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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two patients are described who presented with congestive heart failure and were found to have an atrial septal defect with a pulmonary blood flow approximately twice the systemic blood flow. Most of the usual clinical signs of atrial septal defect were absent, and the diagnosis was established by right heart catheterization and radioisotopic angiography. Both patients had hypertension and coronary artery disease. Atrial septal defect in the adult patient may not be recognized because of associated cardiac disease, including coronary artery disease and hypertension, or pulmonary disease which may obscure the usual clinical signs of a septal defect. Radioisotopic angiography and right heart catheterization should be considered in any patients with heart disease or congestive failure of obscure cause even if the usual diagnostic signs of atrial septal defect are absent.
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PMID:Occult atrial septal defect in adults. 115 34

For the evaluation of myocardial perfusion in patients with left bundle branch block (LBBB), we performed exercise stress (Ex)-redistribution (RD) myocardial tomography with thallium-201 (201Tl) in 23 patients with LBBB and without coronary artery disease (CAD). Myocardial images in patients with LBBB were compared with those of 9 patients with CAD who showed Ex induced transient septal defect. Bull'-eye maps (201Tl distribution maps at Ex and RD and 201Tl washout rate [WOR] map) were made from myocardial tomograms. In 23 patients with LBBB, 15 patients (65%) developed myocardial perfusion abnormality. In 10 (67%) of these 15 patients, transient perfusion defect appeared in the entire septum (diffuse type). On the other hand in 5 patients (33%), localized fixed perfusion defect developed at the boundary between septum and anterior wall (focal type). In focal type, every patient had other disease such as hypertension, aortic stenosis or sick sinus syndrome. While in patients with diffuse type, other diseases were observed in 30% (p less than 0.05) and they were limited to hypertension or diabetes mellitus. These facts suggested that mechanisms of perfusion abnormalities might be different between these two groups. We compared the perfusion abnormality between LBBB diffuse type and CAD. The extent of the defects was not different between two groups. Although apex was included within the defect in 89% of CAD population, apical defect was observed in only 20% of diffuse type (p less than 0.05). Minimal 201Tl WOR and 201Tl uptake ratio of septum to lateral wall indicated that exercise induced septal defect was slighter in diffuse type than CAD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Myocardial perfusion in patients with left bundle branch block and without coronary artery disease]. 160 38

The authors report the case of a 3-month-old infant with a history of interventricular septal defect with pulmonary arterial hypertension. This child had pulmonary symptomatology (dyspnea, recurrent bronchitis, acute attacks of asphyxia) which it was possible to link to a retrotracheal left pulmonary artery by magnetic resonance imaging (MRI). Classical investigations (upper GI barium series and chest X-ray) were suggestive of a bronchogenic cyst type abnormal pulmonary structure. Angiography confirmed the MRI diagnosis. In this case the infant also had tracheal lesions (lower tracheal hypoplasia) which required further evaluation by fibroscopy and bronchography. Thus MRI shows itself to be a useful investigation in the study of basic vascular abnormalities.
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PMID:[Magnetic resonance imaging in the diagnosis of retrotracheal pulmonary artery]. 202 7

Enalapril was used to treat five patients with pulmonary arterial hypertension secondary to congenital cardiopathy, three with ventricular septal defect, one with arterial septal defect, and one with patent ductus arteriosus. The dose of enalapril was 20 mg/day. All patients underwent pretreatment and posttreatment cardiac catheterization. It was concluded that enalapril may be a useful drug in the treatment of pulmonary arterial hypertension secondary to congenital cardiopathy.
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PMID:Hemodynamic changes with enalapril in pulmonary arterial hypertension secondary to congenital heart disease. 302 17

Twenty-five patients with malseptation of the aortopulmonary trunk resulting in aortopulmonary septal defect (window) were evaluated in a unique combined surgical series assembled from two institutions participating in the USA-USSR Health Exchange Program. Typical aortopulmonary septal defect or window (type I) with the connection between the ascending aorta and main pulmonary artery was found in 21 patients. Four had a more cephalad defect (type II) between the ascending aorta and the origin of the right pulmonary artery. Hemodynamics were the consequence of a large left-to-right shunt (mean ratio of pulmonary to systemic flow, 3.0) with right ventricular hypertension (mean right ventricular pressure, 86 mm Hg) and increased pulmonary vascular resistance (mean, 7.4 U) (mean ratio of pulmonary to systemic vascular resistance, 0.33). Angiography may provide patterns that allow preoperative distinction between the two types of aortopulmonary septal defect and provide information important in planning the details of corrective operation. Operative techniques included ligation, direct suture, and patch closure of the aortopulmonary septal defect. The best method appeared to be patch closure by the transaortic approach; real and potential problems were associated with other techniques.
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PMID:Aortopulmonary septal defect: hemodynamics, angiography, and operation. 728 16

