Skip to main content
NCBI home page
Interactive Cardiovascular and Thoracic Surgery logoLink to Interactive Cardiovascular and Thoracic Surgery
. 2012 Mar 28;15(1):102–108. doi: 10.1093/icvts/ivs107

Tricuspid regurgitation after successful mitral valve surgery

Vasiliki Katsi a, Leonidas Raftopoulos b, Constantina Aggeli b, Ioannis Vlasseros a, Ioannis Felekos b,*, Dimitrios Tousoulis b, Christodoulos Stefanadis b, Ioannis Kallikazaros a
PMCID: PMC3380985  PMID: 22457188

Abstract

The tricuspid valve (TV) is inseparably connected with the mitral valve (MV) in terms of function. Any pathophysiological condition concerning the MV is potentially a threat for the normal function of the TV as well. One of the most challenging cases is functional tricuspid regurgitation (TR) after surgical MV correction. In the past, TR was considered to progressively revert with time after left-sided valve restoration. Nevertheless, more recent studies showed that TR could develop and evolve postoperatively over time, as well as being closely associated with a poorer prognosis in terms of morbidity and mortality. Pressure and volume overload are usually the underlying pathophysiological mechanisms; structural alterations, like tricuspid annulus dilatation, increased leaflet tethering and right ventricular remodelling are almost always present when regurgitation develops. The most important risk factors associated with a higher probability of late TR development involve the elderly, female gender, larger left atrial size, atrial fibrillation, right chamber dilatation, higher pulmonary artery systolic pressures, longer times from the onset of MV disease to surgery, history of rheumatic heart disease, ischaemic heart disease and prosthetic valve malfunction. The time of TR manifestation can be up to 10 years or more after an MV surgery. Echocardiography, including the novel 3D Echo techniques, is crucial in the early diagnosis and prognosis of future TV disease development. Appropriate surgical technique and timing still need to be clarified.

Keywords: Functional tricuspid regurgitation, Mitral valve surgery

INTRODUCTION

Tricuspid valve (TV) disease affects ∼0.8% of the general population, and is much more common in certain populations: 35% of heart failure (HF), 30% of severe mitral regurgitation (MR) and up to 50% of mitral valve (MV) surgery patients develop tricuspid regurgitation (TR) to various degrees. TR affects mortality in a significant way, with 1-year survival in patients with absent, mild, moderate and severe TR being ∼91, 90, 70 and 60%, respectively [1].

TR is probably the most common and anticipated complication of left-sided heart valve pathology, especially MV disease. Although the MV is often surgically corrected, either by repair or by replacement with a mechanical or biological prosthetic valve, concomitant management of the regurgitant TV is usually neglected. This is an issue that may be mainly attributed to the fact that there is no clear consensus on the management of patients with concomitant TR.

ECHOCARDIOGRAPHIC ASSESSMENT OF THE TV

The complexity of TV morphology has led to continuous efforts to improve and enhance the various techniques of cardiac valve imaging. Conventional 2D Echo has the inherent limitation of not being able to show all three tricuspid leaflets together in the same view. Thus, the precise evaluation of the whole tricuspid apparatus becomes extremely difficult. On the other hand, real-time 3D Echo (RT-3DE) has the unique capability of obtaining a short-axis plane of the TV, which allows simultaneous visualization of the three leaflets' motion during the cardiac circle and their attachment in the TA (Fig. 1). Furthermore, Anwar et al. [2], comparing conventional 2D Echo imaging and RT-3DE, concluded that RT-3DE is superior in terms of TA imaging, as 2D Echo clearly underestimates TA diameter (30% of the studied patients exhibited an increased TA diameter with 2D Echo vs. 65% with RT-3DE).

Figure 1:

Figure 1:

Open in a new tab

3D imaging of the TV in open (A) and close (B) positions.

One of the most challenging roles of echocardiography is the classification of the TR as mild, moderate or severe. Both conventional 2D Echo techniques and Doppler echocardiography have been the cornerstone of TR degree estimation, since invasive angiographic grading was never embraced as the golden standard (Figs 2–5). 2D Echo imaging can provide valuable information on the actual morphology of the TV and the coaptation depth, which is practically an index of the tethering of the TV leaflets. Doppler imaging, either continuous-waved (CW Doppler) or colour, has been utilized as a qualitative and quantitative method of TR assessment, implementing a variety of signs and indices (Table 1) [3]. Of note, the width of the vena contracta >0.7 cm and systolic flow reversal in hepatic veins are the only criteria suggested by ACC-AHA guidelines for the characterization of TR as severe [4].

Figure 2:

Figure 2:

Open in a new tab

MV replacement (A) without post-surgical MR (B) accompanied by remaining moderate TR (C).

Figure 3:

Figure 3:

Open in a new tab

Moderate MR after aortic valve replacement (A) accompanied by moderate-to-severe TR (B and C).

