Mild tricuspid valve disease is common, and usually clinically silent.1 Moderate and severe tricuspid regurgitation, however, are increasingly recognized as an important marker of morbidity and mortality.2 By far the commonest etiology is secondary or functional tricuspid regurgitation, where the valve leaflets are structurally normal, and regurgitation is primarily a result of annular dilatation in the setting of right or left heart dysfunction or dilatation, or pulmonary hypertension.3 Secondary tricuspid regurgitation is a very dynamic lesion, commonly seen in patients with left-sided valvular disease, ischemic heart disease, and atrial fibrillation. Primary tricuspid disease is most commonly a result of endocarditis, carcinoid heart disease, and rheumatic valve disease, with lead- and catheter-related pathology from cardiac devices as an increasingly recognized cause. Apart from congenital lesions involving the pulmonary valve or the right ventricular infundibulum and carcinoid heart disease, pulmonary valve disease as an acquired condition in adults is extremely rare. The pulmonary valve is the least commonly involved in infectious processes such as rheumatic fever and bacterial endocarditis.
Tricuspid valve disease is present in 15% of the population.4 The tricuspid valve has recently become a more prevalent focus of interest, but used to be described as “the forgotten valve,” reflecting a clinical and research predilection for the left-sided heart valves.5 The most common valve lesion is secondary tricuspid regurgitation,6 also known as functional regurgitation.4 It is characterized by valvular insufficiency in an otherwise structurally normal valve, resulting from annular dilatation caused by right heart dysfunction or dilatation,7 pulmonary hypertension,8 or left heart dysfunction.
The tricuspid valve is the most apically (or caudally) placed valve with largest orifice among the four valves.9 The tricuspid apparatus includes leaflets or cusps, chordae and papillary muscles, and tricuspid annulus in addition to the right atrium and right ventricle (Fig. 51–1).
Relationship of the tricuspid valve to the aortic valve, conduction tissue and other surrounding anatomical structures. AL, anterior leaflet; APC, anteroposterior commissure; ASC, anteroseptal commissure; AVN, atrioventricular node; LCS, left coronary sinus; PL, posterior leaflet; PSC, posteroseptal commissure; RCS, right coronary sinus; SL, septal leaflet.
The tricuspid annulus is oval in shape and becomes more circular when dilated. The annulus has a complex nonplanar shape with the posteroseptal portion being the lowest and the anteroseptal being the highest.9 It tends to become more planar with moderate or severe “functional” tricuspid regurgitation. The annular orifice area is approximately 20% larger than the mitral annulus area, with a major diameter of 3.0 to 3.5 cm in adults. The larger orifice provides for the inflow to occur at lower velocities and lower pressure decreases. Both early and late diastolic velocities are lower than the ...