Although tricuspid insufficiency after chest trauma is

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1 Surgical Treatment of Traumatic Tricuspid Insufficiency: Experience in 13 Cases Wei-Guo Ma, MD, Guo-Hua Luo, MD, Han-Song Sun, MD, Jian-Ping Xu, MD, Sheng-Shou Hu, MD, and Xiao-Dong Zhu, MD Department of Cardiovascular Surgery, Fu Wai Hospital and Cardiovascular Institute, Chinese Academy of Medical Sciences, Beijing, China Background. Traumatic tricuspid insufficiency (TTI) is uncommon and surgical experience is limited. We report our surgical experience with TTI in 13 patients. Methods. From January 2000 through March 2008, we operated on 13 patients with TTI (10 men 3 women; mean age, years). The intervals from trauma to diagnosis and from trauma to surgery averaged 37.4 and 54.4 months, respectively. At operation, the mechanism of TTI was due to anterior chordal rupture in 8, anterior papillary muscle rupture in 3, rupture of anterior papillary muscle and chordae in 1, and anterior leaflet defect in 1. In 7 patients the annulus was dilated. Valve repair was successful in 13 patients. Results. No early or late deaths occurred. Severe hemolysis occurred in 1 patient after tricuspid and mitral valve repairs. At follow-up extending to 9.5 years, 9 patients were in New York Heart Association functional class I, and 4 were in class II. Transthoracic echocardiography demonstrated no or trivial residual regurgitation in 7 patients, mild regurgitation in 4, and mild-to-moderate regurgitation in 2. A significant decrease of the right ventricular end-diastolic dimension ( vs mm; p < 0.001) was observed. The mean transvalvular gradient was mm Hg. Eleven patients were in sinus rhythm. Conclusions. Satisfactory early and midterm outcomes can be achieved for TTI by tricuspid valve repair. Early surgical intervention should be emphasized to achieve good functional results and preserve the right ventricular function. (Ann Thorac Surg 2010;90:1934 8) 2010 by The Society of Thoracic Surgeons Although tricuspid insufficiency after chest trauma is uncommon, it has been reported with an increasing frequency during the past decades, which might in part be ascribed to the increase in the number of traffic accidents, wide spread of better diagnostic procedures such as echocardiography, and a deeper understanding and awareness of this pathology [1, 2]. Nevertheless, the real prevalence of traumatic tricuspid regurgitation is probably underestimated because chronic isolated tricuspid insufficiency is usually well tolerated and most patients experience few or no symptoms early after the trauma [3, 4]. Optimal treatment for this condition ranges from longterm medical therapy to early surgical correction, including valve repair and replacement [5]. In this article we report our experience with surgical treatment of traumatic tricuspid insufficiency in 13 patients between January 2000 and March 2008 and the early and midterm results. Patients and Methods The Ethics Committee of Fu Wai Hospital and Cardiovascular Institute approved this retrospective study and Accepted for publication July 23, Address correspondence to Dr Luo, Department of Cardiovascular Surgery, Fu Wai Hospital, 167 Northern Lishi Rd, Beijing, , China; wgma@yahoo.com. waived the need for individual patient consent for this study. Patients From January 2000 through March 2008, 13 patients (10 men, 3 women) with traumatic tricuspid insufficiency underwent operation at Fu Wai Hospital, Chinese Academy of Medical Sciences in Beijing, China. Their mean age was years (range, 17 to 53 years) and their mean body weight was kg (range, 34 to 92 kg). Table 1 lists their preoperative clinical data. The tricuspid insufficiency was attributed to blunt chest trauma in all patients, including traffic accidents in 9, fall in 2, explosion of a stream boiler in 1, and blow on the chest in 1. The diagnosis of a traumatic cause was based on a history of severe chest trauma combined with one or more operative findings compatible with tricuspid valve trauma, including an avulsed papillary muscle, ruptured chordae tendineae, lacerated valve leaflet(s), and dehiscence of valve leaflet(s) from the annulus. Three patients also had other traumatic cardiac lesions, including 1 each with anterior mitral chordal rupture, anterior mitral valve prolapse, and perforation of the right coronary cusp with left ventricular diverticulum. Early symptoms were exertional dyspnea and fatigue in 9, palpitations in 8, vague chest pain in 7, edema in 2, cough in 1, and dizziness in 1. Physical findings included peripheral edema, hepatic congestion, distention of the external jugular vein, and a loud systolic murmur over 2010 by The Society of Thoracic Surgeons /$36.00 Published by Elsevier Inc doi: /j.athoracsur