Figure 4:

Figure 4:

Open in a new tab

Severe rheumatic MR (A) accompanied by small TR (B).

Figure 5:

Figure 5:

Open in a new tab

Moderate functional ischaemic MR in a patient with PH (A) accompanied by moderate TR (B).

Table 1:

Echocardiographic criteria of TR severity

Mode Criteria
2D TTE TA diameter >3.4 cm (measured in diastole)
 Large coaptation defect
Colour Doppler Vena contracta width >0.7 cm (suggested by ACC-AHA guidelines)
Jet area >10 cm2
Systolic flow reversal in hepatic veins (only when sinus rhythm is present (suggested by ACC-AHA guidelines)
aERO >40 mm2
aPISA radius >9 mm 
aRegurgitant volume >45 ml
CW Doppler Signal density
Open in a new tab

aThis parameter is rarely used in clinical practices.

In spite of the plethora of echocardiographic findings associated with TV and TR, numerous studies have stressed the importance of TV morphology on medical practice, mostly regarding the need for TV repair. The average TA diameter in normal individuals is 21 ± 2 mm/m2 of body surface area (BSA), whereas the average TA circumference is 78 ± 7 mm/m2 BSA. The threshold TA diameter beyond which TR may occur is 27 mm/m2 BSA. Performing TA annuloplasty should be based on the extent of TA dilatation rather than the degree of TR: thus improving the long-term outcome [5]. The extent of TA dilatation that should act as threshold for TV repair surgery is reflected by cut-off points of a diameter of >21 mm/m2 or TA fractional shortening of <25% [6].

MECHANISMS OF TR DEVELOPMENT IN MV DISEASE

The pathogenesis of TR in MV disease is complex and multifactorial (Table 2) [7]. Either in organic (rheumatic fever) or in functional TR (ischaemic or cardiomyopathy), the underlying heart disease leads initially to the gradual development of MR. Rheumatic heart disease may also lead to mitral stenosis (MS). Both MR and MS increase left atrial (LA) pressure, which progressively leads to pulmonary hypertension (PH), right ventricular (RV) dysfunction and enlargement, and, ultimately to TR. Furthermore, the increased LA pressure also causes LA dilatation, which is directly associated with atrial fibrillation (AF) and TA dilatation, the latter practically being the substratum for TR development. Rheumatic heart disease may affect the TV in situ and directly produce TR.

Table 2:

Major determinants of late onset TR

Study Determinant
De Bonis et al. [22] Right chamber dilatation/dysfunction
Mutlak et al. [8] Higher PASPs
Wang et al. [19] Longer time from onset of MV disease to surgery
Boyaci et al. [18] History of rheumatic heart disease
Matsunaga and Duran [15] Ischaemic heart disease
Song et al. [20] Female gender
Song et al. [20] Larger LA size
Kim et al. [21] AF
Shiran and Sagie [7] Prosthetic valve malfunction
Open in a new tab

The mechanisms by which functional TR is developed have been investigated in many studies (Fig. 6). It seems that two parameters are the most important in this pathophysiological process: TA dilatation and TV leaflet tethering (standing for the apical displacement of the TV leaflets). These two phenomena lead to the disruption of the balance among tricuspid leaflet size, annular orifice area and spatial orientation of the valve apparatus, ultimately resulting in impaired leaflet coaptation and TR development [8]. The degree to which each of these two factors affects TR development is controversial.

Figure 6:

Figure 6:

Open in a new tab

Synopsis of major underlying mechanisms for the development of late onset TR.

TA dilatation can result from various pathophysiological processes, including left-sided HF from myocardial or valvular causes, RV pressure and volume overload and dilatation of any of the cardiac chambers. Left ventricular (LV) dysfunction itself impairs RV function, due to a variety of mechanisms and interactions. The shared intra-ventricular septum, the continuity between the muscle fibres of the left and right ventricles and the common biochemical neurohormonal milieu play an important part on this process. The inevitable left-sided chamber enlargement accompanying the left HF and the subsequent MR leads to right-sided pressure overload and enlargement of the right-sided chambers, with TA dilatation and resultant TR [9].

TA dilatation seems to be of much greater importance in the development of late TR compared with preoperative TR. Although grading of TR is highly subjective, depending on RV preload, afterload and contractility, TA diameter is relatively easy and accurate in measurement: with a cut-off point predictive for late TR of >70 mm at the surgical table or of >40 mm or 21 mm/m2 at the echo imaging [10].

