[Tricuspid regurgitation, tricuspid stenosis, tricuspid atresia].
Explore the source record for details and available documents.
SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Tricuspid valve involvement is not uncommon in patients with rheumatic heart disease and is frequently missed on routine clinical examination. We prospectively studied the echocardiographic profile of tricuspid valve disease in 788 consecutive patients with rheumatic heart disease. Out of these patients 9% (70) had tricuspid valve disease and 55.7% (39) of these were of < or = 20 years of age. Of these 60% were females and 40% were males. Their ages ranged from 9 to 64 years (mean 24.2+/-13.6 years). Of these patients, 50% had tricuspid stenosis with or without tricuspid regurgitation whereas 50% had isolated tricuspid regurgitation. Isolated tricuspid stenosis was present in 7.4% of these cases. All patients had associated mitral stenosis. Severe mitral stenosis was present more commonly in patients with juvenile tricuspid stenosis compared to older patients (94.1% vs. 55.6%, P<0.005). Mitral regurgitation was present more commonly in juvenile age group patients compared to older patients (53.8% vs. 25.8%, P<0.01). A combination of mitral, aortic and tricuspid stenosis was present in five cases and four of these were in the juvenile age group. Left ventricular enlargement and dysfunction were present in 28.6 and 14.3% patients, respectively, and the majority of these patients were in the juvenile age group (P<0.05). We conclude that rheumatic tricuspid valve disease occurs early in the course of the disease and progresses faster in India and is always associated with mitral stenosis. Juvenile tricuspid stenosis is more commonly associated with severe mitral stenosis, mitral regurgitation, left ventricular enlargement and dysfunction as compared with older patients.
Explore the source record for details and available documents.
This report concerns a 2-year-old boy who had situs solitus and atrioventricular concordance with double-outlet left ventricle, L-malposition of the aorta, pulmonary stenosis, tricuspid stenosis, hypoplastic right ventricle, ventricular septal defect, and secundum atrial septal defect. These lesions were correctly diagnosed preoperatively, and "correction" was achieved by closing the atrial septal defect and tricuspid valve and performing a Fontan procedure using an antibiotic-sterilized aortic homograft for the conduit. The patient initially did well postoperatively but, despite vigorous diuretic therapy, developed large bilateral pleural effusions necessitating frequent aspiration. He died unexpectedly one month after the operation. Postmortem examination showed the repair to be intact. Despite his death, we are encouraged to consider this operation in such cases in the future.
BACKGROUND: Tricuspid stenosis is a part of the chronically rheumatic heart. Although rare, when tricuspid stenosis does occur, it occurs in the setting of coexistent mitral and aortic valve disease. The natural course of patients with severe tricuspid stenosis is not well defined. The aim of this study is to present close follow-up of patients with chronic rheumatic heart disease and severe tricuspid stenosis. METHODS AND RESULTS: We retrospectively studied 13 patients (11 women and 2 men) with severe tricuspid stenosis who were followed closely for 6 to 31 years. The mean tricuspid pressure gradient ranged from 3 to 9 mm Hg. Twelve patients underwent surgery for mitral and/or aortic valve lesions without complications. Concomitant tricuspid valve surgery was performed on six patients: two De Vega procedures, two Kay plications, and two implantations of Carpentier rings. All these also had leaflet commissurotomy. After surgery, the mean tricuspid gradient decreased in three patients, did not change in two, and increased in one. All 13 patients were treated with diuretics, digoxin, warfarin, and spirinolactone or ACE inhibitors. On their last follow-up visit, every patient had increased jugular venous pressure. Hepatomegaly was found in 6 of 13, leg edema in 4 of 13, and ascites in 1 of 13. CONCLUSIONS: Most tricuspid stenos patients are women with severe mitral and aortic valve disease. After successful repair of the mitral or aortic valve, and regardless of the type of tricuspid valve surgery, severe tricuspid stenosis was found to be very well tolerated by all the patients over many years of follow-up.
Two cases of pulmonary atresia with intact ventricular septum and severe tricuspid stenosis are described in which the initial angiographic diagnosis was tricuspid atresia and pulmonary atresia. Two dimensional echocardiography showed the features of an imperforate tricuspid valve because in each case contrast echocardiography failed to show anterograde flow from the right atrium to right ventricle. Successful radical surgical repair was achieved in one patient with performing a tricuspid valvotomy and inserting an external valved conduit between the hypoplastic right ventricle and the main pulmonary artery. In the second case, an infant died four weeks after tricuspid valvotomy and right ventricular outflow tract reconstruction.
