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

Definitive, if not curative surgery is available for the eight most common congenital cardiac defects-ductus arteriosus, ASD, coarctation, pulmonary valve stenosis, aortic valve stenosis, tetralogy of Fallot, and transposition. The results of surgery for uncomplicated cases of DA, ASD, VSD, and coarctation usually can be determined by clinical means (including chest radiogram and ECG). Postoperative heart catheterization is recommended for evaluation of the patient who has had surgery for pulmonary valve stenosis or artic stenosis and is necessary after tetralogy of Falot or transposition of the great arteries repair to identify the important postoperrative residua and sequelae. The term "curative" surgery probably shoud be reserved for operation for divion of ductus arteriosus unassociated with pulmonary hypertension and performed in childhood. After closure of ASD, patients should continue to be observed for late development of arrhythmias and persistent cardiac enlargement, although the incidence of these problems is low. After VSD closure the patient is still followed at intervals for possible ill effects of the ventriculotomy scar, manifest as arrhythmias, ventricular aneurysm or myocardial insufficiency. The patient with coarctation repair must be observed for a possible late complication from one of the several clinically silent cardiovascular or cerebrovascular anomalies as well as for the change of restenosis or unrelieved hypertension...
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PMID:Residuae, sequelae, and complications of surgery for congenital heart disease. 12 37

Echocardiography is an extremely useful noninvasive technic in the differential diagnosis of a large heart. It may show whether a large heart is due to left ventricular hypertrophy or dilatation, or if it is due to a pericardial effusion. The hypertrophied heart may be further characterized by determining whether it is symmetrical, as caused by aortic stenosis or hypertension, or whether it is assymmetrical, which is characteristic of hypertrophic cardiomyopathy. Similarly, dilatation of the heart may be due to volume overload of the left ventricle secondary to valvular insufficiency, congestive cardiomyopathy or ischemic heart disease; these can be distinguished by echocardiography. As certain types of mitral insufficiency are associated with specific valvular dysfunction, the possible etiology of the mitral insufficiency and therefore of the volume overload of the left ventricle may be determined using echocardiography. Finally, mediastinal tumors may simulate a large heart, and demonstration of normal cardiac dimensions and wall motion can exclude a cardiac etiology for the "large heart."
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PMID:Echocardiography in the differential diagnosis of the large heart. 13 5

Successful correction of severe valvular calcific aortic stenosis is described in which a stented porcine aortic heterograft was placed in the ventricular apex. Creation of a double outlet is a valid alternative approach to relieve left ventricular hypertension, and indication for such a procedure may be encountered unexpectedly. Intramyocardial placement of a durable tissue valve provides a simple and effective option for the cardiac surgeon.
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PMID:Valve placement in the ventricular apex for complicated left ventricular outflow obstruction. 14 54

This report reviews the clinical features of 80 patients with roentgenographically proved mitral annular calcification. The mean age of the group was 73 years, and there was a 2.5 to 1 female to male ratio. Evaluation for underlying cardiovascular disease revealed six patients with severe calcific valvular aortic stenosis; five patients with hypertrophic cardiomyopathy, 11 with mitral prolapse and 33 with significant arterial hypertension (blood pressure greater or equal to 150/96 mm Hg). Eighty-five per cent of the group (68 of 80 patients) had an underlying cardiac disorder associated with either chronically increased left ventricular systolic pressure or abnormal leaflet motion. Other cardiovascular abnormalities occurring as complications secondary to the mitral ring calcification included subacute bacterial endocarditis (three cases), arterial emboli (five episodes) and high grade atrioventricular block (16 cases). Twelve patients had severe mitral regurgitation; successful mitral valve replacement was carried out in four patients (all with myxomatous mitral tissue). Evidence of diffuse conduction system disease, not limited to the area of the cardiac fibrous skeleton, was found frequently (44 patients). Nine patients had sinus node dysfunction and 35 patients had electrocardiographic evidence of distal intraventricular (fascicular) block. Twenty-one patients eventually required pacemakers for management of symptomatic bradyarrhythmias. Atrial fibrillation was present in 23 patients. In this review it was found that calcification of the mitral annulus is frequently associated with or induces serious cardiovascular disease. Since some of these disorders may be modified by appropriate therapy, calcification of the mitral annulus should no longer be ignored as a benign marker of the elderly heart.
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PMID:Calcification of the mitral annulus: etiology, clinical associations, complications and therapy. 15 99

To study the influence of left ventricular (LV) late diastolic filling on the A wave of the LV pressure, simultaneously recorded echocardiographic LV dimensions and high-fidelity LV pressure measurements were taken in 24 patients. Group 1 comprised eight patients without LV hypertrophy (LVH) and LV end-diastolic pressure (LVEDP) less than or equal to 13 mm Hg. Group 2 comprised 16 patients with LVH secondary to aortic stenosis, idiopathic hypertrophic subaortic stenosis, or hypertension and increased LVEDP. Patients in group 2 had significantly thicker left ventricles, decreased mitral E-to-F slopes, and larger A waves in the LV pressure curve. On the basis of end-diastolic chamber stiffness, we divided group 2 into two populations: 12 patients (group 2A) with end-diastolic chamber stiffness similar to that in group 1, and four patients (group 2B) with markedly elevated end-diastolic chamber stiffness. Patients in group 2A had a larger atrial contribution to LV filling than those with markedly abnormal stiffness (group 2B). Therefore, in LVH an increased A wave in the LV pressure may be related to either elevated end-diastolic chamber stiffness or augmented left atrial volume transport.
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PMID:The influence of left ventricular late diastolic filling on the A wave of the left ventricular pressure trace. 15 5

