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

Patients with rheumatic mitral stenosis often have no pulmonary oedema despite considerably increased pulmonary venous pressure. Pulmonary microvascular permeability was measured non-invasively by a previously validated method of double isotope scintigraphy with indium-113m and technetium-99m. This permits calculation of an index reflecting transferrin efflux and thus, indirectly, the microvascular permeability. Fifteen patients with severe mitral stenosis (defined as valve area less than 1.0 cm2) were compared with a control group of 11 patients with mild coronary artery disease. The permeability index was significantly lower in patients with mitral stenosis than in the control group. Furthermore, the extent of reduction of the permeability index correlated with the severity of mitral stenosis as reflected by the Gorlin valve area. This finding may account for the relative resistance of these patients to pulmonary oedema despite chronic pulmonary venous hypertension.
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PMID:Pulmonary microvascular permeability in patients with severe mitral stenosis. 186 52

Small and large airways narrow in LVF and the term cardiac asthma is often used. However, current usage of this term is inconsistent and its meaning is therefore ambiguous. The term is better avoided despite several emerging similarities with bronchial asthma. Airway narrowing may be precipitated by acute elevation of pulmonary or bronchial vascular pressures. This appears to be mainly due to reflex bronchoconstriction. The afferents of this reflex are C-fibers with their endings in the lung parenchyma, bronchi, and pulmonary blood vessels and RAR in the larger airways, and they run in the vagus nerves, as do the efferent bronchoconstrictor fibers. Chronic elevation of pulmonary vascular pressures, as in mitral stenosis, are also associated with airway narrowing. Pulmonary edema (in the absence of vascular hypertension) also causes reflex bronchoconstriction. Bronchial responsiveness to bronchoconstrictor drugs is increased in LVF, partly, at least, due to reflex mechanisms. Bronchial mucosal swelling may also contribute. Narrowing by nonreflex mechanisms definitely occurs and there is direct evidence that decreased lung volume caused by pulmonary edema may cause this. There is little evidence for bronchial narrowing due to the mechanical effect of peribronchial edema, or by swelling of the bronchial mucosa. However, edema foam may terminally cause grave obstruction. Patients with LVF are commonly treated with bronchodilator drugs, but the basis for this approach needs further clarification.
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PMID:Airway obstruction and bronchial hyperresponsiveness in left ventricular failure and mitral stenosis. 192 73

The authors studied the bronchoscopic appearance of bronchial mucosa's vessel contour in pulmonary venous hypertension in 20 patients with mitral stenosis and in 20 with cardiomyopathy and/or aortic vitium. The submucous venous congestion was scored on the base of its extent and severity according to Ohmichi. They have observed a linear relation between the PPA (wedge) and PPA values in patients with mitral stenosis and the total scores indicatory of submucous venous congestion. The mean total scores of patients with mitral stenosis as well as cardiomyopathic patients showing volume-loading of the pulmonary circuit and/or aortic vitium differed to the benefit of the former. Mucosa's vessel contour of grade 3 was found in 12 patients with mitral stenosis and only in 4 cases of cardiomyopathy and/or aortic vitium, so that is more characteristic of mitral stenosis. In spite of this, condition of patients with cardiomyopathy and/or aortic vitium are considered more severe on the base of NYHA values. Taking both patient populations into consideration relation between NYHA-phase and the degree of total scores could not have been proved. Venous congestion on lower part of the left main bronchus was observed in every patient. Appearance of congestive bronchial mucosa has not occurred in pure precapillary pulmonary hypertension.
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PMID:[Bronchoscopic appearance of the bronchial mucosa in pulmonary venous hypertension]. 194 61

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

Plasma atrial natriuretic peptide (ANP), cyclic guanosine monophosphate (GMP) and renin activity (PRA) were measured in 13 patients with mitral stenosis 24 h before and 48 h after balloon valvotomy resulting in a fall in LA pressure from 23.4 +/- 2.2 to 10.5 +/- 0.8 mmHg (P less than 0.01). Before treatment, plasma ANP was higher during ambulation (128.1 +/- 18.5 pg ml-1) than in the supine posture (93.3 +/- 15.0 pg ml-1; P less than 0.01) and did not diminish after return to the erect posture (86.4 +/- 14.1 pg ml-1). A physiological response was restored after valvotomy with ANP plasma levels of 49.2 +/- 7.8 pg ml-1 in the initial ambulant period, 63.1 +/- 12.6 pg ml-1 in the supine posture and 44.6 +/- 8.7 pg ml-1 in the final erect posture. Postural variations of cyclic GMP were parallel to those of ANP. In contrast, LA hypertension did not abolish PRA postural response. During the three successive periods of ambulation, supine posture and erect posture PRA was 5.4 +/- 1.0, 2.8 +/- 0.6 and 5.5 +/- 1.2 ng h-1 ml-1, respectively, before treatment, whereas after treatment the values measured were 10.3 +/- 2.9, 2.3 +/- 0.7 and 7.0 +/- 2.5 ng h-1 ml-1 respectively. Variations of plasma ANP, cyclic GMP and PRA in response to postural changes were also studied in 10 healthy volunteers and in 12 uraemic patients with high plasma ANP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic peptide response to postural changes in patients with left atrial hypertension. 196 7

