Outcome of surgical treatment of post-traumatic tricuspid insufficiency

Objective: To investigate the optimal time and procedure of surgical treatment of traumatic tricuspid insufficiency. Methods: From May 1984 to September 2004, eight patients underwent operation for traumatic tricuspid valve insufficiency. All patients, male, aged from 7 to 67 years [median: 38 years, mean: (38.5±18.1) years]. The intervals between trauma and operation ranged from 1 month to 20 years [median: 19 months, mean: (52.5± 80.3) months)]. In seven patients, tricuspid insufficiency was attributed to blunt chest trauma including vehicle accident in three patients and the other patient is a stab wound. Diagnosis was confirmed by echocardiography. Pre-operative cardiac functions in patients were classified as New York Heart Association ( NYHA ) classes Ⅱ-Ⅳ. During operation, the anterior leaflet of the tricuspid valve was completely or partially flailed as a result of chordal rupture in all patients. Chordal rupture of septal leaflet was found in one patient. Anterior leaflet was perforated in two patients. Septal leaflet was retracted and adherent to ventricular septum in two patients. Valve repair was intended for all patients. Finally, valve repair was performed successfully in 3 patients and tricuspid replacement was performed in 5 patients. Results: No early or late death occurred. With a follow-up through clinical manifestation and echocardiography for 7-129 months [median; 39 months, mean: (53.4±42.8) months], all patients were classified as NYHA class I, without any changes. Conclusions : The satisfactory treatment of traumatic tricuspid insufficiency can be obtained by surgical treatment. Earlier surgery may increase the feasibility of tricuspid valve repair and prevent the deterioration of right ventricular function.     

Diagnosis and treatment of traumatic tricuspid valve insufficiency

Traumatic tricuspid valve insufficiency (TTVI) is a relatively uncommon disease. To summarize the experience in the diagnosis and treatment of TTVI, we have analyzed the clinical data of 3 patients with TTVI who were admitted to the department of cardiac surgery of our hospital between April 1997 to     

Long-term results of bioprosthetic tricuspid valve replacement: an analysis of 25 years of experience

Background

Current knowledge in long-term results of tricuspid valve replacement is limited. Present study reviews our experience from a consecutive series.

Methods

We retrospectively studied the early and late results of 32 consecutive patients (7 male and 25 female; mean age 60.2 ± 18.1 years) undergoing bioprosthetic tricuspid valve replacement between 1985 and 2010. The etiology is rheumatic in 38 %, congenital in 3 %, endocarditis in 9 %, and functional in 50 %. Patients underwent isolated valve replacement. The remaining underwent combined aortic and tricuspid (n = 5, 16 %), mitral tricuspid (n = 15, 47 %), and aortic, mitral, and tricuspid (n = 1, 3 %) valve replacement. Preoperative liver dysfunction was evaluated using Model for End-stage Liver Disease (MELD) score. Mean follow-up was 5.6 ± 6.8 years (ranging from 0 to 25.0 years).

Results

Hospital mortality was 19 %. On univariate logistic regression analysis, NYHA class IV (p = 0.039, odds ratio 11.3, 95 % confidence interval 1.2–112.5), MELD score (>10) (p = 0.011, odds ratio 21.0, 95 % confidence interval 12.0–222.0) and congestive liver (p = 0.05, odds ratio 9.4, 95 % confidence interval 1.0–93.5) were incremental risk factors for hospital death. The 15- and 25-year actuarial survival were 56.5 ± 10.3 % and 45 ± 13.0 %, respectively. Multivariate analysis using Cox proportional hazard model showed MELD score (p = 0.024, hazard ratio 7.0, 95 % confidence interval 2.1–23.9) and postoperative pulmonary hypertension (p = 0.012, hazard ratio 4.4, 95 % confidence interval 1.4–14.1) were significantly associated with decreased survival. At 15 years, freedom rates from tricuspid valve reoperation, anticoagulation-related bleeding, and valve related events were 85.7 ± 13.2 %,95.7 ± 4.3 % and 81.8 ± 13.2 %, respectively. The linearized incidence of structural valve deterioration was 0.50 %/patient-year, anticoagulation-related bleeding was 0.94 %/patient-year, and valve-related events were 1.52 %/patient-year.

