66. Tricuspid Stenosis- Review of CT Surgery

Yogesh B. Patel and Lawrence S. Lee

This chapter is a revision and update of that included in the previous editions of the TSRA Review written by Brian Solomon (2^nd edition) and Lucas M. Duvall (1^st edition).

Anatomy

Please refer to Chapter 45 for in detail description of tricuspid valve anatomy.

Etiology

In the current era, true isolated tricuspid stenosis (TS) is considered a very rare lesion. If tricuspid stenosis (TS) is encountered, it is usually seen in conjunction with tricuspid regurgitation (TR) or other valvular disease (such as mitral disease). As mentioned in previous chapters, tricuspid disease is classified into either organic or functional. Most pathologies associated with TS are organic. TS accounts for only 2.4% of all cases of organic tricuspid valve (TV) pathology and it is most commonly found in young women. Rheumatic heart disease is the most common cause of TS worldwide and it usually with some aspect of mitral stenosis. Other primary causes of TS include carcinoid syndrome and systemic diseases such as systemic lupus erythematous (SLE) or antiphospholipid antibody (APLA) syndrome. Functional or secondary TS is caused by obstruction and narrowing of the TV and can be due to tumors such as atrial myxomas or IVC renal/ovarian tumors. Iatrogenic causes of TS can occur due to fibrosis of valve due to PPM/defibrillator leads or even chest radiation therapy.

Pathophysiology

The lesions of rheumatic disease typically show diffuse fibrous thickening of leaflets, fusion/shortening of chordae and often commissural fusion. The leaflet thickening is different than that of mitral in that calcific deposits are usually absent. The anteroseptal commissure is the most commonly involved commissure.

Carcinoid heart disease occurs in up to 50% of patients with carcinoid syndrome and can be the initial presentation of the syndrome in 20% of cases. It can cause isolated TS but there is usually an aspect of TR associated with the valvular disease. Carcinoid disease affecting the heart valves is characterized by carcinoid plaque which is plaque-like deposits of fibrous tissue onto valve leaflets. The deposits most commonly occur on the endocardium of valvular tissues. Macroscopically, the valve has a white appearance with thickened leaflets and papillary muscles in addition to fused or shortened chordae. The right heart structures are most commonly involved because the lungs inactivate humoral substances which protects the left-sided structures.

Carpentier described a separate classification system for TV disease which describes three types of disease according to the mobility of the leaflets:

Type I – normal leaflet motion with annular dilation
Type II – increased leaflet motion owing to leaflet prolapse (secondary to chordal rupture or elongation)
Type III – reduced leaflet motion due to leaflet thickening, fused commissures or leaflet tethering

TS can be described as a Type III lesion based on the above classification system. A normal tricuspid valve circumference measures 12 to 14 cm and a circumference of less than 10 to 11 cm is generally accepted as TS. The normal valve area of a tricuspid valve is 4 cm² and a valve area less than 1 cm² is classified as severe TS.

Diagnosis of TS

Patients usually present with symptoms related to right-sided heart failure such as fatigue, reduced exertional capacity, and even syncope with exertion. Those with severe TS can develop hepatomegaly, bilateral leg edema, ascites, and abnormal liver function. Similar to TR, symptoms can progress to cardiac cachexia and jaundice. The murmur of TS is described as a low frequency diastolic murmur best heard from the 4^th ICS of the lower left sternal border. The lungs are generally clear to auscultation in patients with isolated TS. Jugular venous pulsations can be seen and a prominent presystolic a wave can be exhibited. The y descent is characterized as slow due to delayed emptying of the RA into the RV.

CXR frequently show nonspecific findings of RA enlargement. On EKG, in patients in sinus rhythm, signs of RA enlargement – tall peaked P waves in leads II, III and avF – are noted.

As with most valvular diseases, echocardiography remains the gold standard for diagnosis of TS. Transthoracic echocardiography (TTE) is more effective at visualizing the TV due to its anatomic position. High velocity and turbulent diastolic flow across the valve are seen on echo. Peak tricuspid inflow velocity during inspiration >1 m/s, inflow time-velocity integral >60 cm, and valve area ≤1 cm² all indicate severe TS.

A mean transvalvular pressure gradient ≥5 mm Hg at normal heart rate is also seen with TS. With TS, pressure halftime by continuous wave Doppler (T_½) can be helpful in determining severity. Longer T_½ translates to greater TS severity, and values ≥190ms are associated with severe TS. A dilated IVC and increased RA size can typically be visualized on echocardiography.

Cardiac catherization can be used to measure a diastolic mean gradient and cardiac MRI can be done to evaluate RV size and function.

Treatment

Currently, there are two options for non-medical treatment of TS: balloon valvotomy and surgery. Balloon valvotomy is recommended for isolated symptomatic severe TS and mild or less TR in patients with high surgical risk. Surgery is recommended for isolated symptomatic severe TS with low-to-moderate surgical risk and severe TS undergoing surgery for left sided valve disease. In patients with high surgical risk and isolated symptomatic severe TS and moderate or greater TR, an individualized assessment of risks/benefits of TV surgery vs. medical therapy is applied.

Similar to other valves, options for TV surgery include repair or replacement. Set up and exposure is identical to surgery for TR. Median sternotomy, right thoracotomy, or robotic approaches can all provide adequate exposure of the TV. Bicaval cannulation with snaring of both cava is done to isolate the right atrium. If only the tricuspid valve needs to be addressed, surgery can be done on a beating heart on cardiopulmonary bypass with mild hypothermia. If aortic cross-clamping is utilized, antegrade cardioplegia is used to achieve arrest. Retrograde cardioplegia is not routinely used; if employed, however, a purse string is placed around the coronary sinus to prevent backflow of cardioplegia into the RA. Incision for the right atriotomy starts close to the right atrial appendage and is continued towards the posterior aspect of the atrium between the right inferior pulmonary vein and the IVC. If the mitral valve also needs to be addressed, a transeptal approach can be utilized.

Repair options for TS are limited; valve commissurotomy can be useful if leaflet fusion is found. The valve is carefully inspected and the incision is started 4-5 mm from the annulus. It is continued apically into the papillary muscle for at least 1cm. Care is taken that the edges of each side the commissurotomy incision are supported by chordae. In the current era, balloon valvotomy has replaced surgical commissurotomy in most cases.

Due to the pathology of TS, TV replacement is usually indicated. Decision of mechanical vs. bioprosthetic valve is individualized to each patient. During replacement, all attempts should be made to preserve the tricuspid valve apparatus. The remainder of the operation proceeds in the usual manner for a tricuspid valve replacement. Care is taken to avoid injuring the conduction system, which lies in the region of the septal leaflet in close proximity to the anteroseptal commissure.

Anatomy

Etiology

Pathophysiology

Diagnosis of TS

Treatment

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