47. Tricuspid Valve Regurgitation- Clinical Scenarios

Emmanuel Moss, MD, and Robert A. Guyton, MD

Concept

  • Indication for intervention on the tricuspid valve
  • Preoperative considerations
  • Choice of intervention – Repair vs. replace
  • Valve choices – bioprosthesis vs. mechanical
  • Critical steps of tricuspid valve repair and replacement
  • Pitfalls and controversies

Chief complaint

“A 45-year-old man presents with a 6-month history of progressive fatigue, shortness of breath and lower extremity edema. Auscultation reveals a holosystolic ejection murmur at the left ventricular apex.”


Differential

The clinical scenario mentioned is typical for congestive heart failure. The causes can be several (CAD, MR, MS, AS, etc.). The peripheral edema and murmur raise concern for tricuspid regurgitation. Other diagnoses to consider include: Cirrhosis, constrictive pericarditis, or restrictive cardiomyopathy.


History and physical

This patient may have valvular disease of any type but most likely has mitral or tricuspid regurgitation. Valvular disease can lead to symptoms of congestive heart failure. It is important to determine the onset and duration of her symptoms as well as the character (asthenia, fatigue, weakness, malaise, peripheral edema). Evaluate for signs of right heart failure (ascites, hepatosplenomegaly, pulsatile liver, peripheral edema, pleural effusions). Late findings include cachexia, wasting and jaundice. Atrial fibrillation is common. Look for evidence of coronary artery disease (chest pain, risk factors, etc).


If TR is high on the differential, then consider primary and secondary causes:

  • Primary (structural). Congenital (e.g., Ebstein, AV canal/cushion defect), rheumatic disease (never isolated), endocarditis (IV drug use and Duke’s criteria), myxomatous degeneration, endocarditis, iatrogenic (e.g., permanent pacemaker (PPM) lead, repetitive myocardial biopsies), carcinoid (see below for explanation), trauma (e.g., chordal rupture from anterior leaflet), valvular tumor.
  • Secondary (functional). Most common form of TV dysfunction. Leaflets are normal. Caused by left sided lesion (e.g., mitral regurgitation), ischemic cardiomyopathy, dilated cardiomyopathy, cor pulmonale.

Tests

  • CXR: cardiomegaly, enlarged RA/RV, pleural effusions.
  • TTE. Transthoracic rather than transesophageal is particularly helpful for evaluating the tricuspid valve. It is used for diagnosis and decisions regarding management PREOPERATIVELY. For functional TR, intraoperative transesophageal echo is unreliable due to changes in vascular tone under general anesthesia, reducing the degree of regurgitation. For regurgitation, a jet that penetrates 2 cm into the RA is mild, 3-5 cm is moderate and systolic flow reversal of the hepatic or caval veins is severe. The grade is often reported as 1-mild, 2-moderate, 3-moderately severe, 4-severe. In addition, a jet radius greater than 9 mm, vena contracta > 0.7, ERO > 0.4 cm2, or regurgitant volume 45 mL indicate severe regurgitation.
  • Need to ask about the size of the annulus and the gradient. Annular size > 40 mm is a rough cut off for a valve that needs intervention. Mean gradient of 3-5 mmHg is considered severe. Also need to inquire on the character of the leaflets (tethered, thickened, prolapsed, flail).
  • TEE. Important for getting more detailed information on the mitral valve. Should also assess pulmonary artery pressure (PAP), right ventricular (RV) function, presence of PFO or ASD (bubble test if there is a doubt), endocarditis (vegetations) or carcinoid lesions.
  • Catheterization: evaluate for any coronary lesions. TR can be due to or result in RV failure. Obtain the cardiac index, LCWP, PAP, RA/RV end-diastolic pressure and CVP. Cardiac index may be unreliable in the setting of TR and you should rely on the EF for assessment of function. Absent X descent, prominent V wave, and ventricularization of RA tracing all support tricuspid disease.


Index scenario (additional information)

“Echocardiogam reveals a left ventricular ejection fraction of 45%, severe mitral regurgitation, moderate pulmonary artery hypertension, and moderate-severe tricuspid regurgitation with normal leaflets and a dilated annulus (45 mm).”


