 Thanks so much. Okay. So hi again, everyone. My name is Marcus Alpatori And I'm an anesthesiologist and CVSU attending at Toronto General with an interest in perioperative echocardiography I'm here to talk to you today about TEE and surgical decision-making in the operating room. I Want to thank you all for attending today and also want to thank the organizers for giving me the opportunity to present It's an honor to close out this inaugural year of this province wide initiative And I'm eager to see how it will continue to grow and evolve in the upcoming years Again, I have to acknowledge the efforts and dedication of both Raphael and Fabio Who really deserve an incredible amount of recognition for bringing us together and organizing these multi-centre echo rounds The feedback we've received so far has been very encouraging And we would like to continue to expand. So please email Raphael or Fabio with any suggestions regarding format or potential topics Or if you know of any other centers that would like to be included We are in the process of getting these rounds accredited So hopefully we will be eligible for CPD credits in the upcoming year. So I have no disclosures or competing interests But in terms of acknowledgements I've had the good fortune to train under some incredibly supportive and experienced mentors that are world-renowned for their expertise in echocardiography A particular thanks goes to Dr. Ahmad Omran, consultant cardiologist who helped to develop this lecture And joins us on the call today to provide additional insights I also want to acknowledge the talented roster of cardiovascular surgeons that we have here at TGH Collaboration and collegiality across the drapes is essential for optimal patient outcomes in all of ours But nowhere is it more important than complex cardiac surgery To that end, I would like to introduce Dr. Mitesh Padiwala, a cardiovascular surgeon here at TGH who specializes in advanced valve repair Mechanical circulatory support and heart transplantation. He's joined the call today to provide a valuable surgical perspective So today's lecture is inspired by the 2020 ASC guidelines entitled The use of transesophageal echocardiography to assist with surgical decision-making in the operating room a surgery-based approach By Alina Nakawara and a roster of international experts that includes our very own Dr. Vegas Prior to the publication of these guidelines There was little instruction on how to best apply existing ASC guidelines to the perioperative setting Most ASC guidelines were developed for cardiologists interpreting trans thoracic images under ideal conditions But as we all know the OR is a very different place a dynamic environment with unique challenges As highlighted by Nakawara hemodynamic fluctuations electrical pacing positive pressure ventilation fluid shifts and surgical maneuvers can all impact echocardiographic evaluation It is still vitally important that we're able to perform rapid thorough and accurate assessments So that we can best inform surgical decision-making Over the course of this lecture, we will review three cases in which TEE was essential to surgical decision-making We will show how TEE can be used to refine diagnoses the technology adjust the surgical plan and assess surgical results We have included evidence-based discussion from the surgical literature where appropriate You will be polled several times throughout the lecture on what you would decide in a given situation So quickly before we get started some important caveats to mention Firstly the optimal surgical technique or approach will depend largely on local expertise and experience Optimal is in quotation marks here as there are often many ways to skin a cat And the technique most likely to succeed is the one most familiar to the surgeon Secondly the 2020 guidelines are comprehensive But obviously can't cover every surgical circumstance or ambiguity that may arise In those cases, we have deferred to the surgical and echocardiographic literature to guide our decision-making Lastly, although the specific surgeries that we are going to discuss may not be performed at your institution The learning points are all broadly applicable So without further ado, let's get right into the first case So our first case involves a 19 year old woman with severe symptomatic mitral regurgitation in the context of lewis-deeds syndrome Lewis-deeds or LDS is a genetic connected tissue disease similar to Marfan's Compared to patients with Marfan syndrome LDS is characterized by a more aggressive vascular course Morbidity and mortality occur at an earlier age with dissections occurring at smaller aortic dimensions Although the management of patients with connected tissue disease is mainly focused on prevention of aortic dissection Mitral valve involvement occurs in 60 to 75 percent of cases and is a considerable source of morbidity Common mitral valve abnormalities include mitral valve prolapse and myxomatous degeneration with severe MR Our patient had undergone