Literature
Clinical Pearls & Morning Reports
Published May 17, 2023
How does tricuspid regurgitation present clinically?
Because tricuspid regurgitation is most frequently diagnosed in patients with coexisting conditions, many clinicians have viewed it as an innocent bystander to the more consequential diseases of the left heart and pulmonary vasculature. Natural history studies highlight the need for early diagnosis of tricuspid regurgitation; survival is progressively shorter with the increasing severity of tricuspid regurgitation, even after adjustment for coexisting conditions. Read the NEJM Review Article here.
Clinical Pearls
Q: Is there anything unique about the chordal attachments that support the tricuspid-valve leaflets?
A: Thinner than mitral-valve leaflets, the tricuspid-valve leaflets are supported by chordae attached to a major anterior papillary muscle along the lateral wall of the midright ventricle, as well as one or more smaller posterior papillary muscles. The anterior papillary muscle supplies chordae to the anterior and posterior leaflets along their line of coaptation, whereas the posterior papillary muscles supply chordae to the posterior leaflet (or leaflets) and the posterior segment of the septal leaflet. The chordal attachments arising either from small septal papillary muscles or directly from the septum are unique to the tricuspid valve and support the anterior segment of the septal leaflet and the adjacent segments of the anterior or posterior leaflet. Given the complex chordal arcades and their attachment sites, the tricuspid valve is sensitive to changes in the position and function of the free wall of the right ventricle, as well as the interventricular septum.
Q: What are some of the predictors of tricuspid regurgitation and its severity?
A: As with other valvular heart diseases, the prevalence of tricuspid regurgitation increases with age. Female sex is an independent predictor of the severity and progression of tricuspid regurgitation. Atrial arrhythmias — in particular, atrial fibrillation — are common in patients with tricuspid regurgitation and occur in both incident and progressive valvular disease. Besides older age, female sex, and atrial fibrillation, other clinical predictors of severe and progressive tricuspid regurgitation include elevated pulmonary-artery systolic pressure and increased left atrial size.
Morning Report Questions
Q: How is tricuspid regurgitation categorized?
A: Primary tricuspid regurgitation occurs as a result of intrinsic valve disease and is attributable to congenital anomalies, infective endocarditis, rheumatic disease, carcinoid heart disease, toxic effects of chemicals, tumors, blunt trauma, or myxomatous degeneration. In patients with secondary tricuspid regurgitation, the intrinsic structure of the leaflets appears normal, but there can be abnormalities of the right atrium, tricuspid annulus, or right ventricle that result in leaflet malcoaptation. Atrial abnormalities are seen in 10 to 25% of patients with secondary tricuspid regurgitation. Patients with ventricular secondary tricuspid regurgitation have dilatation of the right ventricle (mainly the midventricular free wall), leading to apical displacement of the papillary muscles and tethering of the leaflets. Right ventricular dilatation and dysfunction are most frequently due to remodeling in the context of elevated pulmonary-artery pressures resulting from precapillary or postcapillary pulmonary hypertension. Tricuspid regurgitation associated with a lead from a cardiac implantable electronic device is now a distinct category, separate from primary causes.
Q: How does tricuspid regurgitation present clinically?
A: Patients with severe tricuspid regurgitation present with signs and symptoms of chronic right heart failure, including systemic fluid retention, leading to elevated jugular venous pressure, peripheral edema, and ascites; reduced intestinal absorption and anasarca; decreased cardiac reserve, resulting in exercise intolerance, dyspnea, and poor functional capacity; and decreased cardiac output, with progressive end-organ damage caused by a combination of end-organ venous congestion and underperfusion. The signs and symptoms of reduced cardiac output may be mistaken for left heart failure, delaying a timely diagnosis of tricuspid regurgitation.