Conclusion

Preoperative hepatic congestion and liver dysfunction which were indicated by the MELD score >10 were associated with poor outcome for patients undergoing tricuspid valve replacement. The MELD score is useful to predict the morality among these patients.     

Biological or mechanical prostheses in tricuspid position? A meta-analysis of intra-institutional results

BACKGROUND: Tricuspid valve replacement (TVR) is an uncommon procedure. The use of biological vs mechanical prostheses in TVR has pros and cons. Therefore, we debate the choice between the different types of valves by means of a meta-analysis of studies of the last decade. METHODS: The heading "tricuspid valve replacement and (bio* or mec*)" was used to retrieve studies from Medline, Current Contents, and Embase. Eight out of 11 studies met the preset strict criteria: intra-institutional comparison of results of biological or mechanical TVR. Survival of hospital-discharged patients was recalculated to reduce the effect of unbalanced perioperative risk factors on overall survival. Hazard ratio was obtained from actuarial survival graphics comparison and at-risk groups, according to the method described by Parmar. If missing, the number of patients at risk was approximated assuming constant and noninformative censoring. Hazard pooling was done according to study heterogeneity. Bioprostheses were assumed as the gold standard and mechanical prostheses assumed as the challenging device. Therefore, a hazard more than 1 pointed to a higher risk of mechanical prostheses. Our 1998 study was updated for this analysis. RESULTS: In this study, 1,160 prostheses and 6,046 follow-up years were analyzed. The pooled survival hazard ratio of mechanical prostheses versus bioprostheses was 1.07 (0.84 to 1.35, p = 0.60). The pooled freedom from reoperation hazard ratio was 1.24 (0.67 to 2.31, p = 0.67). Pooled survival differences were trivial, favoring mechanical prostheses at 1 (-0.04%) and 15 years (-1.1%) and favoring bioprostheses (+1.8%) at 10 years. CONCLUSIONS: There is not a gold standard in tricuspid prostheses replacement. Prosthetic choice is left to the surgeon's clinical judgment, taking into consideration each patient's characteristics and needs.     

Surgical treatment of tricuspid regurgitation caused by Löffler’s endocarditis

A 25-year-old man with a history of bone-marrow-transplantation for the treatment of Löffler’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.     

Is a tricuspid annuloplasty ring significantly better than a De Vega's annuloplasty stitch when repairing severe tricuspid regurgitation?

A best evidence topic in cardiac surgery was written according to a structured protocol. The question addressed was whether tricuspid valve (TV) repair with an annuloplasty ring leads to an improved outcome over a conventional suture annuloplasty for patients with severe tricuspid incompetence. Altogether, 306 papers were found using the reported search, of which 14 presented the best evidence to answer the clinical question. The author, journal, date and country of publication, patient group studied, study type, relevant outcomes, results and study weaknesses of these papers are tabulated. We found seven studies supporting the use of ring annuloplasty over De Vega's suture annuloplasty. Five studies found no significant difference in outcome between the two techniques. We found only two studies supporting the use of De Vega's suture annuloplasty over ring annuloplasty. Therefore, most of the tabulated studies show good evidence in support of ring annuloplasty compared with De Vega's suture repair for treatment of moderate to severe TV regurgitation. One cohort study identified a 20.4% postoperative failure rate for tricuspid regurgitation (TR) repair and concluded non-application of ring as a predictor for reoperation. One cohort study with a mean follow-up of 17 months reported success rates as high as 97% with ring annuloplasty for TV regurgitation. One large cohort study of 2277 patients with TR who had undergone repair reported a sustained reduction in TR and the rate of recurrence in a 5-year echocardiographic follow-up. One cohort study of 129 patients concluded that ring annuloplasty has the lowest rate of recurrence compared with De Vega's suture repair. An old randomized controlled trial (RCT) on the subject also reported a similar result to the mentioned studies. In contrast, we reviewed one recent study and four older studies and found no significant difference between the two techniques. We reviewed one study that reported De Vega's suture repair as a superior technique to ring annuloplasty. We conclude that there is good evidence supporting ring annuloplasty over conventional De Vega's suture annuloplasty.     

