Severe bioprosthetic MS - How to proceed?

[vector2]

Pt is a 40 yo M, h/o of endocarditis s/p bioprosthetic MVR in 2016, PCI to RCA in 2015, aflutter, congestive hepatopathy, thrombocytopenia, recurrent pleural effusions, LAA thrombus on recent cardiac CT for which he has been on eliquis for 1 month.

He is presenting to you today for a valve-in-valve transseptal TMVR after holding his eliquis for 2 days.

You proceed with a careful induction of GETA. In this hospital cardiology does the TEE and/or TTE for cath lab procedures and here are some of the images they get:

(CW spectral doppler is inverted here)

SPAP is 65-75 mmHg by TR CW jet


I think it’s fair to say that the LAA, despite being on eliquis for 1 mo, is still quite concerning for thrombus, and even if one isn’t going to call it frank thrombus keep mind that when doing transseptal ViV TMVR that a stiff wire frequently heads into the LAA or LUPV and does some scraping. In a 40 yo patient, the interventional cardiologists and CT surgeon were not willing to accept the stroke risk here.

So, given that A/C does not appear to be working, our only option is operative. Take note of the biventricular size and function, the appearance of the bio MVR, and the fact that the mean mitral inflow gradient (not shown) is 20 mmHg.


For residents and fellows first:

What are the echocardiographic findings in the limited images above? What interventions does this patient need? What are your preanesthetic concerns given his surgical and medical history? How are you going to induce? Which monitors and lines? How are you going to come off CPB?

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[MirrorTodd]

Honestly I'm not even sure what veins those are. I wanna say this is a TTE. From the bottom up: parasternal short axis with a significant wall motion abnormality...inferior wall i think. EF 25-30% maybe. 2nd from the bottom is that mod TR? 3rd from the bottom is no idea really. Is that SAM of the mitral valve obstructing LVOT? CW wave dont know what that is. The other ones no idea. Maybe there's a clot in the LAA. I can't tell for sure.
Shifty reply I know, but I have not gotten very good training on echo, and minimal to non one TTE.
Is this TEE and the images are flipped or something? They look weird to me.

 

[MirrorTodd]

Needs a new mitral valve and probably an atrial appendage clipping. Preanesthetic concerns are death on induction. I never know how to answer that question. Induce the same way they did yesterday in the cath slow...very carefully...essentially prop, roc, tube. Pads will already be on obviously, as well as heparin drawn up and bypass machine standing by, surgeon gowned with saw on mayo already tested.
He should've had an a line already from the cath lab procedure, 2x large bore IV, if all goes well on induction, MAC introducer and float a swan.
I don't know of multiple ways to come off bypass. Far as I know, you tell the perfusionist to turn the flows down until they are off. Sometimes you have them give the heart a little volume in between. Should there be more than one way?

 

[JiPo]

I will take a stab at it. Hope I don't sound like an idiot.

Images
1st image TEE = two chamber view (72 degree is closer to commissural view, but can't see the valve all that well), with LAA zoomed in. I see some sludge here, indicating there may be a clot here. I would like to see PW through it to see if is less than 0.4. You see coumadin ridge and left pulmonary vein. You also see LCx artery.

Edit: Now that I look at the image again, there is a clear clot along the coumadin ridge, in addition to the sludge.

2nd image TEE = Same as the first image, but zoomed out to show LV, and angle is cut out less. You see 4 chambers here. Mitral valve opening looks tiny, and you see TV which seem to be opening well.

3rd image TEE = CW across MV in 2 chamber view. I don't know how to interpret this yet.

4th image = This is either TG midpapillary long axis view (cut out to 90 degrees) or TTE image. I am not sure which one, but RV looks grossly larger than LV to the point that RV is bowing into the LV. LV is grossly underfilled.

5th image = ME 4C view. Shows moderate, maybe severe? TR. If I have to guess, this is likely from severe MS -> Pulm HTN -> RV distension/failure -> worsening TR, which could explain congestive hepatopathy with this TR.

6th image = This is TTE. Apical 4C view. Shows TR.

7th image = Either Parasternal short axis on TTE or TG short axis on TEE. Given how well you can see the RV and RV is in the center, not the LV tells me it is likely parasternal short axis TTE. Again shows dilated RV with severely underfilled LV, consistent with severe MS with RV dilation.

What I would like to get
Right heart cath to determined the severity of pulmonary pressure.

Anesthesia plan
In severe MS, I would love to keep them sinus, but that is not an option given the likely clot in LAA. Avoid tachycardia, which leads to avoiding hypotension, which would cause reflex tachycardia. I would induce with etomidate, or titrate in propofol very slowly. Induce with 1-2u of vasopressin bolus. Have esmolol ready just in case. I would use Vaso as pressor of choice throughout the case. Depending on the severity of pulmonary hypertension, I would start milrinone infusion. Coming off bypass could be tricky since LV may not be able to accommodate such large increase in pre-load after it gets a new valve, so would start with generous epinephrine infusion, milrinone infusion, and depending on how RV improves (if it is still dilated and not working too well, would also add flolan). Vaso again will be the pressor of choice, but if maxed out at 0.04, would add phenylephrine.

I probably am wrong on most things here, but thanks for a good case! Fun mental exercise on a weekend morning.

Edit:
Forgot that this is a re-do sternotomy. 5 units of blood in the room, checked. 16g (14g) x2 + cordis or 16g x1 + MAC cordis. Have surgeon cannulate fem A/V so they can easily exchange it for crashing onto bypass if needed during sternotomy.

Also will likely need a TVR as well.

 

[drmwvr]

What I would like to get
Right heart cath to determined the severity of pulmonary pressure.

How would that change anything you said you'd do?

 

[MirrorTodd]

I will take a stab at it. Hope I don't sound like an idiot.

Images
1st image TEE = two chamber view (72 degree is closer to commissural view, but can't see the valve all that well), with LAA zoomed in. I see some sludge here, indicating there may be a clot here. I would like to see PW through it to see if is less than 0.4. You see coumadin ridge and left pulmonary vein. You also see LCx artery.

2nd image TEE = Same as the first image, but zoomed out to show LV, and angle is cut out less. You see 4 chambers here. Mitral valve opening looks tiny, and you see TV which seem to be opening well.

3rd image TEE = CW across MV in 2 chamber view. I don't know how to interpret this yet.

