Tricuspid Stenosis


Tricuspid stenosis is characterized by reduced tricuspid orifice, thereby creating a barrier to the passage of blood from the right atrium to the right ventricle during diastole.

tricuspid valveThe frequency of tricuspid stenosis is perceived differently by different authors. Congenital tricuspid stenosis is rare. Through hemodynamic investigation, the characteristic signs of tricuspid stenosis are found in 3-5% of operated valvulopathy; the disease is more frequent in women.

Etiology of tricuspid stenosis

The most common cause of tricuspid stenosis is rheumatic disease. Only exceptionally it may be the result of endomyocardial fibrosis, carcinoid syndrome, fibroelastoma, valvular vegetation’s or systemic lupus erythematosus. Other causes of obstruction of the right atrioventricular orifice are right atrial tumors (myxomas most common) or tumors extra-cardiac compression.

Rheumatic tricuspid impairment is practically never met as an isolated injury but is attached to mitral injuries, aortic valve or both. The most common tricuspid rheumatic injury is accompanied by mitral lesion. Only about 3-5% of the patients with rheumatic mitral stenosis and a tricuspid rheumatic lesion are clinically manifested. In contrast, nearly half of patients with rheumatic cardiac disease present tricuspid organic changes. At almost 15% there is a certain degree of tricuspid stenosis.

The main lesion is encountered by commissural fusion. The large area of the tricuspid valve lesion makes this more difficult to identify. Cusps are usually thickened and quite mobile, and valvular calcification is rare. When it occurs, is less severe than the left heart valves. There may be a variable degree of shortening and fusion of chordae tendineae, which is generally less marked in comparison with lesions of the mitral subvalvular apparatus. Result a tricuspid valve of a diaphragm aspect, with a central oval aperture and relatively fixed dimensions. Thus, tricuspid valve stenosis will present a degree of regurgitation. As in mitral stenosis, there is a propensity for females, and the range of the incidence is increased, tricuspid stenosis is between 20 and 60 years. There are regions of the world where the incidence of rheumatic tricuspid lesions is higher (for example: India).

Clinical manifestations and diagnosis

Decreased cardiac output causes symptoms such as extreme fatigue and systemic venous congestion that causes jugular turgor, edema peripheral up to anasarca, marked hepatomegaly and ascites. These clinical manifestations contrast with the absence or low-level of dyspnea.

Tricuspid stenosis masks clinical signs of coexisting mitral stenosis. Lack of pulmonary congestion due to “the tricuspid dam” causes lack of hemoptysis, paroxysmal nocturnal dyspnea or episodes of acute pulmonary edema. Actually, the absence of manifestations of congestion in the pulmonary circulation in patients with mitral stenosis should raise the suspicion of tricuspid stenosis. Sometimes another encountered symptom is a waveform feeling in the neck corresponding to the wave from the jugular diagram.

Physical examination is often misleading because of the signs of tricuspid stenosis are partially masked by the signs associated with mitral stenosis. Therefore clinical detection of tricuspid stenosis is needed for this lesion first to be suspected and searched systematically. Jugular pre-systolic wave (wave A), it presents when patients are in sinus rhythm; it can be easily confused with a systolic wave. A pre-systolic hepatic pulsation occurs quite frequently. Sometimes it can be perceived a pre-systolic impulse given to the right of the sternum strong right atrial contraction.

As mentioned above, clinical examination of the chest shows no pulmonary or rales load and are strikingly poor in comparison to often massive edema up to the anasarca with jugular turgor and Scythian.

Therefore, in principle, tricuspid stenosis diagnosis is suggested by the combination of a wave clear and with no evidence of pulmonary hypertension and right ventricular enlargement.

Clinical suspicion may be strengthened by the presence of a diastolic murmur at the lower pole of the sternum, sometimes accompanied by rustling. It is emphasized during inspiration. Auscultation of tricuspid stenosis is similar to that of mitral stenosis, but is often covered by it. The clement of opening sounds usually better from the left parasternal at the lower end of the sternum, as well as diastolic murmur. The latter has a higher tone to diastolic rumble of mitral stenosis. Pre-systolic breath is rough, starts earlier than that of mitral stenosis, and has a crescendo-decrescendo character (appearance – rhombic).

