Tricuspid valve disease involves the atrioventricular valve apparatus that separates the right atrium (RA) from the right ventricle (RV). Tricuspid regurgitation (TR) and tricuspid stenosis (TS) are commonly encountered. Isolated tricuspid valve disease is rare. It most often occurs as a secondary condition. TR is more common than TS and usually develops in association with pulmonary hypertension in patients with mitral stenosis or regurgitation. Most patients with rheumatic tricuspid valve disease present with TR or a combination of stenosis and regurgitation. Rheumatic TS does not occur as an isolated lesion, but it often accompanies mitral and aortic valve disease. Some patients may develop TR in association with trauma or infective endocarditis. TS is nearly always rheumatic in origin. However, congenital tricuspid atresia, RA tumors, tricuspid valve vegetations, the presence of a pacemaker lead, or compression caused by extracardiac tumors may produce a clinical picture similar to that of TS. In addition, in patients with carcinoid syndrome, endomyocardial fibrosis may lead to obstruction of RV inflow, resulting in a clinical presentation similar to that of TS. [1, 2, 3, 4]
For patients with tricuspid valve disease, echocardiography is the preferred examination.  Echocardiography provides excellent images and may be used to detect and quantitate tricuspid regurgitation. It also permits assessment of the dimensions of cardiac chambers, determination of RV and pulmonary pressures, and delineation of associated valvular diseases. If acoustic windows are poor, transthoracic echocardiograms may be suboptimal. In such instances, transesophageal echocardiography is helpful. [6, 7, 8]
In TS, electrocardiograms (ECGs) show tall right atrium (RA) P waves and no RV hypertrophy. Chest radiographs show a dilated RA without an enlarged pulmonary-artery segment.
The echocardiographic changes of the tricuspid valve in TS include the following:
Diastolic doming of the valve
Thickening of the leaflets and restriction in the motion of the leaflets
Reduction in the separation of the commissures of the leaflets
A diminished tricuspid opening
With transesophageal echocardiography, depiction of the details of valvular structure is improved. On Doppler echocardiography, a delayed slope of antegrade flow is seen; such findings compare well with cardiac catheterization findings in the quantification of TS and in the assessment of associated TR. [9, 10]
ECG findings are frequently nonspecific. Incomplete right bundle-branch block, Q waves in lead V1, and atrial fibrillation are often noted.
The main purpose of echocardiographic imaging is to diagnose TR, assess its severity, and estimate pulmonary arterial pressure and the status of RV function. In secondary TR, clinically significant enlargement of the tricuspid annulus, right atrium, and right ventricle are found. In patients with TR caused by endocarditis, echocardiography may reveal vegetations on the valve or a flail valve leaflet. Transesophageal echocardiography may depict the TR vividly. [9, 10]
Doppler echocardiograms depicting TR are provided below.
In TS, radiographs may show marked cardiomegaly with conspicuous enlargement of the right atrium (RA) (ie, prominence of the right heart border), which extends into a dilated superior vena cava and azygos vein; conspicuous dilatation of the pulmonary artery may be absent. Vascular changes in the lungs characteristic of mitral valvular disease may be masked, with little or no interstitial edema or vascular redistribution; however, left atrial enlargement may be present.
In patients with functional tricuspid regurgitation, marked cardiomegaly is usually evident, and the RA is prominent. Evidence of elevated RA pressure may include distention of the azygos vein and the presence of a pleural effusion. Ascites with upward displacement of the diaphragm may be present. Systolic pulsations of the RA may be present on fluoroscopy.
In tricuspid valve disease, findings are generally nonspecfic, and false findings are frequent.
Computed tomography (CT) scans of the heart are rarely needed to delineate structural cardiac abnormalities. The degree of confidence is moderate and the rates of false-positive and false-negative findings are low. [6, 11]
Magnetic Resonance Imaging
Magnetic resonance imaging (MRI) may be helpful in delineating valvular structural abnormalities when echocardiographic assessment is suboptimal. In patients with TR, spin-echo (SE) and cine gradient-echo (GRE) imaging may provide important data. [12, 13] The rates of false-positive and false-negative findings are low. While performing cine GRE imaging, one must remember to keep the echo time somewhat long, because with short eco times, the signal void may be difficult. [6, 11]
The major hemodynamic effect of TR is augmentation of the total stroke volume of the RV. SE MRIs can display the RV myocardium well. SE MRI may be the preferred technique for accurate assessment of RV function, such as measurement of RV end-diastolic, end-systolic, and stroke volumes, as well as the ejection fraction. When the RV wall is thickened and hypokinetic, particularly with ventricular arrhythmias or syncope, MRI may be used to look for RV dysplasia (transdifferentiation of myocardium to fat). In addition to the RV, SE MRI may show enlargement of the RA, vena cava, and hepatic veins.
SE images may show structural abnormalities other than TR, including Ebstein anomaly, pacemaker leads, valvular vegetations, tricuspid prolapse, and carcinoid syndrome.
