 Okay. So hi again, everyone. My name is Marcus Salvatore and I'm an anesthesiologist at CBICU attending at Toronto General Hospital with an interest in perioperative echocardiography. And today we'll be talking about TEE for septal myectomy with a focus on interoperative decision making. I have no disclosures or competing interests and in terms of acknowledgments on the left are my mentors in echocardiography and cardiac anesthesia or world renowned for their expertise. A particular thanks goes to Dr. Ahmad Omran, consultant cardiologist who helped to develop this lecture. I also want to acknowledge the talented roster of cardiovascular surgeons that we have here at the Peter Monkardiac Centre. And to that end, I would like to introduce Dr. Anthony Ralph Edwards, a cardiovascular surgeon here at TGH with specialist expertise in septal myectomy. He's a preeminent authority in the surgical correction of pulmonary cardiomyopathy performing 50 to 70 procedures per year for patients referred from across Canada. He joins the call today to answer questions and to provide a valuable surgical perspective. Thank you, Dr. Ralph Edwards. Thank you, Marcus. Overdid the introduction a little bit. So although we are steering this ecosystem more towards an interactive case review, we will quickly review the guiding tenants of the TEE exam for the surgery. We'll critically appraise cases involving septal myectomy in which TEE was used to refine diagnoses, detect new pathology, adjust the surgical plan and assess surgical results. We'll also interpret TEE findings in the context of the surgical literature and best practices. So HOKUM is the most common inherited cardiac disorder, remarkable for both its genetic and clinical variability. Epidemological studies estimate a prevalence of approximately 0.2% of the population or 1 in 500 individuals. As with most of echocardiography, I find it easier to remember the cardinal features if I understand the key anatomic and structural changes that underlie this disease. The six features listed on the left have the most diagnostic utility whereas those listed on the right are ancillary findings that can be used to support a diagnosis. We will explore these six findings in more depth in the upcoming slides. So although the focus of this talk will be septal myectomy for HOKUM, symmetric and asymmetric ventricular hypertrophy can result from a host of common conditions listed here. As a result, you may be faced with an incidental finding of high LVOT gradients or SAM during the course of routine revascularization or valve surgery. It is important to know how to assess and interpret these findings to determine whether modifications to the surgical plan are necessary. The most common non-genetic cause for asymmetric hypertrophy is a ventricular septal bulge commonly seen in older patients with long-standing hypertension. The prevalence of VSB increases significantly with age and is found in approximately 20% of patients by the age of 80. Although often seen as a benign condition, VSB can still cause high LVOT gradients, SAM, and significant MR with pathological consequences. See review paper by Canepa et al in 2016 for detailed comparison. Nearly any pattern and distribution of LV wall thickening can be observed in HOKUM, with the basal anterior septum in continuity with the anterior free wall being the most common location for LVH. So the TEE perceptal myectomy starts by accurately defining the borders of the intraventricular septum. This relies on four principle measurements, including the distance from the right coronary cusp to the maximal septal thickness. The maximal septal thickness itself, now a clinical diagnosis of HOKUM and adult patients can be established by demonstrating a maximal wall thickness of over 15 millimeters anywhere in the left ventricle in the absence of another cause by hypertrophy in adults. This measurement is crucial but challenging as it is often difficult to distinguish the boundary between the intraventricular septum and the right ventricular endocardium. The myocardial fibrosis that characterizes HOKUM can sometimes yield differences in ecogenic texture which can aid in this distinction. The third is the distance from the right coronary cusp to the distal narrowing and finally the distal narrowing itself. So this brings us to our first poll and thank you Rafael for helping to arrange the interactivity. And the question is which of the following are true and you can select all that apply. So A, measurements should be made in end systole when the gradient is highest, B, measurements should be made in end diastole when the walls are thinnest, CTE overestimates thickness compared to cardiac MRI or D, the surgical resection follows the line from the RCC to the distal narrowing. So I'll give you about five seconds or 10 seconds or so to lock in your answers and then we'll keep moving. Okay I think that's most of the respondents and we'll end the poll there. So the results can bring them up here show that the majority of people feel that