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At least 1,441 records · Page 80Linked to original sources
PubMed1991

[Percutaneous valvuloplasty: a decade of continuous progress].

Percutaneous balloon valvuloplasty is an interventional procedure designed to treat valve stenosis. The indications, techniques and results depend on the valve being opened. It is currently the treatment of choice for pulmonary valve stenosis. It is an excellent alternative to surgery for mitral stenosis in patients with mobile valves and little abnormality of the subvalvular apparatus. In aortic stenosis it constitutes a gratifying palliative procedure in older patients at high surgical risk. Longer observation is needed to better appreciate the results and indications of balloon valvuloplasty.

Aortic Valve Stenosis↗
PubMed2004

Connexin 43 expression and distribution in compensated and decompensated cardiac hypertrophy in patients with aortic stenosis.

OBJECTIVES: Gap junctions (GJ) are important determinants of conduction. In advanced heart failure alterations of the major ventricular GJ protein, connexin 43 (Cx43) are found. However, changes in Cx43 expression during the progression from compensated cardiac hypertrophy to heart failure, especially in humans, have not been studied extensively. The aim of the present study was to investigate changes in Cx43 expression and distribution in compensated and decompensated left ventricular (LV) hypertrophy in pressure-overloaded human hearts with valvular aortic stenosis (AS). METHODS: We measured Cx43 levels by Western blot and quantitative immunoconfocal microscopy of LV septum biopsies from three groups of patients with AS (group I (n=9): ejection fraction (EF)>50%; group II (n=12): EF 30-50%; group III (n=9): EF<30%). LV biopsies from six patients with mitral valve stenosis and two donor hearts served as controls. RESULTS: Only the early phase of LV hypertrophy (AS-I) was characterized by extensive Cx43 lateral staining. As compared to controls, the AS-I group showed a 44.3% increase in Cx43 protein, which was reflected in an augmented number of GJs per 100 microm(2) intercalated disc area (control: 62.5+/-6.4 vs. AS-I: 79.8+/-4, p<0.001) and an increased GJ surface density (control: 0.00547 vs. AS-I: 0.00724 microm(2)/microm(3), p<0.01). Decompensated LV hypertrophy (AS-III) was specified by reduced percentage of the Cx43 signal per myocyte area (control: 1.74% vs. AS-III: 1.31%, p<0.01) or per intercalated disc (control: 18.3% vs. AS-III: 11.3%, p<0.005). Mean GJ area and GJ number per intercalated discs in the AS-III group were decreased significantly by, respectively, 42.5% and 36.4% as compared to control. In addition, decompensated LV myocardium showed a markedly heterogeneous spatial distribution of Cx43. CONCLUSION: The quantity and spatial distribution of Cx43 differs markedly between compensated and decompensated LV hypertrophy in human patients with AS. Upregulation of Cx43 in compensated hypertrophy may represent the immediate adaptive response to increased load, whereas diminished and heterogeneous Cx43 distribution in decompensated hypertrophy may play maladaptive roles culminating in heart failure and ventricular arrhythmias.

Aged↗
PubMed1983

Severe tricuspid valve stenosis. A cause of silent mitral stenosis.

The diastolic rumbling murmur of mitral stenosis (MS) may be attenuated in the presence of low cardiac output, right ventricular enlargement, Lutembacher's syndrome, pulmonary emphysema, and obesity. In this report we would like to stress that the presence of tricuspid stenosis (TS) is an additional significant cause of silent MS. The clinical material consisted of 73 patients with rheumatic TS who had undergone cardiac surgery. Five of these cases had clinical findings of TS without auscultatory findings of MS. They were found to have severe MS at the time of operation and to require mitral valve surgery. At cardiac catheterization the mean diastolic gradient (MDG) across the mitral valve (MV) was less than 3 mmHg and pulmonary arterial systolic pressure was 29-42 mmHg. The MDG across the tricuspid valve was 6-17 mmHg. In conclusion, TS can mask clinical and hemodynamic findings of MS. The reason for this is the mechanical barrier imposed by TS proximal to the MV.

Adolescent↗
PubMed1993

Aortic/mitral obstruction and coarctation of the aorta.

The prevalence, anatomy and physiology, clinical manifestations, laboratory findings, and management of patients with aortic/mitral obstruction and coarctation of the aorta are assessed. Subaortic stenosis reviewed includes discreet membranous and tunnel subaortic stenosis as well as hypertrophic obstructive cardiomyopathy. The discussion of valvular aortic stenosis includes both congenital and acquired forms of the disease. Supravalvular aortic stenosis is described along with coarctation of the aorta. Mitral valvular stenosis includes the congenital as well as acquired variety with focus on the congenital lesion. Current opinion regarding the medical, the cardiac catheterization, interventional, and the surgical approaches to therapy is presented.

Aortic Coarctation↗