4th image = This is either TG midpapillary long axis view (cut out to 90 degrees) or TTE image. I am not sure which one, but RV looks grossly larger than LV to the point that RV is bowing into the LV. LV is grossly underfilled.

5th image = ME 4C view. Shows moderate, maybe severe? TR. If I have to guess, this is likely from severe MS -> Pulm HTN -> RV distension/failure -> worsening TR, which could explain congestive hepatopathy with this TR.

6th image = This is TTE. Apical 4C view. Shows TR.

7th image = Either Parasternal short axis on TTE or TG short axis on TEE. Given how well you can see the RV and RV is in the center, not the LV tells me it is likely parasternal short axis TTE. Again shows dilated RV with severely underfilled LV, consistent with severe MS with RV dilation.

What I would like to get
Right heart cath to determined the severity of pulmonary pressure.

Anesthesia plan
In severe MS, I would love to keep them sinus, but that is not an option given the likely clot in LAA. Avoid tachycardia, which leads to avoiding hypotension, which would cause reflex tachycardia. I would induce with etomidate, or titrate in propofol very slowly. Induce with 1-2u of vasopressin bolus. Have esmolol ready just in case. I would use Vaso as pressor of choice throughout the case. Depending on the severity of pulmonary hypertension, I would start milrinone infusion. Coming off bypass could be tricky since LV may not be able to accommodate such large increase in pre-load after it gets a new valve, so would start with generous epinephrine infusion, milrinone infusion, and depending on how RV improves (if it is still dilated and not working too well, would also add flolan). Vaso again will be the pressor of choice, but if maxed out at 0.04, would add phenylephrine.

I probably am wrong on most things here, but thanks for a good case! Fun mental exercise on a weekend morning.

Edit:
Forgot that this is a re-do sternotomy. 5 units of blood in the room, checked. 16g (14g) x2 + cordis or 16g x1 + MAC cordis. Have surgeon cannulate fem A/V so they can easily exchange it for crashing onto bypass if needed during sternotomy.

Also will likely need a TVR as well.

Answer was far better than mine lol

 

[JiPo]

How would that change anything you said you'd do?

When I was typing my response initially, I was thinking about using the PA numbers to determine whether I should talk to cardiologist/CT surgery about starting milrinone pre-op, but now that you mentioned it, right heart is dilated, but still beating regardless of what the PA pressure is right now, so RHC results won't change my induction plan or management. Plus, I will get a swan anyways after induction, so I will have PA pressure with me. I will start milrinone after induction if I see RV changes on TEE or worsening PA pressure on swan.

 

[greatnt249]

Just out of curiosity, what was the rationale behind doing a valve-in-mitral valve procedure on a 40 y/o with clearly severe prosthetic mitral stenosis (as opposed to redo surgery)?

 

[Hork Bajir]

Great post vector.

As a current CT fellow I’ll give it a shot: moderately depressed LV fxn, RV dilated and severely depressed. LV may or may not perk up a bit when loaded appropriately after fixing the valve. Not gonna call any RWMAs from the images shown here. Critical MS (not gonna calculate a valve area but... small), mild TR, cannot rule out LAA thrombus (wouldn’t definitively call one from these images alone, but also suspicious enough that I’d be loathe to hit the cardio version button unless pt is dying).

Induce slowly with pads on and surgeon in the room. MS is so scary because once you get into a death spiral, few things can bail you out except electricity (for tachyarrythmia), or crashing onto bypass. Coming off bypass will need significant intotropes for the RV; relatively less worried about LV fxn. Fine to try pulmonary vasodilators as there is little harm in doing so, but the high PASP here probably is postcapillary pHTN (unless this is all very longstanding with capillary remodeling). Assume surgeon will visually inspect the LAA while on pump and do what needs doing there. Sucks that a 40 yo is getting a redo MVR... Would put in a mechanical valve unless pt is a pro athlete or something (maybe an ON-X for a bit more wiggle room on the Coumadin).

Also curious how bad the liver function is. If you’re cirrhotic, anticipate bleeding like a stick pig. Plenty of platelets etc.

 

[deleted875186]

Happy I went into pain

 

[Iso4ane]

Just out of curiosity, what was the rationale behind doing a valve-in-mitral valve procedure on a 40 y/o with clearly severe prosthetic mitral stenosis (as opposed to redo surgery)?

Probably his third strike. I.e this was his third valve (Native, 1st bioprosthetic, and this was his 2nd bio prosthetic already.), so retry into the chest to replace that valve would be crazy.

 

[abolt18]

Pt is a 40 yo M, h/o of endocarditis s/p bioprosthetic MVR in 2016, PCI to RCA in 2015, aflutter, congestive hepatopathy, thrombocytopenia, recurrent pleural effusions, LAA thrombus on recent cardiac CT for which he has been on eliquis for 1 month.

He is presenting to you today for a valve-in-valve transseptal TMVR after holding his eliquis for 2 days.

You proceed with a careful induction of GETA. In this hospital cardiology does the TEE and/or TTE for cath lab procedures and here are some of the images they get:

(CW spectral doppler is inverted here)

SPAP is 65-75 mmHg by TR CW jet


I think it’s fair to say that the LAA, despite being on eliquis for 1 mo, is still quite concerning for thrombus, and even if one isn’t going to call it frank thrombus keep mind that when doing transseptal ViV TMVR that a stiff wire frequently heads into the LAA or LUPV and does some scraping. In a 40 yo patient, the interventional cardiologists and CT surgeon were not willing to accept the stroke risk here.

So, given that A/C does not appear to be working, our only option is operative. Take note of the biventricular size and function, the appearance of the bio MVR, and the fact that the mean mitral inflow gradient (not shown) is 20 mmHg.


For residents and fellows first:

What are the echocardiographic findings in the limited images above? What interventions does this patient need? What are your preanesthetic concerns given his surgical and medical history? How are you going to induce? Which monitors and lines? How are you going to come off CPB?

Alright, I want to do this before I read everyone else's responses so I can be honest with myself.