Paraclinical explorations

  • Electrocardiogram does not provide very important data. May be present signs of right atrial hypertrophy, possibly disproportionate to the absence of right ventricular hypertrophy. More frequently are present signs of biatrial hypertrophy. The sinus rhythm is present in more than half of patients.

  • Radiological examination is highly characteristic. It shows a significant increase in the right atrium associated with no evidence of pulmonary hypertension and with clear lung fields. Right atrium, the biggest are found in patients with stenosis and tricuspid regurgitation, which are associated to atrial fibrillation and a mid-right atrial pressure over 12mmHg.

  • Echocardiography may be useful in the diagnosis and assessment of severity of tricuspid stenosis. Unfortunately, due to its position, tricuspid is difficult to assess. Features of tricuspid stenosis are:

  • In 2D mode:

  • tricuspid valve thickening and of the chordae;

  • limiting the opening movement of the diastolic valve (look in the “dome”);

  • Dilatation of the right atrium and of the inferior vena cava.

Tricuspid orifice planimetry is not feasible.

  • At the Doppler exam:

  • The increased diastolic gradient pressure AD / VD;

  • Lengthening the half-life of the pressure (T 1/2) over 420 ms up to 150ms (140ms :90-n);

  • Reduction of the functional tricuspid orifice surface calculated by the empirical formula: ST = 190 / T1/2p.

Tricuspid stenosis flow is usually made ​​within apical, 4 rooms or parasternal left (cross cup cavities centered on the left). Holodiastolic flow is positive and creates a set with the speed of a slower decrease; the higher is the stenosis the less is the severity. Signs of severe tricuspid stenosis evoking Doppler are:

  • The average diastolic gradient> 5mmHg;

  • Functional tricuspid area <2cm ².

Meanwhile, continuous Doppler quantification of stenosis is not sufficiently reliable.

Cardiac catheterization is the essential method for determining severity and to confirm the diagnosis. The main features that can be highlighted hemodynamic by catheter are diastolic transtricuspid gradient over 5 mmHg, increased right atrial pressure and cardiac output decreased. A valvular tricuspid orifice area less than 1.5 cm2 usually causes significant hemodynamic disturbances and significant clinical manifestations. Cardiac index was closely correlated with the tricuspid valve area, as opposed to the pressure in the right atrium.

Differential diagnostic

Tricuspid stenosis must be differentiated from:

  • Diseases which determine right heart insufficiency: mitral stenosis, right atrial myxoma;

  • Hepatic cirrhosis given the hepato-splenomegaly, ascites and edema as well as alteration often severe, the liver function tests due to prolonged the hepatic stasis;

  • Cardiac amyloidosis and other restrictive cardiomyopathies may have a similar clinical and hemodynamic, echocardiographic appearance but is different from the tricuspid stenosis and the endomyocardial biopsy, rectal or gingival, confirm the presence of amyloid deposits;

  • The constrictive pericarditis. In favor of this diagnosis it pleads the following:

1. Physical signs

  • No heart beating or retraction of the systolic peak;

  • Clacment protodiastolic pericardium, which occurs in 0.06-0.12 seconds after the second heart sound;

  • Kussmaul’s pulse pulsus paradoxus;

  • Atrial fibrillation in 30-50% of cases.

2. Chest radiography:

  • pericardial calcification in 5-50% of patients;

  • Normal cardiac silhouette (1/3 of patients) or increased its size (two thirds of patients), pleural effusion or pulmonary stasis aspect;

3. Echocardiography:

  • thickening of the pericardium, which is rarely highlighted;

  • Indirect signs: biatrial dilatation in contrast with ventricles with normal size and contractions dilated of the inferior vena cava and the absence of inspiratory collapse, displacement of the interventricular septum toward the left ventricle during inspiration.

4. Nuclear magnetic resonance and computed tomography are highly relevant for the detection of pericardial thickening;

5. Cardiac catheterization is useful to confirm pericardial restriction;

6. Pericardial biopsy is performed during surgical treatment of pericarditis and is essential in identifying causal tuberculosis or malignancy.

Therapeutic attitude and surgical indications

Basic treatment is surgery in tricuspid stenosis. However, soda restriction and diuretic treatment may cause a significant symptomatic improvement. A period of increased urine output may decrease hepatic congestion improving liver function and reducing the risk of surgery.

