Secondary Tricuspid Regurgitation Research Articles

Right Ventricular Remodeling and Dysfunction With Subsequent Annular Dilatation and Tethering as a Mechanism of Isolated Tricuspid Regurgitation

Secondary tricuspid regurgitation (TR) as a result of pulmonary hypertension and/or left-sided heart disease is caused by tricuspid valve (TV) annular dilatation and tethering of the tricuspid leaflet after right ventricular (RV) dilatation. However, the mechanism of isolated TR without significant pulmonary hypertension remains unknown. The present study investigated the RV function and TV deformations in patients with isolated TR to find out the mechanism and etiology of the disease. Twelve patients with isolated, severe TR were included. RV area, volume, ejection fraction (EF), tenting distance and tenting area were measured. These parameters were compared with 12 age-and gender-matched controls and 12 patients with secondary TR. The cause of isolated TR was incomplete coaptation associated with annular dilatation without other problems. Compared with the controls, RV end-diastolic volumes and annular diameters were significantly larger and RVEF was significantly lower in patients with isolated TR. Tenting area and tenting distance were also significantly higher. However, there were no significant differences in these parameters between patients with isolated and secondary TR. Isolated TR was associated with RV remodeling, systolic dysfunction and resultant annular dilatation and tethering of tricuspid leaflets.

Incidence and Predictors of Late Secondary Tricuspid Regurgitation after Mitral Valve Replacement

Incidence and Predictors of Late Secondary Tricuspid Regurgitation after Mitral Valve Replacement

Secondary Tricuspid Regurgitation or Dilatation: Which Should Be the Criteria for Surgical Repair?

Secondary tricuspid dilatation may or not be accompanied by tricuspid regurgitation (TR). Tricuspid dilatation can be objectively measured whereas TR can vary according to the preload, afterload, and right ventricular function. The purpose of this prospective study was to determine whether surgical repair of the tricuspid valve based on tricuspid dilatation rather than TR could lead to potential benefits. Between 1989 and 2001, 311 patients underwent mitral valve repair (MVR). The tricuspid valve was examined in each patient. Tricuspid annuloplasty was performed only if the tricuspid annular diameter was greater than twice the normal size (> or = 70 mm) regardless of the grade of regurgitation. Patients in group 1 (163 patients; 52.4%) received MVR alone. Patients in group 2 (148 patients; 47.6%) received MVR plus tricuspid annuloplasty. Although not significant there was a difference with regard to hospital mortality (group 1 = 1.8%, group 2 = 0.7%) and actuarial survival rate (Kaplan-Meier: group 1 = 97.3%, 96.2%, and 85.5%; group 2 = 98.5%, 98.5%, and 90.3% at 3, 5, and 10 years, respectively). The New York Heart Association (NYHA) functional class was significantly improved in group 2 (group 1 = 1.59 +/- 0.84; group 2 = 1.11 +/- 0.31; p1). TR increased by more than two grades in 48% of the patients in group 1 and in only 2% of the patients in group 2 (p < 0.001). Remodeling annuloplasty of the tricuspid valve based on tricuspid dilation improves functional status irrespective of the grade of regurgitation. Considerable tricuspid dilatation can be present even in the absence of substantial TR. Tricuspid dilatation is an ongoing disease process that will, with time, lead to severe TR.

Secondary mitral and tricuspid regurgitation accompanying left ventricular systolic dysfunction: Is it important, and how is it treated?

Am Heart J 2002;144:373-6.

Tricuspid valve repair with the Cosgrove-Edwards annuloplasty system: early clinical and echocardiographic results

Background. The use of flexible rings for tricuspid valve repair is becoming popular. The purpose of this study was to evaluate the Cosgrove-Edwards annuloplasty system for tricuspid regurgitation. Methods. From June 1998 to December 2000, 22 patients with significant secondary tricuspid regurgitation underwent tricuspid valve repair with the Cosgrove-Edwards annuloplasty system. All patients had disease of left-sided heart valves in addition to tricuspid disease; 34 concomitant procedures were performed. Twenty-one patients (95.5%) were in preoperative New York Heart Association functional class 3 or 4. The mean follow-up was 19.9 ± 9.7 months. Results. There were two in-hospital nonvalve-related cardiac deaths (9.1%) and one noncardiac death after discharge (4.5%). All survivors were in New York Heart Association functional class 1 or 2; their tricuspid regurgitation was well controlled within grade 1+ and there was a significant reduction of systolic pulmonary artery pressure. Five (83.3%) of the 6 survivors with preoperative pulmonary hypertension had no or trivial residual tricuspid regurgitation. Conclusions. The Cosgrove-Edwards annuloplasty system is very effective in the treatment of secondary tricuspid regurgitation, also in the presence of pulmonary hypertension.