the measurements should be made in end diastole which is correct. That's the time when we make the measurements and TE overestimates thickness compared to cardiac MRI is the other correct answer here. So B and C were correct and the measurements should be made in end diastole when the measurements are thinnest and the myectomy is performed during cardiopulmonary bypass obviously when the heart is completely collapsed. So the measurements that the surgeon uses to make the incisions you want to be in a relaxed state. And then an observational study by Felin et al. in 2017 compared ventricular septal measurements in Holcomb across various imaging modalities and showed only modest correlation between ECHO and MRI measurements. Specifically MRI showed the greatest correlation with trans thoracic ECHO but TE measurements were on average 13% larger than an MRI. So it definitely varies by center but at our institution we perform cardiac MRIs for all patients that are coming from myectomy. So the next feature that we look for is LVO turbulence and gradient and LVO flow tract obstruction either at rest or with provocation is present in approximately 75% of patients with Holcomb. There are two primary mechanisms responsible and the first is decepto hypertrophy with narrowing of the LVO T causing abnormal blood flow dynamics. The second are the anatomic alterations in the mitral valve and apparatus which we will discuss in more detail shortly. The presence of a peak LVO T gradient of over 30 millimeters of mercury is considered to be indicative of obstruction with resting or provoked gradients over 50 millimeters of mercury generally considered to be the threshold for septal reduction therapy. Continuous wave Doppler in the deep trans gastric view will often show a late peaking or dagger shaped trace. This characteristic Doppler profile occurs because the LVO T obstruction is dynamic and sensitive to ventricular loading conditions and contractility. Although ejection begins normally as assistively progresses the outflow tract narrows due to increased pressure and myocardial contraction. This gradient then worsens as the ventricle empties causing the peak gradient to occur late insistently. Now ideally during these surgeries we wish to demonstrate a high baseline LVO T gradient that then resolves in the post pump study following the myectomy. However there are several hemodynamic changes that occur under general anesthesia which may diminish the LVO T gradient such as reduced sympathetic tone, volume loading, vaticardia, and decreased myocardial contractility. As a result the baseline LVO T gradients may be normal or at least under the therapeutic threshold. In these cases we often provoke gradients using one or more maneuvers including valsalva, myocardial irritation to induce pvcs, or debutamine infusions as shown here. The flow turbulence through the LVO T is also what causes the fluttering or early systolic closure of the aortic valve during mid systole. The reasons behind this phenomena are incompletely understood owing to the complex fluid dynamics involved. One of the oldest theories remains the most dominant with Saab-e-Adal from 1982 suggesting that turbulent flow is associated with an increase in the kinetic energy of blood through the LVO T. Because the total amount of energy remains constant the increased kinetic energy occurs at the expense of a reduction of pressure in the LVO T proximal to the aortic valve. The resultant pressure gradient across the aortic valve is what leads to the premature closure. Now mitral valve physiology in patients with HOKOM is abnormal for two principal reasons. The first is abnormal flow dynamics through the LVO T as already described. And the second and commonly underappreciated issue is that the mitral valve is structurally abnormal in these patients. The mitral valve leaflets are often elongated and there is anterior displacement of the papillary muscles in mitral valve apparatus which predisposes these patients to SAM. During early systole the tip of the interior mitral leaflet is dragged into the LVO T by the venturi effect of mid systolic flow. This is termed systolic interior motion or SAM. The displaced anterior mitral valve leaflet results in poor mitral valve leaflet co-optation and eccentric posterior directed MR in mid to late systole. MR severity relates to the degree of LVO T obstruction. Now one of the dogmas of echocardiography is that flow always goes in the direction of restriction. So if the interior mitral leaflet is being pulled interiorly shouldn't the resultant jet also be directed interiorly? Well no, what happens in HOKOM is that the entire co-optation point of the mitral valve moves in the interior direction. It is therefore the shorter posterior leaflet that can't reach the co-optation point acting as the quote-unquote restricted leaflet and the result is a posteriorly directed jet. So our first question for Dr. Ralph Edwards is which features of the baseline TE study are most important to you when performing septomyectomy? I