1st picture is TEE mid-esophageal ~commissural vs 2 chamber view, looking at the LAA which I'd say looks like thrombus present. Also, huge left atrium!
2nd picture is TEE mid-esophageal commissural view, same comment as 1st image. Spontaneous echo contrast.
3rd picture. TEE mid-esophageal 2-chamber view of LV. Pulse-wave doppler of mitral valve. Peak gradient of ~25
4th picture. TTE parasternal long-axis view. Very empty LV, looks like big RV. Both appropriate and expected with the given pathology. High velocity flow through prosthetic MV. AV opens and closes nicely.
5th picture. TEE mid-esophageal 4-chamber with color flow over TV. I'm guessing moderate TR, centrally located most likely just due to RV dilation and the leaflets not coapting. Could get better after correcting MS.
6th picture. TTE apical 4-chamber view with color flow over TV. Bi-atrial enlargement. RV severely dilated, overtaking the apex of the heart. Repeated demonstration of TR, mild-moderate? I see that tricuspid annular plane moving, but a little m-mode and/or calipers would be helpful. I'd guess it's less than 2.7cm
7th picture. TTE, parasternal short-axis mid-LV view showing severely dilated RV, inter-ventricular septal flattening that I THINK is during diastole which should point more toward RV volume overload > RV pressure overload. Small LV relative to RV. I don't have the experience to quantify the LVEF but not horrendous, but also NOT >55%.

This patient needs surgery, the bone is broken... sorry wrong thread.
But seriously I can see why they don't want to stick a catheter into his LA and potentially dislodge the LAA thrombus. I see no other immediate interventions that can or should be done.

I know you said atrial flutter but it looks like he's in sinus rhythm here in these echo images. I'd like for him to stay that way as much as possible for induction. Obviously can still have a stroke but I don't know that we can do much to prevent it at this point.

Surgeon to get A/V groin access prior to induction and stay in room. Defib pads on and hooked up. Art line. Pre-oxygenation. Induce slowly with etomidate and fentanyl with mucho rocuronium. Phenylephrine first line for any BP issues, esmolol in hand to avoid any tachycardia.

RIC vs 14g IV, level 1 hooked up to that. TEE in. IJ MAC+PAC, but I'm only floating the swan to the SVC until we have an open chest. BIS + cerebral oximetry (only because that's what we "always do"here).

Coming off bypass? Milrinone +/- vaso or epi depending on needs for augmenting SVR vs inotropy.

Alright I'm all out of ideas. But hold on for a long and bumpy case.

 

[greatnt249]

Probably his third strike. I.e this was his third valve (Native, 1st bioprosthetic, and this was his 2nd bio prosthetic already.), so retry into the chest to replace that valve would be crazy.

Transseptal perforation to do valve-in-valve is also not ideal with a right heart that looks like that; likely to get a significant right-to-left shunt afterward unless they were planning on closing on the way out.

 

[deleted697535]

Far as I know, you tell the perfusionist to turn the flows down until they are off. Sometimes you have them give the heart a little volume in between. Should there be more than one way?

Holy sh1t!!

 

[vector2]

Just out of curiosity, what was the rationale behind doing a valve-in-mitral valve procedure on a 40 y/o with clearly severe prosthetic mitral stenosis (as opposed to redo surgery)?

Probably his third strike. I.e this was his third valve (Native, 1st bioprosthetic, and this was his 2nd bio prosthetic already.), so retry into the chest to replace that valve would be crazy.

It was his 1st bio valve. And as far as surgical vs tmvr rationale, I would also ask you to think about some of the resource differences between quaternary mothership heart centers and more community-oriented centers, especially as it relates to the most common complication(s) he could potentially face coming off bypass and in the immediate to intermediate postoperative period.


Also, in regard to the procedures this pt might need:

 

[abolt18]

It was his 1st bio valve. And as far as surgical vs tmvr rationale, I would also ask you to think about some of the resource differences between quaternary mothership heart centers and more community-oriented centers, especially as it relates to the most common complication(s) he could potentially face coming off bypass and in the immediate to intermediate postoperative period.


Also, in regard to the procedures this pt might need:

View attachment 324993

Based on this chart, he's getting a concomitant TV ring.

 

[vector2]

Someone had mentioned earlier that the flutter wasn't obvious on the TEE EKG, but he was indeed in flutter.

A couple extra TR clips as he was emerging from anesthesia

Hepatic vein doppler in aflutter might be one of the most esoteric things I've had to think about in awhile:

Figure 20: (a) Hepatic vein Doppler in a case of atrial flutter showing undulations (Marked A) due to repeated atrial contraction and relaxation. (b) Atrial flutter wave occurring simultaneously with QRS produces prominent reversal wave. EXP: Expiration, INSP: Inspiration, AR: Atrial reversal, D: Diastolic forward flow

 

[dannyboy1]

Put patient to sleep carefully. Proceed with surgery. Ionotropes and vasopressors to come off. Transfer to CTICU. go to lunch.

 

[MirrorTodd]

Holy sh1t!!

Is it any surprise that I have no interest in doing a CT fellowship? But I'm always up for learning, so how many ways are there to come off bypass? (Not sarcasm)

 

[Hork Bajir]

Is it any surprise that I have no interest in doing a CT fellowship? But I'm always up for learning, so how many ways are there to come off bypass? (Not sarcasm)

Lol... your answer was like if someone asked “how will you induce this patient” and you answered “by giving some medications until they lose consciousness, and then maybe putting in a breathing tube... is there another way??”

 

[MirrorTodd]

Lol... your answer was like if someone asked “how will you induce this patient” and you answered “by giving some medications until they lose consciousness, and then maybe putting in a breathing tube... is there another way??”

I suppose it's a good thing I'm not taking the boards anytime soon.

 

[Hork Bajir]

It was his 1st bio valve. And as far as surgical vs tmvr rationale, I would also ask you to think about some of the resource differences between quaternary mothership heart centers and more community-oriented centers, especially as it relates to the most common complication(s) he could potentially face coming off bypass and in the immediate to intermediate postoperative period.


Also, in regard to the procedures this pt might need:

View attachment 324993

Not sure I would be telling the surgeon to go after the TV here. Obviously grading TR is super subjective and problematic, but from the images you’ve shown us, I wouldn’t call the degree of TR more than mild to moderate (relatively narrow based jet). Certainly would interrogate with more views. Even if we agreed that it was moderate, this patient would have a sick right heart and a soft indication for TV ring- I’m not convinced that more time on pump to make everything look perfect is really doing this dude any favors. He’s young, and if he’s unfortunate enough not to be in the group of patients where his RV will remodel and the TR will get better after fixing the MV pathology (which we are lousy and predicting), he would probably be a candidate for one of the percutaneous TV interventions coming down the road (versus redo for TV ring in 6 months or so)

 

[greatnt249]

It was his 1st bio valve. And as far as surgical vs tmvr rationale, I would also ask you to think about some of the resource differences between quaternary mothership heart centers and more community-oriented centers, especially as it relates to the most common complication(s) he could potentially face coming off bypass and in the immediate to intermediate postoperative period.