Long-term follow-up after carpentier-Edwards ring annuloplasty for tricuspid regurgitation

Background. Use of flexible rings for tricuspid ring annuloplasty is becoming popular. This study was undertaken to evaluate Carpentier-Edwards (C-E) rigid ring annuloplasty for tricuspid regurgitation (TR), secondary to mitral valve disease and clinical outcome on a long-term basis. Methods. From December 1985 to March 1996, 45 patients with secondary TR underwent C-E ring annuloplasty. Thirty-nine patients (95.1%) were in New York Heart Association (NYHA) functional class III or IV. The mean follow-up was 96.7 ± 48.5 months or 362.6 patient-years. Results. There were three in-hospital and nine late deaths that were not related to tricuspid annuloplasty. Actuarial survival at 10 years was 68.3%. Echocardiographic studies showed that TR was well controlled within grade 2+ in all survivors. Residual pulmonary hypertension (PH) was recognized in 9 of 21 patients (42.9%) with preoperative PH, however, no TR was seen in 6 patients. A TR grade of 2+ was observed in 3 patients. Thirty of the total survivors (96.8%) were in NYHA class I and II, but 1 patient was in NYHA class III. The actuarial rate of freedom from tricuspid valve reoperation after 10 years was 97.5%. Conclusions. C-E ring annuloplasty is acceptable for repair of secondary TR and improvement in clinical status on a long-term basis.

Technical Considerations and Intermediate-Term Results with Modified Devega Tricuspid Annuloplasty

Because of unsatisfactory long-term results with current DeVega tricuspid annuloplasty, 43 patients with secondary tricuspid regurgitation associated with mitral disease were treated with a modified DeVega operation. This procedure continues the suture line to the tendon of Todaro, resulting in almost circumferential traction of the tricuspid annulus. The suture is tied securely around a 29-mm or 31-mm (for women and men, respectively) ball-shaped obturator. Atrioventricular block was not observed. One patient died during the early postoperative period. During a mean(s.d.) follow-up of 5.0(2.0) years, one patient died from causes unrelated to tricuspid regurgitation 2 years after surgery. The mean(s.d.) functional class (New York Heart Association) was 3.1(0.5) on admission and improved to 1.2(0.4) at the end of follow-up. The mean(s.d.) cardiothoracic ratio improved from 67(6) to 60(5)% at 1 month after operation and was 59(5)% at the final examination. Preoperative Doppler echocardiography revealed a mean(s.d.) regurgitation grade of 2.7(0.7). (Grades 1-4 are equivalent to mild, moderate, severe and massive regurgitation, respectively.) At 1 month, regurgitation was corrected almost completely in all patients (grade 0.2(0.4)) and remained significantly improved at follow-up (grade 0.5(0.6)). The actuarial freedom rate at 5 years for moderate or severe regurgitation (> grade 2) was 93%. This modification of the DeVega technique substantially improved early and late tricuspid valve competence.

Are hepatic pulsations in dilated cardiomyopathy with heart failure due to tricuspid regurgitation?