routine surveillance since early childhood when a floppy mitral valve was first diagnosed Over the last three years, she'd become increasingly symptomatic Describing NYHA class 3 symptoms and showing new LV dilatation on echocardiogryph Interoperative TEE confirms severe mitral regurgitation Resulting from myxomatous degeneration of the valve The LV was severely dilated with an LV internal end diastolic diameter of 64 millimeters Despite the degree of dilatation biventricular function was preserved The left atrium is enlarged and the intratral septum bows to the right Consistent with severely elevated left atrial pressures from the MR Turning our attention to the mitral valve, we clearly see myxomatous disease Now we often think of myxomatous disease as a single entity But it actually exists as a continuum from Barlow's disease on one end to fibroelastic deficiency on the other As described by the STCS paper by Adams in 2007 This is more than an academic distinction Where the valve exists on this continuum determines its repairability The degeneration seen in connective tissue disease is surgically and pathologically similar to Barlow's disease Like Barlow's these valves show mixoid infiltration with excess tissue As a result the leaflets are bulky and billowing often with multi-segmental prolapse as shown here Examination of the valve also revealed mitral annular disjunction Or an abnormal atrial displacement of the mitral valve leaflet hinge point visible here The presence of mitral annular disjunction has prognostic value in patients with connective tissue disease As Chevalescu in 2021 published a paper in EHJ that shows that the presence of mad Predicted aortic events at a younger age and the likelihood of needing mitral valve surgery Panning through the valve. We see severe MR originating from two jets One centrally directed and one anteriorly directed 3d imaging shows prolapse of all anterior and posterior leaflet segments Evaluation of the aorta was vitally important in this case as we know that many of these patients will go on to require aortic repair or replacement early in life The aortic valve was competent with an aortic cytosidus diameter of 40 millimeters and an extending aorta diameter of 22 millimeters Interestingly what was not detected on the pre-op echo was a dilated myxomatous tricuspid valve The diameter of the tricuspid valve is 46 millimeters Here we can see the same redundant and voluminous leaflet tissue with multi-segment prolapse that characterize the mitral valve This was an interesting finding as primary tricuspid disease is relatively rare With 75 of tr being functional in nature Here the tr was graded as moderate with at least two jets visualized Closer inspection of the valve also shows tricuspid annular disjunction This is a newly described entity that has gained traction in the literature over the past year We can clearly see that the junction of the atrial wall tricuspid valve leaflet occurs well above the upper limit of the ventricular myocardium The clinical implications of this finding are still being explored But a small single center study by abel in 2021 does not seem to implicate tricuspid annular disjunction in the development of ventricular arrhythmias So this brings us to our first poll Thank you to rafael for helping to set up the polling system and interactivity So given the echo findings the patient age and history of connected tissue disease Which interventions would you recommend? Please select as many options as you think apply Listed here are the most pertinent features of the mitral valve to help with your decision making We will give you the next 30 seconds to lock in your decision 30 seconds marquis Yeah So as the results are tallied let's review the recommendations from the guidelines In their section on mitral regurgitation Nyqoara identified the following features predictive of sam following mitral valve repair A myxomatous mitral valve with redundant leaflet tissue A non-dilated lv Interior and posterior leaflet lengths of over 20 and 15 millimeters respectively measured in mid diastole Ratio between the lengths of the interior and posterior leaflets of less than 1.3 and n systole A short c-set distance of under 25 millimeters A narrow aorta mitral angle of less than 120 degrees A thick basal intraventricular septum of over 15 millimeters An interior displacement of the papillary muscles Although intuitively you would think that the more predictors present the greater the likelihood of sand This assumption has never been proven Our patient has three predictors of sam following repair Before revealing the poll results, I'd like to take a moment to hear from dr. Buddy Walla So matech regardless of what the literature says in reality Do these echocardiographic features influence your management? And how do they weigh compared to direct visual inspection of the valve? So they do weigh into our management in other words if you find these these Echo findings then it makes us alert to the fact the patient is at high risk