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This study clarified the clinical profile and echocardiographic findings of severe idiopathic tricuspid regurgitation (TR). Among 8,538 consecutive ultrasonic examinations, a total of 63 patients had severe TR, which was depicted by color flow mapping as a regurgitant signal more than 4 cm from the tricuspid valve orifice. Thirteen of the 63 patients had no underlying diseases, and these patients with severe idiopathic TR were the subjects of the present study. All 13 patients were over 66 years of age (mean 77.3 +/- 5.6 years old) and had had episodes of right heart failure which responded effectively to diuretics. All 13 patients had atrial fibrillation. Using two-dimensional echocardiography, thickening (77%), prolapse (69%) and malaligned coaptation (54%) of the tricuspid valves were observed. The tricuspid annular diameters, cross-sectional areas of the right and left atria and the right ventricular end-diastolic dimensions were significantly greater than those of the age-and-gender-matched lone atrial fibrillation group and the normal control group (p less than 0.01). The left ventricular dimension and ejection fraction did not differ from those of the matched lone atrial fibrillation group. Other valvular regurgitations were also detected (AR 77%, MR 100%, PR 69%), but the degrees of regurgitation were minimal. We proposed severe TR with tricuspid annular dilatation, right atrial and right ventricular dilatation observed in the aged as a distinct cardiac disease entity.
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PMID:[Clinical evaluation of severe idiopathic tricuspid regurgitation]. 213 28

The clinical and echocardiographic features of right atrial thrombi were examined in 9 patients, 5 men and 4 women aged 16 to 86 years. The 2D echocardiographic diagnosis was confirmed at autopsy (4 cases) or by the association of severe recurrent pulmonary embolism (5 cases). Three patients had associated ischaemic heart disease and on patient had dilated cardiomyopathy. The clinical presentation was: acute cor pulmonale (5 cases including 2 patients which biventricular myocardial infarction), chronic post-embolic cor pulmonale (1 case), tricuspid valve obstruction (1 case), general ill health with pyrexia (1 case) and heparin-induced thrombocytopenia (1 case). Predisposing factors included: absence of anticoagulent therapy (7 cases), previous supraventricular arrhythmias (2 cases) and right ventricular failure (6 cases, including 2 of right ventricular infarction). In 2 patients the thrombi were relatively immobile and had a wide base of implantation on the interatrial septum; in 1 patient, multiple thrombi were observed lining the right heart cavities from the inferior vena cava to the pulmonary infundibulum. In the other 6 patients, the thrombi were very mobile with a visible pedicule of implantation (2 cases) or totally free (4 cases). The variable polylobulated appearances, completely irregular whirling motion and intermittent prolapse into the tricuspid valve were characteristic features of the latter 4 cases. They disappeared spontaneously (2 cases) or after fibrinolytic therapy (2 cases) in under 36 hours. Three patients were operated with one postoperative death. The global hospital mortality was 22%. The present occasional detection of right atrial thrombosis will certainly become more common if patients with pulmonary embolism, right ventricular infarction or deep venous thrombosis are systematically examined by 2D echocardiography in the acute phase of their illness.
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PMID:[Clinical, echocardiographic and evolutive aspects of right atrial thrombosis]. 308 12

Double-chambered right ventricle is an uncommon congenital anomaly consisting of obstruction of the trabecular zone of the ventricle by an elevated, hypertrophied moderator band, with or without additional muscle bundles(s). During an 18 month period (August 1984 to February 1986) 12 patients underwent repair of double-chambered right ventricle. Their ages ranged from 13 months to 12 years (mean 4.4 years). Associated lesions were ventricular septal defect in 11 patients (three closed spontaneously), atrial septal defect in two, left superior vena cava in three, aortic valve prolapse in one, and mild subaortic stenosis in two. Right ventricular outflow tract gradients were from 30 to 165 mm Hg (mean 77.2 +/- 37.3 mm Hg). The initial six patients (Group 1) were treated in the "classical" manner with a right ventriculotomy for muscle resection and ventricular septal defect closure (4/6). All patients survived. Five of the six required pharmacologic support for signs of mild to moderate right ventricular failure. The right ventricular outflow tract gradient postoperatively was 0 mm Hg in five patients and 25 mm Hg in one patient. Oxygen saturations were checked in the right atrium and pulmonary artery in all six patients, and one patient had a step-up of more than 10%. In the next six patients (Group 2) a previously unreported right atrial-pulmonary artery approach was used to avoid a ventriculotomy. The right ventricular outflow tract gradient was 0 mm Hg in five patients and 5 mm Hg in the sixth. A ventricular septal defect was closed in four of the six patients. There were no deaths, and no patient required inotropic support. Follow-up has been from 2 to 20 months. There have been no late deaths, and all patients are asymptomatic. One patient in Group 1 still has signs of a residual ventricular septal defect at 1 year. No patient has echocardiographic evidence of right ventricular outflow tract obstruction. All patients have remained in sinus rhythm with right bundle branch block. No patient has been recatheterized. Repair of double-chambered right ventricle is easily performed without a ventriculotomy. The atrial exposure of the ventricular septal defect is excellent. The muscle bundle(s) can be visualized easily through an initial transverse pulmonary arteriotomy with completion of resection through the tricuspid valve.
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PMID:Surgical repair of double-chambered right ventricle with or without ventriculotomy. 382 Nov 48