Hepatic pulsations are important clinical manifestations of many cardiac disease states associated with severe systemic venous congestion. These hepatic pulsations are related to transmission of dominant right atrial a or v waves to the liver. For example, systolic pulsations of the liver in patients with primary severe tricuspid regurgitation are due to transmission of a prominent right atrial v wave. 1 Presystolic pulsations are due to transmission of a prominent right atrial a wave, seen in patients with tricuspid stenosis, constrictive pericarditis, restrictive cardiomyopathy and pulmonary hypertension. 2 In patients with dilated cardiomyopathy who present with biventricular failure, a pulsatile liver is generally taken as a sign of secondary tricuspid regurgitation, indicating advanced heart failure. The original description of this clinical finding is difficult to pinpoint, but it is taught to medical students and housestaff, and is mentioned in most comprehensive cardiology texts. 2 This study was prompted by the unexpected observation of a pulsatile liver due to a-wave transmission, as assessed with Doppler studies of hepatic venous flow, in a 59-year-old patient with dilated cardiomyopathy being considered for heart transplantation. After this finding in a selected patient, we conducted this prospective study in patients with dilated cardiomyopathy and biventricular failure to assess specifically the frequency of a- versus v-wave transmission to the liver causing clinically detected hepatic pulsations.

Factors influencing the efficacy of DeVega's annuloplasty for secondary tricuspid regurgitation.

DeVega's annuloplasty was performed on 41 patients with tricuspid regurgitation (TR) associated with combined valvular disease and results were assessed based on Doppler echocardiographic findings in an attempt to examine the applicability of this surgical technique. TR was quantitatively evaluated via Doppler echocardiography before and after surgery. Clinical symptoms, cardiac function, and surgical results were assessed, and the severity of left ventricular myocardial degeneration was determined using electron microscopy. There were no differences in the following factors between the TR recurrence and TR improvement groups: previous heart surgery, number of involved valves, presence or absence of a giant left atrium, preoperative New York Heart Association (NYHA) functional class, and type of prosthetic valve (Björk-Shiley vs. St. Jude Medical). We found no differences between these two groups in TR severity and tricuspid annulus diameter measured during surgery. Severity of myocardial degeneration was closely associated with the recurrence of TR. Clinically, most had diminished cardiac function before surgery. DeVega's technique appears to be remarkably effective in patients with well-preserved myocardium because no TR recurrence was detected even in examinations with the most accurate Doppler echocardiography. However, such long-term effectiveness of DeVega's technique cannot be expected in patients with degenerated myocardium.

The Mechanisms and Importance of Tricuspid Regurgitation and Hepatic Pulsations in Dilated Cardiomyopathy: A Review

Secondary tricuspid regurgitation is a common finding in dilated cardiomyopathy, being present in up to 90% of patients studied with Doppler echocardiography. It appears to be primarily due to annular dilatation and loss of the sphincter-like action of the tricuspid annulus during systole. Apical displacement of the papillary muscle and increased chordal tension may also contribute to mal-coaptation of the tricuspid leaflets in systole. Hepatic pulsations generally occur late in dilated cardiomyopathy, indicating hepatic congestion due to progressive biventricular failure. These are thought to result from secondary tricuspid regurgitation and transmission of the regurgitant v wave to the liver. Careful pulsed-Doppler studies of the timing of hepatic pulsations in dilated cardiomyopathy often show them to be presystolic, rather than systolic, suggesting that a mechanism other than tricuspid regurgitation may be responsible. (ECHOCARDIOGRAPHY, Volume 8, March 1991)

Tricuspid valve honk due to pulmonary hypertension secondary to left atrial myxoma

Atricuspid “honk” is a rare and fascinating auscultatory phenomenon that has been heard in patients with congestive cardiomyopathy, 1 a right-sided cardiac pacemaker catheter, 2 tricuspid valve prolapse, 3 cor pulmonale 4 and mitral stenosis with pulmonary hypertension. 5 We report a patient in whom a tricuspid honk was due to a left atrial myxoma causing severe pulmonary hypertension and secondary tricuspid regurgitation.

二次的三尖弁閉鎖不全症の治療とその術後成績 強縫縮ＤｅＶｅｇａ法，術中ＴＲ評価は可能か？

二次的三尖弁閉鎖不全症の治療とその術後成績 強縫縮ＤｅＶｅｇａ法，術中ＴＲ評価は可能か？

二次性三尖弁閉鎖不全症の右室圧 容積関係からみた右室機能の評価ならびに三尖弁弁輪形成術の術後遠隔予後との関連について

二次性三尖弁閉鎖不全症の右室圧 容積関係からみた右室機能の評価ならびに三尖弁弁輪形成術の術後遠隔予後との関連について

A case of primary endocardial fibroelastosis in the left and right side of the heart with associated secondary mitral and tricuspid regurgitation

A case of primary endocardial fibroelastosis in the left and right side of the heart with associated secondary mitral and tricuspid regurgitation

二次的三せん弁閉鎖不全に対するＣａｒｐｅｎｔｉｅｒ ｒｉｎｇによる三せん弁輪形成術の効果

二次的三せん弁閉鎖不全に対するＣａｒｐｅｎｔｉｅｒ ｒｉｎｇによる三せん弁輪形成術の効果

Clinical study on the abnormal flow patterns in Ebstein's anomaly using pulsed Doppler echocardiography.