of sam and it will Change our surgical approach To take that into account in other words, we will conduct maneuvers to try and minimize the risk of sam to compensate for some of these echocardiographic findings We will make the posterior leaflets shorter if we need to we will make sure the co-optation line is posterior We will avoid the use of downsizing rings And so or we'll do a myectomy if that's the case. So it does influence our management In terms of visual inspection of the valve visual inspection of the valve Will only give us the heights of the posterior and anterior leaflets It gives us limited data to Suspect the there would be a higher risk of sam other than the tall posterior leaflet Classically more than 15 millimeters on visual inspection should should alert us to the fact that there is a higher risk of sam Or a co-optation margin that is more mid or or anteriorly located And so the echo findings do influence our management This is very helpful And with myxomatous disease in particular, what are the features that make a repair most challenging? So, you know, if it's isolated to posterior leaflet in one segment, it's easy If it's isolated to posterior segment multi posterior leaflet multi-segment It's a little bit more challenging, but still relatively simple But when it affects both leaflets and there is a relative Difference in the co-optation height in other words one leaflet is prolapsing To a different severity than the other Then that makes the repair more challenging And if there is a features that would increase the risk of sam that also makes the the repair more complex But if it's myxomatous disease surgeons typically Have an easier overall time fixing a valve because there's more leaflet material to play with potentially to resect As opposed to fibroelastic deficiency where, you know, you're limited to Resuspension techniques alone and there's very little leaflet tissue to play with or to remove And if you try to you'll make the valve too small Perfect. Thanks. That's great. So Raphael, if you could put up the poll results So we see that people recommend mitral valve repair looks like 60% in TV repair Some have recommended mitral valve replacement given the features that we've seen Nobody recommends to replace the tricuspid valve and nobody Says that we should replace or touch the ascending area. Okay So let's see how that compares to real life So the mitral valve was repaired in this case on surgical inspection The mitral valve was a Barlow's valve with myxomatous degeneration of all segments The surgeon repaired the valve using a looping technique to place eight neocords to the p1 and p2 segments As well as a 75 millimeter simplicity annuloplasty band A tricuspid annuloplasty was also performed to correct the tr and gross dilatation of the tricuspid valve annulus There was no ascending aorta intervention A small PFO was closed and then left atrial appendage was ligated Now the closure of the appendage is a bit controversial in this patient But it is the common practice of the primary surgeon The only guidelines on surgical closure of the left atrial appendage during concomitant cardiac surgery Are the 2017 sts and 2016 ESC guidelines for the management of atrial fibrillation Both of these documents state that only closure of the sorry only state that closure of the laa is considered reasonable as a class 2a or b recommendation There is no recommendation regarding prophylactic closure of the left atrial appendage for patients and sinus rhythm But this degree of biatrial dilatation at such a young age would definitely predispose the patient to a rhythmia is later in life Unfortunately, echocardiographic evaluation of the repair revealed moderate to severe posteriorly directed MR As severe systolic interior motion of the mitral valve Now the obvious question to ask is whether this persistent MR is caused entirely by dynamic SAM Or whether there is any underlying structural MR from an incomplete or inadequate valve repair As you recall, there were two jets of mitral regurgitation seen in the baseline study One centrally directed and one anteriorly directed There's only one jet visible now and it is posteriorly directed which is consistent with MR from SAM Furthermore, if we slowly scroll through this clip We can see that the MR does not appear until after the T wave in late systole Which is also a feature of SAM related MR So let's see if I can just slow this down here. Okay. So going frame by frame And looking at the ECG at the bottom, we see that the MR starts to appear Just after the T wave So measurements were repeated which show an anterior leaflet measuring 26 millimeters And an intraventricular septum of 13 millimeters 3d evaluation of the valve showed that there really weren't any more prolapsing segments And the length of the posterior annulus to the co-aptation point was 17 millimeters So for our second poll The surgeon turns to you and asks, what do you think I should do? Now the 2020 guidelines predict SAM before repair, but they