What is your diagnosis? Tricuspid valve stenosis (TS).
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Authors report the results of prospective and longitudinal study. The aims of this study were to evaluate among 35 patients, prevalence, diagnosis and treatment aspects of tricuspid stenosis (TS), as well as evolution and pronostical factors. The prevalence of TS was about 4.2%. The main clinical signs were: dyspnoea (94.2%), jugular veinus pulses (42.8%), superior cave syndrom (68.8%), diastolic rumble (74.3%). ECG showed sinus rhythm (51.4%), a right atrial hypertrophy (48.5%). Echocardiography showed tricuspid leaflets thickened (82.8%), a right atrial hypertrophy (48.5%), a mean gradient between right atrial and right ventricle: 8.6 +/- 3.14 mmHg (65.7%) and mean tricuspid area about 1.41 +/- 0.83 cm2 (continuous equation); about 1.74 +/- 1.29 cm2 (Hatle formula) and 1.11 0.84 cm2 (simplified Hatle formula). Aetiology was only rheumatic fever. After a follow-up of 8.53 +/- 6.06 months, the mortality rate was 28.5%. Complications were irreducible heart failure (24 cases), liver failure (2 cases) and stroke (3 cases). Factors associated with mortality were: severity of tricuspid stenosis and pulmonary hypertension, importance of dyspnea and heart failure (p < 0.041).
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Malignant disease is present in the pericardium of 1.5% to 20.6% of patients dying of malignant diseases as was examined postmortem. We present a case of a 57-year-old man with a history of Hodgkin's disease and a sarcoma of gluteus who presented with tachypnea, generalized weakness, and anasarca for 7 days. The echocardiogram revealed the presence of a significant pericardial thickening and localized pericardial effusion resulting from a tricuspid stenosis. A right anterior thoracotomy was performed, and a pericardiectomy (4 x 4 cm) was done. The histologic examination of the pericardium revealed the presence of a metastatic dissemination from a sarcoma. The cause for the clinical presentation and the treatment of malignant pericardial disease are discussed.
A patient developed acute, severe hemodynamic deterioration five days after an aortic valve replacement. Cardiac catheterization revealed a markedly elevated right atrial pressure but a normal right ventricular end-diastolic pressure. Angiography revealed an extrinsic mass causing compression of the right atrium and the tricuspid anulus. A large clot overlying the right atrium and ventricle was found at emergency surgery. Postoperative cardiac tamponade may result in an atypical hemodynamic presentation when there is selective compression of one chamber or of a valve anulus.
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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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Anatomic and functional features of the normal and abnormal mitral valve are reviewed. Of 1,010 personally studied necropsy patients with severe (functional class III or IV, New York Heart Association) cardiac dysfunction from primary valvular heart disease, 434 (43%) had mitral stenosis (MS) with or without mitral regurgitation (MR): unassociated with aortic valve stenosis or regurgitation or with tricuspid valve stenosis in 189 (44%) patients, and associated with aortic stenosis in 152 (35%), with pure (no element of stenosis) aortic regurgitation in 65 (15%) patients, and with tricuspid valve stenosis with or without aortic valve stenosis in 28 (6%) patients. The origin of MS was rheumatic in all 434 patients. Of the 1,010 necropsy patients, 165 (16%) had pure MR (papillary muscle dysfunction excluded): unassociated with aortic valve stenosis or regurgitation or with tricuspid valve stenosis in 97 (59%) patients, and associated with pure aortic regurgitation in 45 (27%) and with aortic valve stenosis in 23 (14%) patients. When associated with dysfunction of the aortic valve, pure MR was usually rheumatic in origin, but when unassociated with aortic valve dysfunction it was usually nonrheumatic in origin. Review of operatively excised mitral valves in patients with pure MR unassociated with aortic valve dysfunction disclosed mitral valve prolapse (most likely an inherent congenital defect) as the most common cause of MR. Excluding the patients with MR from coronary heart disease (papillary muscle dysfunction), mitral prolapse was the cause of MR in 60 (88%) of the other 68 patients, and a rheumatic origin was responsible in only 3 of the 68 patients, all 68 of whom were greater than 30 years of age. Mitral anular calcification in persons aged greater than 65 years is usually associated with calcific deposits in the aortic valve cusps and in the coronary arteries. Because calcium in each of these 3 sites is common in older individuals residing in the Western World, it is most reasonable to view mitral anular calcification in older individuals as a manifestation of atherosclerosis. Mitral anular calcium appears to be extremely uncommon in persons with total serum cholesterol levels less than 150 mg/dl. Mitral anular calcium may produce mild MR and, if the deposits are heavy enough, MS.
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