TA dilation, leaflet tethering, or both, can lead to secondary or functional TR.

With functional TR, the TA becomes larger, flatter and more circular [5]. The annulus becomes more circular with TR worsening due to the dilation of the TA preferentially along its free wall distance. Specifically, there is greater enlargement of the TA antero-posterior diameter (antero-septal commissure to posterior leaflet distance) than the medio-lateral diameter (septal-to-anterior leaflet distance) [5] (Fig. 10.5). This is likely due to the anterior high point of the TA being adjacent to the fibrous skeleton of the heart, providing more resistance to dilation than along the free wall. The ratio between the antero-posterior dimension and the annular height is a dimensionless index reflecting the TA remodelling (“stretch”) in dysfunctional TV, which increases markedly in functional TR in comparison with controls (13 ± 5 vs. 4 ± 1, p < 0.0001) and together with TA area and circularity, are independent determinants of functional TR severity [5].

TA dilation is a constant feature in patients with functional TR and is poorly correlated with the severity of TR. Annular dilation is a reliable marker of TV dysfunction and a sign that the valve is prone to leak later on. In contrast with functional TR which may improve after the reduction of pulmonary pressures (i.e. after mitral valve surgery or after thromboendarterectomy in patients with chronic thromboembolic pulmonary hypertension [2]), TA dilation persists and will not return to normal values. The persistence of TA dilatation may explain why almost 40% of patients who underwent mitral valve surgery successfully may develop severe functional TR several years later despite absence of pulmonary hypertension [13]. However, almost 1 out of 2 patients without significant TA dilation at the time of mitral valve surgery (≥70 mm intraoperatively in Dreyfus series [14]) will still develop late TR, suggesting either that intraoperative TA diameter is an imperfect predictor of late TR, or that there are multiple contributing factors to TR late development in addition to TA size.

Functional TR is frequently associated with advanced stages of left-sided valve disease, myocardial or pulmonary diseases leading to increased pulmonary pressures, right ventricular dilation and/or dysfunction [3, 15]. Thus, it is an established belief that the dilation of right ventricle is the first mandatory step towards the TR development and univocally responsible for TA enlargement, even before significant TR is present [16]. However, this theory does not explain the occurrence of functional TR in chronic atrial fibrillation or its relatively low incidence in some conditions evolving with significant right ventricular dilatation (corrected tetralogy of Fallot, arrhythmogenic cardiomyopathy etc) [17, 18] . Using 3D echocardiography-derived measurements of right heart chambers and TA in 59 patients with functional TR of various etiologies, we have found that right atrial volume was actually the most consistent determinant of TA area [19]. This may explain, at least in part, the onset of FTR in patients with dilated right atrium, but relatively small right ventricle (atrial fibrillation subgroup), and the absence of significant regurgitation in those with severely enlarged right ventricles, but preserved right atrial volumes (tetralogy of Fallot subgroup).

In patients with functional TR, there is also an impairment of TA “sphincteric” function and dynamics, with a significant decrease (up to 50%) in the systolic shortening of TA area and diameters [5].

Despite its importance for the diagnosis and therapy of functional TR, the sizing of TA remains an elusive goal. The best methodology for the noninvasive measurement of TA size is not clearly defined, and present thresholds for surgical annuloplasty based on TA diameter by conventional echocardiography are actually supported by limited evidence and have been questioned by several recent papers [20, 21].

So far, several approaches have been used to size the TA in vivo in TR studies. Dreyfus et al. have proposed the intraoperative sizing of TA from the antero-septal commissure to the antero-posterior commissure, and the 70 mm cut-off for defining significant TA dilation [14]. Performing an annuloplasty in all patients with TA above this threshold improved New York Heart Association functional class and prevented progression of functional TR at long-term follow-up. This approach was deemed reliable and reproducible by Dreyfus and coworkers [14], yet it has been criticized by others [20] due to its large variability with various degrees of TA stretching since the heart is unloaded and still during surgery.

Dreyfus et al. suggested that the intraoperative 70 mm diameter threshold corresponds to a 40 mm diameter measured in diastole by transthoracic 2D echocardiography between mid-anterior and mid-septal annulus in apical 4-chamber view [14, 22] (Fig. 10.2). This assumption actually has never been demonstrated experimentally and has been challenged recently by several recent 3D echocardiography studies showing that: (1) TA diameter in conventional 4-chamber view may represent the distance between septal leaflet and either anterior or posterior leaflet [23, 24] (Fig. 10.5); (2) the TA size by 2D echocardiography and surgical measurements correlate only modestly, and the difference between the two is much smaller (roughly 3 mm) [20] than the difference suggested in the seminal papers of Dreyfus GD et al. (30 mm) [14]; (3) 1 out of 5 healthy subjects have TA annulus >40 mm and would qualify for annuloplasty based on conventional 2D TA diameter [12]; (4) newer abnormality threshold for TA dilation could be larger—42 mm or 23 mm/m² [20].

Since the TA is a dynamic structure with an asymmetric saddle shape, even small variations in the angle of the ultrasound beam (Fig. 10.2) or in the timing of measurements can result in considerable discrepancies in TA size [12]. Although the TA measurement from apical four-chamber view seems to be preferred, being recommended by guidelines and different authors as more feasible and reproducible than other views [8, 20], the best way and timing to measure the TA by conventional echocardiography still remain controversial [22] and require stronger evidence.

Two-dimensional echocardiography , either transthoracic or transesophageal, may underestimate the TA size. 3D echocardiography probably offers a more accurate evaluation of TA dilation by its ability to yield anatomically sound, quantitative measurements such as TA area, as well as true maximal and minimal diameters, irrespective of their spatial orientation [3]. In addition, semi-automated modeling of TV based on 3D echocardiography data offers unique quantitative measures of TA size and leaflet tenting volume, which account for the non-planarity of TA, as well as the asymmetry and inter-subject variability of leaflet size and tethering [25] (Fig. 10.3). Finally, current technology allows to obtain 3D prints of TV models and directly appreciate their different sizes and complex shapes (Figs. 10.6 and 10.7), elevating our impressions from textured flat-panel coloured perspectives to actual exploration of the complex geometry of the TV, with the potential to guide personalized care of patients with functional TR [26.]

It can be foreseen that 3D echocardiography will become the standard technique for assessing the TV geometry and accurately measuring TA dimensions [22]. If so, there are a few caveats that have to be considered.

First of all, since 3D echocardiography provides larger values for TA annulus size than 2D echocardiography (Fig. 10.2), specific abnormality thresholds of TA should be used if measurements are obtained by 3D echocardiography. Secondly, due to the non-planarity of TA, software-derived semi-automated measurements (Fig. 10.3) may provide different results than manual measurements of TA diameters and area planimetry performed on a 3D slice of TA (Fig. 10.5). Thirdly, preliminary data using dedicated algorithms specifically developed for TA quantification showed that TA reference values should be gender-specific and indexed by body surface area, suggesting that the “one-size-fits-all” approach suggested for 2D TA diameter no longer holds true for 3DTA measurements. Finally, despite the use of a dedicated software algorithm applied on 3D echocardiographic data is the only way to account for TA non-planarity and peculiar geometry, at present there is no such software commercially available.

Other studies used either multi-detector computed tomography (MDCT) or magnetic resonance imaging (CMR ) for measuring the TA size. Interestingly, the antero-posterior TA dimension by MDCT, and not the septal-lateral dimension, was an independent determinant of TR severity [9]. However, their clinical use of CMR and MDCT is limited at present for patients with unsatisfactory quality images.