don't give much additional guidance on what to do if you have SAM post repair So the options are a attempt medical management with volume expansion reduction in heart rate increased peripheral resistance reduced contractility and discontinuation of any ionotropes revised repair by shortening the anterior leaflet revised repair by shortening the posterior leaflet perform a myectomy replace the mechanical with sorry replace the valve with mechanical valve replace the valve with a low-profile bioprosthetic epic valve Or insert a larger annular plastic ring Again choose all options that you feel are correct We'll give you 30 seconds That's 30 seconds there when the pool okay So take a look at the results Also, it's good a lot of variability in terms of answers here. So attempt medical management 80 feel that we should do that some recommendations for interior posterior leaflet lengthening my sorry shortening of myectomy replace with the mechanical valve And a larger annular plastic ring nobody thinks we should replace with the tissue valve given the patient's age. Good okay So in lieu of ASC recommendations, we defer to the surgical literature for guidance on the management of sand There are two papers. I would recommend if you're interested in a bit of a deeper dive The first is a 2012 paper by Ibrahim that talks about the various ideologies of sand And outlines the strengths and weaknesses of various surgical repair techniques More useful for us as anesthesiologists and ecocardiographers is a 2015 paper by Al Fieri That specifically addresses the management of sand after mitral valve repair In this paper Al Fieri outlines a comprehensive algorithm for the medical and then surgical management of sand found in the or According to non-published data Al Fieri states that approximately 30 of patients will have resolution of sand with volume expansion and discontinuation of ionotropes That number increases to 80 with administration of beta blockers and increased afterload using vasopressors or manual occlusion techniques In all patients with transient sand medical management is then maintained in the post-operative period to prevent recurrence The late clinical outcomes of patients who had transient sand were favorable Therefore Al Fieri concludes that conservative management of intraoperative transient sand is considered a reliable policy The conclusion is supported by a small 2015 study by Cooperstein et al and JTCS Which showed that post repair sand occurs in about eight percent of patients But less than one percent requires surgical re-intervention Of those patients with transient medically managed sand Only five percent showed significant sand on follow-up stress at echocardiography In our case medical management was attempted but unsuccessful With the mr persisting despite ionotrope discontinuation volume expansion esmol and svr augmentation The decision was made to go back on pump and revise the repair Now the nature of the repair to us non-surgeon seems interesting Like many of you, I would have thought that the most direct method would be to resect or shorten the interior leaflet Thereby minimizing the amount of excess tissue that is drawn into the lbot by the venturi effect However, the surgeons will almost always choose placement of cordae over leaflet remodeling as this technique better preserves native valve anatomy By placing additional neocords in the posterior leaflet The co-optation point of the mitral valve moves towards the posterior annulus and away from the lbot Although we continue to see turbulent flow through the lbot the sam has resolved and there is no residual mr The diameter of the mitral valve now measured 42 millimeters and continuous wave doppler interrogation reveals low gradients with no evidence of stenosis Due to the degree of turbulence pulse wave doppler was performed with a sampling envelope in the lbot Which showed very low gradients and we proceeded with chest closure Follow-up trans thoracic echo performed on postoperative day four showed a global reduction of lb systolic function with an lvef of 38 This is a well recognized sequelae of mitral valve repair even in patients with normal preoperative lb function In an observational study from JTCS in 2014 Quintana et al showed that 18 percent of patients with normal lb function will develop persistent systolic dysfunction post repair Of these patients only 31 percent will recover their baseline ejection fraction at five years Importantly, there was no sam detected only trivial mr and no stenosis of the mitral valve The tricuspid repair was also performing well So I think just in the interest of time we'll go through cases first and then we can have a question and answer session at the end Just to make sure that we get through all the lecture content So on to the next case Our second case involves a 50 year old patient with critical symptomatic stenosis of a bicuspid aortic valve This was recently identified after suffering two recent syncopal events within the same month Preoperative workup