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

We report 100 cases of mitral commissurotomy in children, 15-years-old or less, suffering from rheumatic mitral stenosis. Mitral stenosis in children is characterised by the severity of functional impairment and the considerable radiological, electocardiological and haemodynamic changes, with pulmonary arterial hypertension which is always present and often well marked. The early results of mitral commissurotomy are very satisfactory with clinical improvement and a low mortality. But, in the long term, we have seen progressive deterioration in the clinical state of these patients resulting from re-stenosis or from the progression of another valve lesion. Three problems have been discussed. First, the progression of the rheumatic process which seems to account to a large extent for the late failures of mitral commissurotomy in children. Secondly, the problem of tricuspid insufficiency, which is often associated with mitral stenosis in childhood and which usually disappears during the post-operative period. Finally, the problem of pre-capillary pulmonary arterial hypertension which always showed a tendency towards regression.
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PMID:[Mitral commissurotomy in children. Apropos of 100 cases]. 10 82

The prostaglandin synthetase inhibitor indomethacin was given orally or intravenously to pregnant ewes. This resulted in the fetal pulmonary to systemic arterial mean blood pressure difference across the ductus arteriosus rising significantly, presumably secondary to constriction of the ductus arteriosus. The pressure difference was due to pulmonary arterial hypertension, and not due to a fall in systemic arterial mean blood pressure. Fetal arterial blood gas tensions and pH values were normal throughout. In five experiments the pressure difference could be promptly but temporarily reversed by the administration of PGE1 into the fetal inferior vena cava. Indomethacin was present in fetal blood, and maternal plasma prostaglandin levels were suppressed. Indomethacin administration during pregnancy causes constriction of the fetal ductus arteriosus and fetal pulmonary arterial hypertension which, if severe, may cause rapid fetal death. It is possible that this mechanism may be one cause of persistent pulmonary hypertension or tricuspid insufficiency or both in the newborn infant.
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PMID:Constriction of the fetal ductus arteriosus after administration of indomethacin to the pregnant ewe. 43 Mar 14

The prostaglandin synthetase inhibitor indomethacin was given orally or intravenously to pregnant ewes. This resulted in a significant rise in the fetal pulmonary-to-systemic arterial mean blood pressure difference across the ductus arteriosus, presumably secondary to constriction of the ductus arteriosus. In five experiments the pressure difference could be promptly but temporarily reversed by the administration of prostaglandin E1 (PGE1) into the fetal inferior vena cava. Fetal lungs from study and control animals were fixed by perfusion at measured pulmonary arterial mean blood pressure, and fifth-generation resistance vessels were studied. The medial width/external diameter ratio was significantly increased in the study vs the control lungs due to increased smooth muscle and decreased external diameter. In addition, study fetuses had acute degenerative myocardial changes in the tricuspid valve papillary muscles, the right ventricular free wall and the interventricular septum. Similar changes were not seen in control fetuses. Indomethacin administration during pregnancy causes constriction of the fetal ductus arteriosus, fetal pulmonary arterial hypertension, and right ventricular damage. If severe, this may cause rapid fetal death. If less severe, in the newborn infant, this mechanism may be one cause of persistent pulmonary hypertension due to vasoconstriction and increased pulmonary arterial smooth muscle and/or tricuspid insufficiency due to papillary muscle infarction.
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PMID:Hemodynamic, pulmonary vascular, and myocardial abnormalities secondary to pharmacologic constriction of the fetal ductus arteriosus. A possible mechanism for persistent pulmonary hypertension and transient tricuspid insufficiency in the newborn infant. 44 54

The etiology of chronic congestive heart failure (CHF) after repair of tetralogy of Fallot was determined in 102 patients consecutively catheterized 1 to 12 years postoperatively. Chronic CHF was observed in 36/102 patients. The most prevalent abnormality leading to congestive failure (31/36) was a large residual ventricular septal defect alone or in combination with other lesions. All postoperative patients with pulmonary to systemic flow ratios greater than 2:1 (25/102) had congestive failure and evidence of biventricular dysfunction. Significant tricuspid regurgitation (N = 11) and persistent systemic to pulmonary artery shunts (N = 6) contributed to volume overload and congestive failure in the patients with large residual ventricular septal defect. Isolated severe residual right ventricular outflow tract obstruction was a common cause of chronic CHF. Pulmonary artery hypertension was present in 20/36 patients with CHF. The increased pulmonary pressure was not wholly due to an increased pulmonary flow since 7/20 patients had pulmonary vascular resistance greater than 3 mm Hg/L/min/m2. Our findings indicate that persistent or chronic congestive heart failure in postoperative tetralogy of Fallot patients requires bilateral cardiac catherterization since an identifiable and surgically correctable lesion is nearly always present.
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PMID:Chronic congestive heart failure after repair of tetralogy of Fallot. 87 25

This is a report of the echocardiographic findings in a 9-year-old white female with primary pulmonary arterial hypertension confirmed by catheterization and later at autopsy. The reported findings of an absent "a" wave, a flat diastolic E to F slope, and a midsystolic closure of the pulmonic valve were observed. In addition, tricuspid valve prolapse was noted. Prolapse of the tricuspid valve may be part of the mechanism of tricuspid insufficiency in a patient with pulmonary hypertension.
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PMID:Echocardiographic findings in a patient with primary pulmonary hypertension. 126 Aug 55

