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

The condition of patients with transposition of the great arteries, intact ventricular septum and severe pulmonary vascular disease is inoperable with present techniques. In a series of 260 surgically treated patients with transposition of the great arteries and intact ventricular spetum, 5 had severely increased pulmonary vascular resistance, and all 5 died; postmortem examination confirmed the presence of severe pulmonary vascular disease. The concept of the "palliative Mustard" procedure was applied in two children with transposition of the great arteries, intact ventricular spetum and pulmonary vascular disease who underwent the Mustard operation with creation of a ventricular septal defect. The postoperative course was uneventful in both patients. Thirteen and 5 months, respectively, after operation, both are physically active and have respective arterial oxygen saturation levels of 94 and 92 percent.
Am J Cardiol 1976 Oct
PMID:Mustard operation and creation of ventricular septal defect in two patients with transposition of the great arteries, intact ventricular septum and pulmonary vascular disease. 6 23

Lung specimens of 27 patients under six months of age with complete transposition of the great arteries (TGA), obtained at autopsy, were studied histologically. No evidence of hypertensive pulmonary vascular disease was found in patients under four months of age (23 patients), while obstructive intimal proliferations were seen in 2 patients, aged four and five months, with TGA and VSD. Since pulmonary vascular lesions in transposition with VSD appear early in infancy, timely palliative procedures, such as banding of the pulmonary artery, are strongly indicated when the radical corrective operation is to be postponed.
G Ital Cardiol 1976
PMID:[Complete transposition of the great arteries: hypertensiol pulmonary vascular disease in the first six months of life (author's transl)]. 6 99

More than 1,100 patients underwent a systemic-pulmonary arterial shunt operation at the Children's Memorial Hospital, Chicago, from 1946 to 1974. Of these patients, 294 were studied to assess the presence of pulmonary vascular disease and the time of its occurrence after surgery. They were selected either because lung tissue was available for histologic grading of pulmonary vascular disease (114 patients) or because hemodynamic studies were performed after the shunt operation (180 patients). The shunts, all patent at the time of the study, ranged in duration from 1 month to 23 years. After a subclavan-pulmonary arterial shunt (75 patients) there was little evidence of advatients) pulmonary vascular disease in either histologic C2 of 25 patients) or hemodynamic (1 of 50 patients) studies. After an aortic-pulmonary arterial shunt (44 Waterston, 175 Potts) there was small likelikhood of advanced pulmonary vascular disease with a shunt duration of less than 5 years (1 of 35 histologic, 0 of 27 hemodynamic studies). With a shunt duration of more than 5 years the incidence of advanced pulmonary vascular disease increased significantly (15 of 54 histologic, 17 of 103 hemodynamic studies). A mean pulmonary arterial pressure of 50 mm Hg or greater strongly suggests the presence of advanced pulmonary vascular disease. When a systemic-pulmonary arterial shunt has provided effective palliation with decreased pulmonary pressure there is small likelihood that advanced pulmonary vascular disease will develop, even with a long shunt duration of 20 to 25 years.
Am J Cardiol 1977 May 04
PMID:Pulmonary vascular disease after systemic-pulmonary arterial shunt operations. 6 97

The incidence and time of occurrence of pulmonary vascular disease were studied in 67 children with the complete form of atrioventricular (A-V) canal defect. Advanced pulmonary vascular disease begins to develop during the first year of life, with intimal fibrosis (grade 3 cahnges) noted between age 6 months to 1 year. Vascular dilatation with plexiform lesions (grade 4 changes) can be found by age 1 year. These changes can be found in some patients in spite of hemodynamic findings usually considered to indicate lesser degrees of vascular disease. After age 2 years advanced pulmonary vascular disease is commonly found and may persist after surgical correction of the defects. A similar rapid progression of pulmonary vascular disease was noted in 40 children who had a large ventricular septal defect without A-V canal in whom systemic pressure was transmitted directly to the pulmonary vascular bed. Thirty-six of the 67 children had trisomy-21. No difference was noted in the speed of progression of pulmonary vascular disease between these children and those without trisomy 21. Palliative or corrective surgery should be performed in these patients by age 1 year to prevent development of advanced pulmonary vascular disease.
Am J Cardiol 1977 May 04
PMID:Pulmonary vascular disease in complete atrioventricular canal defect. 6 98

Twenty-seven patients with truncus arteriosus and previous pulmonary arterial banding were evaluated 1 1/2 to 14 years (mean 7 years) after banding. Ages at the time of cardiac catheterization ranged from 3 to 18 years (mean 9 years). Current symptoms were severe in five patients and were related to truncal valve incompetence or decreased pulmonary blood flow (or both) rather than to age, duration of palliation or band location. Twenty-one of 22 patients with two pulmonary arteries were considered to be in a hemodynamically operable state at the time of study. The condition of three of five patients with a single pulmonary artery was subsequently found inoperable because of severe pulmonary vascular disease in the lung supplied by the single pulmonary artery. In patients with two pulmonary arteries, demonstration of low pressure in at least one normal-sized pulmonary artery established operability. Postoperative pressure measurements correlated well with preoperative prediction of operability, with 19 of 20 patients having a pulmonary arterial pressure less than 70 percent of systemic levels after repair. Bilateral pulmonary arterial binding may be more effective than central arterial banding (which frequently produces severe obstruction to the right pulmonary artery) in preventing pulmonary vascular obstructive disease in patients with truncus arteriosus who have two pulmonary arteries. Patients with truncus arteriosus and a single pulmonary artery with pulmonary arterial banding remain at high risk for the development of pulmonary vascular obstructive disease.
Am J Cardiol 1976 Nov 04
PMID:Truncus arteriosus and previous pulmonary arterial banding: clinical and hemodynamic assessment. 13 85