2 Ann Thorac Surg MA ET AL 2010;90: SURGERY FOR TRAUMATIC TRICUSPID INSUFFICIENCY 1935 Table 1. Preoperative Clinical Data Patient Profile No. or Mean SD (Range) Sex Male 10 Female 3 Age, y (17 53) Weight, kg (34 92) Duration from trauma, mon To diagnosis 37.4 (15 d 25 y) To operation 54.4 (50 d 25 y) Cause of trauma Traffic accident 9 Fall 2 Explosion 1 Blow on the chest 1 Early symptoms Exertional dyspnea and fatigue 9 Palpitations 8 Vague chest pain 7 Edema 2 Cough 1 Dizziness 1 NYHA functional class I 3 II 4 III 6 Electrocardiogram Sinus rhythm 11 Atrial fibrillation/flutter 2 Right bundle branch conduction 7 delay RV end-diastolic dimension, mm (25 55) Cardiothoracic ratio ( ) NYHA New York Heart Association; RV right ventricle; SD standard deviation. exposed through an oblique right atrial incision. At operation, the mechanism of tricuspid insufficiency was due to anterior chordal rupture in 8, anterior papillary muscle rupture in 3, rupture of anterior papillary muscle and chordae in 1, and defect of the anterior leaflet in 1. The annulus was dilated in 7 patients (Table 2). Tricuspid valve repair was achieved in all patients by using one or more of the following valve repair techniques (Table 2): 1. papillary muscle reimplant to the right ventricular free wall with interposition of a 5-0 polytetrafluoroethylene (PTFE) suture or with a pledgeted 4-0 Prolene suture (Ethicon, Somerville, NJ) in 2; 2. artificial chordae implant using a 5-0 PTFE suture to the right ventricular free wall or the anterior papillary muscle in 4; 3. double orifice technique by anchoring the free edge of the anterior leaflet to the facing edge of the septal leaflet with 2 stitches of pledgetted mattress 5-0 Prolene suture in 4; 4. leaflet plication, in which the leaflet with ruptured chordae tendineae was sewn to the adjacent normal leaflet, in 7; 5. de Vega annuloplasty in 5; 6. implantation of a Carpentier-Edwards annuloplasty ring (Baxter International Inc, Irvine, CA) in 5; 7. Kay s commissuroplasty in 1; and 8. repair by autologous pericardial patch in 1. After reconstruction, the competence of repair was tested by injecting saline solution through a catheter into the right ventricle and confirmed by transesophageal echocardiography after weaning from cardiopulmonary bypass. Additional procedures included mitral valve repair in 1, mitral valve replacement in 1, and closure of the defect in right coronary cusp and left ventricular diverticulum in 1. the left lower sternal border that increased with inspiration. The mean interval between chest trauma and diagnosis of tricuspid insufficiency was 37.4 months (median, 6 months; range, 15 days to 25 years). The mean duration from trauma to surgery was 54.4 months (range, 50 days to 25 years; median, 15 months). Before operation, 11 patients were in sinus rhythm, 1 patient was in atrial fibrillation, and 1 was in atrial flutter. Electrocardiograms showed complete or incomplete conduction delays of the right bundle branch type in 7 patients. The preoperative New York Heart Association functional class was I in 3 patients, II in 4, and III in 6. The preoperative diagnosis of tricuspid regurgitation was made echocardiographically in all patients. Surgical Techniques Operations were performed through a median sternotomy under cardiopulmonary bypass with aortic and bicaval cannulation at moderate hypothermia, with the ascending aorta cross-clamped. The tricuspid valve was Table 2. Operative Findings and Techniques of Tricuspid Valve Repair Findings and Repairs Mechanism of tricuspid regurgitation Anterior chordal rupture 9 Anterior papillary muscle rupture 4 Posterior chordal rupture 2 Anular dilation 7 Anterior leaflet defect 1 Techniques of repair Leaflet plication 7 Polytetrafluoroethylene chordae implant 4 Papillary muscle reimplant 2 De Vega annuloplasty 5 Annuloplasty with Carpentier-Edwards ring 5 Double orifice repair 4 Kay s commissuroplasty 1 Repair by autologous pericardium 1 No.

