Abstract
Proper tricuspid valve (TV) function is essential to unidirectional blood flow through the right side of the heart. Alterations to the tricuspid valvular components, such as the TV annulus, may lead to functional tricuspid regurgitation (FTR), where the valve is unable to prevent undesired backflow of blood from the right ventricle into the right atrium during systole. Various treatment options are currently available for FTR; however, research for the tricuspid heart valve, functional tricuspid regurgitation, and the relevant treatment methodologies are limited due to the pervasive expectation among cardiac surgeons and cardiologists that FTR will naturally regress after repair of left-sided heart valve lesions. Recent studies have focused on (i) understanding the function of the TV and the initiation or progression of FTR using both in-vivo and in-vitro methods, (ii) quantifying the biomechanical properties of the tricuspid valve apparatus as well as its surrounding heart tissue, and (iii) performing computational modeling of the TV to provide new insight into its biomechanical and physiological function. This review paper focuses on these advances and summarizes recent research relevant to the TV within the scope of FTR. Moreover, this review also provides future perspectives and extensions critical to enhancing the current understanding of the functioning and remodeling tricuspid valve in both the healthy and pathophysiological states.
Highlights
The tricuspid valve (TV) regulates blood flow on the right side of the heart between the right atrium (RA) and right ventricle (RV) throughout cardiac cycles
Echocardiography is most frequently employed for diagnosing functional tricuspid regurgitation (FTR), but cardiac magnetic resonance imaging (CMRI) and computed tomography (CT) are increasingly used as a complement [53]
A study by Hammarström et al (1991) [97] used 2DE to measure human annulus parameters with three primary observations: (i) an average annular diameter of 22.5 mm, (ii) the greatest motion occurring along the lateral point of the TV annulus, and (iii) a hinge-point of the annulus movement occurring on the septal side
Summary
The tricuspid valve (TV) regulates blood flow on the right side of the heart between the right atrium (RA) and right ventricle (RV) throughout cardiac cycles. TR is considered primary when there is some type of structural abnormality or damage to the TV apparatus as the primary cause of the TR [2] Congenital diseases, such as Ebstein’s anomaly and hypoplastic left heart syndrome (HLHS), and acquired diseases (e.g., tricuspid leaflet flail resulting from chordae rupture) fall into this category. The TV annulus will lose its saddle-like geometry to become more flattened [9,10] These alterations will continue to progress, resulting in papillary muscle displacement, leaflet tethering, a reduced coaptation of the TV leaflets, and the formation or worsening of FTR [4,5,6,9,10]. It has been shown that the MV leaflet VICs are stiffer than the cells in the TV leaflets, implying a correlation between the VIC-regulated collagen biosynthesis and transvalvular pressure loading [52]
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