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

An African youth who had died from primary pulmonary hypertension was suspected of having ingested a herbal remedy containing the seeds of the local plant Crotalaria laburnoides. Consequently powdered seeds of this plant were fed to 20 Wistar albino rats for 60 dyas to see if this would induce ventricular hypertrophy and associated hypertensive pulmonary vascular disease. At the end of the experimental period right ventricular hypertrophy, medial hypertrophy of the pulmonary trunk and 'muscular pulmonary arteries', and muscularization of the pulmonary arterioles had developed in a proportion of the test animals. These are the morbid anatomical features pathognomonic of a raised pulmonary arterial pressure and show that the seeds of Crotalaria laburnoides contain an agent capable of inducing pulmonary hypertension in rats. This study suggests the value of seeking a history of ingestion of herbal remedies and drugs in cases of unexplained pulmonary hypertension in man.
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PMID:A pulmonary hypertension-producing plant from Tanzania. 12 2

Clinical studies have suggested that patients with Down syndrome have precocious development of pulmonary hypertension, even in the absence of congenital heart disease. To examine the pathologic basis of this impression, we studied 82 patients with Down syndrome autopsied at The Johns Hopkins Hospital from 1913 to present. The patients ranged in age from 26 hours to 25 years; 41 (50%) were female. Atrioventricular canal defect was present in 40 patients, nine of whom also had pulmonary stenosis. Eight had isolated ventricular septal defect and seven had other malformations. Histologic sections of the lung from each patient were studied and the degree of hypertensive pulmonary vascular disease graded. Age and sex-matched controls without cardiovascular manifestations, all other autopsied patients with atrioventricular canal defect not associated with Down syndrome, and age-matched patients with ventricular septal defect or other malformations were similarly studied for pulmonary vascular changes. Comparison of the 27 patients with Down syndrome and no cardiovascular malformations with normal controls showed no differences, with one notable exception: an 8-month-old child with Down syndrome had severe HPVD secondary to idiopathic pulmonary hypertension. HPVD in patients with the various cardiovascular malformations was similar for those groups with Down syndrome and those without, when HPVD was considered as a function of the patients' age and the type of malformation. We conclude that, in general, patients with Down syndrome have no predisposition to develop severe or precocious hypertensive pulmonary vascular disease.
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PMID:Hypertensive pulmonary vascular disease in Down syndrome. 15 39

Most cardiovascular problems in pregnant women arise from the complications of preexisting chronic conditions (e.g., rheumatic and congenital heart disease) and hypertensive vascular disease. Regular supervision of these patients is essential to detect incipient pulmonary congestion or disturbances of cardiac rhythm. Even if the pregnancy has been uncomplicated, hospital admission 1-4 weeks before the due date is recommended to ensure optimal conditions for labor. Vaginal delivery at term with adequate sedation and use of forceps to shorten the 2nd stage of labor is the perferred mode. Induction of labor may be indicated in hypertensive vascular disease or in cases where adjusting or discontinuing drug therapy calls for precise timing of delivery. Eisenmenger's disease and primary hypertension are potential medical indications for pregnancy termination. The distribution pattern of organic heart disease encountered in pregnant women has changed in the past 20 years, with a decrease in rheumatic and an increase in congenital heart disease. The incidence of chronic rheumatic heart disease in pregnant women fell from 3.5% of all deliveries at Newcastle General Hospital in 1942-51 to 1.1% in 1962-71. Acute pulmonary edema in mitral stenosis is currently a major risk during pregnancy. There is no optimal stage of pregnancy for valvotomy, nor evidence that this procedure induces miscarriage in the early weeks. Pregnancy has become less hazardous in severe forms of congenital heart disease as more patients with these disorders have undergone cardiac surgery prior to pregnancy. Pregnancy is not believed to have any effect on the longterm course of rheumatic heart disease. Patients with aortic stenosis, coarctation of the aorta, primary pulmonary hypertension, Fallot's tetralogy, Eisenmenger's syndrome, and surgically untreated cyanotic lesions require special attention during pregnancy. The outlook for women who become pregnant after an acute cardiac infarction episode depends on the functional state of the heart at the time of pregnancy and the presence or absence of angina pain. There has been a gradual decline in perinatal mortality, especially in cases complicated by rheumatic heart disease.
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PMID:Cardiac disorders. 34 Jan 1

Autopsy observations suggested that lesions of hypertensive pulmonary vascular disease (HPVD) due to elevated venous pressure differ from those with arterial hypertension only. Clinical and pathologic features were reviewed in patients from the Hopkins autopsy files with proved pulmonary hypertension; 50 had venous HPVD due to left-sided congestive heart failure, 50 had arterial HPVD due to congenital malformations, and 15 had idiopathic pulmonary hypertension (IPH). The two forms of HPVD have consistent distinctive histologic changes. In venous HPVD intimal fibroelastosis (IFE) develops in veins and arteries with retention of normal lumen diameters. Intensity of IFE correlates with severity and duration of venous hypertension. Arterial HPVD has IFE in conducting arteries, but the characteristic lesion is cellular intimal proliferation in regulatory arterioles, producing progresssive irreversible lumenal narrowing. Glomoid and angiomatoid lesions appear with prolonged severe arterial hypertension. They do not occur in venous HPVD. Hypertensive arteritis may develop with either form of HPVD. IPH has arterial-type HPVD. IFE of venous HPVD appears to be a response to increased mural tension. Arteriolar intimal cellular proliferations seen in arterial HPVD may be produced by blood flow boundary layer separations. IPH may be explainable as protracted inappropriate pulmonary arteriolar constriction.
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PMID:The pathogenesis of the two forms of hypertensive pulmonary vascular disease. 99 86