I must admit that I'm a little confused by the second statement regarding resource differences. It would seem to me that if a system has the resources available to have a structural interventional cardiologist at their institution that they would also have cardiac surgery available as back-up in case something goes sideways with the procedure. So ultimately it boils down to which is the most appropriate intervention for the patient, which depends on a number of variables, but one that I didn't see mentioned was what was the suspected etiology of the severe mitral stenosis?

I've actually seen a similar case to this before, but I'll hold off on commenting on what was done unless someone asks so as not to hamper the discussion.

 

[vector2]

I must admit that I'm a little confused by the second statement regarding resource differences. It would seem to me that if a system has the resources available to have a structural interventional cardiologist at their institution that they would also have cardiac surgery available as back-up in case something goes sideways with the procedure. So ultimately it boils down to which is the most appropriate intervention for the patient, which depends on a number of variables, but one that I didn't see mentioned was what was the suspected etiology of the severe mitral stenosis?

I've actually seen a similar case to this before, but I'll hold off on commenting on what was done unless someone asks so as not to hamper the discussion.

I think you misunderstood what I said, as I wasn't referring to doing the TMVR without CT surgery present (to my knowledge there aren't any institutions that would do a TMVR like this without perfusion and CT surgery hanging around in the building somewhere).

I am talking about the resource differences between taking a guy for reop CT surgery at a quaternary center vs. taking this guy for reop CT surgery at a more community-oriented center "especially as it relates to the most common complication(s) he could potentially face coming off bypass and in the immediate to intermediate postoperative period.

In regard to the etiology of this bioprosthetic MV stenosis, the durability of bio valves is around 10-15 years but degeneration is markedly accelerated in younger patients due to a more pronounced immunologic response to the valve and enhanced calcification of the valve.

 

[Hork Bajir]

I think you misunderstood what I said, as I wasn't referring to doing the TMVR without CT surgery present (to my knowledge there aren't any institutions that would do a TMVR like this without perfusion and CT surgery hanging around in the building somewhere).

I am talking about the resource differences between taking a guy for reop CT surgery at a quaternary center vs. taking this guy for reop CT surgery at a more community-oriented center "especially as it relates to the most common complication(s) he could potentially face coming off bypass and in the immediate to intermediate postoperative period.

...Are you referring to the need for potential MCS?

 

[vector2]

Not sure I would be telling the surgeon to go after the TV here. Obviously grading TR is super subjective and problematic, but from the images you’ve shown us, I wouldn’t call the degree of TR more than mild to moderate (relatively narrow based jet). Certainly would interrogate with more views. Even if we agreed that it was moderate, this patient would have a sick right heart and a soft indication for TV ring- I’m not convinced that more time on pump to make everything look perfect is really doing this dude any favors. He’s young, and if he’s unfortunate enough not to be in the group of patients where his RV will remodel and the TR will get better after fixing the MV pathology (which we are lousy and predicting), he would probably be a candidate for one of the percutaneous TV interventions coming down the road (versus redo for TV ring in 6 months or so)

I would encourage you do your own lit search to determine what's actually the evidence that someone like this who has significant RV/TVA dilatation and functional TR will reliably improve vis a vis remodeling/improved TR/improved RV function after the left-sided valve is fixed.

I'd also like to see what @bigdan @sevoflurane @dchz @Twiggidy think about ringing this guy's TV while on pump

 

[greatnt249]

In regard to the etiology of this bioprosthetic MV stenosis, the durability of bio valves is around 10-15 years but degeneration is markedly accelerated in younger patients due to a more pronounced immunologic response to the valve and enhanced calcification of the valve.

So the thought process is to put another tissue valve in the guy? The reason I bring this up is that it is indeed possible to thrombose a bioprosthetic valve, which would make a catheter-based approach to replacement less than ideal. I could see why maybe when he initially got his mitral valve that they might have been worried about him following up with anticoagulation for life, but if he's been on the straight and narrow and now looking at a redo valve replacement, it should be considered how to give the guy the best shot at potentially not needing any future cardiac surgeries.

 

[dchz]

I would encourage you do your own lit search to determine what's actually the evidence that someone like this who has significant RV/TVA dilatation and functional TR will reliably improve vis a vis remodeling/improved TR/improved RV function after the left-sided valve is fixed.

I'd also like to see what @bigdan @sevoflurane @dchz @Twiggidy think about ringing this guy's TV while on pump

I'm honored to be mentioned. I would like to include @sethco in the discussion as well. He's much more experienced in this stuff than me even though he much more often offers financial advice.

My knowledge of evidence on improvement of 2ndary TR after left sided repair is 0. As in I don't ever recall any paper that i've read on this purpose nor have I had extensive experience in this specific situation. So I will refrain from commenting as if I have any clue what's going on. I usually err on the conservative side until I see more convincing info.

As far as the TR, given the left sided pathology, i'm not convinced it needs a ring (or partial ring) from the info I have in your initial post. However, I need more data, including the TV annulus size and more than 1 view of the TR and intra op hep vein PW. At the point of pre-pump TEE given the 1 image, I'd involve the surgeon and cardiologists on the discussion. The official recommendation says put in a ring if it's > 4cm even if it's not severe TR, but in real life people don't stick very strictly to that.

As far as the post pump TV echos in your 2nd post, am i crazy or are you doing a TTE as he's emerging from anesthesia??? I see systolic reversal of the hepatic vein flow and a solid TR jet, which is suggestive of severe TR... if this TTE is done pre op, I would certain be more convinced to intervene on the TV, but if he's emerging from anesthesia... i'm not sure i'd crack open the chest again if he's hemodynamically stable.

 

[abolt18]

I'm honored to be mentioned. I would like to include @sethco in the discussion as well. He's much more experienced in this stuff than me even though he much more often offers financial advice.

My knowledge of evidence on improvement of 2ndary TR after left sided repair is 0. As in I don't ever recall any paper that i've read on this purpose nor have I had extensive experience in this specific situation. So I will refrain from commenting as if I have any clue what's going on. I usually err on the conservative side until I see more convincing info.