In order to test the hypothesis that delayed mitral valve opening (MO) with regard to endsystolic dimension (t DS-MO) is specific for hypertrophic obstructive cardiomyopathy (HOCM), LV echograms of patients with different forms of LV hypertrophy due to chronic pressure overload (CPO; aortic stenosis + arterial hypertension, n = 24) and hypertrophic obstructive cardiomyopathy (n = 24) were recorded, digitized and compared with those of normals (N :n = 28(. In patients with HOCM (93 +/- 37 ms; p less than 0.0001) and CPO (66 +/- 31 ms; p less than 0.0001) the time t DS-MO was significantly delayed compared with N (13 +/- 15 MS), due to abnormal relaxation. This prolonged relaxation time resulted in an abnormal diameter increase (delta D) during the isovolumic relaxation phase (HOCM: 4.0 +/- 2.2 MM/CPO: 3.0 +/- 1.8 mm; p less than 0.0001/N:0.6 +/- 0.5 mm) and the rapid filling phase (HOCM 7.6 +/- 2.7 mm; p less than 0.0001/CPO 9.2 +/- 2.9 mm; p less than 0.05 / N: 10.7 +/- 2.2 mm). The echocardiographical signs of an abnormal relaxation are not specific for HOCM, they can be seen in different forms of secondary LV hypertrophy and are accompanied by changes in the diastolic filling pattern.
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PMID:[Left ventricular relaxation and filling abnormalities in patients with HOCM and left ventricular pressure overload (author's transl)]. 15 91

Septal and left ventricular posterior wall (LVPW) thicknesses and their ratios were studied at the left ventricular outflow tract and left ventricular cavity in 66 patients with echocardiographically diagnosed left ventricular concentric hypertrophy, 20 with idiopathic hypertrophic subaortic stenosis (IHSS), and 34 normal subjects. Concentric hypertrophy was due to hypertension in 41 subjects and to valvular disease in 15 subjects. Septal thickness in normal subjects was related to body surface area (p less than 0.02). In 12% of normal subjects, 39% of patients with concentric hypertrophy and 95% with IHSS, the septal/LVPW ratio was greater than or equal to 1.3. Thirty-two percent of patients with hypertension, 78% with aortic stenosis, and 60% with aortic insufficiency had septal/LVPW ratios greater than or equal to 1.3 at left ventricular midcavity level. In conclusion, a septal/LVPW thickness ratio of greater than or equal to 1.3 is common in patients with concentric left ventricular hypertrophy and may also occur in normal subjects. A ratio greater than or equal to 1.5 may be more specific for genetically determined asymmetric septal hypertrophy.
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PMID:Interventricular septal thickness and left ventricular hypertrophy. An echocardiographic study. 15 45

The authors report a clinical and phonocardiographic study of functional aortic systolic murmurs in 26 elderly patients, in 19 of which the lesion was confirmed pathologically. Systolic murmurs radiating across the chest in elderly have the same clinical characteristics as aortic stenosis from which they may, however, be distinguished owing to the: absence of a thrill during systole. The brief duration and the proto-meso-systolic position of the murmur with early inscription of maximal oscillations on the phonocardiogram. Conversion of the second aortic sound. Almost constant absence of a diastolic murmur. Normal carotid arteriogram, including normal ejection time after correction and time of half rise. "Innocent" systolic murmurs are due to calcification of the aortic valve without stenosis, and/or dilatation of the ascending aorta. There is no systolic pressure gradient between the left ventricle and the aorta during cardiac catheterisation. No lesions were found in the mitral valve suggesting mitral incompetence, therefore, we consider the term mitro-aortic murmur used by Huchard should be dropped; Radiation of the murmur from the apex of the heart up into the neck may be explained by the simultaneous occurrence of anatomical changes due to age and/or hypertension and by the vibratory nature of the murmurs which become propagated above and below their origin, as shown by the intracardiac recordings.
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PMID:[Functional aortic systolic murmurs in the elderly]. 17 95

The Williams and Beuren's syndrome associates a particuliar facies, a mental debility, a supravalvular aortic stenosis, and frequent vascular anomalies of pulmonary artery as well as aorta and its branches. Relations between this syndrome and congenital idiopathic hypercalcemia seem now determined; the hypertension which has been frequently observed in this last case, seems more unusual in the case of Williams and Beuren's syndrome. The authors report a case about this syndrome in which the hypertension seemed linked to a stenosis of the left renal artery and which has been treated surgically. A year later the result is satisfactory but the evolutive potential of arterial lesions described in this syndrome does not necessory lead to a final recovery. Besides there are in this disease hypertensions which are relevant to an other etiology (more especially aortic hypoplasia) and stenosis of renal arteries without hypertension.
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PMID:[Williams-Beuren syndrome and renovascular arterial hypertension]. 21 3

The authors presented a case of the Williams and Beuren's syndrome, special by the existence of aorta coarctation, high blood pressure, nephrotic syndrome and renal dysplasia. The Williams-Beuren's syndrome is characterised by the association of facial anomalies, mental retardation and supra-valvular aortic stenosis. The case presented in this study demonstrates: -- the symptomatic diversity of the Williams and Beuren's syndrome; -- and the relationship of this syndrome and severe idiopathic hypercalcemia of the infant. The etiopathogenesis is also discussed.
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PMID:[Williams and Beuren's syndrome with hypertension and associated renal abnormalities (author's transl)]. 22 86


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