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This three-part article examines the histologic and morphologic basis for stenotic and purely regurgitant tricuspid valves. In Part I, conditions producing tricuspid valve stenosis are reviewed. In over 90% of stenotic tricuspid valves, the etiology is rheumatic disease. In isolated tricuspid stenosis, the etiology is either carcinoid or congenital. Rare causes of tricuspid stenosis include active infective endocarditis, metabolic or enzymatic abnormalities (Fabry's, Whipple's disease), and giant blood cysts.
This three-part article examines the histologic and morphologic basis for stenotic and purely regurgitant tricuspid valves. In Part I, conditions producing tricuspid valve stenosis were reviewed. In Part II, conditions producing pure tricuspid regurgitation are discussed. In contrast to the relatively few causes of tricuspid stenosis, the causes of pure (no element of stenosis) tricuspid regurgitation are multiple. Some of the conditions producing pure regurgitation include floppy tricuspid valves, infective endocarditis, papillary muscle dysfunction, rheumatic disease, and Ebstein's anomaly.
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Explore the source record for details and available documents.
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This three-part article examines the histologic and morphologic basis for stenotic and purely regurgitant tricuspid valves. In Part III, morphometric analysis of tricuspid valve annular circumference, leaflet area, and the product of annular circumference and leaflet area are shown to be useful in establishing etiology for the purely regurgitant tricuspid valves and in assessing the anatomic basis of pure tricuspid regurgitation in the presence of mitral stenosis.
We report the anatomic and hemodynamic details of severe stenosis of a bioprosthetic tricuspid valve studied by transthoracic and transesophageal echocardiography. This patient also had antegrade systolic flow across the tricuspid valve due to a combination of severe tricuspid valve stenosis and poor right ventricular systolic function.
A case of calcified tricuspid valve stenosis resulting from a complication of ventriculoatrial shunt implantation is presented. Tricuspid valve repair or replacement was not possible because of the prohibitive risk of damaging the right atrioventricular junction and conductive pathways. This rare lesion was treated successfully by insertion of an external right atrial-right ventricular valved conduit. The role of echocardiography in the detection of such a lesion is emphasized and the etiologic and therapeutic aspects are discussed.
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.
Congenital tricuspid valve stenosis in the absence of other valvular abnormalities is rare. In this report we describe a patient with congenital tricuspid valve stenosis, ostium secundum atrial septal defect, and electrocardiographic left anterior fascicular block, who presented with paradoxical emboli. This case, as well as previous case reports, suggests that congenital tricuspid stenosis with ostium secundum atrial septal defect is associated with left anterior fascicular block.
Endocardial pacemaker leads may cause tricuspid valve regurgitation, but only four cases of tricuspid stenosis without endocarditis have been reported. A 77-year-old woman had received three endocardial leads when aged 44, 57, and 72 years. One lead pushed up the septal leaflet of the tricuspid valve from below the valve, then adhered to the leaflet, and was positioned against the ventricular septum. Tricuspid valve stenosis and moderate regurgitation were separately detected by transthoracic echocardiography. The tricuspid valve orifice area was 0.93 cm2 at cardiac catheterization. An excessive loop of a ventricular lead, especially a subvalvular loop, can cause opening limitation of the tricuspid valve, and the entangling of the lead in the subvalvular structures can easily induce reactive fibrosis and adhesions.
This report describes the first successful case of tricuspid valve stenosis by percutaneous double balloon valvuloplasty in Mexico. The gradient decreased from 5 to 0 mmHg, with an increase in valve area by echocardiography and improvement of the jugular vein pulse and disappearance of symptoms. The feasibility of the balloon percutaneous valvuloplasty was demonstrated unequivocally.
Tricuspid valve stenosis and occlusion of superior vena cava are severe complications to Port-a-cath. In a child with SLE, symptoms started to develop about five to seven years after Port-a-cath insertion and cyclophosphamid injections. The patient developed hepatomegaly with abdominal and venous distension. Open heart surgery was necessary to remove the catheter. At operation it was found that the catheter was placed adjacent and through the tricuspid valve. The valve was severely stenosed with thrombus formation. The catheter and thrombus were removed, commissurotomy and bicuspidization of the valve and chordeal replacement performed to achieve an acceptable functional result. The superior vena cava was repaired with a pericardial patch. Retrospective analyses of the echocardiograms and chest x-rays show that the catheter was nearly related to the tricuspid valve and with the tip in the right ventricle. In such circumstances it is recommended with early withdrawal of the catheter, and in patients with immunological disease the indwelling time should be considered and limited.
Tricuspid and mitral valve flow area was determined from an apical four-chamber view. Doppler signals were recorded from normal subjects and patients with tricuspid and mitral valve stenosis by using a pulsed Doppler unit. The location of sample volume was chosen at the ventricular side of the valve orifice and within the right ventricular tract. This was done with the aid of an integrated cardiac imaging facility. The analog signal at the output of the Doppler unit was sampled and digitized using an analog/digital interface board and transferred to a personal computer. The data were then analyzed using the Fast Fourier Transform (FTT) and autoregressive (AR) modeling methods of spectral analysis and all the sonograms were obtained. Statistical comparison between the FFT and AR methods was made. The results show that the AR method offers a superior performance over the FFT method as regards the assessment of tricuspid and mitral valve stenosis.
OBJECTIVE: To describe surgical treatment of tricuspid valve stenosis using the Fontan procedure in a young dog. STUDY DESIGN: Case report. SAMPLE POPULATION: One client-owned dog RESULTS: A six month old female Labrador retriever was diagnosed with tricuspid obstruction. The dog had a displaced tricuspid valve and small right ventricle and had progressed to right-sided (backward) cardiac failure. A Fontan procedure (connection of the right atrium to the pulmonary artery with a prosthetic conduit) was performed. Within three days the right atrial pressure had dropped from a preoperative value of 33 mm Hg to 8 mm Hg and the ascites was significantly reduced. The dog died suddenly two months after surgery. Postmortem examination of the heart showed a greatly enlarged right atrium and hypoplastic right ventricle. The tricuspid valve leaflets were fused and displaced ventrally leaving an opening measuring 3x5 mm between the chambers. The conduit was intact with no evidence of leakage or thrombosis. CONCLUSIONS: Palliation of tricuspid stenosis using the Fontan procedure can be performed in dogs. Sudden death may occur and is most likely because of cardiac arrythmias.
The rare congenital anomaly of pulmonary valve stenosis and massive tricuspid valve insufficiency with intact ventricular septum is a lethal condition without reported survival after attempted treatment. In a neonate suffering from this syndrome, the pulmonary valve stenosis was relieved by rupturing the fused valve with a balloon catheter introduced transvenously. The desperate condition of the patient quickly improved after this procedure, with subsequent disappearance of the tricuspid valve incompetence. Balloon rupturing of fused valves at angiography may represent a therapeutic alternative in cases in which surgical valvulotomy is associated with a high mortality.