The whole process of late functional TR evolution in relation to TA dilatation could be considered to have three distinct phases [10]. At first, increased RV volume leads to dilatation of the TA (phase 1). During this phase, TR may or may not be present, depending on the degree of TA dilation and TV leaflets' coaptation. Over time, the progressive enlargement of the RV and the subsequent dilatation of the TA lead to significant TR due to the failure of the leaflets' coaptation (phase 2). If TV repair is attempted during these two phases, annuloplasty alone seems to be enough. Finally, the progressive enlargement and eccentricity of the RV lead not only to TA dilatation, but also to tethering of the TV leaflets, due to the attachment of the papillary muscles of TV to the free wall of the RV (phase 3). Coaptation depth can be used as an index of TV tethering, with a cut-off point of ≥0.8 cm. At this phase, TV repair must be performed, not only by single annuloplasty, but also with a procedure to overcome tethering effects (e.g. augmentation of anterior tricuspid leaflet to increase its surface of coaptation with the septal and posterior leaflets) [11].

TR IN PH

PH does not seem to be significantly related to functional TR, at least in ischaemic heart disease [12, 13]. PH is generally associated with TR and it has been shown that pulmonary thromboendarterectomy, with its subsequent lowering of pulmonary artery pressure (PAP), leads to regression of the co-existing TR [14]. Nevertheless, PAP may not be affected after MV repair, probably due to permanent damage of the pulmonary vasculature, or even non-detected ischaemic LV failure [15]. On the one hand, successful MV repair eliminates the passive component of PH and decreases the reactive pulmonary arteriolar vasoconstriction in a time interval of 1 week to several months. On the other hand, the passive component of PH may be hindered by prosthetic valve mismatch, suboptimal results of mitral MS repair by balloon valvotomy or significant residual MR. Furthermore, pre-existing pulmonary arteriolar medial hypertrophy leads to persistent or recurrent PH [7]. Nevertheless, Kaul et al. [16] observed that patients with severe PH before MV surgery exhibited late TR at a lesser extent during follow-up, better functional capacity and a significantly improved survival rate compared with those without severe PH. This controversial observation can be potentially attributed to the fact that severe PH is associated with good RV function, whereas patients with non-severe PH exhibit worse RV function, and often organic TR.

Nevertheless, the clinical significance and the role of PH in functional TR remain controversial. Pulmonary artery systolic pressure (PASP) is a strong determinant of TR, but many patients with high PASP do not exhibit significant TR [8]. TR regression after PASP lowering is a very common observation in patients with thromboembolic pulmonary vascular disease undergoing pulmonary thromboendarterectomy [14], or patients with MV stenosis undergoing percutaneous mitral balloon commissurotomy. Mutlak et al. [8] found that high PASP constitutes only one of the various risk factors that finally led to TR development. Such risk factors include age and female gender, possibly due to lower tolerance of the TV apparatus to elevated PASP and to potential dependency of cardiac remodelling in response to PH on age and gender. Right chamber enlargement, LA enlargement, implantation of pacemaker leads and organic MV disease (probably due to occult organic TV disease) are also included. Additionally, in patients with higher PASP (≥70 mmHg), parameters like RA size, TA diameter and TV tethering were worse with increased severity of TR.

TR AFTER LEFT-SIDED VALVE SURGERY

TR is closely associated with functional ischaemic MR. Up to 30% of ischaemic MR patients undergoing MV repair surgery exhibit significant TR: in 57% of them, it is completely ignored during surgery [15]. Moreover, 50% of patients who had a previous MV repair surgery for functional MR exhibit significant TR during follow-up, ranging from 25% at <1 year, 53% between 1 and 3 years and 74% over a >3-year follow-up period. The incremental incidence of TR after ischaemic MR repair is mainly attributed to ischaemic remodelling cardiomyopathy of these patients, resulting in LV and RV geometric changes, with dilatation of the TA [15]. RV pressure overload secondary to the pre-existing MV disease may also have a part in this pathophysiological altering of the RV geometry and the consequent TA dilatation. Nevertheless, the catalytic role of ischaemia in the development of TR is undisputable, since only 16% of patients undergoing MV repair surgery, for non-ischaemic MR , exhibit grade 3+ to 4+ TR at the 8-year follow-up period [13].

The incidence of TR in functional ischaemic MR patients undergoing MV repair is not affected, either by pre-existing PH or by any residual postoperative MR. It is not even affected by whether or not TR is surgically treated during MV surgery: using either single suture or flexible ring techniques. On the other hand, preoperative TA dilatation may well be a predictor of late TR, as preoperative and follow-up TA dimensions are significantly larger in patients with late TR. These patients also tend to be older in age, thus suffering from RV pressure overload for a longer period of time [15].

Pre-existing TR is an adverse clinical marker in patients undergoing percutaneous balloon mitral valvuloplasty, regardless of the success of the procedure, with a poor prognosis [17]. Independent of pre-existing TR, late functional TR is also a very common epiphenomenon after MS surgery. A higher grade of TR in patients undergoing MV replacement for rheumatic MS is associated with more advanced MV disease, higher PAP, more severe preoperative TR and preoperative signs of RV failure [18].