Is tricuspid valve replacement a catastrophic operation?

Objective: Tricuspid valve replacement (TVR) has a high postoperative mortality, despite recent advances in perioperative care. We report the results of our experience in TVR with an emphasis on early mortality and morbidity and long-term follow-up. Methods: Between October 1994 and August 2007, 80 consecutive TVRs were performed in 78 patients. The mean age was 48 ± 14 (range: 20–70) years. The underlying disease of the patients was classified as rheumatic (n = 54), congenital (n = 12), endocarditis (n = 10) or degenerative (n = 4). Previous cardiac surgery had been performed in 40 patients (50%). Isolated TVR was performed in 24 patients (30%). Results: Hospital mortality occurred in one patient (1.4%). Postoperative morbidities included intra-aortic balloon pump (n = 5), bleeding re-operation (n = 4), delayed sternal closure (n = 3), acute renal failure (n = 3), subdural haematoma (n = 3), extracorporeal membrane oxygenation (n = 1), mediastinitis (n = 1) and pacemaker insertion (n = 4). In 42 patients, ventilator support was needed for more than 72 h. Based on multivariate analysis, age (p < 0.001) and the cardiopulmonary time (p = 0.004) were the identified risk factors. Follow-up was completed in all patients with a mean duration of 56 ± 37 (range: 0–158) months. During the follow-up period, there were seven deaths (8.8%), including five cardiac deaths. The 5- and 8-year survival rates were 95 ± 3% and 79 ± 9% and event-free survival rates were 76 ± 6% and 61 ± 9%, respectively. Based on multivariate analysis, the only identified predictors of late deaths was a postoperative low cardiac output (p = 0.024). Conclusions: TVR can be performed and low operative mortality can be achieved thorough optimal perioperative management in the current era.     

A case for anatomic correction in atrioventricular discordance? Effects of surgery on tricuspid valve function

OBJECTIVE: To assess tricuspid valve function in atrioventricular discordance after palliative procedures (pulmonary artery banding and Blalock-Taussig shunt) and corrective procedures (anatomic and physiologic repair). METHODS: Tricuspid valve dysfunction was assessed by transthoracic echocardiography and graded as no regurgitation (0), mild (1), moderate (2), and severe (3) before and after palliative and corrective procedures performed in 97 patients with atrioventricular discordance between 1988 and 1999. Thirty-two percent had an isolated ventricular septal defect, 43% had a ventricular septal defect and pulmonary stenosis, and 16% had pulmonary stenosis. Twenty-six patients underwent pulmonary artery banding and 28 had a Blalock-Taussig shunt. Seventy patients underwent physiologic and 19 underwent anatomic repair. Six patients underwent one-ventricle repair. RESULTS: After pulmonary artery banding, the tricuspid regurgitation score decreased from 1.7 +/- 0.8 to 0.9 +/- 0.6 (P <.001). In patients who underwent a Blalock-Taussig shunt, the tricuspid regurgitation score increased from 0.7 +/- 0.5 preoperatively to 1.4 +/- 0.6 postoperatively (P <.001). After physiologic repair, there was no significant change in the tricuspid regurgitation score; however, 7 patients required additional repair or replacement. The regurgitation score was significantly reduced from 1.5 +/- 0.8 to 0.4 +/- 0.5 (P <.001) after anatomic repair. The operative mortality in patients who underwent physiologic repair was 7% as compared with 0% in the anatomic repair group (P =.59). The median follow-up was 3.2 years. CONCLUSIONS: Right ventricular volume loading (shunt) worsens tricuspid regurgitation, whereas volume reduction (banding) or left-to-right septal shift (anatomic repair) has beneficial effects. We have not observed a significant change in the tricuspid regurgitation score after physiologic repair. Anatomic repair can be performed in selected patients with atrioventricular discordance and provides superior functional results.     