Cine GRE imaging
Cine GRE images are used to determine the severity of TR by demonstrating the area of the signal void of the regurgitant jet traveling into the RA in systole. It is best imaged in the 4-chamber view and the coronal oblique view displaying the RA and the RV.
As with Doppler echocardiography, velocity-encoded (VENC) MRI permits assessment of the severity of regurgitation by determining the maximum velocity (Vmax) in the regurgitant jet with velocity measurements in a plane parallel to the jet (in-plane measurement). The velocity measurement may then be used to calculate pulmonary arterial systolic pressure (PPA) by adding RA pressure (PRA, which is empirically taken to be 10 mm Hg) to the RV and RA pressure gradient (P). For this purpose, the following modified Bernoulli equation is used: PPA = 10 + (4 X Vmax2).
Tricuspid stenosis (TS)
The echocardiographic changes of the tricuspid valve in TS resemble those observed in the mitral valve in mitral stenosis (see the images below). Two-dimensional echocardiography characteristically shows the following:
Diastolic doming of the leaflets (especially the anterior tricuspid valve leaflet)
Thickening of leaflets and restriction in the motion of the other leaflets
A reduction in the degree of separation of the tips of the leaflets
A reduction in the diameter of the tricuspid orifice
Doppler echocardiography shows a prolonged slope of antegrade flow; Doppler echocardiography compares well with cardiac catheterization in the quantification of TS and in the assessment of associated TR.
The goal of echocardiography is to detect TR, to estimate its severity, and to assess pulmonary arterial pressure and RV function. In patients with TR secondary to dilation of the tricuspid annulus, the right atrium (RA), right ventricle (RV), and tricuspid annulus usually appear greatly dilated on echocardiography. Evidence suggests that in patients with TR, RV diastolic overload with paradoxical motion of the ventricular septum occurs to a degree similar to that observed in patients with an atrial septal defect. 
Exaggerated motion and delayed closure of the tricuspid valve are evident in patients with Ebstein anomaly. Prolapse of the tricuspid valve resulting from myxomatous degeneration may be evident on echocardiography. Echocardiographic indications of tricuspid valve abnormalities, especially TR, as evidenced on Doppler examination, may be seen in most patients with carcinoid heart disease. In patients with TR caused by endocarditis, echocardiography may reveal vegetations on the valve, or it may show a flail valve.
Transesophageal echocardiography is useful in the detection of TR.
Contrast echocardiography involves rapid injection of saline indocyanine green dye or sonicated human albumin (Albunex) into an antecubital vein while a 2-dimensional echocardiogram is recorded. The injection produces microcavities that are readily visible on echocardiography and that travel normally as a bolus through the circulation. In TR, these microcavities may be seen to travel back and forth across the tricuspid orifice and to pass into the inferior vena cava and hepatic veins during systole.
Pulsed Doppler echocardiography reveals systolic flow from the RV to the RA; it is a sensitive technique for detecting and quantifying TR. Reverse flow may also be recorded in the inferior vena cava and hepatic veins. The peak velocity of TR flow is useful in the noninvasive estimation of RV (and pulmonary arterial) systolic pressure.
Color-flow Doppler imaging is a sensitive and specific method for assessing TR; it is helpful in selecting patients for surgical treatment and in evaluating postoperative results.
The degree of confidence in echocardiography is high, and false findings are rare.
Patients who present with congestive heart failure may require assessment of tricuspid valve and LV function by use of a first-pass technique (ie, multiple-gated acquisition [MUGA] scanning). The degree of confidence is moderate, and findings may be nonspecific.
Angiography performed after the injection of contrast material into the RA, with imaging in the 30° right anterior oblique projection, characteristically shows the following:
Thickening of the leaflets
Decreased mobility of the leaflets
A diastolic jet through the constricted orifice
Thickening of the normal atrial wall
In patients with TR, there is often an elevation of RA and RV end-diastolic pressures, whether the condition is the result of organic disease of the tricuspid valve or is secondary to RV systolic overload. The RA pressure tracing usually reveals an absence of the x descent and a prominent v or c-v wave (ventricularization of the atrial pressure). The absence of these findings essentially excludes moderate or severe TR.
As the severity of TR increases, the contour of the RA pressure pulse increasingly comes to resemble that of the RV pressure pulse. An increase in RA pressure on deep inspiration or no change in RA pressure on deep inspiration, rather than the usual decrease, is a characteristic finding. Measurement of the pulmonary arterial (or RV) systolic pressure may be helpful in determining whether the TR is primary (ie, caused by disease of the valve or its supporting structures) or functional (ie, secondary to RV dilatation).
A pulmonary arterial or RV systolic pressure less than 40 mm Hg suggests a primary cause, whereas a pressure greater than 55 mm Hg suggests that TR is secondary. Intermediate values are not helpful. In many instances, right ventriculography may be helpful in the diagnosis and quantitative assessment of TR.
The degree of confidence in angiography is high, and false findings are rare.