Only 75% of severe tricuspid regurgitation is classified as functional, or related primarily to pulmonary hypertension, right ventricular dysfunction, or a combination of both. Non-functional tricuspid regurgitation occurs when there is damage to the tricuspid leaflets, chordae, papillary muscles, or annulus, independent of right ventricular dysfunction or pulmonary hypertension. The entities that cause non-functional tricuspid regurgitation include rheumatic and myxomatous disease, acquired and genetic connective tissue disorders, endocarditis, sarcoid, pacing, RV biopsy, blunt trauma, radiation, carcinoid, ergot alkaloids, dopamine agonists, fenfluramine, cardiac tumors, atrial fibrillation, and congenital malformations. Over time, severe tricuspid regurgitation that is initially non-functional, can blend into functional tricuspid regurgitation, related to progressive right ventricular dysfunction. Symptoms and signs, including a falling right ventricular ejection fraction, cardiac cirrhosis, ascites, esophageal varices, and anasarca, may occur insidiously and late, but are associated with substantial morbidity and mortality. Attempted valve repair or replacement at late stages carries a high mortality. Crucial to following patients with severe non-functional tricuspid regurgitation is attention to echo quantification of the tricuspid regurgitation and right ventricular function, patient symptoms, and the physical examination. Keynote Lecture Series
Review of non-functional tricuspid regurgitationMore than 75% of severe tricuspid regurgitation is classified as functional or related to pulmonary hypertension or right ventricular dysfunction or dilatation, rather than independent abnormalities of the tricuspid valve components: leaflets, annulus, chordal attachments, and papillary muscles. An understanding of non-functional tricuspid regurgitation mandates an appreciation of functional tricuspid regurgitation because the former may ultimately be worsened by some of the same forces that propel the latter (1,2).The anatomy of the tricuspid valve lends itself to functional impairment. Unlike the dense, separate, fibrous structure, with two fibrous trigones, that surrounds the mitral valve, the tricuspid annulus, with only a right fibrous trigone, blends into the right atrial fibro fatty structures and is more susceptible to dilate or not reduce appropriately in size during systole, with either right atrial or right ventricular dilatation. Only two papillary muscles, albeit with an additional posterior commissural chord, supply three leaflets. The chordal attachments to the anterior leaflet arise largely from the anterolateral papillary muscle, not both papillary muscles, and there is a reliance on attachments to the moderator band and free wall. The smallest leaflet, the septal leaflet, is relatively fixed. Right ventricular expansion can readily tether or restrict the anterior leaflet. The posterior leaflet can become restricted via an interesting mechanism: the posteroseptal portion of the valve is more apically ...