Two cases of hypertensive pulmonary vascular disease with Raynaud's phenomenon are reported. One is a 32-year-old housewife of primary pulmonary hypertension with some immunological disorders and the other is a 28-year-old female of systemic lupus erythematosus. It may be considered that some immunological process could play a role in the etiology of some cases of primary pulmonary hypertension and the relationship of pathogenesis between these 2 cases was discussed.
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PMID:Case report. Two cases of pulmonary hypertension with Raynaud's phenomenon. Primary pulmonary hypertension and systemic lupus erythematosus. 116 Jan 86

Case report of a 5 year old boy with a well diagnosed primary pulmonary hypertension, combined with anomalies of the pulmonary arteries of the left upper lobe of the lungs with angiographically loopy appearance. Congenital heart and vascular disease did not exist; AV-fistulae were not found. There is no proof of a connection between the anomalies of the pulmonary arteries and pulmonary hypertension. There was no similar case in the current literature to be found.
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PMID:[Primary pulmonary hypertension and abnormalities of pulmonary arteries]. 126 79

The pulmonary circulation of the rat is widely used as an animal model for studies of human pulmonary hypertension. It is not difficult to understand its appeal. The species is a small laboratory animal which is readily accommodated in decompression chambers for studies for simulated high altitude. It is also very susceptible to the action of the metabolites of pyrrolizidine alkaloids which rapidly lead to severe pulmonary vascular disease in the absence of intrinsic heart and lung disease, thus suggesting its value as an animal model of primary pulmonary hypertension. However, these obvious advantages of the rat pulmonary circulation are outweighed by the fact that its pathological reactions to hypoxia and noxious dietary agents differ significantly from those found in human disease. This can lead to erroneous conclusions as to the nature of the remodelling of the human pulmonary vasculature in pulmonary hypertension.
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PMID:The rat is a poor animal model for the study of human pulmonary hypertension. 155 66

A kindred with a familial hemoglobinopathy and familial primary pulmonary hypertension with autosomal dominant transmission has been identified. Affected family members were obvious from their cyanosis due to a reduced affinity for oxygen by the hemoglobin variant. The mother and one child had clinical pulmonary hypertension, whereas two siblings had cyanosis and preclinical pulmonary vascular disease as evidenced by abnormal perfusion lung scans and elevated levels of fibrinopeptide A in the face of normal pulmonary hemodynamics. In one, pulmonary hypertension could be induced with exercise. The studies on this family support the hypothesis that primary pulmonary hypertension may be initiated by abnormalities of the pulmonary vascular bed that predispose to in situ thrombosis. The possible common genetic transmission of the two diseases offers the speculation that the gene that confers predisposition to pulmonary hypertension may be located near the gene responsible for beta globulin.
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PMID:Familial pulmonary hypertension in association with an abnormal hemoglobin. Insights into the pathogenesis of primary pulmonary hypertension. 170 27

Fourteen patients with pulmonary vascular disease, either primary pulmonary hypertension or the result of cardiac defects, underwent balloon atrial septostomy (BAS) over the period of July 1981 to June 1988 because of symptoms of syncope, fatigue, right heart failure, and cardiac arrest. Ages ranged from 4 mo to 50 yr. Two moribund patients died within 24 h of the septostomy due to severe hypoxemia and unrelieved low cardiac output; three others died 2 wk to 35 mo later; the remaining 9 patients have improved symptomatically and are alive 11 to 96 mo after septostomy. One received a heart and lung transplant 19 mo later. We conclude that, in patients with symptomatic cor pulmonale secondary to pulmonary vascular disease, atrial septostomy can improve symptoms and may serve as a palliative bridge to heart and/or lung transplantation.
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PMID:Effects of atrial septostomy in patients with terminal cor pulmonale due to pulmonary vascular disease. 172 34

We describe clinical and postmortem findings in a 44-year-old man with pulmonary hypertension and infection with the human immunodeficiency virus (HIV-1). Plexogenic angiopathy and veno-occlusive lesions were present, in addition to a mild, patchy pulmonary interstitial lymphoid infiltrate. The clinical data for 14 previously reported cases of HIV-associated primary pulmonary hypertension are summarized. We speculate that these vascular changes may be due to damage from a specific immune response to HIV.
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PMID:Primary pulmonary hypertension and human immunodeficiency virus infection in a non-hemophiliac man. 174 Mar 4


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