showed no significant flow limiting coronary artery disease, but a small rca He has no other significant past medical history The baseline echo shows a bicuspid aortic valve with moderate lv hypertrophy Long axis view shows a calcified valve with turbulence and approximate ascending aorta The annulus of the ascending aorta matched with the preoperative ct with a measured diameter of 29 millimeters There was no dilatation of the ascending aorta The short axis view shows up a cuspid valve with fusion of the right and non coronary cusps Trans gastric views and Doppler measurements reveal severe as with a maximum measured velocity 4.89 meters per second and peak and mean gradients of 96 on 64 millimeters of mercury respectively There's mild ai Ava by continuity equation is 0.69 inflow and outflow as well as short axis arch views Show a well functioning pulmonic valve with an annulus of 30 millimeters And this brings us to our third poll Given the valve characteristics a severely calcified bicuspid aortic valve and the age of the patient in 50 years What intervention would you recommend? Select all options that you think apply won't give you 30 seconds. I think this was supposed to be a single choice Oh, sorry, I apologize. Yeah, I feel a single choice. That's 37 Okay, take a look at the results Okay, so mechanical aortic valve and 40 The 24 by prosthetic and a Ross 30. Okay, good so After much deliberation it was decided to proceed with the Ross procedure A Ross procedure entails replacement of the aortic valve with the patient's own pulmonary valve Followed by the implantation of a cadaveric pulmonic valve homographed The 2020 ACC AHA guidelines have a grade 2b recommendation For a Ross procedure and patients under 50 years of age who prefer a bioprosthetic avr and have the appropriate anatomy Although long-term durability data from experience centers is excellent There are additional risks including the potential long-term failure of two valves As well as the perils that accompany coronary valve re-implantation similar to the mental procedure Coronary implantation can be avoided using the sub coronary technique initially described by Ross But this is rarely done to the different dimensions and commissure distribution Particularly in patients with aortic insufficiency or a bicuspid or unicuspid aortic valve Failure after Ross is most attributable to regurgitation of the neo aortic valve in the second decade after the operation 50% of pulmonary homographs will require re-intervention within 10 to 20 years In order for a patient to be eligible for the Ross procedure The annular diameters of the pulmonic pulmonic and aortic valves have to be within two millimeters of each other with these measurements Sorry, but these measurements are largely derived from the preoperative cta As you saw in the preoperative workup We had good annular match with both diameters being approximately 29 millimeters And when you come off pump and are evaluating the outcome of the Ross procedure There are no specific guidelines or recommendations for echocardiographic evaluation of the neo aortic valve In lieu we use the assessment algorithm proposed by van overshell for aortic valve repair The likelihood of AI after repair or Ross is low If one the level of cusp co-optation occurs above the aortic annulus Two the effective co-optation height is greater than nine millimeters and reaches the middle of the sinus of alzalva And three the length of cusp opposition is over four millimeters Although we can't measure the effective height in this image due to poor visibility of the annulus The co-optation length alone measures eight millimeters indicating a very low likelihood of regurgitation Remember that the pulmonary autographed is harvested and implanted as a conduit attached to a short piece of pulmonary artery And so pair of avial elix cannot occur Doppler interrogation of the deep trans gash review shows that the neo aortic valve is free of stenosis or regurgitation With a max velocity under two meters per second and peak immune gradients of 14 and six millimeters of mercury respectively The pulmonic valve is replaced with a cadaveric cryo preserved pulmonary homeographed Although it is available in various sizes The homeographed is always oversized to the largest available or 28 millimeters Due to the risk of pulmonary conduit stenosis as first reported by renani and omeran in 2000 A low gradient is crucial here as peak Doppler gradients will typically double within the first week following surgery After evaluating the valves we return to the four chamber view to see that the rv was increasingly dilated and showing signs of moderate to severe dysfunction Contractility at the base was preserved, but the remainder was largely achinetic A short axis mid papillary view of the left ventricle showed a d-shaped septum in both systole and diastole Suggesting rv pressure and volume overlap And this brings us to our fourth poll Given this new finding of progressive rv dysfunction. What would you recommend to