think the goals of the procedure are obviously to relieve the obstruction and to do this we want to remove the bulk of the in the septum that's causing the narrowing. The goal is to try and reduce the septal thickness to about one centimeter. So I'd like to know what the maximal thickness is of the septum to gauge how much I want to remove. The other thing that I need to know is sort of the shape of this this obstruction whether it's very focal and limited or whether it's more generalized and involves the entire septum. The short high obstructions are fairly easily resected with a very limited you know, resection but the long ones that involve most of the septum you have to be able to get below the mitral valve leaflet, anterior mitral leaflet so that there's no flow acceleration in the region of the anterior leaflet of the mitral valve so that you don't get SAM. So to do this we can either say that I want to make the the resection about one centimeter longer than the length of the anterior leaflet or go one centimeter below the SAM septal contact point. So the SAM septal contact point, the morphology of the septum and the thickness of the septum are the things that are interesting to me. I must say however I don't make my decisions based on the intraoperative transsophageal echo. I find that oftentimes this exaggerates the thickness of the septum and I use the preoperative surface study to guide the resection, the vast majority of cases. Thanks so much and we're looking to have a clip here of a surgical mimic to be being performed. Dr. Ralph Edwards would you mind just walking us through this procedure? I know this isn't let me just to disclaimer this isn't Dr. Ralph Edwards's procedure himself but he's agreed to kind of walk us through the major steps. I know I know you tend to perform a different series of incisions and that video is also available online but you just let me know when you'd like me to get started or if there's any preamble that you'd like. This is a pretty fast clip so I don't think I'm going to really be able to talk while it's running. The myectomy classically spans between the the middle of the right coronary sinus and the lateral border of the mitral valve annulus and how I do this is I follow the hinge point of the the right and left cusps of the aortic valve and make an incision about two millimeters below this right up to the commissure and I make the first cut about two millimeters deep and then I sort of distract that that cut line into the outflow tract and then make a identical cut parallel to it but at the base of the first cut so that you're kind of making a cut that's going straight up and depending on how much you need to resect you keep on doing this until you've achieved the thickness that you'd like to resect and then I put the retractor in this groove that I've created and then carry the resection into the ventricle. Having said that I then make an incision on the the medial border of the the mitral annulus and perform a resection below the membranous septum to sort of meet the the first resection and this is the extended myectomy. I think that this can be done without too much increased risk for heart block and I do this pretty much as a standard routine now the the problem with this operation is it's a debulking procedure so anywhere that you can get muscle mass out of the outflow tract improves your your results. Perfect thanks. So the post myectomy study seeks to confirm that the resection was adequate with reduction or resolution of the LVOT gradients and any related SAM. An adequate resection results in persistent obstruction and symptoms while excessive or poorly placed myectomy can produce the atrogenic heart block and ventricular septal defects with morbidity and mortality rates reported as high as 6 however in sharp contrast data collected from dedicated Holcomb centers have shown remarkably decreased operative mortality of around 0.4% explained primarily by surgical experience technique improved myocardial preservation and decreased pump times. The table here shows an average of the complication rates reported in literature however notably in 2017 a retrospective review of the TGH experience including Dr. Ralph Edwards spanning 291 myectomies over four years the authors reported a permanent pacemaker requirement in approximately 5% of patients and mortality of 0.3% with no iatrogenic VSDs highlighting the advantages of designated Holcomb centers. So without further ado let's get into the first case. So our first patient is a 65 year old female that had Holcomb diagnosed as an incidental finding in 2020 during a workup for hypertension. She reported a two to three year history of worsening dyspnea and exertional fatigue with NYHA class 3 symptoms. Coronary angiogram shows multi-vessel coronary disease and her TTE shows an intraventricular septum of 18 millimeters with resting gradient of 67 millimeters of mercury and moderate SAM. She had mildly synodic mitral valve and a mean gradient of six millimeters of mercury. Here is her four