As far as the TR, given the left sided pathology, i'm not convinced it needs a ring (or partial ring) from the info I have in your initial post. However, I need more data, including the TV annulus size and more than 1 view of the TR and intra op hep vein PW. At the point of pre-pump TEE given the 1 image, I'd involve the surgeon and cardiologists on the discussion. The official recommendation says put in a ring if it's > 4cm even if it's not severe TR, but in real life people don't stick very strictly to that.

As far as the post pump TV echos in your 2nd post, am i crazy or are you doing a TTE as he's emerging from anesthesia??? I see systolic reversal of the hepatic vein flow and a solid TR jet, which is suggestive of severe TR... if this TTE is done pre op, I would certain be more convinced to intervene on the TV, but if he's emerging from anesthesia... i'm not sure i'd crack open the chest again if he's hemodynamically stable.

I think he was waking up from the GA that was induced for the valve-in-valve procedure. The one during-which the other TEE images were found. That was my impression.

 

[vector2]

I think he was waking up from the GA that was induced for the valve-in-valve procedure. The one during-which the other TEE images were found. That was my impression.

Yes, @dchz those were upon a wakeup on spontaneous ventilation (including the HV doppler) after the TMVR was aborted

 

[Hork Bajir]

@vector2 its been a while since I looked into the literature on this, but last time I looked I remember my ‘take home point’ being that we suck at predicting whose TR will get better after fixing the left sided valve lesion, and whose will not. In some cases the TR does improve after fixing the MV disease... We just don’t know if that will be the case for this dude. Care to save me the time and link me to whatever specific paper you’re referencing?

Also as an aside- I know I suck at grading TR, but honestly are this images really showing severe regurgitation??? I’m not used to looking at images with the green turbulence mapping so that might be throwing me off, but the vena contracta looks not that bad

 

[vector2]

@vector2 its been a while since I looked into the literature on this, but last time I looked I remember my ‘take home point’ being that we suck at predicting whose TR will get better after fixing the left sided valve lesion, and whose will not. In some cases the TR does improve after fixing the MV disease... We just don’t know if that will be the case for this dude. Care to save me the time and link me to whatever specific paper you’re referencing?

Also as an aside- I know I suck at grading TR, but honestly are this images really showing severe regurgitation??? I’m not used to looking at images with the green turbulence mapping so that might be throwing me off, but the vena contracta looks not that bad

Some of the reason those recommendations in valve guidelines are almost never Class Ia is because there are so few randomized trials, and most of the data when we are thinking about TVR at the time of left sided surgery come from retrospective cohorts.

For instance if you look at Functional tricuspid regurgitation at the time of mitral valve repair for degenerative leaflet prolapse: the case for a selective approach, you'll see a retrospective study looking at TR after MVr in which the TV was left alone and even grade 3 TR got better with MVr.

And then in Secondary tricuspid regurgitation or dilatation: which should be the criteria for surgical repair?, they retrospectively looked at pts undergoing MVr who had TV annuloplasty when TVA diameter was greater than twice normal, regardless of the grade of TR. Those who had TV annuloplasty had less future worsening of TR and better funtional status.


All right, so what about the gold standard of prospective, randomized controlled trials testing this repair-based-on-diameter notion?

---------------------
J Thorac Cardiovasc Surg. 2012 Mar;143(3):632-8.

Prophylactic tricuspid annuloplasty in patients with dilated tricuspid annulus undergoing mitral valve surgery
Umberto Benedetto 1, Giovanni Melina, Emiliano Angeloni, Simone Refice, Antonino Roscitano, Cosimo Comito, ******** Sinatra

Abstract
Objective: Progression of functional tricuspid regurgitation is not uncommon after mitral valve surgery and is associated with poor outcomes. We tested the hypothesis that concomitant tricuspid valve annuloplasty in patients with tricuspid annulus dilatation (≥40 mm) prevents tricuspid regurgitation progression after mitral valve surgery.

Methods: We enrolled 44 patients undergoing mitral valve surgery (both repair or replacement) showing less than moderate (≤+2) tricuspid regurgitation and dilated tricuspid annulus (≥40 mm) at preoperative echocardiography. They were randomized to receive (n = 22) or not receive (n = 22) concomitant tricuspid annuloplasty (Cosgrove-Edwards annuloplasty ring; Edwards Lifesciences, Irvine, Calif) at the time of mitral valve surgery. Clinical and echocardiographic follow-up was 100% completed at 12 months after surgery.

Results: Preoperative clinical and echocardiographic characteristics were comparable in the 2 groups. Operative mortality was 4.4% (1 death in each group). At 12 months follow-up, tricuspid regurgitation was absent in 71% (n = 15) versus 19% (n = 4) of patients in the treatment and control groups, respectively (P = .001). Moderate to severe tricuspid regurgitation (≥+3) was present in 0% versus 28% (n = 6) of patients in the treatment and control groups, respectively (P = .02). Pulmonary artery systolic pressure significantly decreased from baseline in all cases (P < .001) and was comparable in the 2 groups (41 ± 8 mm Hg vs 40 ± 5 mm Hg; P = .4). Right ventricular reverse remodeling was marked in the treatment group (right ventricular long axis: 71 ± 7 mm vs 65 ± 8 mm; P = .01; short axis: 33 ± 4 mm vs 27 ± 5 mm; P = .001) but only minimal in the control group (right ventricular long axis: 72 ± 6 mm vs 70 ± 7 mm; P = .08; short axis: 34 ± 5 mm vs 33 ± 5 mm; P = .1). The 6-minute walk test improved from baseline in both groups (P < .001), but this improvement was greater in the treatment group (+115 ± 23 m from baseline vs +75 ± 35 m; P = .008).

Conclusions: Prophylactic tricuspid valve annuloplasty in patients with dilated tricuspid annulus undergoing mitral valve surgery was associated with a reduced rate of tricuspid regurgitation progression, improved right ventricular remodeling, and better functional outcomes.

Prophylactic tricuspid annuloplasty in patients with dilated tricuspid annulus undergoing mitral valve surgery - PubMed

Prophylactic tricuspid valve annuloplasty in patients with dilated tricuspid annulus undergoing mitral valve surgery was associated with a reduced rate of tricuspid regurgitation progression, improved right ventricular remodeling, and better functional outcomes.

pubmed.ncbi.nlm.nih.gov

---------------------



You are right in that grading TR using VC is full of uncertainty, much of it because it's load dependent and also because no matter what view you're using you're probably cutting across commissures in a weird way. And in this patient he's got flutter, so even though @dchz points out that he looks like he has hepatic vein systolic reversal (a usually specific sign of severe TR), it's kind of hard to know what to make of it here.