Surgical indication to the tricuspid stenosis is putted when the tricuspid valve area is less than 2 cm2 and the average pressure gradient in diastolic trans-tricuspid is over 5 mmHg. Usually the final decision on surgical treatment of tricuspid stenosis is taken on the operating table.

In case of coexistence of tricuspid stenosis and mitral stenosis, tricuspid stenosis resolution is irrational, because it is due to the pulmonary congestion precipitation and its manifestations.

Because tricuspid stenosis is almost always accompanied by a degree of impairment, digital commissurolysis may not result in significant hemodynamic improvement, only to turn into a severe stenosis insufficiency. A reconstruction of the tricuspid valve to transform the competent bicuspid valve it can be a solution. This can be achieved through commissures only at the level commissurotomy anterior septal and posterior septal. Commissurotomy at the level antero-posterior commissure does not indicate an increased risk of subsequent severe regurgitation.

In case of a severely deformed tricuspid replacement with a valve prosthesis is required. At the moment, however there are many controversies both regarding to prosthetic indication and to the type of prosthesis best suited for this position. A number of variables have been associated to the need for prosthetic tricuspid. These include jugular venous distension level, severity of tricuspid insufficiency determined by ultrasound, heart surgery history and association with tricuspid stenosis.

It can excise the tricuspid valve or it can be left in place. In case of excision the valve is allowed a 2-3 mm sponge from the ring. This is especially important at the septal cusp level to avoid injury management system. If the tricuspid valve is left in place, it preserves the subvalvular structures, allowing the management system to avoid injuries. If possible obstruction is suspected by previous valve right ventricular outflow tract, the central valve portion can be excised by chordae facility.

Tricuspid valve replacement with a homograft is more complicated and is mostly with a mitral valve. Fixing the papillary muscles is either intracavitary (in the right ventricle) or through the right ventricular wall. It requires experience to appreciate a good chordae length. The ring is set with a monofilament suture line. It is placed an annuloplasty ring to prevent expansion and to ensure proper coaptation of the cusps. Special care is needed to achieve the suture to prevent conduction disturbances.

Regarding the type of prosthesis that is most suitable for prosthetic tricuspid opinions are divided. Many authors prefer biological prostheses been given better strength under low pressures at the right heart level. However bio degeneration in younger patients and their calcification represent a problem. The risk of thrombosis of mechanical prostheses in the tricuspid position is bigger than the prosthesis from the left heart. Frequently, thrombosis develops gradually, and intravenous thrombolysis is highly effective. Mortality for re-interventions is quite small.

Recent studies with double-disc mechanical prostheses St. Jude have provided encouraging data, allowing the surgeon to confidently recommend a mechanical valve to young patients without contraindications to anticoagulation. This strategy will avoid past situations in which patients received a bio prosthetic implant on the right side and a mechanical prosthesis on the left side of the heart.

Bio prostheses, porcine or pericardial tissue have a proper functioning in the tricuspid position. Studies show a longer period of life without structural dysfunction or tricuspid replacement in comparison with the mitral position.

Nakano et al reported the absence of structural degeneration of 100% of patients with Carpentier-Edwards pericardial xenograft at 9 years but to non-structural disturbances at 72.8%. The cause of non-structural dysfunction was pannus formation (organized thrombotic material) on the face of the ventricular cusps. This discovery is often subclinical. Follow-up echocardiography revealed an incidence of 35% of the anatomical findings in patients followed for at least 5 years. Guerra reported similar changes in explanted porcine pig valve. Explanted valves in tricuspid position had a lower degree of degeneration and calcification compared with explanted valves in the mitral position. The study reports pannus formation on the ventricular tricuspid valve cusps. Pannus interferes with the pliability and the functioning of the cusps.

The study published in 2001 by Nakano about bio-prosthetic valve in the tricuspid position reports the absence of indication of reoperation at 63% of 48 patients who were followed 18 years. The absence of structural damages was recorded at 96% of patients but structural dysfunction occurred at 77%. Surgical re-intervention of bio-prosthetic replacement was required previously placed to 12 of 58 survivors. To 6 of the 12 patients, the primary indication was prosthetic dysfunction and 7 showed pannus on the face ventricular cusps.


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