Pathophysiology

Tricuspid regurgitation due to primary structural valvular abnormalities is rare, but will occasionally be seen due to rheumatic heart disease, myxomatous disease (prolapse), infective or marantic endocarditis, carcinoid heart disease, anorectic drugs, trauma, Marfan’s syndrome, or Ebstein’s anomaly. In addition, the tricuspid valve can be damaged during placement of leads for pacemakers or implantable cardioverter‐defibrillators or during right ventricular biopsies in heart transplant recipients.

In contrast, secondary functional tricuspid regurgitation is commonly encountered as a consequence of conditions associated with increased pulmonary arterial pressures, such as left ventricular systolic or diastolic dysfunction, mitral regurgitation, mitral stenosis, primary pulmonary disease, or primary pulmonary hypertension. Dilatation of the tricuspid annulus may also be seen in right ventricular infarction or in dilated cardiomyopathies.

The backward flow of blood from the RV to the RA is often clinically subtle due to the relatively compliant RA and the more conspicuous manifestations produced by the underlying primary disease process. Nevertheless, as the regurgitation becomes more severe, the signs and symptoms of elevated systemic venous pressure become evident and, in severe disease, cardiac output is diminished.

Hemodynamic changes detected by physical exam

Symptoms and signs are often due to associated left‐sided heart disease or pulmonary disease but, if there is significant tricuspid regurgitation, signs of this are generally evident on the physical exam. As with any cause of right heart failure, there are likely to be congestive findings on physical exam such as pedal edema, ascites, and hepatic enlargement.

Inspection of the jugular veins will generally demonstrate both distention correlating with elevated RA pressure, and a distinct and prominent CV wave reflecting systolic regurgitant flow into the RA. The typical murmur is holosystolic and located at the left sternal edge. Augmentation of the murmur with inspiration helps to distinguish tricuspid from mitral regurgitation.

Hemodynamic changes detected by echocardiography

Two‐dimensional (2D) and Doppler echocardiography are invaluable in the evaluation of tricuspid regurgitation [1]. The 2D portion of the study evaluates the structure of the valvular apparatus, but, as already noted, this is normal in the overwhelming majority of cases. RA and RV size, however, give important clues to the duration of the volume and pressure overload.

The Doppler component of the study yields specific hemodynamic information. Color flow and pulse‐wave examination reveal the presence, direction, and magnitude of the regurgitant jet. Detection of systolic flow reversal in the inferior vena cava and hepatic veins is generally indicative of severe tricuspid regurgitation. Finally, continuous‐wave Doppler and the modified Bernoulli equation can be used to estimate the RV and pulmonary artery systolic pressures. In tricuspid regurgitation, the gradient between the RV and the RA during systole equals four times the square of the velocity. This gradient is then added to the estimated right atrial pressure (the jugular venous pressure) to estimate RV systolic pressure. In the absence of pulmonic stenosis, this also equals pulmonary systolic pressure. It is important to recognize that this calculation estimates the severity of the pulmonary hypertension, not the volumetric severity of the tricuspid regurgitation itself.

Hemodynamic changes evident at catheterization

In the cardiac catheterization laboratory, the findings associated with tricuspid regurgitation are most evident in the RA pressure tracing (Figure 13.2). The normal RA waveform consists of an A wave associated with atrial contraction, a C wave associated with ventricular contraction, and a V wave associated with rising atrial pressure just prior to opening of the tricuspid valve. With volumetrically important tricuspid regurgitation, there is a large systolic wave in the right atrial tracing, reflecting retrograde ejection of blood and consequent transmission of pressure from the RV to the RA. This waveform is variously termed an S wave or a CV wave, as it occurs during systole and subsumes the normally independent C and V waves. The magnitude of the systolic wave is determined by both the severity of the regurgitation and the compliance of the RA [2].

Catheterization data do not allow definitive distinction between structural and functional tricuspid regurgitation. However, severe tricuspid regurgitation associated with relatively low RV and PA systolic pressures (less than 40 mm Hg) are more likely to be at least partially due to organic valvular disease. On the other hand, tricuspid regurgitation associated with very high RV systolic pressures is much more likely to be functional.

Treatment

In the case of functional tricuspid regurgitation, the mainstay of therapy is treatment of the condition causing pulmonary hypertension. This may be medical therapy as, for example, in the setting of left ventricular failure, or procedural as, for example, in the setting of mitral stenosis. Diuretics may be useful for refractory fluid retention. With structural valve disease, tricuspid valve repair or replacement is appropriate for patients who are either refractory to medical therapy or undergoing surgery for coexistent mitral valve disease. Often a prosthetic ring is used for annuloplasty. If valve replacement is necessary, bioprostheses are favored because the tricuspid valve may be relatively prone to thrombosis.

Pathophysiology

Acquired tricuspid stenosis is uncommon. Most cases are due to rheumatic heart disease, carcinoid heart disease, or stenosis of a prosthetic valve initially placed for tricuspid regurgitation. When rheumatic tricuspid stenosis is present, it is generally associated with mitral stenosis, which accounts for most of the presenting signs and symptoms. The signs and symptoms of tricuspid stenosis may be mimicked by tumors (myxoma or metastasis) or vegetations that obstruct RV inflow.