3 1936 MA ET AL Ann Thorac Surg SURGERY FOR TRAUMATIC TRICUSPID INSUFFICIENCY 2010;90: Follow-Up Before discharge, all patients underwent electrocardiogram, transthoracic echocardiography, and chest roentgenograph evaluation. After discharge, the patients were followed-up by regular outpatient visits, and routine transthoracic echocardiography was performed to evaluate the competence of repair. Statistical Analysis Statistical analysis was performed by using SPSS 11.5 software (SPSS Inc, Chicago, IL). The results are expressed as the mean standard deviation, and 2-tailed paired t test was used to compare continuous variables. Any p value of less than 0.05 was considered statistically significant. Results The cardiopulmonary bypass time averaged minutes (median, 93; range, 60 to 185 minutes) and the mean clamp time was minutes (median, 55; range, 34 to 160 minutes). Intraoperative transesophageal echocardiography showed satisfactory results of reconstruction in all patients (regurgitation less than 2/4 and a transvalvar pressure gradient less than 4 mm Hg). The mean intensive care unit stay was hours (median, 32; range, 14 to 144 hours) and mean time to extubation was hours (median, 12; range 3 to 40 hours). The mean postoperative hospital stay was days (median, 8; range, 6 to 23 days). Before discharge, chest roentgenograph showed a remarkable decrease of the cardiothoracic ratio from preoperatively to postoperatively (p 0.05). All patients survived their operations, and no late death had occurred at the latest follow-up. In the patient who underwent repair of the mitral and tricuspid valves, severe hemolysis occurred at postoperative day 5. Reoperation had to be performed to replace the mitral valve with a 27-mm mechanical valve. The hemolysis resolved after mitral valve replacement, and he was discharged 10 days later uneventfully. At follow-up extending to 9.5 years (median, 6.5; mean, years), 9 patients were in New York Heart Association functional class I, and 4 were in class II. Among the 11 patients who were in sinus rhythm preoperatively, sinus rhythm persisted in 9 patients, and atrial flutter developed in 2 patients postoperatively. In the 2 patients who were in atrial flutter or fibrillation preoperatively, sinus rhythm developed after the operation and persisted at the latest follow-up. Echocardiography showed that all patients had reduction of the tricuspid regurgitation grade (no or trivial regurgitation in 7, mild in 4, and mild-to-moderate in 2) and a significant decrease of the right ventricular end-diastolic dimension from mm preoperatively to mm postoperatively (p 0.001). The mean and peak pressure gradients across the tricuspid valve were mm Hg (range, 1.4 to 3.8 mm Hg) and mm Hg (range, 2.3 to 6.1 mm Hg), respectively. The left ventricular ejection fraction was Comment Although traumatic tricuspid regurgitation after blunt chest trauma was reported by Williams early in 1829 [6], the first surgical correction was performed by Cooley in the late 1950s [7]. Because this condition often progresses slowly and its clinical course is usually subtle [8], patients are often asymptomatic and can tolerate it for a long time [3]; thus, traumatic tricuspid insufficiency was easily neglected or misdiagnosed in the early years [9, 10]. Some patients become cyanotic due to stretching of the right atrium with resultant enlargement of a patent foramen ovale and right-to-left shunt. The finding of cyanosis in combination with cardiomegaly, right heart enlargement, and right bundle branch block may lead to a misdiagnosis as the Ebstein anomaly [9, 11]. However, with an increased clinical awareness of this potential complication after blunt chest trauma and widespread use of echocardiography, traumatic tricuspid insufficiency has been rising in prevalence and is diagnosed much earlier [12 14]. Blunt chest trauma is responsible for 90% of cases [1]. In our series, all cases were ascribed to blunt chest trauma, with traffic accidents being the cause in 9 of 13 (69.2%), and the interval between trauma and diagnosis averaged 37.4 months (range, 15 days to 25 years). Clinically, in patients with a history of severe blunt chest trauma who present with palpitation, dyspnea, and complete or incomplete right bundle branch blockade on electrocardiogram, traumatic tricuspid insufficiency should be highly suspected. Preoperative diagnosis was established in all 13 patients in this series by echocardiography, which not only allows for visualization of valvular and subvalvular structures and evaluation of tricuspid regurgitation but also provides useful information for making surgical decisions [15 17]. In our hospital, we now recommend echocardiography for patients who have sustained severe blunt chest trauma to detect tricuspid insufficiency or myocardial contusion as early as possible. To date, the surgical experience regarding this valve disease is limited to case reports or short series involving less than 25 patients [4], and a sketchy examination of the English literature has revealed approximately 130 cases of traumatic tricuspid insufficiency treated surgically [5, 18 20]. Surgical indications are not clearly defined [21] and depend on the patients symptoms and the type of anatomic lesions [1, 8, 19]. Our experience with surgical treatment of traumatic tricuspid insufficiency dated back to 1969 when the senior author (X.D.Z.) performed a successful repair in a man with traumatic tricuspid regurgitation [personal communication, 2009]. In practice, we prefer valve repair to replacement to avoid the complications inherent in heart valve prosthesis and anticoagulation and have adopted different repair techniques depending on the specific