Clinical, experimental and pathologic studies strongly indicate that hypertension is a major factor in coronary heart disease, sudden death, stroke congestive heart failure and renal insufficiency. The deleterious effect of the elevated blood pressure on the cardiovascular system appears to be due mainly to the mechanical stress placed on the heart and blood vessels. Humoral factors and vasoactive hormones such as angiotensin, catecholamines and prostaglandins may play a role in the pathogenesis of hypertensive cardiovascular disease but this role has not yet been defined and is probably secondary. Hypertension and the resulting increase in tangential tension on the myocardial and arterial walls, leads to the development of hypertensive heart disease and congestive heart failure as well as hypertensive vascular disease that affects not only the kidneys but also the heart and brain. Hypertensive vascular disease involves both large and small arteries as well as arterioles and is characterized by fibromuscular thickening of the intima and media with luminal narrowing of the small arteries and arterioles. The physical stress of hypertension on the arterial wall also results in the aggravation and acceleration of atherosclerosis, particularly of the coronary and cerebral vessels. Moreover, hypertension appears to increase the susceptibility of the small and large arteries to atherosclerosis. Thus the patient with hypertension is a candidate for both hypertensive and atherosclerotic vascular disease of the coronary and cerebral vessels leading to occlusive disease of both the large and small arteries and resulting in myocardial infarction and stroke. Other major complications of hypertensive vascular disease include rupture and thrombotic occlusion of blood vessels, especially in the brain. Disease of the arterial media, which begins in childhood with the deposition of calcium in the vessels, may be an important cause of arterial hypertension. This form of hypertension may manifest itself in adults as arteriosclerotic hypertension and lead to cardiovascular complications very similar to those of essential hypertension. The relation of arteriosclerotic hypertension to nutritional factors, including dietary salt intake, deserves study.
Am J Cardiol 1976 Nov 23
PMID:Role of hypertension in atherosclerosis and cardiovascular disease. 13 91

The history and the physical examination are still at the basis of the approach of the patient suffering from intermittent claudication. The history makes clear the specific symptom and its localization. The evolution of the disease, the social and professional handicap are defined. Other troubles and other localizations of the vascular disease are recognized and the nature of the risk factors etablished. The physical examination indicates the pattern and the distribution of the vascular lesions and orientates the pathogenic investigations. A rough assessment of the insufficiency of the cutaneous and muscular circulation is also possible.
Acta Cardiol 1979
PMID:[Intermittent claudication. Introduction to clinical diagnosis]. 31 82

Postoperative changes in the medial thickness of the small pulmonary arteries and the degree of pulmonary vascular disease were estimated histometrically and histopathologically in three cases of late death after total correction of complete transposition of the great arteries with large ventricular septal defect and pulmonary hypertension. In the postoperative course of two of the three cases extreme medial hypertrophy of the small pulmonary arteries as well as severe pulmonary vascular disease were found. In the third case, the thickening of the media was mild and pulmonary vascular disease had not progressed owing to a residual ventricular septal defect. Examination of three additional cases of late death and 15 autopsy cases of complete transposition of the great arteries revealed that hypertrophy of pulmonary arterial media after radical surgery for complete transposition of the great arteries is a common phenomenon. In cases of complete transposition of the great arteries with severe pulmonary hypertension, the deveopment of marked hypertrophy of the media accompanied by pulmonary vascular disease after total correction is usually seen and seems to be the most likely cause of death in the postoperative period.
Am J Cardiol 1979 Aug
PMID:Quantitative analysis of postoperative changes in the pulmonary vasculature of patients with complete transposition of the great arteries and pulmonary hypertension. 46 66

The effects of pulmonary vascular disease on the results of surgical closure of single large ventricular septal defects are reviewed. Hospital mortality in infants was not affected by the presence of preoperative pulmonary vascular disease. The late results were clearly related to age at operation, preoperative pulmonary vascular resistance, and pulmonary artery pressure. Probability of event analysis allows selection of the optimal age for elective repair of large ventricular septal defects.
Adv Cardiol 1978
PMID:Surgical implications of pulmonary hypertension in congenital heart disease. 61 18

1. In the presence of normal coronaries, it is possible to find--or not CAI, in patients with arteriosclerose cardiopathy. 2. When coronary obstructions are present, we also could find a clear dominance of CAI. It is necessary to emphasize the fact that every patient of these series who suffered of trivascular coronary illness presented CAI. 3. When CAI shows in at rest ECG of a patient clearly showing ischemic cardiopathy, more often than not we also find important coronary obstructions, but when this sign is not present it doesn't necessarily mean that we should discard the possibility of a vascular disease, it only points to us the presence of a trivascular coronary pathology. 4. Frequently we find a CVP between normal levels when CAI is not present. 5. We found CAI in every patient showing dysinesia and also in most of the patients with dysinergia.
Arch Inst Cardiol Mex
PMID:[Changes of the P wave in ischemic cardiopathy. Electrocardiographic correlation]. 72 43


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