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1/30. Isolated tricuspid valve regurgitation resulting from severe annular dilatation: case report.

    A rare case of isolated tricuspid regurgitation (TR) in a 65-year-old man is presented. echocardiography revealed enlargement of the right atrium, dilatation of the tricuspid valve annulus without thickening or prolapse of the leaflets, and an intact atrial septum. No downward displacement of the tricuspid septal leaflet was observed by echocardiography. Mild mitral regurgitation and severe TR were detected on color flow Doppler studies. cardiac catheterization indicated elevated right atrial pressure, with a pronounced V-wave. No left-to-right shunt was detected at the right atrium. At surgery, severe annular dilatation of the tricuspid valve (without organically diseased or deformed tricuspid leaflets) was observed, and tricuspid annuloplasty with a prosthetic ring performed. Postoperative echocardiography and right ventriculography showed trivial TR.
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2/30. Surgical treatment of tricuspid regurgitation caused by Loffler's endocarditis.

    A 25-year-old man with a history of bone-marrow-transplantation for the treatment of Loffler's endocarditis underwent surgery for massive tricuspid regurgitation with paroxysmal atrial flutter. Dense fibrosis in the right ventricular endocardium with complete obliteration of the apex was seen intraoperatively, and the right ventricular cavity was diminished. Annular dilatation of the tricuspid valve and entrapment of the posterior leaflet to the endocardial fibrosis were also seen. Annuloplication at the posterior leaflet was performed. In addition, the right atrial free wall was widely resected and the septal and inferior vena cava-tricuspid valve isthmi were cryoablated for the treatment of atrial flutter. Postoperative catheterization revealed rather high right ventricular end-diastolic pressure. However, tricuspid regurgitation disappeared with the increased cardiac output. atrial flutter could not be induced by repetitive stimulation in the postoperative electrophysiological examination.
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3/30. Idiopathic annular dilation: a rare cause of isolated severe tricuspid regurgitation.

    The management of patients with severe tricuspid regurgitation (TR) requires the clinician to clarify the mechanism of regurgitation. Primary disorders of the tricuspid valve, either congenital or acquired, may be readily identified by echocardiography. Severe TR most often results from left-sided heart disease and secondary pulmonary hypertension. Cardiomyopathic processes may also cause right ventricular failure and functional TR. We report three patients with severe TR due to idiopathic annular dilation. The tricuspid valves were otherwise normal on surgical inspection, and the pulmonary pressures were not significantly elevated. Each patient was aged over 65 years and had chronic atrial fibrillation with preserved left ventricular systolic function. Surgical treatment was associated with marked clinical improvement. Clinicians should recognize this unusual but treatable cause of right-sided congestive heart failure.
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4/30. Pulsation, systolic thrill and murmur in femoral veins secondary to severe tricuspid regurgitation.

    We report on a case of pulsatile femoral veins with a systolic thrill and murmur in a 26-year-old patient who exhibited severe tricuspid regurgitation. The pulsatile nature of the veins may result from the 'ventricularization' of venous pressure with each pressure pulse. The observed systolic thrill and murmur may be due to the systolic reversal of substantial regurgitant flow in the venous system of the lower limbs. This case also demonstrates that severe tricuspid regurgitation can have far-reaching manifestations.
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5/30. Platypnea-orthodeoxia in a patient with ostium primum atrial septal defect with normal right heart pressures.

    We describe an adult patient with an ostium primum atrial septal defect (ASD) and a patent foramen ovale (PFO) with normal right heart pressures who presented with platypnea and orthodeoxia. A dilated aortic root encroaching into the region of the ASD and PFO, along with a tricuspid regurgitant jet moving into the left atrium through the ASD found on the transesophageal echocardiogram may have been responsible for orthodeoxia. Surgical closure of these defects resulted in the disappearance of both platypnea and orthodeoxia.
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6/30. Arterial switch operation after Mustard procedures in adult patients with transposition of the great arteries: is it time to revise our strategy?