chamber view which clearly demonstrates the gross asymmetric myocardial hypertrophy. Focus on the mitral valve shows clear SAM as well as severe mitral annular calcification with decreased leaflet mobility especially at the base of both the interior and posterior mitral valve leaflets. Clips of the aortic valve show the characteristic turbulence through the LVOT as well as the aortic valve fluttering and early systolic closure. Unexpectedly inspection of the mitral valve revealed that compared to the baseline study the degree of MR had increased to severe. Furthermore the jet was centrally directed as opposed to the posteriorly directed eccentric jet characteristic of SAM. This raised the possibility that a component of the MR was related to primary mitral valve dysfunction or structural abnormality in the valve itself. This freeze frame of the mitral valve further supports this possibility as we see at least moderate MR by vena contracta beginning in early systolic far before the appearance of the SAM as demonstrated here. Continuous wave Doppler gradients through the mitral valve shows reduced mitral valve gradient compared to baseline with a mean gradient of three millimeters of mercury. Inspection of the tricuspid valve revealed moderate TR directed towards the intratral septum as well as an elevated RVSP. The RV appears thickened suggesting that the elevated pulmonary pressures were chronic. The pulmonary hypertension in this case likely resulted from a combination of MR, MS, and diastolic dysfunction. So our second poll and Raphael, if you could help, what would you recommend to the surgeon regarding mitral valve intervention in this case? We'll put it up for 15 seconds. We recommend no intervention required. All MR is second to SAM. You would recommend to repair the mitral valve, replace the mitral valve, or discontinue bypass and reassess the mitral valve after my activity. Okay, so I'll show you our polls here which suggest that the majority of people feel that we should discontinue bypass and reassess after my activity. And Tony, from a surgical perspective, which features of the mitral valve or MR would make intervention more likely in your opinion? Well, I think obviously if you see that there's a structural abnormality in the valve that would indicate that it's much more likely that you're going to have to replace the valve. Also, the timing of the mitral regurgitation, mitral regurgitation that's related to SAM occurs late insistently. So if you click through the frames, once if there's mitral regurgitation before there's turbulence in the outflow tract, that would suggest intrinsic mitral regurgitation and a valve, the majority of the problem being related to the valve. And then an atypical appearance to the regurgitant jet also would push you towards thinking that this was a valve related problem and maybe not so much related to SAM. Having said all this, the loading conditions and effects that anesthetic have on mitral regurgitation are variable in different patients and sort of difficult to predict and knowing what the MR looked like before on the surface study can go a long way to guiding you in the operating room as well. Thanks. Okay, so we did what the audience suggested in this case, which was only last month actually. And a septomyectomy was performed spanning the medial and lateral borders of the mitral valve annulus. Specimen was approximately eight millimeters in thickness and carried five centimeters into the ventricle. The lateral attachments of the popular muscle heads were fully mobilized in a secondary cord or a strut cord between the anterior leaflet and the outflow tract were divided. SVG was performed to the LAD and OM1 in order to treat the coronary obstructions that were identified in the preoperative angiogram. And then the plan was to perform the myectomy, discontinue bypass, re-evaluate the mitral valve for MR. So the post-myectomy study revealed complete resolution of the high LVOT gradients. The clip on the left shows high velocity but laminar flow through the LVOT and that's often characteristic of these patients upon discontinuation of bypass. If any provocation was required to elicit gradients during the baseline study, then you should again repeat those same provocation maneuvers as part of the post-myectomy evaluation to yield a meaningful comparison. To everyone's surprise, detailed examination of the mitral valve revealed complete resolution of the MR from severe initially to now trace without any intervention besides the myectomy performed. The resolution of the MR was also associated with reduction in the RBSP and pulmonary pressures from 61 down to 46. So our third question for the audience is why was the MR centrally directed in this case or why didn't appear in the as the eccentric posterior directed jet that's so characteristic of Holcomb and Sam? And Raphael, if you could put up the poll. So the options are because of the severity of the MR, the mitral annular, annular calcification that was seen, the length of the anterior