4 Ann Thorac Surg MA ET AL 2010;90: SURGERY FOR TRAUMATIC TRICUSPID INSUFFICIENCY 1937 valve anatomy and underlying pathology during the operation [5, 22]. In the case of leaflet laceration, an interrupted or running double-headed Prolene suture was used to repair the leaflet directly. For ruptured anterior papillary muscle, a double-headed pledgeted Prolene suture was used to reimplant the papillary muscle in situ. Chordae tendineae rupture is the most common cause in tricuspid injury; in some cases, the ruptured chordae tendineae was affixed on the right ventricular free wall, whereas in other cases, the leaflet with ruptured chordae tendineae was sewn to the neighboring normal leaflet. In 4 patients, the anterior leaflet with ruptured chordae tendineae was anchored to the septal leaflet edge-to-edge (doubleorifice repair) as described by Alfieri and associates [5]. The efficacy of the double orifice was proved by our experience and that of others [23, 24]. Annuloplasty is a critical component of virtually all mitral and tricuspid valve repairs because it can correct annular dilatation, increase leaflet coaptation by decreasing the dimension of the annulus, reduce tension on suture lines, and prevent future annular dilatation [25, 26]. In the 9 patients with annuloplasty in our series, 5 were achieved using the de Vega technique and 4 with a Carpentier-Edwards annuloplasty ring. Our experience also confirmed the excellent long-term results of the simple de Vega annuloplasty [27, 28]. In the review of 74 surgical cases by Alfieri and associates [5], chordal rupture was the most frequent cause of traumatic tricuspid regurgitation, occurring in 41 (55.4%); other causes were papillary muscle rupture in 20 (27%) and leaflet rupture in 11 (14.8%). Nevertheless, it is noteworthy that all patients in this series had anterior leaflet pathology. Anterior chordal rupture was seen in 9 (69.2%) and anterior papillary muscle rupture in 4 (30.8%). This finding corroborates our idea that restoration of the anatomy and function of the anterior leaflet is essential to successful valve repair. To that end, the lesions of the anterior leaflet should be corrected as completely as possible, and the annular size should be reduced properly so that the anterior leaflet could coapt more sufficiently. It is generally believed that the development of moderate-to-severe right heart failure has been the indication for surgical intervention, and if the operation is delayed, the papillary muscles, the chordae tendineae, and the involved leaflet(s) are frequently found in a contracted and atrophic state, precluding valve repair [18]. In 1 patient who was operated on 18 months after the trauma, there was a defect in the anterior leaflet at the anteroseptal commissure, and the leaflet was contracted with thickening and fibrosis; however, there were no such findings in patients with longer intervals between trauma and intervention. We speculate that the contraction and atrophy of valvular and subvalvular tissues is not only associated with the interval from trauma to surgery but is also patient-specific. Nevertheless, patients with moderate regurgitation or more should be operated on as soon as possible. A shorter duration between trauma and operation is advantageous in terms of feasibility of tricuspid valve repair. Although more than half of our patients had delayed operations because of economic reasons or poor medical care conditions, such as postponed referrals, the interval from trauma to surgical repair (mean, 54.4 months; median, 15 months) was still much shorter than the Mayo Clinic series (mean, 16 years; median 17 years) [18]. This is probably one important factor for the higher rate of valve repair in our patients. Despite the small number of patients in this series, the functional benefits of earlier intervention are evident for patients with traumatic tricuspid insufficiency, and surgical repair should be performed as early as possible once the diagnosis is made. Early repair can not only prevent right ventricular dysfunction but also limit right atrial dilatation and thereby increase the likelihood of maintaining or restoring sinus rhythm. In this series, the 2 patients who had preoperative atrial fibrillation or atrial flutter reverted to sinus rhythm postoperatively, with no ablation procedures during the operation. The exact mechanism for this finding is unclear and needs further observation; the conversion to sinus rhythm might result from the decrease of right atrial pressure and from the reduction of right atrial dimensions after successful repair. Although valve repair is generally superior to replacement, especially for children and adolescents in whom normal growth is expected [29], the choice of repair vs replacement is diversified in the literature. In a recent Chinese series, valve replacement had to be done in 5 of 8 patients (62.5%) [30] in contrast to 6 of 33 (18%) from the Mayo Clinic experience [19]. In our series, valve repair was successful in all 13 patients (100%), with satisfactory early and midterm outcomes. The rate of successful repair is comparable to that of Alfieri and associates [5, 20]. In conclusion, our experience shows that a comprehensive use of various tricuspid valve repair techniques can often be performed for traumatic tricuspid insufficiency with low risk, allowing symptomatic relief with excellent midterm outcomes. Early operation should be emphasized to achieve good functional results and preserve the right ventricular function. References 1. Vayre F, Richard P, Ollivier JP. 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