 So next we have Dr. Annette Vegas and Annette and I go way back where we're resins together in the Toronto program. Annette is a vital force behind the Toronto perioperative echocardiography symposium. She is an attending in the CDICU at TGH and she has devoted a considerable part of her career to developing web-based educational materials of teaching both transesophageal and transthoracic echocardiography. Annette has extensively published journal articles and book chapters, authored textbooks and co-edited textbooks related to echocardiography. She's a professor of anesthesiology and an elected fellow of the American Society of Echocardiography. The title of the Dr. Vegas presentation is Pathophysiology and Assessment of Functional TR. Greetings and welcome. My name is Annette Vegas and I'm an anesthesiologist from Toronto, Canada. This session is entitled Pathophysiology and Assessment of Functional Tricuspid Regurgitation. I have the following disclosures. I received book royalties from Springer International and a speaker on Arrarium from Abbott. This talk will focus on the mechanisms and assessment of functional tricuspid regurgitation or FTR. We will begin by looking at some definitions, identify conditions that cause FTR, examine the pathophysiology of FTR, and highlight some key echocardiographic features of FTR related to the tricuspid valve. And finally look at FTR disease progression and management. Primary tricuspid regurgitation results from tricuspid valve leaflet disease and is uncommon. Functional tricuspid pathology or FTP is geometrical distortion of the normal spatial relationships of the tricuspid valve structure that may lead to valvular dysfunction. Functional tricuspid regurgitation follows from functional tricuspid pathology related to right ventricular remodeling, tricuspid annulus dilatation, and leaflet tethering. Functional tricuspid regurgitation can be categorized either by the mechanism associated with the morphologic abnormality of the tricuspid apparatus or by the etiology. Mechanisms that cause functional tricuspid regurgitation include left heart disease causing post capillary pulmonary hypertension, pulmonary hypertension causing pre capillary pulmonary hypertension, right ventricular dysfunction, or idiopathic that is unrelated to any of the previously described mechanisms, but often results from atrial remodeling. There are many potential etiologies associated with each mechanism. Left sided heart diseases include systolic and diastolic heart failure, aortic or mitral valve disease. Those causing pre capillary pulmonary hypertension include chronic lung disease, pulmonary thromboembolism, and primary pulmonary hypertension. Those causing primary right ventricular dilatation and or dysfunction, such as large left to right shunt, primary right ventricular dysplasia, and right ventricular ischemia or infarction. And finally, idiopathic associated with long standing atrial fibrillation and or heart failure with preserved ejection fraction. This 2015 paper by Dreyfus et al is an easy read and nicely summarizes the development assessment diagnosis and treatment of functional tricuspid regurgitation. This talk will focus on the first two parts looking specifically at structural changes in the tricuspid valve and the echocardiographic assessment. We will not spend time talking about tricuspid regurgitation assessment or the surgical management, which are ably covered in other sessions. Though the pathophysiology of functional tricuspid regurgitation evolves from many etiologies. It revolves around common mechanisms that remodel the heart, specifically the left heart, pulmonary vasculature and right heart, right ventricle and right atrium. There are changes in the 3D geometry and dynamics of the tricuspid annulus and leaflets, which we will examine more closely in the upcoming slides. In the presence of pulmonary hypertension and increased RV afterload. The first casualty is the RV, which remodels in the longitudinal direction, leading to mild eccentric tricuspid annulus dilatation and leaflet malcoaptation. Further dilatation distorts the RV, which undergoes a spherical deformation causing leaflet tethering and papillary muscle displacement with loss of leaflet coaptation and incomplete leaflet closure, worsening FTR. Without pulmonary hypertension, there is often right atrial enlargement. The right atrium dilates and remodels. This is leading to market tricuspid annulus dilatation along the RV free wall. There is mild RV remodeling with widening at the RV base and retention of the conical longitudinal shape. There is no leaflet tethering and leaflet length is normal. We have now conducted an elegant in vitro experiment on porcine hearts to determine the effect of annular dilatation and papillary muscle displacement in functional tricuspid regurgitation. Isolated annular dilatation moves the anterior and posterior annular segments laterally creating a gap between the three leaflets closer to the subdom. The anterior leaflet tries to cover the enlarged gap, but residual leaflet length is insufficient. A 40% increase in annular area