In six patients with clinically unsuspected right atrial thromboemboli the diagnosis was made with two-dimensional echocardiography. Five patients had pulmonary emboli, and one had systemic embolization. Three patients had congestive cardiomyopathy, two with tricuspid regurgitation; of the remaining three, one had cor pulmonale complicated by tricuspid regurgitation, one had thrombophlebitis and one had no discernible cardiac illness. Four patients had dizziness or syncope, four had dyspnea, three had chest pain, three had hypotension and tow had cyanosis. Five patients were treated with thrombolytic or anticoagulant therapy, or a combination of the two. In three patients, surgical removal of the thrombus was undertaken because of recurrent pulmonary emboli or tricuspid regurgitation, or both, and progressive right heart failure. The thromboemboli were removed in all three, but one patient died. On two-dimensional echocardiography, four of the six patients' thromboemboli were snake-like, unattached to the right atrium and prolapsed freely across the tricuspid valve into the right ventricle in diastole and back into the right atrium in systole. The other two patients' thromboemboli were attached to the right atrium and did not prolapse across the tricuspid valve. Our cases, together with a review of other reports, suggest that right atrial thromboemboli: 1) can be accurately diagnosed by two-dimensional echocardiography; and 2) result from two different pathophysiologic mechanisms developing a) in situ, either on a foreign body or secondary to reduced cardiac output, or b) as a result of an embolus from systemic vein thromboses.
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PMID:Right atrial thromboemboli: clinical, echocardiographic and pathophysiologic manifestations. 649 Oct 71

Although myasthenia gravis (MG) is frequently mentioned in standard textbooks and journal articles as a rare cause for pulmonary hypertension and right heart failure, no case can actually be found in the literature. The case described in this report is the first documented case of chronically decompensated MG manifesting itself as pulmonary hypertension, severe right heart failure, and functional prolapse of both the mitral and tricuspid valves. Interestingly, no hepatic biochemical abnormalities were present in spite of significant congestive hepatomegaly.
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PMID:Rare cardiopulmonary complications of chronically decompensated myasthenia gravis. 742 Apr 43

A 70-year-old woman who had fatiguability due to right heart failure seven years after receiving blunt chest trauma in a road traffic accident presented to our hospital. Preoperative echocardiography revealed severe tricuspid regurgitation resulting from prolapse of the anterior leaflet. The valve was repaired by chordal replacement with expanded polytetrafluoroethylene sutures and DeVega annuloplasty. At three months after surgery, the patient is in good clinical condition, and repeat echocardiography revealed only mild tricuspid regurgitation.
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PMID:Valve repair with chordal replacement for traumatic tricuspid regurgitation. 942 37

A 66-year-old male was brought to our hospital following a car accident. He had subarachnoid hemorrhage, multiple rib fractures, and left hemopneumothorax. He was referred to the Cardiology Department for elevated troponin levels (42 ng/ml, reference 0-1 ng/ml). The electrocardiogram was free of ischemia, whereas the transthoracic echocardiography revealed dilated right heart chambers, enlarged tricuspid annulus and coaptation failure of the tricuspid valvular leaflets. There was rupture on the subvalvular apparatus of the anterior leaflet of the tricuspid valve with accompanying prolapse, causing severe tricuspid valvular regurgitation. The patient did not present right ventricular failure signs and symptoms; he was referred to surgery after the resolution of associated thoracic and cranial injuries.
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PMID:Posttraumatic tricuspid valve injury and severe tricuspid valve regurgitation. 2421 91

A 66-year-old woman who had myasthenia gravis (MG) admitted for type II respiratory failure and right heart failure. Although she had neither ptosis, eye movement disorder, nor diplopia, she had orbital muscles weakness, reduction of gag reflex, dysarthria, dysphagia, and mild proximal muscle weakness. Blood tests showed anti-striated muscle antibodies (anti-titin antibody and anti-Kv1.4 antibody). A muscle biopsy of the left biceps showed a marked variation in fiber size, mild mononuclear cell infiltration was seen surrounding blood vessels in perimysium and nemaline bodies in some fibers. Immunohistochemical stains showed many muscle fibers express HLA-ABC. The patient was diagnosed as sporadic late-onset nemaline myopathy (SLONM) with MG, and treated by tacrolimus. After treatment, her respiratory function gradually improved and she discharged. In the case of atypical MG, measurement of anti-striated muscle antibody or muscle biopsy should be considered.
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PMID:[A case of sporadic late-onset nemaline myopathy associated with myasthenia gravis positive for anti-titin antibody and anti-Kv1.4 antibody]. 3253 68