The objective of this study was to determine the long-term survival pattern and variables affecting long-term survival and complications occurring during follow-up of patients with Eisenmenger syndrome. A retrospective study of patients diagnosed with Eisenmenger syndrome were followed up. A tertiary care centre was used and it provided superspeciality services in various disciplines. The subjects included 201 patients with Eisenmenger syndrome--diagnosed by a combination of echocardiography and a peripheral arterial oxygen saturation study and/or cardiac catheterisation with or without angiocardiography--worked up and followed up for variable duration over a period of 16 years from 1976 to 1992. One hundred nine patients were females and 92 were males--age of presentation varied from 3 months to 62 years (mean +/- standard deviation 19.23 +/- 12.62 years). A total of 12 different anatomic lesions were seen--the most common three being ventricular septal defect (33.33%), aterial septal defect (29.85%), and patent ductus arteriosus (14.23%). History, physical examination, chest skiagram and electrocardiogram established only the presence of pulmonary arterial hypertension except where differential cyanosis indicating ductus was discernible or the degree of splitting of second heart sound provided some clue to the level of shunt. Contrast echocardiography, completed in 25.4% established the level of shunt in all patients. In others the diagnosis was confirmed by cardiac catheterisation. Twenty patients died during a mean follow-up period of 54.6 +/- 54.47 months. Sudden cardiac deaths (30%), congestive heart failure (25%) and haemoptysis (15%) were the most predominant causes of death. Only one patient died during puerperium.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prognosis for patients with Eisenmenger syndrome of various aetiology. 796 Feb 65

Atrioventricular septal defect with cor triatriatum is a rare combination, with only nine cases reported so far. Cor triatriatum, a potentially correctable cause of pulmonary arterial hypertension in atrioventricular septal defect patients, was missed in a few earlier case reports, leading to death and subsequent diagnosis at autopsy. We report the case of 3-year-old female child with this combination (partial atrioventricular septal defect with cor triatriatum) wherein the final diagnosis was made at cardiac catheterization. Successful surgical correction was performed.
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PMID:Atrioventricular septal defect with cor triatriatum: case report and review of the literature. 956 22

Thirty patients with complete atrioventricular septal defect were operated upon between 1989 and 1996 at our institute. Their ages ranged from two months to 24 years (mean age 2.81 years). All patients had severe pulmonary arterial hypertension except one who had associated pulmonic stenosis. Four patients had severe atrioventricular valve regurgitation and another six had moderate regurgitation. Five patients had Down's syndrome. The cleft in the left atrioventricular valve was closed in all but seven patients. There were five (16.66%) in-hospital deaths which included two patients in whom the cleft was left open. Follow-up ranged from three months to eight years. All patients were evaluated by 2D echocardiography in the immediate post-operative period and three to six monthly subsequently. One patient progressed to moderate and another to severe left atrioventricular valve regurgitation during follow-up. In both the patients the cleft had been left open. All other patients continue to have stable left atrioventricular valve status, that is, none or trivial to mild regurgitation. In view of late deterioration of the left atrioventricular valve regurgitation only in those patients where the cleft was left open, we suggest complete closure of the cleft in all complete atrioventricular canal defects.
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PMID:Routine cleft closure in repair of complete atrioventricular septal defects. 1005 78

Williams syndrome is a genetic disorder associated with characteristic facies, supravalvar aortic stenosis, peripheral pulmonary stenosis, mental retardation, hypertension, premature aging of skin, and congenital cardiac defects. Many cardiac defects such as bicuspid aortic valve, mitral valve regurgitation, coarctation of the aorta, and ventricular or atrial septal defects are linked to the syndrome. Complete atrioventricular septal defect has rarely been associated with Williams syndrome and only one necropsy case has been reported in the literature. The long term follow up of Williams syndrome associated with complete atrioventricular septal defect is reported. During a 10 year follow up period, the pressure gradient in the ascending aorta did not increase despite narrowing of the ascending aorta as identified on an aortogram.
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PMID:Williams syndrome associated with complete atrioventricular septal defect. 1269 80

Turner syndrome is a condition usually associated with reduced final height, gonadal dysgenesis, and thus insufficient circulating levels of female sex steroids, and infertility. A number of other signs and symptoms are seen more frequently with the syndrome. With respect to cardiac function, congenital malformations of the heart and the great vessels, hypertension and ischemic heart disease, and increased risk of aortic dissection are all conditions that the pediatrician or the physician caring for females with Turner syndrome should keep in mind. Many girls and adolescents with Turner syndrome receive growth hormone (GH) treatment, which has so far been an effective and well-tolerated therapy. Nevertheless, because of the experience from acromegaly, the physician should monitor blood pressure and perform echocardiography, together with clinical examinations by a cardiologist at regular intervals. During adulthood most women with Turner syndrome are faced with premature menopause and the need for female hormone replacement therapy (HRT). During clinical evaluation of girls and women with Turner syndrome, these conditions and complications should be kept under surveillance. Here the cardiovascular complications of Turner syndrome are reviewed. The risk of congenital heart defects such as bicuspid aortic valves, aortic coarctation, other valve abnormalities, and septal defect is increased. Likewise, the risk of aortic dissection at a young age is increased, as is the risk of hypertension, ischemic heart disease, and stroke. GH therapy does not seem to adversely affect the heart, although longer-term follow-up studies are needed. In short-term studies, HRT lowers blood pressure, while any effect on the risk of ischemic heart disease has not been evaluated. Treatment with GH and HRT are discussed in relation to the heart and great vessels. Presently, the pathophysiology of the congenital cardiovascular malformation in Turner syndrome is unexplained, although different theories exist. Recommendations for clinical practice are given, including life-long surveillance of cardiac function, aortic diameter and blood pressure.
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PMID:Turner syndrome and the heart: cardiovascular complications and treatment strategies. 1472 55


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