mitral valve leaflet that the valve was rheumatic and restricted, the degree of LA dilatation or the obtuse order mitral angle. Those are the options that you have there. I'll just give you 10 seconds. Okay, so we have the highest degree of respondents probably for MAC degree of LA dilatation and anterior mitral valve leaflet length. Okay, so the correct answer is the jet was anteriorly directed due to MAC. This is a rare finding and reported in only three out of 93 patients in a case series investigating MR and Holcomb from 2000. So the in terms of the follow up echo on postoperative two, it showed preserved the left particular function, only mild MR and an RBSP of 35, which continued to improve after the surgery. Okay, now on to our second case, which involves aortic stenosis and a fibromuscular ridge. So not a classic Holcomb case, but we just want to talk about septal macadamies and asymmetric hypertrophy and other conditions as well. So this patient is a 72 year old male that was referred for moderate aortic stenosis. He was otherwise healthy, but complained worsening exertional dyspnea over the last year. His peak radiant on surface echo was 89 millimeters of mercury with an aortic valve area of 1.2 centimeter squared. He also had mild AI but otherwise preserved by ventricular function. And although he was referred for a Tavi assessment, because he didn't have any additional comorbidities, he was thought he was best served with surgical aortic valve replacement. So the four chamber view here demonstrates the gross hypertrophy affecting both the right and left ventricle. The short axis of the aortic valve shows a very stenosed but clearly tricuspid aortic valve with three raffae. The midisophageal long axis view shows marked flow turbulence through the LVOT with the presence of a small but discreet fibromuscular ridge. This was an unexpected finding not diagnosed during the preoperative TTE. Continuous wave doppler from the deep transcastric view revealed a peak aortic valve gradient of 59 millimeters of mercury, whereas the LVOT gradient only measured the mean of nine millimeters of mercury. Here we have three features that are combining to contribute to the LVOT gradient and high velocities, namely the aortic stenosis, the fibromuscular ridge and the gross concentric hypertrophy resulting from long-standing AS. In terms of the surgery that was performed, this was a non septomyectomy surgeon that was performing this ad hoc procedure and aortic valve replacement was performed with a 23 millimeter alveolus bioprosthesis and then the ad hoc component was the resection of this discreet fibromuscular ridge with myectomy. After discontinuation of bypass, repeat assessments showed preserved LV function, but unfortunately with persistent turbulence through the LVOT despite the aortic valve replacement. Continued assessment showed an additional concerning finding not seen in the preoperative study. I'll give you a few seconds to make your assessment from these limited images. So our fourth question is what is your assessment of the surgical intervention? And Raphael, if you could put up the poll. So is this pervalveric leak related to the tissue aortic valve that was placed? Is this prosthetic valve stenosis or stuck leaflet? Is this a residual LVOT gradient? Is this a septal perforator? Or is this a eatrogenic VSD? I won't give you 10 seconds. Okay, the polls ended and 81% say that this is a VSD and that is the right answer. So color interrogation in the minisophageal four chamber view clearly shows a restricted VSD in the perimemberness region at the site of the myectomy. The defect measures 0.6 centimeters using color flow Doppler or sorry continuous wave Doppler. A freeze frame of the inflow outflow view confirms the size and continuous wave Doppler demonstrates peak velocities over four meters per second. Now a quick pause to demonstrate the difference between VSDs and unroofed unroofed septal perforators. I feel that the similarities between these two entities are often over emphasized as they have distinct qualities that make them easy to tell apart in most cases. On the left, we have a VSD which clearly shows high velocity turbulent flow during systole moving from the LV towards the RV or away from the probe. Conversely, on the right, we see unroofed septal perforators with low velocity diastolic flow into the left ventricle. So Tony, from a surgical perspective, how is this complication best managed? Well, I don't think you can you can leave it. I think you have to close the the defect that you've created. Sometimes if these things are small, you can you can find them and put a a pledged stitch and just bring it together that way. If it's larger or or the the muscle around it is won't take a stitch all that well, then probably a patch on the surface of the outflow tract in the left ventricle is the way to go and make the patch redundant so that the pressure is sort of distributed over a large patch area so that the patch is pushed into the the defect during systole and you get