Wang et al. [19] studied the incidence of late TR after left-sided valve replacement, observing that 30% of these patients progressively developed TR (25.1% significant TR). This resulted in increased morbidity and mortality in the immediate and late postoperative period. In their study, PH and TA dilatation have been shown to be significant risk factors for late TR.

TA dilatation and decreased systolic reduction in annulus size have been associated with poor prognosis [6]. Furthermore, quite a few clinical conditions have been associated with late secondary TR development as independent risk factors [19, 20]. A long period from left-sided valve disease onset till surgery is a classic risk factor. It seems that LA enlargement, with an associated decrease in its contractility, implies an important increase of the RV afterload and adverse RV remodelling. AF, acting as a surrogate of disorder of atrial contractile function, increases the preload and afterload of RV. These alterations of the haemodynamic condition of the RV, in conjunction with the mechanical and electrical remodelling of both atria, lead to RV remodelling and progressive TR. Additionally, Kim et al. [21] have demonstrated that the Maze procedure reduces the incidence and severity of TR over time, if it is combined with left-sided valve surgery. On the other hand, Song et al. [20] associated AF with late TR, whereas in previous studies, they did not associate the Maze procedure with better prognosis. Female gender may be indirectly associated with a higher prevalence of late TR due to relatively higher prevalence of MV rheumatic involvement [20]. Rheumatic fever may cause pancarditis, rendering the RV more susceptible to subclinical damage and more vulnerable to progressive dysfunction and geometry changes after exposure to the haemodynamic changes provoked by left-sided valve lesions.

De Bonis et al. [22] investigated the evolution of TR after MV replacement for functional MR specifically in dilated cardiomyopathy (DCM) and showed that 18% of patients who exhibited preoperative TR ≤ 2+, without tricuspid annuloplasty during MV surgery, developed or had a progression of their TR ≥ 2 grades during follow-up. TR at discharge of higher grade and existing preoperative RV dysfunction were ominous factors for TR progression. Similar to previous studies, they noted TA dilatation as the underlying mechanism, but they also underlined the significance of tethering of the tricuspid leaflets due to RV dilatation, leading to a coaptation depth of >0.5 cm. A natural history of DCM, LV/RV dysfunction with HF, PH with the consequent increase in RV afterload, recurrence of functional MR after repair, ICD or pacemaker implantation and lack of reverse remodelling after operation act as underlying risk factors for TR development over time [22].

EFFECT OF MV SURGERY ON TR

In the early years of left-sided heart valve surgery, the most common approach was leaving the TV untouched, irrespective of the size of the regurgitation [23]. It was believed that severe TR would resolve after surgical correction of the MV, due to the positive haemodynamic effect that left-sided heart valve repair would produce. However, Braunwald et al. [23] had arrived at this conclusion by studying relatively young patients, with good RV function implied by the high PASP, the relatively low right atrial pressures and a short follow-up period of 30 months, which was later proved to be insufficient for predicting the possible future development of TR. In general, TR after MV surgery may potentially subside in patients with younger age, functional TR, smaller preoperative MV area, severe PH, larger resolution of PH after valvotomy and no AF [24].

However, Shafie et al. [25] have shown that pre-procedural TR is a predictor of poor outcome in patients undergoing balloon mitral valvotomy for MS. Severe postoperative TR is more often registered with more severe MV disease, higher pulmonary vascular resistance and a smaller increase in MV area after valvotomy. It is associated with lower overall survival, more frequent HF and greater need for a repeat of valvotomy or MR [17]. Furthermore, Groves et al. [26] have shown that isolated and severe TR after MV repair is associated with reduced exercise duration, maximal oxygen consumption and anaerobic threshold, despite the postoperative good natural or prosthetic valve function. Residual or recurrent TR progressively leads to RV dilatation and, subsequently, to intra-ventricular shifting towards LV, compression of LV, restricted filling of LV, increased LV diastolic and pulmonary pressure: all of these phenomena compiling the so-called restriction dilatation syndrome [27].

However, all the previously mentioned findings refer to ischaemic, rheumatic or mixed valve disease. A recent paper by Yilmaz et al. [28] attempted to evaluate postoperative TR in patients undergoing isolated MV repair for degenerative mitral prolapse. According to the authors, clinically significant TR progression was unlikely to occur in the specific patient population. Their data also suggested that in the absence of significant RV failure, surgical intervention for functional TR repair is rarely needed in patients undergoing isolated MV repair for degenerative MV disease.