I think some of the literature has helped in that it really appears that TV annular dilatation (let's not open the can of worms yet about the accuracy of diameter measurements in TEE vs TTE) is more important than severity of TR, which means in this case it's not nearly as important to me whether the TR is moderate or severe (although for the record cards read it as moderate on the TEE and severe on the TTE). The $64,000 question is what was this guy's TV annulus diameter, and in the apical 4ch with right-sided focus it was like 5 cm.

Beyond the fact that his annulus is dilated, what else can we look at to gauge if his TR is going to worsen? Per this review, "Risk factors for persistence or progression of TR include tricuspid annulus dilatation (>40 mm or 21 mm/m2 on transthoracic echocardiogram [TTE], or >70 mm on direct intra-operative inspection), significant RV dysfunction or dilatation, significant tricuspid leaflet tethering, atrial fibrillation or pulmonary hypertension at the time of left-sided valve surgery, rheumatic or functional aetiology of mitral disease or history of right heart failure."

This guy has pretty much got all of them, either directly or with pathologies that have similar sequelae. Ultimately, even if it complicates the pump run a bit, I don't see how you avoid banding the TV.

 

[Ronin786]

@vector2 its been a while since I looked into the literature on this, but last time I looked I remember my ‘take home point’ being that we suck at predicting whose TR will get better after fixing the left sided valve lesion, and whose will not. In some cases the TR does improve after fixing the MV disease... We just don’t know if that will be the case for this dude. Care to save me the time and link me to whatever specific paper you’re referencing?

Also as an aside- I know I suck at grading TR, but honestly are this images really showing severe regurgitation??? I’m not used to looking at images with the green turbulence mapping so that might be throwing me off, but the vena contracta looks not that bad

I'm not sure about the validity in atrial flutter, but I think there's flow reversal in the hepatic veins which is consistent with severe TR.

 

[deleted697535]

Is it any surprise that I have no interest in doing a CT fellowship? But I'm always up for learning, so how many ways are there to come off bypass? (Not sarcasm)

Well the long answer is an entire career of knowledge and experience... Im but a young padawn in cardiac so i'll be brief...

1 - What blood & products do you need, Are lytes ok, calcium, K, temp? For Deep hypothermia this can be a disaster. how is the ROTEM if you go that way
2 - whats been fixed, what do you need to check for? - this list is endless. Paravalvular leaks, stenosism new RWMAs etc etc
3 - what pressor/inotrope/pulm vasodilator do you need?
4 - pace or no
5 - is the RV dead or the LV or both? do you need to leave chest open for a few days? Need MCS, impella, IABP?

The worst of the worst i could imagine is probably a post transplant, congenital heart disease (think quad-do sternotomy, and very small patient with difficult anatomy), that been on milrinone at home (hence profound vasoplegia), with a VAD (hence bleeding), poor donor heart protection, with like 4 wood unit PVR (think basically bordering on prohibitive risk) that is anuric periop (think screwed electrolytes)

Aka last week! 3rd transplant of the week

For this we did 50 mins reperfusion after x clamp off, dob 10, mil 0.125, norepi 0.4, epi 0.1, vaso 4, meth blue, iNO with ICU vent in OR, hydrocort, paced aai 90 for Right heart, Vasc Cath placed in OR and CRRT started the second we landed in ICU. Volume given back from perfusion was 100mls at a time max. Very nearly left chest open

Actually did well


In general however you're right, if you did dob 5, norepi 0.1 and pace at ddd 80 for everyone, plus wait 10 mins til after x clamp off, then give 250 mls volume back at a time, tell perfusion to come down on flows by 1 Litre and hold 1 minute for 5 minutes probably 90% of patients will come off pump.

The rest well, they wont...

 

[sevoflurane]

I suppose it's a good thing I'm not taking the boards anytime soon.

It’s all good my dude. Delicious case with lots to talk about. Somehow i missed vectors post until I woke up a few minutes ago and was perusing sdn posts. This is the exact type of case that draws me to CT. Mental AF until you start doing something- then it’s game on.

 

[sevoflurane]

Well the long answer is an entire career of knowledge and experience... Im but a young padawn in cardiac so i'll be brief...

1 - What blood & products do you need, Are lytes ok, calcium, K, temp? For Deep hypothermia this can be a disaster. how is the ROTEM if you go that way
2 - whats been fixed, what do you need to check for? - this list is endless. Paravalvular leaks, stenosism new RWMAs etc etc
3 - what pressor/inotrope/pulm vasodilator do you need?
4 - pace or no
5 - is the RV dead or the LV or both? do you need to leave chest open for a few days? Need MCS, impella, IABP?

The worst of the worst i could imagine is probably a post transplant, congenital heart disease (think quad-do sternotomy, and very small patient with difficult anatomy), that been on milrinone at home (hence profound vasoplegia), with a VAD (hence bleeding), poor donor heart protection, with like 4 wood unit PVR (think basically bordering on prohibitive risk) that is anuric periop (think screwed electrolytes)

Aka last week! 3rd transplant of the week

For this we did 50 mins reperfusion after x clamp off, dob 10, mil 0.125, norepi 0.4, epi 0.1, vaso 4, meth blue, iNO with ICU vent in OR, hydrocort, paced aai 90 for Right heart, Vasc Cath placed in OR and CRRT started the second we landed in ICU. Volume given back from perfusion was 100mls at a time max. Very nearly left chest open

Actually did well


In general however you're right, if you did dob 5, norepi 0.1 and pace at ddd 80 for everyone, plus wait 10 mins til after x clamp off, then give 250 mls volume back at a time, tell perfusion to come down on flows by 1 Litre and hold 1 minute for 5 minutes probably 90% of patients will come off pump.

The rest well, they wont...

Noice.

 

[sevoflurane]

great case @vector2
Heading up to the tahoe this morning to catch the remenants on this storm.
Briefly, this guy is in dire straits. Undefiled LV/ biventricular failure, mean ms of 25, congestive hepatopathy, redo sternotomy, stroke risk.... all bad things. Postinduction IABP at the very least with possibly progressing to intra-op rvad, ecmo, etc. As for TV, it’s a tossup btw ringing it and making him better vs right atriotomy/longer pump run and your ability to wean a RHF patient.

Good case bruh. Following.

