Tricuspid regurgitation

Tricuspid regurgitation (TR)
Trivial (small) TR is frequently detected by echocardiography in normal subjects, and should never be interpreted as an abnormal finding. 
Pathological TR is more often secondary (not due to a disorder of the valve structure) and less often it is attributed to a primary (structural) valve lesion. 
Secondary TR is due to annular dilatation and increased tricuspid leaflet tethering and is caused by:
1) Right ventricular (RV) pressure overload (usually caused by pulmonary hypertension as a consequence of left sided heart disease, chronic pulmonary disease, connective tissue disease, congenital heart disease, or idiopathic pulmonary hypertension) 
2) RV volume overload (dilatation of the right ventricle due to an atrial septal defect, or due to intrinsic right ventricular disease with systolic dysfunction, as in right ventricular cardiomyopathy).

Primary TR (caused by structural alterations of the valve) can be caused by
 Infective endocarditis (especially in intravenous drug addicts),
Myxomatous disease (leading to prolapse of the valve leaflets)
Rheumatic heart disease,
Iatrogenic causes (
occasionally TR occurs after pacemaker implantation or after endomyocardial biopsy)
Carcinoid syndrome
( carcinoid syndrome, is  a type of neuroendocrine tumor, usually in the small bowel or appendix, with metastases to the liver, which releases serotonin metabolites into the bloodstream. These metabolites are responsible for the formation of endocardial plaques in the right heart chambers. Involvement of the tricuspid valve causes thickening and immobilization of the leaflets, resulting in significant tricuspid regurgitation and, less often tricuspid stenosis.)
Ebstein’s anomaly is a congenital malformation characterized by apical displacement of the annular insertion of the septal and posterior leaflets of the tricuspid valve and atrialization of a portion of the ventricular myocardium.
Endomyocardial fibrosis,
Ergot-like drugs,
Thoracic trauma
Often, even severe TR can be tolerated for a long period of time without significant symptoms. Symptoms of the causative disorder may be present. Eventually, severe TR will produce symptoms of right heart failure, such as fatigue, exercise intolerance, edema, vague abdominal discomfort due to hepatomegaly.
Physical examination in TR
The most common physical signs of severe TR are prominent v waves in the jugular veins and a pulsatile liver. Both these signs are due to regurgitation of right ventricular blood into the systemic veins. 
The systolic murmur of TR is heard at the lower left sternal border and at the xiphoid area. The holosystolic murmur of tricuspid regurgitation (TR) is often soft (and may be absent in many cases of severe TR, if flow is not turbulent enough) and it becomes louder on inspiration.
In severe cases peripheral (ankle or leg) edema, or even ascites may be present.
Frequent findings are an incomplete right bundle branch block and atrial fibrillation.
Echocardiography in tricuspid regurgitation (TR)
TR is identified using color flow mapping of the systolic
regurgitant jet in the right atrium.
Evaluation of the pulmonary systolic pressure from the measurement of the peak velocity of the TR jet should be carried out in all cases. This may be inaccurate in the presence of severe TR (with a large regurgitant volume) because this leads to a lower pressure difference (pressure gradient) between the right ventricle and the right atrium .
The presence of associated lesions, particularly left ventricular systolic or diastolic dysfunction and lesions of the left-sided cardiac valves, should be assessed.
In primary TR, valve morphology can help determine the etiology: vegetations in endocarditis, leaflet retraction and thickened leaflet tips in rheumatic valve disease, prolapsing thickened leaflets in myxomatous disease, a flail leaflet in myxomatous or post-traumatic valve involvement.
In secondary TR annular dilatation or leaflet tethering is observed:
Significant tricuspid annular dilatation is defined in the apical 4 chamber echocardiographic view by a diastolic diameter ≥40 mm , or >21 mm/ mof body surface area. 
Significant tethering of the valve, in secondary TR, is characterized by a coaptation distance > 8 mm. This is the distance between the tricuspid annular plane and the point of coaptation of the valve leaflets in mid-systole from the apical 4-chamber view.
Evaluation of the right ventricular (RV) dimensions and function should be performed.  Indications of RV systolic dysfunction are: Tricuspid annular plane systolic excursion (TAPSE) <15 mm,
 pulse wave TDI-derived peak systolic velocity of the lateral tricuspid annulus <11 cm/s, and
 RV end-systolic area >20 cm2
Tricuspid regurgitation (TR) severity is estimated from the extent of the jet, or better by vena contracta width (vena contracta is the narrowest portion of the jet, near its origin from the valve leaflets). In many cases, just a visual estimate can allow judgment on the severity of regurgitation.  In case of TR with an eccentric jet, a large eccentric jet reaching the posterior wall of the right atrium indicates significant TR.  Conversely, small jets and a normal size of the right atrium and right ventricle usually indicate mild TR.
Regurgitant jet area correlates roughly with the severity of regurgitation:mild <5 cm2 
moderate 6-10 cm2
severe >10 cm2.  

Other more accurate indications of severe TR are:
Vena contracta ≥ 7 mm

In continuous wave Doppler examination of TR, a dense/triangular TR Doppler signal with early peaking.
PISA radius >9 mm, at color Doppler examination with baseline shift, with a Nyquist limit (aliasing velocity) of 28 cm/s towards the direction of the regurgitation.
Effective regurgitant orifice area (EROA) ≥40 mm².
Regurgitant Volume ≥45 ml/beat.
In severe TR, enlargement of the right atrium, right ventricle, and inferior vena cava is almost always present.

Diuretics improve signs of congestion. Specific therapy of the underlying disease is necessary, when feasible.
Surgery (usually tricuspid annuloplasty with a prosthetic ring) is indicated in :
Symptomatic patients with severe primary TR without severe right ventricular dysfunction. 
In asymptomatic or mildly symptomatic patients with severe isolated primary TR and progressive right ventricular (RV) dilatation or progressive deterioration of RV function (class IIa indication).
In patients with severe (indication class I) or moderate (indication class IIa) primary TR, or moderate secondaryTR with dilated annulus (for limits of annular diameter see above) undergoing left-sided valve surgery.
The surgical operation performed is usually annuloplasty with a prosthetic ring, but in advanced forms of tethering and RV dilatation, or in a severe valve deformity that cannot be corrected, valve replacement should be considered. Valve replacement is performed with large bioprostheses (these are preferred than mechanical valves in the tricuspid position).

Tricuspid regurgitation (color doppler echocardiography). A video-link (by dr Luke Howard) :