Successful management of multiple permanent pacemaker complications – infection, 13 year old silent lead perforation and exteriorisation following failed percutaneous extraction, superior vena cava obstruction, tricuspid valve endocarditis, pulmonary embolism and prosthetic tricuspid valve thrombosis

A 59 year old man underwent mechanical tricuspid valve replacement and removal of pacemaker generator along with 4 pacemaker leads for pacemaker endocarditis and superior vena cava obstruction after an earlier percutaneous extraction had to be abandoned, 13 years ago, due to cardiac arrest, accompanied by silent, unsuspected right atrial perforation and exteriorisation of lead. Postoperative course was complicated by tricuspid valve thrombosis and secondary pulmonary embolism requiring TPA thrombolysis which was instantly successful. A review of literature of pacemaker endocarditis and tricuspid thrombosis along with the relevant management strategies is presented. We believe this case report is unusual on account of non operative management of right atrial lead perforation following an unsuccessful attempt at percutaneous removal of right sided infected pacemaker leads and the incidental discovery of the perforated lead 13 years later at sternotomy, presentation of pacemaker endocarditis with a massive load of vegetations along the entire pacemaker lead tract in superior vena cava, right atrial endocardium, tricuspid valve and right ventricular endocardium, leading to a functional and structural SVC obstruction, requirement of an unusually large dose of warfarin postoperatively occasioned, in all probability, by antibiotic drug interactions, presentation of tricuspid prosthetic valve thrombosis uniquely as vasovagal syncope and isolated hypoxia and near instantaneous resolution of tricuspid prosthetic valve thrombosis with Alteplase thrombolysis.     

Should the tricuspid valve be replaced with a mechanical or biological valve?

A best evidence topic in cardiac surgery was written according to a structured protocol. The question addressed was whether patients requiring tricuspid replacement should have a mechanical or a biological valve. Using the reported search, 561 papers were identified. Thirteen papers represented the best evidence on the subject. The author, journal, date and country of publication, patient group studied, study type, relevant outcomes, weaknesses, results and study comments were tabulated. We conclude that there are no major differences between the insertion of a mechanical or biological tricuspid valve. Aggregating the available data it is found that the reoperation rate is similar with bioprosthetic degeneration rate being equivalent to the mechanical thrombosis rate. Conversely up to 95% of patients with a bioprosthesis still receive anticoagulation. Survival in over 1000 prostheses pooled by meta-analysis was equivalent between biological and mechanical valves.     

Do pulmonary artery catheters cause or increase tricuspid or pulmonic valvular regurgitation?

There are few quantitative data on the extent or mechanism of pulmonary artery catheter (PAC)-induced valvular dysfunction. We hypothesized that PACs cause or worsen tricuspid and pulmonic valvular regurgitation, and tested this hypothesis by using transesophageal echocardiography. In 54 anesthetized adult patients, we measured color Doppler jet areas of tricuspid regurgitation (TR) in two planes (midesophageal [ME] 4-chamber and right ventricular inflow-outflow views) and pulmonic insufficiency (PI) in one plane (ME aortic valve long-axis view), both before and after we advanced a PAC into the pulmonary artery. Regurgitant jet areas and hemodynamic measurements were compared by using paired t-test. There were no significant changes in blood pressure or heart rate after passage of the PAC. After PAC placement, the mean PI jet area was not significantly increased. The mean TR jet area increased significantly in the right ventricular inflow-outflow view (+0.37 +/- 0.11 cm(2)) (P = 0.0014), but did not increase at the ME 4-chamber view. Seventeen percent of patients had an increase in TR jet area > or =1 cm(2); 8% of patients had an increase in PI jet area >/=1 cm(2). IMPLICATIONS: In patients without pulmonic or tricuspid valvular pathology, placement of a pulmonary artery catheter (PAC) worsened tricuspid regurgitation, which is consistently visualized in the right ventricular inflow-outflow view, and often not seen in the midesophageal 4-chamber view. This is consistent with malcoaptation of the anterior and posterior leaflets. PAC-induced pulmonic insufficiency was rarely detected in the midesophageal aortic valve long-axis view. We conclude that a PAC is very unlikely to be the sole cause of severe tricuspid regurgitation or pulmonic insufficiency.