CONSERVATIVE AND SURGICAL TREATMENT OF FUNCTIONAL TR

Late TR treatment still remains controversial. In general, late TR is difficult to treat; loop diuretics and spironolactone are still standing as mainstream therapy, while chronic dialysis may play a role in very advanced clinical conditions. Because of the intrinsic limitations of Braunwald's approach, leaving the TV intact during MV surgery, TR repair or replacement has begun to be deployed concomitantly with MV surgery: based mainly on the severity of the regurgitation, with a consensus that higher degrees of TR should be surgically corrected. Nevertheless, the best time for TV surgery still needs to be clarified; in early stages, when there are few symptoms, it seems unjustifiable to proceed to such type of surgery, whereas, in late stages, when RV dysfunction has been rendered irreversible, it is practically of no use [7].

Moreover, there is great controversy on the appropriateness criteria of concomitant TV repair during functional MR surgery. Currently, the guidelines for less-than-severe TR provide vague indications for intervention. Dreyfus et al. [5] found no significant difference in the 10-year survival or cardiac-related event-free survival, between patients with and without concomitant TV repair during MV repair surgery. Nonetheless, they observed a significant improvement of NYHA class along with lower late TR grade, if TR had been surgically treated. Furthermore, moderate or greater functional TR impairs the mid-term survival and functional status of patients operated for functional MV disease. As TR is virtually an index of underlying RV dysfunction and/or PH and might mask the decreased RV contractility, tricuspid annuloplasty should be mandatory in case of at least moderate functional TR [29]. Additionally, Navia et al. [30], while conducting a retrospective analysis of 1700 patients, proposed that concomitant TV repair is a reasonable approach, especially for patients with RV remodelling and RV failure. This is also verified by other authors who recommended TR annuloplasty in cases of tricuspid annulus dilatation, despite the severity of TR [31, 32].

Among the various surgical techniques, TV repair seems to be superior, whereas TV replacement is worse, due to the inevitable degeneration of the valve over time or thrombotic phenomena. Moreover, according to some investigators [33], the difference in mortality between the two surgical techniques could be attributed to the comorbidities of patients undergoing surgery and the elective/non-elective status of the procedure. RV dysfunction has been proposed as a potential contributor to operative mortality after TV replacement for TR [34]. Yet, difficulties assessing preoperative RV function have prevented clarification of the influence of RV dysfunction on operative mortality. Therefore, TV replacement is reserved for organic disease. There are various TV repair techniques, three of which are the most frequently applied: (i) plication of the posterior leaflet resulting in a bicuspid TV (Kay's annuloplasty), (ii) purse string suture around the anterior and posterior annulus (De Vega annuloplasty) and (iii) annuloplasty with ring or band [1]. There is controversy over the best surgical technique for TV repair. It seems that annuloplasty with a ring, either semi-rigid or flexible, is associated with improved survival, longer event-free survival and greater freedom from recurrent TR [35].

Tricuspid annuloplasty during MV surgery, even though it restrains the development and/or deterioration of TR, constitutes a solid solution for the late postoperative TR problem [19]. Izumi et al. [36] found that the proportion of patients having undergone tricuspid annuloplasty concomitantly with MV surgery was significantly greater in those with late severe TR compared with those without. It seems that TV annuloplasty may lead to deformation of the tricuspid annulus and valve leaflets, resulting in valve insufficiency. The failure of De Vega technique may be attributed to the distention of the anteroseptal commissure produced by the pulling away of the anterior annulus from the commissure, and the anterior leaflet is thrown into multiple folds, thus resulting in an uneven coaptation with the septal leaflet, or even to suture avulsion or breakage [19]. Although tricuspid annuloplasty improves functional capacity and NYHA class of patients undergoing rheumatic MV disease surgery, the event-free survival is shorter and the rate of re-hospitalization higher in those who exhibit significant TR at follow-up compared with those without [18].

In general, TV replacement has a worse prognosis in comparison with annuloplasty, with an operative mortality ranging from 6 to 26%, being worse in patients with NYHA Class III or IV, congenital heart disease or reoperation.

The interrelationship of the TV with MV has been reflected in the guidelines pertaining to the surgical management of TV regurgitation. According to the ACC/AHA guidelines, TV repair is classified as a Class I indication for severe TR in patients with MV disease requiring MV surgery, and as a Class IIb indication even in less than severe TR in patients undergoing MV surgery when there is PH or TA dilatation. However, it is not indicated (Class III) when PASP is <60 mmHg in the presence of a normal MV, with no symptoms [4].

On the other hand, there are factors associated with adverse outcomes after TR surgery and these should always be taken into consideration. Specifically, low functional status (NYHA IV) is related to increased postoperative mortality. Additionally, deterioration of RV systolic function is associated with adverse post-surgical outcomes. The RIMP ratio has been proposed as a useful echocardiographic marker for predicting mortality after TR surgery [37]. According to the same investigators, older age was not related to increased mortality and it should not be held as a restriction for surgery when needed. Therefore, TR surgery should be undertaken before severe compromise of LV or RV function.