a good approximation and closure. And is there a difference if you approach this repair from the left ventricle or from the right ventricle? Well, you it depends on obviously where the the the hole is. Some locations are more difficult than others. The typical location actually for a VSD is in the RVOT just at the base of the outflow tract below the the pulmonary valve as you're making the incision sort of curve around. Sometimes you have a tendency to flare and get deeper as as you as you go around the corner so that's probably the most common place and that's fairly amenable to a pledged repair in the in the RVOT things that are in in a different location are probably best dealt with with a patch placed from the from the left ventricle. Thanks so much. Okay and poll number five. How will a pair of membranous VSD affect your hemodynamic measurements? Ralph, I hope you could put up the poll. I'll give you 10 seconds to answer. Okay and poll results. 56% say underestimate LVOT gradient and 56% say RV and pressure volume overload. Sorry, I realized I changed the final answer after submitting these to RAFAO so that's my fault, but both of those both of those answers are correct. Okay, so in terms of the case to follow up, the VSD was repaired with a pledged suture as only suggested. The post opera of day three echo unfortunately show persistent residual peak LVOT gradients of 30 millimeters or mercury as well as a persistent three to five millimeter restrictive VSD with left to right shunt peak gradient of 60 which was decided to manage conservatively although there was a referral made to the structural heart team for assessment and they also thought that conservative management was best in this case. The meteoric valve gradient was 14 millimeters mercury with no AI but this will also be underestimated in the context of a pair of membranous VSD. There's preserved LV function and the patient was discharged home on post opera day 10. Okay, for our last case we're going to be discussing a hokum combination of hokum and aortic insufficiency. So our third case involves a 69 year old female with an incidental finding of a murmur during work up for cataract surgery. She had worsening symptoms over the past four years and she's now NYHA class three meeting criteria for intervention. No Frank heart failure symptoms but a trans thoracic surface echo showed intraventricular septum of 18 millimeters with a resting gradient of 74 millimeters of mercury and moderate sand. There was only trivial AI detected on the preoperative study. In the four chamber view we see the characteristic hypertrophy as well as an increased amount of regurgitation through the aortic valve compared to the preoperative study and now being graded is mild. A focus long access view of the aortic valve shows that the aortic valve is structurally normal that the AI jet is central without prolapse or billowing and although it appears eccentric in this view I think that's only because the septum is bulging into the LVOT otherwise it would appear as a centrally directed jet. So in terms of the surgical details the aortic valve was tri leaflet and the leaflets were thickened but mobility was not impaired. There was calcification noted at the base of the left coronary cusp. A septal myectomy was performed spanning between the medial and lateral borders of the mitral valve annulus. The specimen was approximately one centimeter in thickness and carried 3.5 centimeters into the ventricle and secondary cordae between the anterior leaflet of the mitral valve and the outflow tract were divided. The lateral aspects of the popular muscle heads were mobilized. Examination of the aortic valve post myectomy though now reveals a second jet of AI that's extremely eccentric directed towards the right coronary cusp implicating an issue with either the left or non coronary cusp. This is a new jet that wasn't present in the preoperative study. So the options here we'll get into with the next poll but I'm just going to let you take a look and examine these views and just as a reference point the bottom jet is likely the original central co-optation jet and the jet closer to the anterior mitral valve leaflet is the new jet arising post myectomy. Here's additional views including the short axis view which show the two jets and finally a 3d unfortunately the color isn't there wasn't color added to this image in particular but shows at least a 3d view with the arrow directed towards the left coronary cusp. So the question for the audience for poll number six is what is the mechanism for the worsening AI post myectomy? Is it RCC prolapse? Is it left coronary cusp restriction? Is it remodeling of the LVOT? Left coronary cusp perforation or central co-optation defect? I'm going to give you 10 seconds to answer. So the majority of respondents at 80% said the left coronary cusp perforation and that is the correct answer. So the AI autotomy was reopened and the valve was inspected and there was a tear present between the border of the calcification at the base