occurs before coaptation reserve is exhausted and regurgitation develops. Papillary muscle displacement either individually or combined can lead to significant tricuspid regurgitation in the absence of tricuspid annular dilatation. Right ventricular dilatation displaces the anterior papillary muscle, left ventricular dilatation displaces the septal and posterior papillary muscle, and by ventricular dilatation displaces all papillary muscles. In septal or posterior papillary muscle displacement, the septal leaflet mobility increases creating a central malcoaptation because the septal leaflet is too short. In a mixed picture of annular dilatation and all papillary muscle displacement, the coaptation line alters towards the free wall. So what about humans? Utsunomaya examined the changes in tricuspid bell geometry and functional tricuspid regurgitation using 3D trans thoracic echo in 51 patients. He found that patients with idiopathic functional TR have a larger right atrium, more tricuspid annular dilatation with modest increases in RV dimensions and papillary muscle displacement causing poor leaflet coaptation but less leaflet tethering. In torrential TR with AF, there is an extensive right heart remodeling with apical displacement of the papillary muscle tips further dilating the tricuspid annulus with leaflet tethering at the free edges. Contrast that in patients with RV dysfunction in sinus rhythm. The RA is not as large, but there is RV remodeling with displaced papillary muscles and leaflet tethering. Thus, patients with idiopathic functional tricuspid regurgitation have leaflet coaptation at the annular plane. In contrast to those with RV remodeling, we'll have tethered leaflets that co-apt below the annular plane. We have already heard a bit about normal tricuspid valve anatomy and function, but to emphasize the tricuspid annulus is not discreet and lax fibrous tissue being composed of endocardium, epichardium and adipose tissue along the RV free wall, which is where the tricuspid annulus dilates. The tricuspid annulus is a complex dynamic 3D structure that differs from the more symmetric saddle shaped mitral annulus. The tricuspid annulus is elliptic with 3D echo data confirming a non-planar shape with two high points, antro-septal and posturalateral, and two low points, antro-lateral and postural septal. The tricuspid annular area and perimeter changes significantly during the cardiorespiratory cycle, decreasing by 35% to a minimum in systole and increasing to a maximum in late diastole. Tricuspid annulus circularity is augmented during systole, with the tricuspid annulus returning to a more oval shape in diastole. There are no age related annular differences, but women have greater indexed perimeters and long axis dimensions. Novel artificial intelligence based semi-automated tricuspid valve alert analysis software called Autovalve Analysis can analyze the tricuspid annulus in real time. Echocardiography provides a robust option for assessing both the etiology and pathology associated with functional tricuspid regurgitation. Specific assessment for functional tricuspid pathology involves determining tricuspid annular dimensions and the degree of tricuspid valve leaflet tethering. I will leave the assessment of right ventricular function to a talk later today. Remember that functional tricuspid regurgitation is less about the amount of tricuspid regurgitation and more about the underlying structural changes. Surgical intervention may occur even in the absence of tricuspid regurgitation. Tricuspid annular shape and size is a surrogate marker of severity and ethnicity of functional tricuspid regurgitation. Like the mitral valve, the fibrous trigones fix the septal leaflet, so the tricuspid annulus primarily dilates along the free wall at the anterior and posterior leaflet attachments. Thus, with functional tricuspid regurgitation, the annulus becomes larger, more planar, circular, with a larger septal lateral distance than anterior posterior distance. The normal annular shape with high and low points becomes intermediate in shape in functional tricuspid regurgitation with only one high point anterior and with advanced functional tricuspid regurgitation has no distinct high point. It may be demonstrated using CT that in healthy patients during systole, the entire annulus is flexible and moves vertically towards the right ventricular apex, reducing the tethering height, thus permitting adequate leaflet co-optation. In functional tricuspid regurgitation, the tricuspid annulus was less flexible with restricted longitudinal movement, increasing the distance between the annular plane and the ventricular apex, increasing the tethering distance of the tricuspid leaflets. Utsanamana compared these parameters for atrial and ventricular related tricuspid regurgitation using 3D TEE. 3D tricuspid valve parameters in atrial related tricuspid regurgitation had a larger AP diameter, annular area, and annular orientation from a more dilated and posteriorly displaced annulus. In ventricular related tricuspid regurgitation, tending volume and all leaflet tethering angles were larger. Current guidelines recommend measuring the tricuspid annulus in diastole from the 2D apical 4-chamber view. Normal tricuspid valve annulus diameter in adults is 28 millimeters with significant tricuspid annular dilatation defined by diastolic diameter of greater than 39 millimeters or 2.1 centimeters per meter squared. 