Clinical, hemodynamic and operative findings of 125 children, up to the age of 12 years, were analysed to determine if the severity of pulmonary venous and arterial hypertension correlated with the severity of rheumatic mitral stenosis. Moderately severe to severe pulmonary venous and arterial hypertension was found in almost three-quarters of the patients. Operative findings indicated critical mitral stenosis in 69% of the cases. In India, following rheumatic fever, some patients follow an unusually rapid course in developing mitral stenosis severe enough to require operative treatment, even at the age of six years.
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PMID:Severity of rheumatic mitral stenosis in children. 174 1

Sneddon's syndrome consists of livedo reticularis and cerebral vascular accidents with no evidence of systemic disease responsible for the livedo. The syndrome has been assimilated to a subgroup of systemic lupus erythematosus (SLE) with presence of antibodies directed against phospholipids. Recently, a significant increase in the frequency of cardiac valve diseases has been demonstrated in some SLE patients with livedo reticularis, cerebral vascular accidents and antiphospholipid antibodies. We report the case of a 26-year old woman who had been presenting for 6 years with idiopathic livedo reticularis. Her history was remarkable for the occurrence of 2 cerebral ischaemic accidents at the ages of 23 and 26 years, generalized convulsive seizures at 22 years, and hypertension of pregnancy with 2 miscarriages. Biopsy of the livedo showed normal histological patterns, but electron microscopy detected an obliterating endothelial proliferation and endothelial cells with numerous Weibel-Palade bodies. Laboratory signs of SLE, as well as antiphospholipid antibodies were absent. At the age of 26 years, cardiac abnormalities were heard at auscultation for the first time, and echocardiography showed that they were due to a fairly loose mitral stenosis. According to Burton's criteria our patient had all the typical features of Sneddon's syndrome. The finding of mitral stenosis--an emboligenic cardiopathy that is potentially responsible for cerebral vascular accidents--raises the problem of its relationship with Sneddon's syndrome. The association does not seem to be fortuitous, since our case is very similar to the cases of SLE or antiphospholipid antibody syndrome associated with cardiac valve lesions. However, this case is particular in that 6 years after the onset of the disease there was still no sign of SLE and of antiphospholipid antibodies.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Livedo reticularis, cerebrovascular disorders and mitral disease: a new cause of Sneddon's syndrome?]. 208 86

The atrial natriuretic factor (ANF) is a hormone whose effects and mode of secretion have been determined. But its exact role in the regulation of volemia in comparison with that of the renin-angiotensin system is still to be defined. Studies of human diseases associated with an increase of ANF plasma concentration may help reach this goal. The mechanisms resulting in elevated ANF plasma concentrations (increase of secretion, decrease of catabolism of the hormone) and the effects of these high levels of ANF on renal functions and circulation are analysed in chronic cardiac failure, mitral stenosis, pulmonary artery hypertension, acute tachycardias, chronic and acute renal failures and in the course of cardiac transplantation. The therapeutic usefulness of drugs inhibiting ANF catabolism (blockers of the clearance receptors for ANF and inhibitors of the enzymes degrading ANF) is also considered.
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PMID:[Atrial natriuretic factor. Role in the physiopathology of cardiac and renal diseases]. 213 35

Right ventricular function was studied in 9 patients with mitral valve stenosis who underwent mitral valve replacement (St. Jude Medical valve 29-31 mm) (MVR). The right ventricular systolic pressure/end-systolic volume index (RVSP/ESVI) correlated well with right ventricular ejection fraction (RVEF) in the normal control group thus it considered to be a index of right ventricular contractility. At rest, RVEF in the MVR group was significantly lower than that in the control group. However there was no difference in the RVSP/ESVI between both groups. In the MVR group, the total pulmonary resistance index (TPRI) and mean pulmonary arterial pressure (mPAP) were higher than those in the control group. During exercise, the RVSP/ESVI became higher in both groups, but RVEF did not increase in the MVR group. In the control group, RVEF became higher during exercise. In addition, TPRI and mPAP increased in the MVR group but the control group did not show significant changes during exercise. In conclusion, low RVEF after MVR, which reflects pump function of the right ventricle, was not caused by contractile dysfunction of the right ventricle but mainly by excess afterload due to irreversible pulmonary vascular resistance persisting after operation as a result of chronic pulmonary vascular hypertension.
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PMID:[Right ventricular dysfunction of mitral valve stenosis]. 221 74

30 patients (24 fm, 6 m) with angiographically proven mitral stenosis as well as 10 healthy controls were investigated by wedge catheterism and thallium-201-scintigraphy to calculate the heart-lung quotient of the isotope. All patients with mitral stenosis could be discriminated from controls by a pathological increase of isotope concentration in the lungs. 4 groups could be subdivided: the first consisted of 8 patients with normal pulmonary artery pressure of x = 13.06 mm Hg and a normal heart-lung quotient less than 1.1. The second group of 15 patients showed passive pulmonary hypertension with a PAm of x = 27.57 mm Hg and heart-lung quotients between 1.1 and 1.4. A third group of 9 patients showed PAm of 36.76 mm Hg with reactive hypertension and a HLQ between 1.4 and 1.6. The last group of patients showed pulmonary hypertension of x = 45 mmHgPAm and a heart-lung quotient of greater than 1.6. Scintigraphy alone allowed classification of the patients, so the value of this method is proven for pre- and postoperative strategy.
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PMID:[Scintigraphic quantification of pulmonary pressure increase in mitral valve stenoses based thallium uptake by the lung]. 232 33


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