In order to evaluate the usefulness of echocardiography in detection and characterization of pulmonary arterial hypertension (PAH) in scleroderma patients, we performed M-mode, two-dimensional, and Doppler echocardiography in 71 patients with progressive systemic sclerosis (PSS) and related syndromes: mixed connective tissue disease (MCTD) and overlap syndromes. We estimated systolic pressure gradients across the tricuspid valve from the peak velocity of tricuspid regurgitation (TR) by color-flow guided continuous wave Doppler. TR velocities of analyzable quality for gradient estimation were obtained in 28 patients (39%), of whom 12 showed PAH (peak TR velocity > or = 2.5 m/sec). In comparison, analyzable TR was recorded in 19 (35%) of 55 patients with left-sided cardiac disease. None of the 12 with Doppler-estimated PAH showed left ventricular dilatation or decreased fractional shortening by M-mode and two-dimensional measurements. Nonsimultaneous cardiac catheterization confirmed PAH in 8 of 9 with Doppler-estimated PAH and in 3 of 12 without analyzable TR who had hemodynamic study. Doppler-estimated right ventricular systolic pressures (RVSP) correlated well with catheterization-measured pulmonary arterial systolic pressures (PASP) (< 0.01). Our results indicate that Doppler echocardiography is useful in detecting subclinical PAH and estimating PASP in patients with collagen vascular disease. The results of pulmonary function studies suggest that PAH in MCTD is mainly caused by pulmonary vasculopathy.
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PMID:Echocardiographic evaluation of pulmonary arterial hypertension in patients with progressive systemic sclerosis and related syndromes. 143 24

Between 1974 and 1990, 58 patients underwent tricuspid valve replacement with porcine bioprostheses (Hancock 42, Carpentier-Edwards 16) during multiple valve replacement (double, 21; triple, 37). Perioperative mortality was 12%; 16 patients died later, mostly from cardiac causes. Actuarial survival (1 patient lost to follow-up) was 81% +/- 11% at 5 years, and 60 +/- 17% at 10 years. Reoperation because of Hancock prosthesis deterioration was performed in 2 patients at 11 and 15 years, respectively. At last follow-up (mean 108 +/- 48 months), 82% of survivors (28/34) were functionally improved. Doppler echocardiography was performed in 29 patients in February 1991. In 21 patients, after 88 +/- 40 months of follow-up, the bioprosthesis was normal, there was no leaflet malformation, no significant tricuspid regurgitation and the mean diastolic transprosthetic gradient (DTPG) was 3.8 +/- 1.7 mmHg. In 7 patients (follow-up: 129 +/- 40 months, P less than 0.05), there was moderate dysfunction (all Hancock prostheses) with leaflet sclerosis, tricuspid regurgitation grade 2, and mean DTPG 5.7 +/- 1.8 mmHg (P less than 0.05). Only 1 patient (Hancock prosthesis implanted in 1981) had severe tricuspid prosthesis stenosis with very thickened leaflets and mean DTPG 13 mmHg. Pulmonary artery hypertension (most often fixed) was present in 11 patients, associated with a poor functional result and a significantly higher DTPG. We conclude that porcine bioprostheses in tricuspid position have an acceptable long-term durability and satisfactory performance. Prosthetic dysfunction correlates with the length of follow-up of patients and with the presence of fixed pulmonary artery hypertension.
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PMID:Long-term results of porcine bioprostheses in the tricuspid position. 161 May 94

An 18-year-old black woman presented with marginally compensated right heart failure, severe pulmonary hypertension, tricuspid incompetence, and right atrial myxoma. Catheterization suggested a substantial reactive component to her P-HTN, especially to nifedipine. Initial management consisted of excision of two right atrial myxomas and tricuspid annuloplasty, and postdischarge management with nifedipine, 30 mg four times daily. Emergency pulmonary thromboendarterectomy was required two weeks later for acute cor pulmonale. It is suggested that concomitant procedures are mandatory in this setting because of the otherwise accelerated adverse pathophysiology of obliterative pulmonary vascular obstructive disease.
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PMID:Long-term severe pulmonary hypertension associated with right atrial myxoma. 162 75

We report the case of a six-day-old male infant exposed in utero to a prostaglandin synthetase inhibitor, who presented pulmonary arterial hypertension, tricuspid insufficiency, and electrocardiographic signs of diffuse myocardial ischemia. The necropsy showed organizing infarction of the anterior and posterior right papillary muscles (probably occurred in utero) with complete rupture of the former, besides abnormal muscularization of the intraacinar pulmonary arterioles (persistent fetal circulation of the newborn). The authors suggest a possible relation between the myocardial ischemic and pulmonary hypertensive lesions since the prostaglandin synthetase inhibitor can induce precocious pulmonary arteriolar muscularization and constriction of the arterial duct, leading to right ventricular overload, thus facilitating the occurrence of papillary and subendocardial ischemia.
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PMID:Post-ischemic rupture of the anterior papillary muscle of the right ventricle associated with persistent pulmonary hypertension of the newborn: a case report. 162 31

Certain clinical and morphologic findings are described in 67 patients (aged 23 to 76 years [mean 52]; 55 women [82%]) who had mitral valve replacement for mitral stenosis (with or without associated regurgitation), and simultaneous tricuspid valve replacement for pure tricuspid regurgitation (58 patients) or tricuspid stenosis (all with associated regurgitation; 9 patients). Of the 58 patients with pure tricuspid regurgitation, 21 had anatomically normal and 37 had anatomically abnormal (diffusely fibrotic leaflets) tricuspid valves. Among these 58 patients, no clinical or hemodynamic variable was useful before surgery in distinguishing the group without from that with anatomically abnormal tricuspid valves. All 9 patients with stenotic tricuspid valves had anatomically abnormal tricuspid valves. The latter group had a lower average right ventricular systolic pressure (tricuspid valve closing pressure) than those with pure tricuspid regurgitation, and none had severe pulmonary arterial hypertension (present in 20 [30%] of the 58 patients with pure tricuspid regurgitation).
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PMID:Clinical and anatomic observations in patients having mitral valve replacement for mitral stenosis and simultaneous tricuspid valve replacement. 195 Nov 27


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