Finally, a significant problem regarding TR surgery is the presence of pacing leads through the TV. As a common rule, it is recommended that the leads should first be extracted and then replaced by an epicardial pacing device. However, according to long-term follow-up studies, the leads should remain in place if the device functions properly, as long as the leads do not interfere with the prosthetic valve [38]. Moreover, the effect of trans-venous leads through the TV on TR itself is minimal, even in growing children with congenital heart disease [39].

CONCLUSIONS

Late onset TR after successful MV surgery is a significant clinical entity as it displays a great impact on patient prognosis. This is illustrated by the intense research that has been conducted over the last years by numerous investigators, which has not only shed light on various aspects of this major clinical problem, but has also led to diversities according to current literature.

To date, controversy still exists on when to operate on TR, especially when it is concomitant with MR. Moreover, the advent of new percutaneous devices may provide solutions for patients who develop late onset TR and cannot undergo major cardiothoracic surgery with high mortality rates.

Conflict of interest: none declared.

References

  • 1.Chan KM, Zakkar M, Amirak E, Punjabi PP. Tricuspid valve disease: pathophysiology and optimal management. Prog Cardiovasc Dis. 2009;51:482–6. doi: 10.1016/j.pcad.2008.08.009. [DOI] [PubMed] [Google Scholar]
  • 2.Anwar AM, Geleijnse ML, Ten Cate FJ, Meijboom FJ. Assessment of tricuspid valve annulus size, shape and function using real-time three-dimensional echocardiography. Interact CardioVasc Thorac Surg. 2006;5:683–7. doi: 10.1510/icvts.2006.132381. [DOI] [PubMed] [Google Scholar]
  • 3.Tribouilloy CM, Enriquez-Sarano M, Bailey KR, Tajik AJ, Seward JB. Quantification of tricuspid regurgitation by measuring the width of the vena contracta with Doppler color flow imaging: a clinical study. J Am Coll Cardiol. 2000;36:472–8. doi: 10.1016/s0735-1097(00)00762-2. [DOI] [PubMed] [Google Scholar]
  • 4.Bonow RO, Carabello BA, Chatterjee K, de Leon AC, Jr, Faxon DP, Freed MD, et al. American College of Cardiology/American Heart Association Task Force on Practice Guidelines. 2008 focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to revise the 1998 guidelines for the management of patients with valvular heart disease). Endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol. 2008;52:e1–142. doi: 10.1016/j.jacc.2008.05.007. [DOI] [PubMed] [Google Scholar]
  • 5.Dreyfus GD, Corbi PJ, Chan KM, Bahrami T. Secondary tricuspid regurgitation or dilatation: which should be the criteria for surgical repair? Ann Thorac Surg. 2005;79:127–32. doi: 10.1016/j.athoracsur.2004.06.057. [DOI] [PubMed] [Google Scholar]
  • 6.Colombo T, Russo C, Ciliberto GR, Lanfranconi M, Bruschi G, Agati S, et al. Tricuspid regurgitation secondary to mitral valve disease: tricuspid annulus function as guide to tricuspid valve repair. Cardiovasc Surg. 2001;9:369–77. doi: 10.1016/s0967-2109(00)00147-2. [DOI] [PubMed] [Google Scholar]
  • 7.Shiran A, Sagie A. Tricuspid regurgitation in mitral valve disease incidence, prognostic implications, mechanism, and management. J Am Coll Cardiol. 2009;53:401–8. doi: 10.1016/j.jacc.2008.09.048. [DOI] [PubMed] [Google Scholar]
  • 8.Mutlak D, Aronson D, Lessick J, Reisner SA, Dabbah S, Agmon Y, et al. Functional tricuspid regurgitation in patients with pulmonary hypertension: is pulmonary artery pressure the only determinant of regurgitation severity? Chest. 2009;135:115–21. doi: 10.1378/chest.08-0277. [DOI] [PubMed] [Google Scholar]
  • 9.Rogers JH, Bolling SF. The tricuspid valve: current perspective and evolving management of tricuspid regurgitation. Circulation. 2009;119:2718–25. doi: 10.1161/CIRCULATIONAHA.108.842773. [DOI] [PubMed] [Google Scholar]
  • 10.Dreyfus GD, Chan KM. Functional tricuspid regurgitation: a more complex entity than it appears. Heart. 2009;95:868–9. doi: 10.1136/hrt.2008.159970. [DOI] [PubMed] [Google Scholar]
