In contrast to aortic or mitral diseases, there has been far less discussion on indications for tricuspid valve repair or replacement. Despite the fact that tricuspid regurgitation (TR) can result in significant symptoms, it remains undertreated. Patients are rarely referred for isolated surgical repair, or replacement, and most surgeries are performed in the context of other planned cardiac surgery. In this article, we will review the causes and natural history of untreated severe TR, indications and surgical approaches for correction of TR.
Causes, Assessment and Natural History
Approximately 80 % of cases of TR are functional due to right ventricular (RV) enlargement resulting in annular dilation, or leaflet tethering.1 RV dilatation is secondary to left heart failure, other valvular causes, RV volume or pressure overload. Less-common causes of TR are organic and include rheumatic, congenital, endocarditis, traumatic/iatrogenic, pacemaker or defibrillator leads interfering with leaflet coaptation, or myxomatous degeneration of the tricuspid valve. A unique cause of TR is isolated TR, the result of marked tricuspid annular dilatation due to degenerative condition of the annulus and/or right atrium.1,2
With TR, patients may experience fatigue and decreased exercise tolerance as a result of decreased cardiac output or the ‘classic symptoms’ of right-sided heart failure from elevated right atrial pressures, such as peripheral oedema, ascites, congestive liver and decreased appetite. Atrial fibrillation is also common as a result of right atrial enlargement. Echocardiography is routinely used to assess the severity of TR in clinical practice. This is performed in an integrative manner using color Doppler, assessing the morphology of continuous wave Doppler recordings across the valve, pulsed wave Doppler of the hepatic veins, measurement of vena contracta width and calculation of effective regurgitant orifice (ERO) using the proximal-isovelocity-surfacearea (PISA) method.3 Serial assessments of TR must be interpreted in the patient’s clinical context, because severity can be affected by multiple factors, such as volume status, respiratory cycle and after-load.4
Without treatment, TR may deteriorate over time, leading to worse symptoms, biventricular heart failure and death. Several trials investigated the impact of TR, in and by itself, or in conjunction with other valvar diseases, on survival and cardiac outcomes.5–8 In a large retrospective analysis of <5,000 patients by Nath et al.,8 it was shown that severe (and even moderate) TR is associated with worse survival even when adjusted for pulmonary artery systolic pressure (PASP), left ventricular ejection fraction (LVEF), RV size and function. The limitations of all these studies were that the considerable matter of multiple co-morbidities affected survival (severe pulmonary hypertension, poor LV function, organic valve disease right and left-sided), so that it was difficult to prove whether TR in and by itself independently affects survival, or is it a surrogate for associated conditions.