with a 2-month history of exertional dyspnea. She had a normal pulmonary function test, arterial blood gas analysis and CT scan of the chest. On CPET she was found to have a higher than normal physiological dead space to tidal volume ratio, increased ventilatory equivalent for the elimination of CO(2) (V(E)/VCO(2)), persistently positive arterial-end-tidal PCO(2 )difference at peak exercise, and a low anaerobic threshold suggestive of pulmonary vascular disease. She was subsequently diagnosed with pulmonary embolic disease by her ventilation/perfusion scan and pulmonary arteriogram. This report highlights the importance of recognizing the hallmarks of unsuspected pulmonary vascular disease on CPET.
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PMID:Abnormalities on cardiopulmonary exercise test in a dyspneic patient. A case report of unsuspected pulmonary embolism. 1245 9

This study assesses the incidence and prevalence of cryptogenic fibrosing alveolitis (CFA) in a well-defined and stable Norwegian population of 250,000 inhabitants during a period of 15 years. We conducted a file survey of all patients (n = 376) aged 16 years or older with a clinician's diagnosis of pulmonary fibrosis (ICD 8: 517 and ICD 9: 515 and 516). Cases with a history of exposure to fibrogenic agents or with collagen vascular disease were excluded and the remaining 158 cases were defined as CFA. The average annual incidence of hospitalised CFA was 4.3 per 100,000. No change was observed in the annual incidence during the 15-year study period. The prevalence was 19.7 and 23.9 per 100,000 by 31.12. 1991 and by 31.12. 1998, respectively. The incidence increased considerably and significantly with age. No significant gender differences were observed. The lack of gender differences and the increase with age were also found when the diagnosis of CFA was exclusively based on cases with hospital file records of breathlessness, bilateral crackles and bilateral shadows on chest radiograph.
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PMID:Incidence and prevalence of cryptogenic fibrosing alveolitis in a Norwegian community. 1269 5


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