    BACKGROUND: After the Mustard or Senning procedure, adults with transposition of the great arteries may have right ventricular failure and require consideration of new therapies. A 2-stage arterial switch operation (ASO) may be performed as an alternative to heart transplantation. This procedure is relatively successful in children, but little is known about the 2-stage ASO in adults. We report our experience in adults undergoing pulmonary arterial banding as the first stage of a planned 2-stage arterial switch procedure after a failed Mustard operation. methods AND RESULTS: Three adult patients with systemic right ventricular failure late after Mustard procedures embarked, through pulmonary artery banding, on a course toward a 2-stage arterial switch at the Toronto General Hospital. Baseline clinical characteristics as well as preoperative hemodynamics were reviewed. Immediate perioperative and postoperative events, hemodynamic measurements, and clinical outcomes were also recorded. Two patients were banded acutely such that their morphologic left ventricular to right ventricular (LV/RV) systolic pressure ratios were >0.65 after the initial banding procedure. The subpulmonary left ventricle failed in both cases. In contrast, the third patient had a more gradual approach to pulmonary artery banding (PAB), with an initial LV/RV pressure ratio of 0.5, which eventually led to a successful conversion to an arterial switch procedure. CONCLUSIONS: Our evidence suggests that in adult patients expected to undergo a 2-stage arterial switch procedure after a failed Mustard operation, acute PAB achieving near-systemic subpulmonary LV pressure leads rapidly to ventricular failure and failure of this treatment strategy. A more gradual approach to PAB may be required to achieve a successful outcome.
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7/30. Tricuspid valve repair in a case with congenital absence of left thoracic pericardium.

    We present a case of severe tricuspid valve insufficiency because of disruption of the anterior tricuspid leaflet with congenital absence of left thoracic pericardium. Findings suggest that tricuspid valve disruption was a result of distorted right ventricular geometry because of luxation of the heart into left thoracic cavity. Tricuspid valve could be repaired by reinsertion of anterior tricuspid leaflet and De-Vega annuloplasty. Normal hemodynamic was obtained and weaning from cardio pulmonary bypass was possible by lifting the heart in orthotopic position using increased positive end expiratory pressure. Postoperative course was uneventful.
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8/30. Traumatic tricuspid regurgitation resulting in protein-losing enteropathy: a case report.

    Protein-losing enteropathy (PLE) with hypoproteinemia is an uncommon but serious complication of congestive heart failure. Reports of patients with PLE resulting from severe tricuspid regurgitation (TR) caused by trauma are rare. A 66-year-old male diabetic patient had a chest contusion as a result of a road traffic accident, and one year later suffered from progressively generalized edema. Examination revealed severe TR with a high central venous pressure and PLE with serum protein deficiency. Treatment with albumin administration and diuretic therapy proved ineffective, and consequently the TR was corrected by valve replacement. Postoperatively, the serum protein level gradually returned to normal. Surgical intervention successfully improved this patient with severe TR and PLE resistant to medical treatment.
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9/30. Stenting of a stenotic aortic homograft in pulmonary position after the Ross procedure.

    Pulmonary autograft replacement of the aortic valve (Ross procedure) has potential advantages, with favorable rates of survival and freedom from reoperation. The procedure itself, however, involves insertion of a homograft in the pulmonary position. The development of severe homograft stenosis is an uncommon but clinically important complication. We report the case of a young female who developed a symptomatic homograft stenosis a year after she underwent the Ross procedure. The lesion was stented successfully and the homograft's patency, together with a markedly improved pressure gradient, was still maintained eight months after percutaneous stenting.
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10/30. Tricuspid valve malfunction and ventricular pacemaker lead: case report and review of the literature.

    Pacemaker implantation can be associated with several complications, including myocardial perforation with or without pericardial effusion, venous thrombosis, vegetations of the tricuspid valve (TV) or pacing lead, and tricuspid regurgitation (TR). The TR is thought to be derived from deformity or perforation of the TV by the pacing lead or secondary to atrioventricular discordance with asynchronous ventricular pacing. Severe TR can be deleterious to the patient because it raises the central venous pressure by increasing the right sided preload. Chronically, the increase in right sided blood volume can result in an increase in the right atrial pressure leading to a decrease in venous return and low cardiac output. Severe TR from leaflet adhesion to the pacemaker lead has not been reported before. With the aging of the population and the expanding use of pacemakers and implantable cardioverter defibrillators (ICD) in clinical practice, this complication may be seen more frequently. We present a patient diagnosed with severe TR, years after his pacemaker implantation. His TR was thought to be caused by adhesion of the tricuspid valve to his pacemaker lead.
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