 

[greatnt249]

great case @vector2
Heading up to the tahoe this morning to catch the remenants on this storm.
Briefly, this guy is in dire straits. Undefiled LV/ biventricular failure, mean ms of 25, congestive hepatopathy, redo sternotomy, stroke risk.... all bad things. Postinduction IABP at the very least with possibly progressing to intra-op rvad, ecmo, etc. As for TV, it’s a tossup btw ringing it and making him better vs right atriotomy/longer pump run and your ability to wean a RHF patient.

Good case bruh. Following.

Earlier in the thread I mentioned having a very similar case a few months ago where a young(er) patient came in with borderline cardiogenic shock after being found to have a mitral gradient of 30 mmHg through the bioprosthetic valve on TTE at one of the satellite hospitals. Right heart looked about as well the one above. Everyone was worried about what induction and intubation would do to the patient. I'm not an anesthesiologist so I can't speak to the approach regarding induction strategy, but ultimately surgeon decided to put the patient on VA ECMO in the OR and try to stabilize before attempting surgery. Two days later, underwent induction and follow-up TEE. Densest spontaneous contrast in left atrium I've ever seen. Took old valve out and found clot in all three cusps on the ventricular side of the prosthesis and got a new mechanical valve figuring warfarin would probably factor into longterm therapy anyway. Survived surgery and is apparently doing well.

 

[abolt18]

Some of the reason those recommendations in valve guidelines are almost never Class Ia is because there are so few randomized trials, and most of the data when we are thinking about TVR at the time of left sided surgery come from retrospective cohorts.

For instance if you look at Functional tricuspid regurgitation at the time of mitral valve repair for degenerative leaflet prolapse: the case for a selective approach, you'll see a retrospective study looking at TR after MVr in which the TV was left alone and even grade 3 TR got better with MVr.

And then in Secondary tricuspid regurgitation or dilatation: which should be the criteria for surgical repair?, they retrospectively looked at pts undergoing MVr who had TV annuloplasty when TVA diameter was greater than twice normal, regardless of the grade of TR. Those who had TV annuloplasty had less future worsening of TR and better funtional status.


All right, so what about the gold standard of prospective, randomized controlled trials testing this repair-based-on-diameter notion?

---------------------
J Thorac Cardiovasc Surg. 2012 Mar;143(3):632-8.

Prophylactic tricuspid annuloplasty in patients with dilated tricuspid annulus undergoing mitral valve surgery
Umberto Benedetto 1, Giovanni Melina, Emiliano Angeloni, Simone Refice, Antonino Roscitano, Cosimo Comito, ******** Sinatra

Abstract
Objective: Progression of functional tricuspid regurgitation is not uncommon after mitral valve surgery and is associated with poor outcomes. We tested the hypothesis that concomitant tricuspid valve annuloplasty in patients with tricuspid annulus dilatation (≥40 mm) prevents tricuspid regurgitation progression after mitral valve surgery.

Methods: We enrolled 44 patients undergoing mitral valve surgery (both repair or replacement) showing less than moderate (≤+2) tricuspid regurgitation and dilated tricuspid annulus (≥40 mm) at preoperative echocardiography. They were randomized to receive (n = 22) or not receive (n = 22) concomitant tricuspid annuloplasty (Cosgrove-Edwards annuloplasty ring; Edwards Lifesciences, Irvine, Calif) at the time of mitral valve surgery. Clinical and echocardiographic follow-up was 100% completed at 12 months after surgery.

Results: Preoperative clinical and echocardiographic characteristics were comparable in the 2 groups. Operative mortality was 4.4% (1 death in each group). At 12 months follow-up, tricuspid regurgitation was absent in 71% (n = 15) versus 19% (n = 4) of patients in the treatment and control groups, respectively (P = .001). Moderate to severe tricuspid regurgitation (≥+3) was present in 0% versus 28% (n = 6) of patients in the treatment and control groups, respectively (P = .02). Pulmonary artery systolic pressure significantly decreased from baseline in all cases (P < .001) and was comparable in the 2 groups (41 ± 8 mm Hg vs 40 ± 5 mm Hg; P = .4). Right ventricular reverse remodeling was marked in the treatment group (right ventricular long axis: 71 ± 7 mm vs 65 ± 8 mm; P = .01; short axis: 33 ± 4 mm vs 27 ± 5 mm; P = .001) but only minimal in the control group (right ventricular long axis: 72 ± 6 mm vs 70 ± 7 mm; P = .08; short axis: 34 ± 5 mm vs 33 ± 5 mm; P = .1). The 6-minute walk test improved from baseline in both groups (P < .001), but this improvement was greater in the treatment group (+115 ± 23 m from baseline vs +75 ± 35 m; P = .008).

Conclusions: Prophylactic tricuspid valve annuloplasty in patients with dilated tricuspid annulus undergoing mitral valve surgery was associated with a reduced rate of tricuspid regurgitation progression, improved right ventricular remodeling, and better functional outcomes.

Prophylactic tricuspid annuloplasty in patients with dilated tricuspid annulus undergoing mitral valve surgery - PubMed

Prophylactic tricuspid valve annuloplasty in patients with dilated tricuspid annulus undergoing mitral valve surgery was associated with a reduced rate of tricuspid regurgitation progression, improved right ventricular remodeling, and better functional outcomes.

pubmed.ncbi.nlm.nih.gov

---------------------



You are right in that grading TR using VC is full of uncertainty, much of it because it's load dependent and also because no matter what view you're using you're probably cutting across commissures in a weird way. And in this patient he's got flutter, so even though @dchz points out that he looks like he has hepatic vein systolic reversal (a usually specific sign of severe TR), it's kind of hard to know what to make of it here.

I think some of the literature has helped in that it really appears that TV annular dilatation (let's not open the can of worms yet about the accuracy of diameter measurements in TEE vs TTE) is more important than severity of TR, which means in this case it's not nearly as important to me whether the TR is moderate or severe (although for the record cards read it as moderate on the TEE and severe on the TTE). The $64,000 question is what was this guy's TV annulus diameter, and in the apical 4ch with right-sided focus it was like 5 cm.

Beyond the fact that his annulus is dilated, what else can we look at to gauge if his TR is going to worsen? Per this review, "Risk factors for persistence or progression of TR include tricuspid annulus dilatation (>40 mm or 21 mm/m2 on transthoracic echocardiogram [TTE], or >70 mm on direct intra-operative inspection), significant RV dysfunction or dilatation, significant tricuspid leaflet tethering, atrial fibrillation or pulmonary hypertension at the time of left-sided valve surgery, rheumatic or functional aetiology of mitral disease or history of right heart failure."