  • 11.Dreyfus GD, Raja SG, John Chan KM. Tricuspid leaflet augmentation to address severe tethering in functional tricuspid regurgitation. Eur J Cardiothorac Surg. 2008;34:908–10. doi: 10.1016/j.ejcts.2008.07.006. [DOI] [PubMed] [Google Scholar]
  • 12.Sagie A, Schwammenthal E, Padial LR, Vazquez de Prada JA, Weyman AE, Levine RA. Determinants of functional tricuspid regurgitation in incomplete tricuspid valve closure: Doppler color flow study of 109 patients. J Am Coll Cardiol. 1994;24:446–53. doi: 10.1016/0735-1097(94)90302-6. [DOI] [PubMed] [Google Scholar]
  • 13.Matsuyama K, Matsumoto M, Sugita T, Nishizawa J, Tokuda Y, Matsuo T. Predictors of residual tricuspid regurgitation after mitral valve surgery. Ann Thorac Surg. 2003;75:1826–8. doi: 10.1016/s0003-4975(03)00028-6. [DOI] [PubMed] [Google Scholar]
  • 14.Sadeghi HM, Kimura BJ, Raisinghani A, Blanchard DG, Mahmud E, Fedullo PF, et al. Does lowering pulmonary arterial pressure eliminate severe functional tricuspid regurgitation? Insights from pulmonary thromboendarterectomy. J Am Coll Cardiol. 2004;44:126–32. doi: 10.1016/j.jacc.2003.12.058. [DOI] [PubMed] [Google Scholar]
  • 15.Matsunaga A, Duran CM. Progression of tricuspid regurgitation after repaired functional ischemic mitral regurgitation. Circulation. 2005;112(9 Suppl.):I453–7. doi: 10.1161/CIRCULATIONAHA.104.524421. [DOI] [PubMed] [Google Scholar]
  • 16.Kaul TK, Ramsdale DR, Mercer JL. Functional tricuspid regurgitation following replacement of the mitral valve. Int J Cardiol. 1991;33:305–13. doi: 10.1016/0167-5273(91)90360-2. [DOI] [PubMed] [Google Scholar]
  • 17.Sagie A, Schwammenthal E, Newell JB, Harrell L, Joziatis TB, Weyman AE, et al. Significant tricuspid regurgitation is a marker for adverse outcome in patients undergoing percutaneous balloon mitral valvuloplasty. J Am Coll Cardiol. 1994;24:696–702. doi: 10.1016/0735-1097(94)90017-5. [DOI] [PubMed] [Google Scholar]
  • 18.Boyaci A, Gokce V, Topaloglu S, Korkmaz S, Goksel S. Outcome of significant functional tricuspid regurgitation late after mitral valve replacement for predominant rheumatic mitral stenosis. Angiology. 2007;58:336–42. doi: 10.1177/0003319707302495. [DOI] [PubMed] [Google Scholar]
  • 19.Wang G, Sun Z, Xia J, Deng Y, Chen J, Su G, et al. Predictors of secondary tricuspid regurgitation after left-sided valve replacement. Surg Today. 2008;38:778–83. doi: 10.1007/s00595-007-3721-3. [DOI] [PubMed] [Google Scholar]
  • 20.Song H, Kim MJ, Chung CH, Choo SJ, Song MG, Song JM, et al. Factors associated with development of late significant tricuspid regurgitation after successful left-sided valve surgery. Heart. 2009;95:931–6. doi: 10.1136/hrt.2008.152793. [DOI] [PubMed] [Google Scholar]
  • 21.Kim HK, Kim YJ, Kim KI, Jo SH, Kim KB, Ahn H, et al. Impact of the maze operation combined with left-sided valve surgery on the change in tricuspid regurgitation over time. Circulation. 2005;112(9 Suppl.):I14–9. doi: 10.1161/CIRCULATIONAHA.104.524496. [DOI] [PubMed] [Google Scholar]
  • 22.De Bonis M, Lapenna E, Sorrentino F, La Canna G, Grimaldi A, Maisano F, et al. Evolution of tricuspid regurgitation after mitral valve repair for functional mitral regurgitation in dilated cardiomyopathy. Eur J Cardiothorac Surg. 2008;33:600–6. doi: 10.1016/j.ejcts.2008.01.011. [DOI] [PubMed] [Google Scholar]
  • 23.Braunwald NS, Ross J, Jr, Morrow AG. Conservative management of tricuspid regurgitation in patients undergoing mitral valve replacement. Circulation. 1967;35(4 Suppl.):I63–9. doi: 10.1161/01.cir.35.4s1.i-63. [DOI] [PubMed] [Google Scholar]
  • 24.Hannoush H, Fawzy ME, Stefadouros M, Moursi M, Chaudhary MA, Dunn B. Regression of significant tricuspid regurgitation after mitral balloon valvotomy for severe mitral stenosis. Am Heart J. 2004;148:865–70. doi: 10.1016/j.ahj.2004.05.017. [DOI] [PubMed] [Google Scholar]
  • 25.Shafie MZ, Hayat N, Majid OA. Fate of tricuspid regurgitation after closed valvotomy for mitral stenosis. Chest. 1985;88:870–3. doi: 10.1378/chest.88.6.870. [DOI] [PubMed] [Google Scholar]