Treatment/management

This scenario addresses combined tricuspid and mitral valve disease. In addition to mitral valve (MV) repair or replacement, this patient meets criteria for tricuspid valve repair with an annuloplasty ring. This patient has several risk factors for persistent and progressive TR following mitral valve surgery. If the TV is deemed irreparable at the time of surgery, it is reasonable to consider replacement with a mechanical valve, depending on the patient’s preference and other anticoagulation concerns. Although bioprostheses deteriorate at a slower rate in the tricuspid position, this patient will likely require a future intervention (whether surgical or transcatheter), while risk of thrombosis with bileaflet mechanical valve is greatly decreased compared to older models (ball-cag, tilting disk).

 
Indications for surgery: ACCF/AHA guidelines

  • Class I
    • TV repair for severe TR in patients requiring MV surgery (level B).
  • Class IIa
    • TV repair or replacement for severe, SYMPTOMATIC, primary TR (level C).
    • TV replacement is reasonable when not amenable to repair.
  • Class IIb
    • Annuloplasty may be considered for less than severe TR in patients undergoing MV surgery when there is pulmonary hypertension or tricuspid annular dilation. (level C).
  • Other suggested indications for concomitant repair (not AHA): End-systolic annular dimension > 40 mm or intraoperative measurement of anteroseptal to anteroposterior annulus > 70 mm (Dreyfus et al, 2005).
  • Endocarditis. Not addressed in AHA guidelines. Generally accepted indications include: 1) severe TR with persistent sepsis, 2) vegetation > 15 mm, 3) persistent vegetation or sepsis despite med tx, 4) Recurrent pulmonary embolism.


Operative steps

  • Critical anatomy: 3 leaflets (septal, posterior, anterior). Septal annulus relatively fixed, annulus dilates posteriorly > anteriorly. AV node contained in triangle of Koch (between coronary sinus, septal annulus, tendon of Todaro).
  • Intraop TEE (assess valve function and dimensions, PFO), median sternotomy, aortic and bicaval cannulation with caval snares.
  • Cardioplegia: cross clamp, antegrade +/- retrograde. For retrograde – after clamping, run antegrade, caval snares are tightened, right atriotomy, handheld retractor, purse string around coronary sinus, insert cannula and inflate balloon, pull back cannula until arrested by purse string (maximize distribution).
  • Left sided lesions addressed first.
  • Tricuspid valve can be addressed with the aorta clamped or the heart beating (PFO, if present, must be closed before releasing the cross clamp). Advantages of beating heart include assessment of iatrogenic conduction disturbances, reduce cross-clamp time. Concern with beating heart is ejection of air in the presence of an undetected interatrial communication and the added challenge of performing a precise annuloplasty on the beating heart.
  • Oblique atriotomy directed posteriorly from appendage toward the right inferior pulmonary vein and inferior vena cava.
  • On septal annulus, sutures are placed through the base of the septal leaflet to avoid damage to the AV node.

Annuloplasty techniques

  • Ring annuloplasty
    • Interrupted mattress sutures leaving a gap at koch’s triangle (roughly 1 cm from the anteroseptal commissure to midpoint on the septal leaflet. Be careful with the sutures near the anteropostero commisure. These can injure the RCA. Several rings available, with semi-rigid incomplete ring being the most commonly used (e.g., Edwards Classic, Edwards physio, MC3). Favored over flexible band.
    • Methods of selecting ring size: 1) Using sizer, measuring the septal leaflet and surface area of leaflet tissue arising from anterior pap muscle, or 2) 30-32 mm for female, 32-34 mm for male.
    • Suture annuloplasty (DeVega). Simpler and faster, however, may have increased long-term risk of recurrence compared to rings. Both limbs of a pledgeted 2–0 Prolene running from anteroseptal commissure along the RV free wall portion of the annulus to the posteroseptal commissures.
    • Posterior leaflet plication (Kay). Obliterates the posterior leaflet.

Replacement

  • Preservation of native valve leaflets, similar to mitral valve.
    • Sutures near the AV node placed through the septal leaflet.

Endocarditis

  • Excise vegetations until healthy tissue. Close gaps primarily or with patch.
    • Consider annuloplasty if valve competence is in question.
    • Replace valve if extensive destruction.
    • 2-stage replacement may be considered in IVDU (intravenous drug users), with normal RV function and PAP.

Intra-operative valve assessment. Fill RV with saline with a bulb syringe and assess coaptation. TEE to assess repair on CPB.

Potential questions/alternative scenarios

“What elements will influence your decision to address the TV in a patient undergoing mitral valve surgery?”

