**4. Diagnosis of tricuspid regurgitation**

According to the 2020 AHA guidelines, TTE can differentiate primary TR (abnormal valve leaflets) from STR (normal valve leaflets) for left ventricularrelated valve or myocardial disease. PA systolic pressure can be measured by TEE. Characterization of the severity of TR-related regurgitation is based on an integrative assessment of multiple parameters, as recommended by the American Society of Echocardiography and European Association of Echocardiography, but many limitations still remain. In patients with TR undergoing left-heart valve surgery, an annular diastolic diameter >40 mm (or >21 mm/m2 ) indicates an increased risk of permanent or progressive TR after isolated mitral valve surgery. PA systolic pressure is estimated from maximal TR velocity. TR velocity for evaluation of RV systolic function is challenged by variation in RV loading condition as well as geometric and image acquisition constraints. Normal RV systolic function is defined by various parameters, including tricuspid annular plane systolic excursion (TAPSE) >16 mm, TV systolic. Other imaging modalities, such as magnetic resonance imaging and CT scanning, can provide more accurate information about the status of the RV [23].

Again according to the AHA guidelines invasive measurement of cardiac index, right–sided diastolic pressures, pulmonary artery pressures, and pulmonary artery pressures and pulmonary vascular resistance, as well as right ventriculography, can be useful when clinical and noninvasive are discordant or inadequate in patients with TR [23].

While TR is one of the main right-sided pathologies that cause right heart failure (RHF), tricuspid stenosis (TS) is a rare etiology for RHF. The increased volume load induces cardiac dilatation, thereby stretching the walls of the cardiac chambers, causing dilation of the tricuspid annulus and enhance the regurgitation of the blood. Therefore, as RHF increases over time, the progressive deterioration of TV functions becomes trapped in a vicious cycle that advances the heart failure. Signs of this pathological mechanism can be seen on echocardiography, and patients with severe TR have right heart enlargement. Other signs observed may include enlargement or pulsation of the inferior vena cava and/or hepatic veins. In addition, the TAPSE can be measured to detect subtle ventricular dysfunction: TAPSE < 8.5 mm is associated with right ventricular ejection fraction less than 25%. If RHF is suspected, investigations including electrocardiogram, natriuretic peptides, and echocardiogram are used to confirm the diagnosis [24].

Echocardiography is routinely used in clinical practice to assess the severity of TR. This includes color doppler flow mapping in at least 2 orthogonal planes, assessment of vena contracta width, flow convergence calculations, and the direction and size of the jet. In addition, the morphology of continuous wave doppler recordings across the valve and pulsed wave doppler of the hepatic veins can be used [25]. Serial evaluations of TR should be interpreted in the clinical context of the patient because, as with functional mitral regurgitation, severity volume status and afterload may be affected by many factors such as The RV shape is complex compared to the left ventricle, appearing as a crescent in cross-section and triangular when viewed from the side [26].


### **Table 3.**

*2020 ACC/AHA guideline for the management of patients with valvular heart.*

Disease recommendations for intervention timing for TR intervention (Level A: High quality evidence from more than 1 rondomised clinical trial (RCT) or metaanalyses of high –quality RCTs or one or more RCTs corroborated by high-quality registry studies. Level B-R: Moderate-quality evidence from 1 or more RCT sor meta-analyses of moderate-quality RCTs. Level B-NR: moderate –quality evidence from 1 or more well-designed, well-executed nonrandomized studies observational studies, or registry studies or meta-analysis of such studies. Level C-LD: Randomized or nonrandomized observational or registry studies with limitations of design or execution or meta-analyses of such studies or physiological or mechanistic studies in human subjects. Level C-EO: Consensus of expert opinion based on clinical experience.) (**Table 3**) [23].

By using experimental models it has been estimated that left ventricle contractions contribute 20% to 40% of RV systolic pressure and volume output [27]. And also both two ventricles share same biochemical environment, by this way any systemic and local neurohormonal parameters result in improvements in biventricular function. Importantly, left-sided heart failure with chamber enlargement and mitral regurgitation can cause right-sided pressure overload, RV dilation, tricuspid annulus enlargement, and resultant TR. This mechanical step initially led to the concept that surgical or medical treatment of the leftsided abnormality would result in secondary recovery or improvement in TR. Although there is improvement in TR, this is not always the case [11]. Dreyfus et al have shown that a paradigm advocating treatment of only the proposed "primary" lesion, such as mitral valve disease, will not directly correct tricuspid annular dilation or improve right ventricular function, which are key determinants of functional TR. In their study, the TV annulus was evaluated visually in 311 patients who underwent mitral valve repair between 1989 and 2001. Tricuspid annuloplasty was performed selectively only in patients with twice the tricuspid annular diameter (as measured from anteroseptal commissure to

anteroposterior). New York Heart Association class were significantly improved in those who underwent TV annuloplasty. In-hospital mortality and actuarial survival rate were similarly improved in patients undergoing TV annuloplasty, supporting the notion that TV annuloplasty improves patient outcomes during mitral valve repair [18].

In 2020 report by Tirone [28] for degenerative MR they found no correlation between tricuspid annulus of ≥40 mm on the development of postoperative TR following mitral valve repair. They concluded that a preoperative echocardiographic diameter of tricuspid annulus ≥40 mm is not associated with the development postoperative TR after mitral valve repair for degenerative MR. Furthermore, in their report of extended outcomes of mitral valve repair for degenerative MR, they found that patients were only 2.5% likely to develop severe TR at 20 years after surgery, but the probability increased to 20.8% when moderate-intensity TR was added. It was also very disturbing to find an accumulated new incidence of atrial fibrillation of 32.4% over 20 years. The development of these two adverse events was not associated with repeat MR and may have been interdependent. The reporter recommends that tricuspid annuloplasty should be performed during mitral valve surgery when there is moderate or severe tricuspid regurgitation and in patients with atrial fibrillation or a dilated right ventricular cavity (systolic diameter ≥30 mm), even in the absence of significant tricuspid regurgitation [18, 29].
