Quantificatiob of Tricuspid Regurgitation: Beyond Geometrical Assumptions
6 الي 8 مرداد 1395، مشهد - ايران
Presentation Type: Speech
So far, we have approached the patient with functional tricuspid regurgitation by transferring the concepts and echocardiographic parameters developed for patients with mitral regurgitation. Even the cut off values of the effective regurgitant orifice area (EROA) for severe tricuspid regurgitation are the same (40 mm2) without accounting for the different anatomy of the two valve apparati and the peculiar hemodynamic environment in which the tricuspid valve is working. The tricuspid valve is a three leaflet valve and the orifice of the tricuspid regurgitant valve is neither circular nor flat. Therefore, the geometric assumptions needed to use the PISA formula to calculate the EROA or to measure the diameter of the vena contracta are not met in functional tricuspid regurgitation (FTR). For the same reasons, and as it has been demonstrated by three-dimensional echocardiography, the shape of the proximal isovelocity surface is not a hemisphere. Accordingly, a single radius cannot account for the size and the complex shape of the PISA. In addition, the right ventricle is a volume pump and the regurgitant volume in FTR varies greatly during the systolic period (larger at proto- and end-systole and smaller at mesosystole), with loading conditions (e.g. diuresis or volume overload, or even patient position can dramatically change the severity of the regurgitation), and with respiratory cycle. By simply measuring parameters, which do not have any solid anatomic and functional ground, taken at one point during cardiac systole, we are oversimplifying a complex pathophysiological problem. Accordingly, we need to re-think the pathophysiology of FTR. Tricuspid annulus dilation is only one of the mechanisms that creates FTR. Papillary muscle displacement and leaflet tethering are also involved. The different mechanisms have a different role in FTR associated to different pathophysiological conditions (e.g. FTR in pulmonary hypertension vs. FTR in chronic atrial fibrillation). In addition, the role of the right atrial volume as a determinant of tricuspid annulus size has been ignored so far. Finally, all measurements we perform should be related to the hemodynamics (right ventricular and right atrial volumes, pulmonary pressure) of the patient at the time of the echocardiographic study, integrated over time throughout systole and with respiratory phase.