  • 26.Groves PH, Lewis NP, Ikram S, Maire R, Hall RJ. Reduced exercise capacity in patients with tricuspid regurgitation after successful mitral valve replacement for rheumatic mitral valve disease. Br Heart J. 1991;66:295–301. doi: 10.1136/hrt.66.4.295. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 27.Antunes MJ, Barlow JB. Management of tricuspid valve regurgitation. Heart. 2007;93:271–6. doi: 10.1136/hrt.2006.095281. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 28.Yilmaz O, Suri RM, Dearani JA, Sundt TM, III, Daly RC, Burkhart HM, et al. Functional tricuspid regurgitation at the time of mitral valve repair for degenerative leaflet prolapse: the case for a selective approach. J Thorac Cardiovasc Surg. 2011;142:608–13. doi: 10.1016/j.jtcvs.2010.10.042. [DOI] [PubMed] [Google Scholar]
  • 29.Calafiore AM, Gallina S, Iacò AL, Contini M, Bivona A, Gagliardi M, et al. Mitral valve surgery for functional mitral regurgitation: should moderate-or-more tricuspid regurgitation be treated? A propensity score analysis. Ann Thorac Surg. 2009;87:698–703. doi: 10.1016/j.athoracsur.2008.11.028. [DOI] [PubMed] [Google Scholar]
  • 30.Navia JL, Brozzi NA, Klein AL, Ling LF, Kittayarak C, Nowicki ER, et al. Moderate tricuspid regurgitation with left-sided degenerative heart valve disease: to repair or not to repair? Ann Thorac Surg. 2012;93:59–69. doi: 10.1016/j.athoracsur.2011.08.037. [DOI] [PubMed] [Google Scholar]
  • 31.Van de Veire NR, Braun J, Delgado V, Versteegh MI, Dion RA, Klautz RJ, et al. Tricuspid annuloplasty prevents right ventricular dilatation and progression of tricuspid regurgitation in patients with tricuspid annular dilatation undergoing mitral valve repair. J Thorac Cardiovasc Surg. 2011;141:1431–9. doi: 10.1016/j.jtcvs.2010.05.050. [DOI] [PubMed] [Google Scholar]
  • 32.Bianchi G, Solinas M, Bevilacqua S, Glauber M. Which patient undergoing mitral valve surgery should also have the tricuspid repair? Interact Cardiovasc Thorac Surg. 2009;9:1009–20. doi: 10.1510/icvts.2009.217570. [DOI] [PubMed] [Google Scholar]
  • 33.Guenther T, Noebauer C, Mazzitelli D, Busch R, Tassani-Prell P, Lange R. Tricuspid valve surgery: a thirty-year assessment of early and late outcome. Eur J Cardiothorac Surg. 2008;34:402–9. doi: 10.1016/j.ejcts.2008.05.006. [DOI] [PubMed] [Google Scholar]
  • 34.McGrath LB, Gonzales-Lavin L, Bailey BM, Grunkemeier GL, Fernandez J, Laub GW. Tricuspid valve operations in 530 patients: twenty-five-year assessment of early and late phase results. J Thorac Cardiovasc Surg. 1990;99:124–33. [PubMed] [Google Scholar]
  • 35.Rahimtoola SH. The year in valvular heart disease. J Am Coll Cardiol. 2008;51:760–70. doi: 10.1016/j.jacc.2007.11.032. [DOI] [PubMed] [Google Scholar]
  • 36.Izumi C, Iga K, Konishi T. Progression of isolated tricuspid regurgitation late after mitral valve surgery for rheumatic mitral valve disease. J Heart Valve Dis. 2002;11:353–6. [PubMed] [Google Scholar]
  • 37.Topilsky Y, Khanna AD, Oh JK, Nishimura RA, Enriquez-Sarano M, Jeon YB, et al. Preoperative factors associated with adverse outcome after tricuspid valve replacement. Circulation. 2011;123:1929–39. doi: 10.1161/CIRCULATIONAHA.110.991018. [DOI] [PubMed] [Google Scholar]
  • 38.Molina JE, Roberts CL, Benditt DG. Long-term follow-up of permanent transvenous pacing systems preserved during tricuspid valve replacement. Ann Thorac Surg. 2010;89:318–20. doi: 10.1016/j.athoracsur.2009.03.037. [DOI] [PubMed] [Google Scholar]
  • 39.Webster G, Margossian R, Alexander ME, Cecchin F, Triedman JK, Walsh EP, et al. Impact of transvenous ventricular pacing leads on tricuspid regurgitation in pediatric and congenital heart disease patients. J Interv Card Electrophysiol. 2008;21:65–8. doi: 10.1007/s10840-007-9183-0. [DOI] [PMC free article] [PubMed] [Google Scholar]

Articles from Interactive Cardiovascular and Thoracic Surgery are provided here courtesy of Oxford University Press

RESOURCES