This guy has pretty much got all of them, either directly or with pathologies that have similar sequelae. Ultimately, even if it complicates the pump run a bit, I don't see how you avoid banding the TV.

Somehow I missed this post.

Post-op images? How'd he do?

Thanks for the good discussion and awesome images. Would love to see your answers to the original questions posted.

 

[sevoflurane]

Tell us how it went @vector2 .

Nice discussion on TV replacement. Points out that imaging alone is not the sole determinant. How dilated was the hepatic vein/inferior VC?

And just to contrast your TR echo here is one I had recently.

 

[abolt18]

Tell us how it went @vector2 .

Nice discussion on TV replacement. Points out that imaging alone is not the sole determinant. How dilated was the hepatic vein/inferior VC?

And just to contrast your TR echo here is one I had recently.

View attachment 325262

That's normal, right?

 

[Dexmetaketapropofol]

Great case, thank you for showing us. During my experience with the Triluminate trial (pilot study for Triclip), Dr. R Hahn has given us better objectivity for TR assessment. We currently use a 5 stage grading system relying more on 3D VC. Are you guys using this system routinely? I'd place a link but a little tied up right now.

I agree, there's no way to get through this case without a TV annuloplasty just for the fact of the hepatic congestion and the pressurized caval system irrespective of the echo findings.

 

[sevoflurane]

Great case, thank you for showing us. During my experience with the Triluminate trial (pilot study for Triclip), Dr. R Hahn has given us better objectivity for TR assessment. We currently use a 5 stage grading system relying more on 3D VC. Are you guys using this system routinely? I'd place a link but a little tied up right now.

I agree, there's no way to get through this case without a TV annuloplasty just for the fact of the hepatic congestion and the pressurized caval system irrespective of the echo findings.

Not currently.
We repair, replace or do a valvectomy based on traditional methods of quantifying TR.

Interested in 3D VC link.

Separately, we are seeing a ton of bad valves due to IV drug abuse. Don’t know if it’s covid related (people staying home/ loss of jobs).

Talk about a dilated IVC and hepatic congestion. Had this gem yesterday.

IVC measured 3.2 cm.

 

[vector2]

For everyone, the 5 stage grading system he's referring to (mild moderate severe massive torrential) is described here

The Conundrum of Tricuspid Regurgitation Grading

Findings from early percutaneous tricuspid intervention trials have shown that the severity of tricuspid regurgitation (TR) far exceeded the current definition of severe TR. Also, the improvement in the amount of TR following tricuspid intervention is ...

www.ncbi.nlm.nih.gov

 

[Dexmetaketapropofol]

For everyone, the 5 stage grading system he's referring to (mild moderate severe massive torrential) is described here

The Conundrum of Tricuspid Regurgitation Grading

Findings from early percutaneous tricuspid intervention trials have shown that the severity of tricuspid regurgitation (TR) far exceeded the current definition of severe TR. Also, the improvement in the amount of TR following tricuspid intervention is ...

www.ncbi.nlm.nih.gov

Thank you, saved me the rummaging the internet

 

[vector2]

Somehow I missed this post.

Post-op images? How'd he do?

Thanks for the good discussion and awesome images. Would love to see your answers to the original questions posted.

Heh, I phrased the OP as a bit of a red herring because I, in fact, really was asking what people would do. This guy's CT surg clinic visit isn't until 1st week of Jan but I'm obviously going to update the thread once he actually goes to surgery.

...Are you referring to the need for potential MCS?

great case @vector2
Heading up to the tahoe this morning to catch the remenants on this storm.
Briefly, this guy is in dire straits. Undefiled LV/ biventricular failure, mean ms of 25, congestive hepatopathy, redo sternotomy, stroke risk.... all bad things. Postinduction IABP at the very least with possibly progressing to intra-op rvad, ecmo, etc. As for TV, it’s a tossup btw ringing it and making him better vs right atriotomy/longer pump run and your ability to wean a RHF patient.

Good case bruh. Following.

This is the billion dollar question right here. Given the moderate-severe TR, severe RV dilation, and severe RV dysfunction- how many folks here would try to come off on epi, milrinone, nitric etc and just see how it goes vs just plan to immediately wean off pump to RVAD? If the plan is the former, what do you think about closing the chest?

 

[drmwvr]

milrinone or NO....pick one..I'd go NO....epi goes without saying...IABP...Ecmo/open chest based on how the guy declares himself....take a deep breath, bro....

 

[anes121508]

I'm not sure about the validity in atrial flutter, but I think there's flow reversal in the hepatic veins which is consistent with severe TR.

Theres a list of crap that messes with hepatic vein flow. Same concepts as pulm v flow and all the different things that cause blunting or reversal. Fib/ flutter on that list.

 

[anes121508]

Great case, thank you for showing us. During my experience with the Triluminate trial (pilot study for Triclip), Dr. R Hahn has given us better objectivity for TR assessment. We currently use a 5 stage grading system relying more on 3D VC. Are you guys using this system routinely? I'd place a link but a little tied up right now.

I agree, there's no way to get through this case without a TV annuloplasty just for the fact of the hepatic congestion and the pressurized caval system irrespective of the echo findings.

Has she posted a video or a paper specifically on her method of 3D vca measurement?

I ask because I think some of the hesitancy for people to do this is that it’s relatively new and people aren’t comfortable with it. Even those that had recent fellowships, I find that there can be more variability in obtaining the 3D vca measurement than other simple metrics.

 

[anes121508]

Heh, I phrased the OP as a bit of a red herring because I, in fact, really was asking what people would do. This guy's CT surg clinic visit isn't until 1st week of Jan but I'm obviously going to update the thread once he actually goes to surgery.






This is the billion dollar question right here. Given the moderate-severe TR, severe RV dilation, and severe RV dysfunction- how many folks here would try to come off on epi, milrinone, nitric etc and just see how it goes vs just plan to immediately wean off pump to RVAD? If the plan is the former, what do you think about closing the chest?

I’ve had this similar case twice now I think. Precisely approach coming off I’ve taken. One wildcard is milrinone. I like that you bring up the chest closure. Our surgeon typically makes the decision to leave it open if he wants, but if we attempt to close it’s another decision point.