your surgeon? The options are a the rv dysfunction is likely due to a long pump run and potentially pacing so proceeded with expectant management only b Doppler and epichardial ultrasound of the rca and pulmonic valve c go back on bypass to examine the rca button D medical management with inotropes and nitric oxide Or e go direct to cath lab from the ur Again, select all the options that you feel apply That's 30 seconds. So when the pull So as we tell the results another question for dr. Buddy wallop So matech rv dysfunction in the post bypass period is common particularly after a long pump run during coronary revascularization surgery How do you differentiate transient post pump dysfunction from true rca ischemia potentially warranting graft revision? you're right, this is uh This is common But the distinguishing feature for me is when I look at the heart if it is transient post pump dysfunction When the heart's re-perfusing unloaded the dysfunction typically gets better So it's resolving in this case you are showing progressive dysfunction And so that that in combination with the fact that a coronary button was constructed would have Raised the concern that this was actually ischemia the other thing I look at is the evolution of the ecg So it's it's the direction in which these evolutions occur if the if the ecg changes are resolving Then I think it's post pump dysfunction that's resolving if the function visually is improving Then typically I just chalk it up to post pump dysfunction But if it is the other way around where it's worsening with time, especially with the heart unloaded then you know after obviously excluding air or or CO2 embolus Then I'd be worried about true ischemia Thanks, let's look at the poll results now Okay, good another multiple or kind of a split crowd, which is good So, uh 40 expected management Doppler and epicardial ultrasound of the rca 40 back on bypass to examine the rca button 50 and medical management planitropes Or in nitric 27 direct cath lab from the war as 5. Okay So we began by inspecting the rca button off pump with Doppler and epicardial ultrasound visual inspection confirmed that there was no obvious kink But the surgeons released some overlying tissue that might have been exerting some compressive effects the Doppler signal was present epicardial ultrasound showed turbulent rca flow But an accurate doppler interrogation for velocity could not be performed Following this brief period of minute manipulation and evaluation the rv function improved with minimal line atropic support The patient tolerated protamine without issue and both valves continued to function well The chest was closed without incident And the patient was brought to cvsu in stable condition The patient was extubated shortly after surgery and progressed well in the immediate post-operative period Unfortunately around 12 hours after surgery the patient became progressively hypotensive Pressure requirements increased Urine output dropped and the cvp rose precipitously ECG showed marked st elevations in v2 and v3 The surgeon was informed and suspecting a recurrent rca issue The patient bypassed the cat lab and emergently returned to the or for exploration Te showed preserved lv and valve function of moderate rv dysfunction The rv was not excessively dilated and there was no significant tr Given the te findings an rca kink was diagnosed And the surgeons proceeded with aortic coronary bypass of the rca using an svg graft rv function was promptly restored with a good result Unfortunately follow-up trans thoracic echo on post-operative day five continued to show moderately reduced rv function Whether this represents myocardial stunning or permanent non-recoverable injury is too early to tell The valves however both continued to work well So and going through to our last case case three This case three represents a common problem that i'm sure we've all faced through our respective institutions A 49 year old man presented to hospital in acute pulmonary edema In the weeks preceding this he experienced increasing difficulties with leg edema paroxysmal nocturnal dyspnea and orthopnea ECG showed an interlateral STEMI an emergent cath showed high-grade left main nrca disease He was scheduled for urgent cabbage following a week of diuresis and afterload reduction Baseline echo showed an enlarged lv with severely reduced function and associated ischemic mr A basal septal aneurysm was identified likely second to the recent informed Echo cardiography also showed moderate rv dysfunction Here are the trans gastric views that show the true extent of the dilatation With an internal diameter of almost 70 millimeters Inspection of the mitral valve was challenging as the large distended ventricle distorted the anatomy and dominated the imaging planes In carpentier 3b disease or secondary ischemic mr Mitral leaflets are anatomically normal but pulled apically in the lv as a result of outward displacement of the papillary muscles This results in systolic restriction and incomplete