of the leaflet and the more normal leaflet. This was repaired with a pledged 70 proline suture and the pledged material was pericardium. Reassessment of the aortic valve following the repair showed that now the original central co-optation is unchanged compared to the baseline study and the new regurgitating jet from the perforated left coronary cusp has been repaired and resolved completely. Again examination of the short axis view reveals that that second color jet is no longer visible. So the follow up on post-operative day four showed a normal LV size and systolic function. The basal septum myectomy site measured five millimeters and no perforated or VSD flow was seen and there was mild to moderate AI that was detected in the post-operative study with an AI pressure half time of around 430 milliseconds. So for Tony the question was how can you minimize the risk of injury to the aortic valve during my myectomy in that video we saw that that ROS retractor is directly over the RCC and in this case it was an LCC injury but is there anything that can be done to try to minimize the likelihood? Well I don't know I've done literally thousands of these cases and there's a I can only remember two cases where patients have had injury to the aortic valve or had the AI that this was the only case where we discovered it after the fact. With the ROS retractor if you have a assistant that sort of balances their weight against the aortic valve and then if the valve slides out from under the retractor I've had the right coronary cusp evolved basically and that was one case and now I instruct the the assistant on how to hold with a static hold where you just place the retractor fix it in place and if the heart slides away it slides away and we reposition it and that's the only time I've had that happen and that was fortunately repairable the tear was right at the insertion of the leaflet and it could be sewn back and actually with long-term follow-up it's been it was okay. This more recent one I think the you know the delusional cardiac surgeon answer to this is that in the region where the hole was in the left coronary cusp there was a calcific plaque and it's possible that deforming the valve in in some way with the forceps while I was doing the myectomy maybe I was a little bit too forceful and it's it's caused this this tear or the the calcification actually cut through the the more normal leaflet adjacent to it or it's also possible that I did it with with the knife I mean I've done a lot of these and it isn't the problem so I'm not really sure fortunately it was relatively easy to fix it's just a matter of really keeping track of multiple things while you're you're doing this you have to sort of stay focused on the end of the blade all the time and and you know have your retractor assistant aware that they shouldn't pull harder if things are are slipping but this is not a common not a common problem. So it seems in reviewing the the literature in the initial moral series it seems to suggest that the AI that or the rate of AI that he reports was actually higher than is reported anywhere now currently with modern techniques. Was there anything specific that she sort of go ahead? Well that the it used to be that people would open the aorta with what they call the hockey stick incision and typically the incision would go along the sinus tubular junction and then drop into the non-cornery sinus which is perfect if you're replacing an aortic valve because the the sinus tubular junction is is narrowed and you oftentimes can't get the prosthesis through it if you just cut transversely but when you sew up these incisions that transverse the stj you alter the anatomy of the valve and you you cause prolapse and leaking of the valve so I think older series probably they weren't quite aware of that they used to think that it had something to do with lack of support of the non the right coronary cusp because of the myectomy that was performed or possibly dilating the valve by using the retractors but I think it's more distortion of the valve created by traversing the the stj now the incisions are one centimeter above the stj and never drop across it so it's it's not so much of a problem. Perfect thanks so much. Okay and that brings us to the end of our talk. Dr. Alvarez or Tony would you like to add anything to what we've discussed today? I think I think there's a lot of nuances to this disease there are a lot of presentations that sort of mimic the physiology but you arrive there at very much different anatomic substrates anywhere from you know elongation of the aorta and you know hypertensive cardiomyopathy to calcification of the posterior leaflet and movement of the anterior leaflets or the co-optation point forward more into the outflow tract and there are multiple ways to get to the same physiologic effect and sometimes these things sort of play into what you do about fixing it. Perfect thanks I really appreciate you being involved today in answering our questions and now we can open it up to the