3D echocardiography provides a more robust method to evaluate dimensions and geometric changes in the tricuspid annulus over the cardiac cycle. 3D TEE can obtain a short axis plane of the tricuspid valve accurately measuring various tricuspid annular axes. The maximum dimensional change occurs along the postrolateral androceptile axis at end diastole, which 2D imaging cannot reliably measure. Specific custom software is available that creates tricuspid valve annular models that help understand pathology and may provide additional information. Though I have to say even mitral models have a limited role in clinical practice. Normal leaflet co-optation occurs at the level of the annulus or just below it with a co-optation length or height of 5 to 10 millimeters. Recall that the two major mechanisms in functional tricuspid regurgitation relate to right atrial and right ventricular remodeling. Compare normal right heart size and function to patients with predominantly atrial enlargement and tricuspid annular dilatation. In the setting of primarily eight annular dilatation, there is less right ventricular remodeling allowing better leaflet co-optation at the annular plane. With right ventricular remodeling, there is leaflet tethering, resulting in leaflet co-optation below the annular plane in the right ventricle. Quantitative assessment of the degree of tethering includes measuring tethering height, area, and angle. Tethering height is the distance of leaflet co-optation from the plane of the tricuspid annulus. The area between the leaflets and the annular plane is the tethering area. The tethering angle is the angle between the annular plane and the leaflet. Significant leaflet tethering is present if the tethering distance is greater than 8 millimeters, tenting area greater than 1.6 centimeter squared, or the angle is greater than 28 degrees. 3D echo can estimate tenting volume. A significant value is greater than 2.3 cc. There is a growing appreciation that functional tricuspid regurgitation is important because patients are symptomatic with a poor quality of life from decreased cardiac output and right heart failure. More importantly, the presence of functional tricuspid regurgitation, no matter the severity, reduces survival with increased mortality, independent of age, 5-ventricular systolic function, right ventricular size, and pulmonary artery pressure. Functional tricuspid regurgitation can progress over time and can be described in stages, though these are not linear. Patients are heterogeneous with varying degrees of leaflet tethering, annular dilatation, and right heart modeling. Treatment options need to take into account these findings. This algorithm approaches the management of tricuspid regurgitation based on severity and symptoms. There are 3 management options, medical, surgical, or the growing fields of percutaneous intervention. The presence of moderate mitral regurgitation may allow the patient to be considered for surgery provided the surgical risk is not high. Previous 2014 AHA guidelines suggest surgical interventions for tricuspid regurgitation in patients undergoing left heart surgery. For all grades of functional tricuspid regurgitation from mild to severe with pulmonary hypertension and tricuspid annular dilatation. Updated 2020 guidelines are based on the presence of severe tricuspid regurgitation or progressive tricuspid regurgitation with tricuspid annular dilatation. We know that functional tricuspid regurgitation may progress over time. There is no guarantee functional tricuspid regurgitation will improve despite an intervention. After mitral valve surgery significant functional tricuspid regurgitation can develop late after several years. The most important risk factors associated with a higher probability for the development of late functional tricuspid regurgitation involve clinical echocardiographic and surgical factors. In addition, these are some of the predictors that have been identified for unsuccessful tricuspid valve repair. Importantly pre-op and non-interoperative tricuspid regurgitation severity and the degree of leaflet tethering are key risk factors. Surgical technique also factors in. This is a nice segue into the next talk. So in summary from this talk one can appreciate there are many causes of functional TR the mechanisms relate to right heart modeling. Tricuspid annular dilatation leaflet tethering and papillary muscle displacement determine the presence and severity of functional TR echocardiography is a robust assessment tool. Tricuspid valve models are not ready for prime time. Intervention depends on functional tricuspid pathology and not just annular size or the amount of tricuspid regurgitation. Thank you very much. And thank you and that is a beautiful segue into our next talk.