mitral leaflet closure This is what is described as a tethered valve The degree of tethering is often asymmetric with the p3 scallop tethered more apically than p1 Now if you evaluate the degree of mr using jet area alone, you will severely underestimate the degree of regurgitation This is because the la pressures are incredibly high here and the ability of the lv to contract and generate pressure is severely compromised The venic contractor is a more reliable measure for grading the degree of mr in this case Which measures measures seven millimeters In addition, the 2020 ASC guidelines recommend using ero of over 0.4 centimeter squared A regurgitant volume of over 60 mils and a regurgitant fraction of over 50 as criteria for severe mr Accurately grading the severity of ischemic mr is vitally important as the new england paper by smith in 2014 Showed that repair of moderate ischemic mr was associated with reduced prevalence of regurgitation But an increased risk of stroke at one year additional mitral valve measurements include a mitral valve annulus of 5.3 centimeters Attempting height of 1.3 centimeters Attempting area of 4.8 centimeters an interior mitral valve angle of 30 degrees and a posterior mitral valve angle of 54 degrees So poll number five is what would you recommend regarding mitral valve intervention? The characteristics of the valve are listed here to help with your decision The options are do nothing as you expect the mitral regurgitation to improve with remodeling of the lv Be mitral valve repair or see mitral valve replacement This is a single choice poll 30 seconds 21 answers. How in the poll? So as we talk about the results another question for dr. So matech, what variables do you weigh most heavily when deciding to address the mitral valve in a patient with ischemic mr? So As a general rule we avoid leaving the or after a cabbage with severe mr So if they show up to the or and they actually truly have severe ischemic mr Then you ought to do something about it. The moderate as you pointed out is is a gray zone And in those patients I would base my decision making on their pre operative presentation If they come in with congestive heart failure or symptoms of dyspnea consistent with their mr Then you ought to You know do something to at least repair The valve or reduce the the mr In terms of you know our previous strategy of repairing severe mr. I think that's By the try the cts net trial has gone by the wayside The strongest predictor of failure is what you showed in this patient Which is the basal aneurysm. So patients with a basal dysfunction or basal aneurysm have have a very high Rhea or current rate of mr And so the te does influence our decision based upon the presence or absence of a basal aneurysm If the valve is severely tethered then a repair is unlikely to to work Um, and so those are are finer points that that do help us Um, in terms of does there seem to be a long-term outcome difference? I think there is in the symptomatic patient There's no good data to suggest that there's a survival benefit But in the patients that I've previously left moderate mr For a variety of reasons. I've almost always regretted it because in their post-op follow-up They often if not always have some degree of Dyspnea and you wonder whether you could have made them just that much better by reducing their mr Thanks, so let's look at the poll results now Oh split like 333 perfect, okay So let's start with the decision of whether to intervene or not the 2020 AHA guidelines for the management of patients with valvular heart disease outlines a treatment algorithm For patients with secondary mr There is no proof that surgical correction of chronic secondary mr is effective in prolonging life But observational studies and a sub study of the randomized stitch trial Suggest that it is wise to address the mitral valve during cabbage when secondary mr is severe As we have a patient with severe mr undergoing cabbage surgical mitral valve correction in this case is a 2a recommendation The issue of whether to repair or replace the valve affected by ischemic mr Is much more challenging and it's a question that has dominated at the literature over the past 10 years The debate centers around two main questions One are there any valve characteristics which can predict repair failure? mb Is there a longevity or quality of life benefit to repair versus replacement? Many studies have looked at echocardiographic predictors of recurrent ischemic mr following repair with varying results Listed here are two papers which summarize these previous studies nicely and synthesize this synthesize it into usable algorithms The decision to repair or replace becomes much easier here when we realize that our patient exhibited almost every predictor of mitral repair failure described in literature These include a basal aneurysm basal dyskinesia an interior leaflet angle of 25 degrees a posterior leaflet angle of over 45 degrees a tenting height of over 11 millimeters A tenting area of over 2.5 