Decision to operate often a difficult clinical dilemma because improvement with repair of left-sided lesions remains unpredictable. In general, moderate to severe TR or any structural TR should be addressed concomitantly with left sided lesions. LV function, RV function, degree of pulmonary hypertension, tricuspid annulus size, and tricuspid valve morphology must all be assessed. The presence of preoperative right heart failure is a strong indication for addressing TR. Some advocate repair of even mild disease without risk factors for progression. If LV and RV function are near normal, the TV annulus is not dilated, pulmonary vascular resistance is low, and a good result is expected from MV repair, then progressive tricuspid regurgitation is less likely. When weaning from CPB, if TR persists and elevated RAP > LAP is encountered with an underfilled well-contracting LV, TV repair should be performed.


“What type of prosthesis would you use for TV replacement?”

Similar to mitral and aortic valve prosthetic valve planning, decision is based on age, anticoagulation considerations, and social issues. Incidence of valve thrombosis was considered prohibitive with older mechanical prostheses (ball-cage and tilting disk) but is not the case with bileaflet valves. However, bioprostheses have better freedom from structural valve deterioration than in mitral position, and unlike mechanical valves, they do not limit the implantation of a transvalvular PM lead in the future.


“Under what circumstances can TV excision without replacement be considered?”

In endocarditis and extensive destruction or an active IVDU. PAPs and RV must be near normal. Replacement can be performed months to years later. Early morality 12%, with hepatic failure frequently playing a role. Survival is 60% at 15 years, with 50% of patients having RV failure. Approach has fallen out of favor.


“When coming off pump following TV replacement, the RV dilates, CVP is high, and PAP decrease. How do you manage this?”

Routine checklist of possible causes of RV failure post CPB (metabolic, air embolism…) and TEE for anatomic assessment. Rule out RVOT obstruction due to redundant billowing of anterior leaflet tissue – If this is the case, central portion of anterior leaflet may be excised while maintaining chordal attachments. If ST changes are noted in the inferior leads, then consider RCA occlusion with the mattress sutures and perform a bypass to the right with vein. Even when all goes well after TVR, there may be an element of RV dysfunction which is treated in the ICU with inotropes (epinephrine or milrinone), fluid restriction, diuresis and pressors. Chemical unloading of the heart can be achieved with milrinone or nitroglycerin drip. An IABP can further help to unload a struggling RV in more severe cases and improve RCA perfusion. Note that you do not always have the luxury of Swan-Ganz monitoring after tricuspid valve surgery. It cannot be used if placing a mechanical valve. It is not ideal when placing a tissue valve. It can be used after a repair, but it would be best if it were manually inserted by the surgeon under direct visualization. This may factor into your selection process as well. A sick patient with poor EF may be better off with 1-2+ residual TR after a repair and a PA catheter for ICU management than no TR with a mechanical valve but no PA catheter.

“What are the risk factors for recurrence of TR following TV repair?”

No ring used, improper placement of the ring (usually by rotation), severity of baseline TR, residual TR at first operation, persistent pulmonary hypertension, residual left sided lesions, transvalvular PPM lead.


“What factors influence operative mortality in TV surgery?”

Preoperative functional class, ejection fraction, prior valve surgery, older age, excision without replacement

“When should tricuspid valve repair be performed in patients who have undergone a previous mitral valve surgery?”

No consensus exists. Historically, operative mortality for reoperative TV surgery has been relatively high, making the benefit over medical therapy unclear. Waiting for the development of severe symptoms before TV repair in this setting has resulted in poor results, reinforcing the belief that this is a high-risk operation. Some now advocate early reintervention in mildly symptomatic patients, hoping to decrease operative risk. Effectiveness of this approach has not been proven.

“Coming of CPB you notice complete heart block (CHB).”

The sutures near the anteroseptal commissure can easily damage the AV node. This can also occur from radial force with the prosthetic valves. If both the mitral and tricuspid were replaced, then the chance of recovery is lower. Giving the patient time to recover in the ICU is reasonable but make sure that you have 2 sets of properly functioning ventricular pacing wires as well as a set of atrial wires. Eventually the patient may require an endocardial or epicardial permanent pacemaker. Endocardial pacers can be placed percutaneously into the atrium and through the coronary sinus to achieve ventricular conduction. If the coronary sinus cannot be cannulated, then worse case scenario they can traverse the repaired valve. If the patient had a tissue valve placed this can be harder but is still possible. Epicardial lead placement is another alternative and avoids a foreign object across the fresh repair/replacement. But you need to balance this decision with the risk of returning to the OR and be able to describe how you reoperate for an epicardial lead. If a mechanical valve is in place and you end up with heart block, then you will not be able to cross it with endocardial wires and the coronary sinus route or epicardial route may be needed ultimately.