Observations on the atrial systolic murmur, the tricuspid opening snap, and the right atrial pressure pulse of tricuspid stenosis are presented, based on catheter manometer intracardiac sound and pressure recordings in five patients with hemodynamically significant tricuspid stenosis. The manometer-recorded right atrial pressure pulse of tricuspid stenosis differed from the normal, with (1) elevation of right atrial pressure, (2) different morphologic features (tall, spiky A wave complete before C; small V wave with an interruption, the tricuspid opening snap notch at termination of the gradual Y descent; a diastolic plateau, the relatively flat diastolic segment of the right atrial pressure pulse following the tricuspid opening snap notch prior to the next A wave), and (3) the relative lack of right atrial pressure and right atrial pressure pulse response with normal respiration. The atrial systolic murmur, recorded in the right ventricular inflow tract, was complete by S1; the crescendo-decrescendo atrial systolic murmur configuration paralleled the right ventricular-right atrial diastolic pressure gradient at the time of the atrial A wave. The right atrial contraction-relaxation process, as reflected by the right atrial A wave ascent and descent, was complete at the onset of ventricular systole with P-R intervals of 170 to 200 msec. Thus, the timing and configuration of the atrial systolic murmur reflected the timing and completion of the right atrial contraction-relaxation process prior to the onset of right ventricular systole and the configuration of the tricuspid diastolic pressure gradient. The tricuspid opening snap was recorded in the right ventricular inflow tract and occurred at the time of a notch at the termination of the Y descent of the right atrial pressure pulse V wave, while right atrial pressure exceeded right ventricular pressure. The sound-pressure events were consistent with angiographic and echocardiographic studies, which showed doming or ballooning of the mobile, fused, stenotic tricuspid valve into the right ventricle during the Y descent of the right atrial pressure pulse. The tricuspid opening snap occurred at the time of the termination of the diastolic movement of the fused tricuspid unit into the right ventricle. These observations are presented within the framework of previous studies in order to trace the development of medical ideas about the pathophysiologic basis for the sound and pressure events of tricuspid stenosis.
Congenital tricuspid stenosis is an uncommon congenital anomaly and usually associated with other lesions such as severe pulmonic stenosis or atresia. Sometimes, it is difficult to diagnose this malformation non-invasively, but the differential diagnosis from tricuspid atresia is essential for the surgical considerations. Described here were three patients with congenital tricuspid stenosis who were successfully diagnosed by contrast echoangiography using peripheral venous injection of the contrast medium. Contrast echoes appeared in the right atrium initially and then in the right ventricle through the stenotic tricuspid valve. In conclusion, contrast echoangiography is mandatory in the diagnosis of this entity.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Isolated congenital tricuspid valve stenosis is a rare entity. The modalities of definitive treatment have been surgical repair or replacement. We present the first reported patient with congenital tricuspid stenosis successfully treated by percutaneous balloon valvotomy. This appears to be an alternative to surgery when the anatomy, as demonstrated by echocardiography, is suitable.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Two-dimensional echocardiography has proved to be reliable in the diagnosis of mitral, aortic and pulmonary stenosis. Its role in the diagnosis of rheumatic tricuspid stenosis is still being defined; therefore, the tricuspid valve echograms of 147 patients with rheumatic heart disease were examined. Thirty-eight of these patients also underwent hemodynamic evaluation. Tricuspid stenosis was defined echocardiographically as diastolic anterior leaflet doming, thickening and restricted excursion of the other two tricuspid leaflets and decreased separation of the leaflet tips. Using these criteria, the sensitivity and specificity of the echocardiogram in detecting tricuspid stenosis were 69 and 96%, respectively, in the group of 38 patients who had both echocardiographic and hemodynamic evaluations. However, when the smaller group of 17 patients who had simultaneous right atrial and right ventricular pressure recordings were considered separately, there was complete agreement between the echocardiographic and hemodynamic data. Thus, the two-dimensional echocardiogram is a sensitive and specific test for diagnosing rheumatic tricuspid stenosis. In addition, these data provided an opportunity to determine the prevalence of tricuspid stenosis in this group of patients with chronic rheumatic valvular disease. Tricuspid stenosis was present in 14 (9.5%) of the total group of 147 patients who had two-dimensional echocardiograms, and in 10 (26.3%) of the 38 who had both echocardiographic and hemodynamic studies. In patients with rheumatic heart disease about to undergo cardiac catheterization, an echocardiographic study should prove useful in making the diagnosis of tricuspid stenosis.
Explore the source record for details and available documents.
Tricuspid valve dysfunction occurs frequently in patients with rheumatic heart disease and is usually manifested as functional or organic tricuspid regurgitation. Rheumatic tricuspid stenosis is less common and occurs characteristically in the presence of concomitant mitral valve disease. In this report, we describe the clinical and echocardiographic findings in a patient with isolated rheumatic tricuspid stenosis and a right-to-left shunt across the interatrial septum, likely as a result of a patent foramen ovale, resulting in central cyanosis. This case illustrates an interesting association of tricuspid stenosis and an interatrial right-to-left shunt suggestive of a reverse Lutembacher's physiology.