centimeters squared and an lv and systolic volume of over 145 millimeters But outside of this specific case does the literature support mitral valve repair in the cases severe ischemic mr The ctsn working group has aggressively pursued the answer to this question in a series of papers published in the new england journal of medicine In 2014 accurate all observed no significant difference and left ventricular reverse remodeling or survival at 12 months Between patients who underwent mitral valve repair and those who underwent mitral valve replacement A long-term follow-up studied by goldstein in 2016 Showed no significant between group difference and left ventricular reverse remodeling or survival at two years Mitral regurgitation occurred more frequently in the repair group Resulting in more heart failure related to adverse events and cardiovascular admissions These publications in general make the prospect of repair much less attractive What is not clear is whether candidates for repair were selected with echocardiographic predictors of failure in mind Perhaps there is a subset of the ischemic mr population that may benefit from repair So applying the full breadth of ctsn criteria We proceeded with acb with mechanical mitral valve replacement owing to the patient's young age The decision to replace the valve was further supported by the intraoperative finding of an infarcted medial papillary muscle Although there was no frank flail seen on the baseline echo Three vessels were bypassed including a suprancial lemograph to the lad in d1 and an svg graph to the piv A 29 millimeter mechanical mitral valve was implanted The pfo was closed and the laa excluded Given the high risk of both af and appendage thrombus in the years to come Although the patient will have a lifelong anticoagulation requirement So now it's time to evaluate the mechanical mitral valve And continuous wave doppler interrogation reveals the following double envelope trace So our sixth poll is this When interrogating the mitral valve, which is true regarding the double envelope phenomenon The options are a this is a ghosting artifact b this is a reverberation artifact c this is a true hydraulic phenomenon D the largest envelope is the true envelope Or e the densest envelope is the true envelope and this is a multi-choice Poll question you can select all the ones that you feel are are true That's 30 seconds. Oh and the poll again Let's take a look at the results So ghosting reverberation hydraulic phenomenon kind of split And most if not all look at the densest envelope is the true envelope So the debate regarding the double double envelope was recently hashed out by libel in 2019 in a letter to the editor in jcva Wybel's letter was in response to a publication by couture at all which referred to the double envelope as reverberation artifact Going to the large amount of flow passing through the mitral valve at high cardiac outputs A different group in an online communication to the american college of cardiology Suggested the second doppler envelope seen when interrogating the mitral valve inflow is a ghosting But if it were ghosting or reverberation through the high flow Why wouldn't it also affect other structures with even higher velocities such as the aortic valve? Secondly, if you compare the envelope sizes, you will appreciate that the ratios between the envelopes are never consistent with reverberation or duplication artifact Which would require an exact doubling of the spectral envelopes What they highlight and something I had never appreciated in my own practice Is that the double envelope is only apparent when the continuous wave doppler interrogation line is pointed towards the septum Changing your angle to avoid the septum often will resolve the double envelope altogether This supports the theory that the second envelope represents flow acceleration of the mitral inflow wall jet along the septum Back to our case inspection of the valve revealed a well seated mechanical valve in the mitral position with characteristic washing jets Continuous wave doppler orient towards the septum revealed a double envelope tracing Tracing the densest jet revealed a peak gradient of 8 and a mean gradient of 3 These gradients did not increase with faster pacing or augmented svr Follow-up tte on post operative day 7 showed significant recovery of lv function following revascularization With lvef improving to 45 Peak and mean gradients through the mitral valve were slightly higher at 18 over 5 as expected There was only trivial mr noted Unfortunately the rv function could not be assessed But there were no clinical indicators of rv failure or dysfunction And that brings us to the end of our presentation on te and surgical decision making and you are As well as the end of our first year of multicenter echo teaching series Thank you all for your participation and attention And i'll now hand it over to rafael to field any additional questions And dr. Badiwala and dr. Olman are both on the call to help add additional insights