“A patient with tricuspid valve endocarditis and a PPM for heart block undergoes a combined mitral/TV repair. How do you handle the pacer leads?”

The original wires should be removed in the setting of bacteremia and endocarditis. You have no way of knowing if it was the wires themselves that caused the infection or will seed a new infection. Some advocate debriding the wires or inspecting them, but the safest thing would be to remove them. Epicardial wires can be placed on the RV. Transvenous atrial wires can be placed later if needed. Place temporary wires as well since you will not be relying on the epicardial lead until it is connected, and a formal device check is performed. Be familiar with the procedure for epicardial lead placement (5-O prolene to fasten the RV lead, tunnel the lead through the left intercostal space a safe distance away from the mammary and out to an area in the skin where you make a subcutaneous pocket for the device.). If you are concerned about the degree of bacterial burden intraop and feel that the epicardial lead could get infected then you can wait a few days post op on antibiotics and place an endocardial lead through the coronary sinus, repaired valve or tissue valve.


“A patient with a prior history of brady syndrome and a PPM comes to the OR for a TVR.”

Note that in the absence of endocarditis the wires can be left either around the sewing ring or through the valve itself accepting a slightly higher risk of recurrent TR. For a younger patient it may be worth placing the wire in the epicardial position since you would like to minimize the chance of recurrent TR. For a mechanical valve you will need to remove the wire and replace later or use an epicardial wire.


“After replacing the tricuspid valve, you feel the need to determine PAP and CI due to worsening hypotension.”

You cannot float a swan in the setting of a mechanical valve, and it is not advised after a tissue valve. It can be done with caution in the setting of a repair. An alternative is to use the CVP with venous saturations and echo data to help guide your management. It can be placed through a tissue valve carefully if necessary.


“Coming of CPB you notice 2+ TR. The patient has extensive comorbidities, 4+ MR which you have just fixed and a low EF.”

The management must weigh the risks of going back on CPB and arresting the heart against the risks of leaving behind residual TR. For this patient the most prudent course of action would be to leave the regurgitation alone. 2+ residual TR will rarely be a good reason to replace the valve. The exception to this would be a younger patient with primary tricuspid disease and evidence of early right heart failure. For that patient you would want to remove as much of the regurgitant volume as possible.


“What is carcinoid valvular disease and how is the tricuspid valve managed with this disease process?”
Carcinoid tumors are serotonin-secreting tumors of the Kulchitsky cells of the GI tract. They can metastasize to liver where serotonin and other vasoactive hormones are excreted, affecting the right sided cardiac valves and pulmonary bed. Carcinoid syndrome leads to focal or diffuse fibrous tissue deposits on the endocardium of valve cusps and cardiac chambers. White fibrous carcinoid plaques present on the ventricular side of the TV cusps cause adherence to the RV wall, preventing leaflet coaptation. Tricuspid valve replacement is required. Involvement of the pulmonic valve may necessitate its replacement as well. In the absence of an ASD or VSD, left sided heart valves are not affected due to inactivation by monoamine oxidase as it passes through the lungs.


Pearls/pitfalls

  • Decision to intervene should be based on PREOPERATIVE TTE.
  • Incomplete rings avoid suture placement near the triangle of Koch.
  • For TV replacement, suture near AV node should be placed at base of septal leaflet, not in the annulus.
  • Rule out PFO before performing TV repair with beating heart.
  • Consider need for epicardial pacemaker lead at the time of surgery, particularly if implanting a mechanical valve.
  • Risk of PPM following TV replacement is 6-10%, commonly following combined TV and MV procedures.


Suggested readings

  • Bonow RO, Carabello BA, Kanu C, et al: ACC/AHA 2006 guidelines for the management of patients with valvular heart disease. Circulation 2006; 114:e84-e231.
  • Chikwe J, Ayanwu AC. Surgical Strategies for Functional Tricuspid Regurgitation. Semin Thoracic Surg 2010;22:90-96.
  • 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; 79:127-132.
  • Duran CMG. Surgical Treatment of Tricuspid Valve Disease. Selke FW, del NIdo PJ, Swanson SJ (eds). Sabiston and Spencer – Surgery of the Chest. 2010; 1241-1258.
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