Tricuspid Valve Regurgitation
1. When does Tricuspid Valve (the largest and the most apically positioned of the four valves in the heart) start regurtitating?
What is the expected changes in its orifice area, from its mean value of around 8 cm2?
To what extent (or fraction), annulus and diameter of Tricuspid Valve changes from their mean values, of around 11 cm2(annulus); and 28 mm (diameter) respectively?
2. Whether any reduction, which remains to be more than 25% in the tricuspid annular area with ventricular systole – always leads to Tricuspid Regurgitation?
3. Whether any changes in the tricuspid annular plane systolic excursion (TAPSE) along the longitudinal axis of RV remains to deviate significantly from the mean value of 16 mm, would it always lead to Tricuspid Regurgitation?
4. Since Tricuspid Regurgitation (TR) remains to be highly dependent on annular dilation, can we expect a significant TR even @ 30%? Or, Should it always exceed 40%?
5. Feasible to capture the markers of fine delineation between
(a) tricuspid annulus diameter during diastole becoming greater than 34 mm; and
(b) tricuspid annulus diameter during systole becoming greater than 32 mm –
leading to a significant TR?
6. Feasible to capture the mechanical responses of anterior, posterior and septal leaflets? Whether the presence of additional leaflets in TV would create any excess friction?
Can we expect eccentric TR (asymmetrical leaflet coaptation) as against central TR (symmetrical) even with 3 TV leaflets?
7. Feasible to capture the coupled hemodynamic and mechanical responses associated with nearly 25 chordal insertions into the tricuspid valve with roughly 7 passing to the anterior leaflet, 6 to the posterior leaflet, 9 to the septal leaflet and 3 inserting into the commissural areas?
8. Since, blood flow from right ventricle into the pulmonary circulation remains dependent on a low-impedance, highly distensible pulmonary vasculature, how much enhancement in pulmonary artery pressure produce tricuspid annular-right atrial dilation; and how much enhancement in pulmonary artery pressure would cause RV dilation?
9. Are there early stage symptoms either for
(a) primary tricuspid regurgitation (resulting from the direct involvement of TV associated with congenital heart disorders such as Ebstein’s anomaly, or, acquired disorders, or, diseases of TV including myxomatous degeneration of TV, endocarditis, carcinoid syndrome, rheumatic heart disease and chest irradiation);
or
(b) functional/secondary tricuspid regurgitation associated with TV annulus dilation and leaflet tethering due to RV remodeling (resulting from ischemic/non-ischemic cardiomyopathies, aortic or mitral valvular disease, or, pulmonary-disease/pulmonary-vascular disease)?
10. When exactly, the dilation of RV causes a shift of the interventricular septum towards LV- with increasing TR?
Severe primary Isolated tricuspid regurgitation is usually associated with huge RV dilation ( increased Annual size at systole and diastole) while severe secondary TR ( with or without left side heart disease ) with RV dilation without severe RV or LV dysfunction and Severe PAH