Pulsed Doppler echocardiography (PDE) was performed in 10 patients with Ebstein's anomaly and 10 cases of tricuspid regurgitation secondary to mitral stenosis. Distal atrialized right ventricle (ATRV): In all patients with Ebstein's anomaly, tricuspid regurgitation flow was recognized by PDE. In this lesion with moderate tricuspid regurgitation, a widely dispersed dot pattern was recorded during systole However, in the cases with severe tricuspid regurgitation a relatively smooth dot pattern was recognized. In the case with marked delay in pressure rise in the right ventricle, PDE showed a bimodal regurgitant flow pattern. The interval between the onset of QRS and that of tricuspid regurgitant flow with right ventricular pressure rise was measured. The interval corrected for heart rate ranged from 0.10 to 0.35 with an average of 0.19 +/- 0.08 sec. In the subjects with secondary tricuspid regurgitation, it ranged from 0.07 to 0.11 sec. This interval was significantly prolonged in Ebstein's anomaly as compared to that in secondary tricuspid regurgitation (p less than 0.001). Proximal ATRV: Tricuspid regurgitant flow was detected in 6 to 10 patients with Ebstein's anomaly. The disturbed flow was less apparent in the proximal ATRV than in the distal ATRV.

Echocardiography: Clinical application in combined mitral stenosis and mitral régurgitation ∗

The echocardiogram was typically abnormal in patients with mitral valve disease. In the patient with combined mitral stenosis and mitral regurgitation, when the slope of the E wave was generally less than 50 mm./sec., dominant mitral obstruction and mild mitral reflux was diagnosed by left heart catheterization and cineradiography. When the slope was generally greater than 60 mm./sec., dominant mitral regurgitation was noted. The slope of the E wave was increased with increasing mitral reflux. Echocardiography was helpful in differentiating the pansystolic murmur of tricuspid regurgitation from mitral regurgitation. The echocardiogram is characteristic for mitral valve obstruction in the patient with severe mitral stenosis and secondary tricuspid regurgitation. In patients with aortic and mitral valve disease, the echocardiogram demonstrated the pathologic findings at the mitral valve. Echocardiography was also helpful in the detection of “silent” mitral stenosis and mitral regurgitation. Also, the systolic murmur of left ventricular outflow tract obstruction was differentiated from mitral regurgitation by echocardiography. In the former the slope was normal, and in patients with mitral reflux the slope was characteristically abnormal. The size of the cardiac chambers was determined by the “A” presentation. Right ventricular enlargement was suggested by the increased distance from the anterior chest wall to the most anterior portion of the mitral valve and left ventricular enlargement by an increased distance from the chest wall to the posterior wall.

Simultaneous Repair of Mitral and Tricuspid Valves Through Right Atrium and Interatrial Septum

Secondary tricuspid regurgitation is frequently responsible for serious downgrading of the clinical status of patients whose only primary rheumatic valvular lesion is of the mitral valve. In some instances the signs of tricuspid insufficiency disappear during the period of medical preparation for standard mitral commissurotomy. In others the disturbed dynamics which result from the tricuspid failure cannot be reversed and the patient must be operated upon for the mitral lesion in spite of the defect. If sufficient benefit accrues from the surgery to diminish right-heart work load, the tricuspid ring shrinks as right ventricular distention disappears. Tricuspid valvular sufficiency then results as a more or less delayed benefit of mitral valve commissurotomy or repair. The question arises as to whether repair of the tricuspid regurgitation accomplished at the same time as repair or commissurotomy of the mitral valve would be beneficial in terms of providing more rapid and certain improvement