10.01.2025 Recording Grand Rounds

Name: 10.01.2025 Recording Grand Rounds
Uploaded: 2025-10-08T20:01:38.54Z
Duration: 1 h 6 min 6 s

October 08, 2025

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ID: 13496
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02:08Might have a little bit
02:09more. Okay.
02:10Alright. Good afternoon, everyone. We'll
02:12get started right on time.
02:14So for those of you
02:15who haven't met, I'm Patty
02:16Chung. I'm an assistant professor
02:18in the basic science department
02:19of cardiology,
02:21and I'm part of the
02:21Grand Rounds committee.
02:23And so please, text in
02:24if you haven't already. Just
02:26a reminder of the upcoming
02:27Grand Rounds events.
02:31The next few guest speakers
02:32we're going to have, is
02:33next week we'll have doctor
02:34Rajesh
02:36Vedantan from NYU,
02:38followed by another ambulatory case
02:40conference and, doctor Mark Palatier
02:42from Yale's own cardiac surgery
02:43department
02:44and doctor Mark Petrie. So
02:45please put these events on
02:46your calendars.
02:47A quick remind reminder that
02:49CVM faculty retreat is this
02:51upcoming Monday, October sixth. Everyone
02:53should have received a calendar
02:54invite, so please do your
02:55best to attend.
02:56And so with that, we'll
02:57kick off this case.
02:59So, it's my great pleasure
03:00to introduce
03:01two leaders of our discussion
03:03today. First is doctor Tarek
03:05Ali of the MBA who
03:06is an assistant professor of
03:07medicine at Yale. He's originally
03:09from Connecticut and earned,
03:11his college degree from Harvard
03:13University,
03:13his medical degree from Brown
03:15University, and completed his MBA
03:16at Harvard Business School. He
03:18trained in internal medicine at
03:19the hospital of the University
03:21of Pennsylvania,
03:22followed by fellowships in cardiovascular
03:23medicine at Tufts Medical Center
03:25and critical care medicine at
03:26the Mayo Clinic in Rochester.
03:28His clinical and research interests
03:30focus on acute cardiovascular care,
03:32quality and process improvements, and
03:34care delivery operations.
03:35Joined by doctor Tarek Ali
03:37today is doctor Divya Iyer,
03:38MD, who is a third
03:39year clinical cardiovascular medicine fellow.
03:42She is also a Connecticut
03:43native who attended University of
03:44Connecticut for college and medical
03:46school before completing her internal
03:47medicine residency at the Mount
03:49Sinai Hospital. Her interest in
03:51cardiology include providing excellent clinical
03:53and procedural care to a
03:54diverse patient population,
03:56ensuring health equity, and mentoring
03:58underrepresented
03:59trainees into the field. And
04:01doctor Iyer is planning to
04:02pursue a fellowship in cardiac
04:03electrophysiology
04:04next year. So with that,
04:05I'd love to really welcome
04:07doctor Ollian Iyer for presenting
04:08today's case.
04:15Hi, everyone.
04:17So
04:18I'm really excited about today's
04:20case. Divya is gonna be
04:21presenting a case that's inspired
04:23by,
04:24a case that we faced
04:25at our at our hospitals.
04:27There are some elements that
04:29are,
04:30changed and modified for educational
04:32purposes,
04:33to help with driving,
04:35education points.
04:36But I am really excited
04:38that with our new form
04:39with this new series, we're
04:40gonna be trialing a format,
04:42where we're gonna have assistance
04:44of our other experts
04:46for to help Divya in
04:47our discussion of this case.
04:49We have doctor Robert McNamara,
04:51who's our professor of medicine,
04:53who's also the director of
04:54echocardiography
04:55here to help us think
04:56through this case.
04:57Doctor Carlos Davila, who is
05:00really a triple threat in
05:01terms of interventional heart failure
05:03as well as structural,
05:04cardiology.
05:06And he will be helping
05:07us through this case. And
05:08then Nikhil Sikant is another
05:10assistant professor of medicine,
05:12also the assistant profess program
05:14director for the cardiology program
05:15as well as the associate
05:16program director for the heart
05:18failure,
05:20fellowship program.
05:21So without ado, I will
05:23introduce Divya to walk us
05:24through our case.
05:32Hello, everyone. Good morning.
05:36Okay.
05:38Alright. So good afternoon.
05:40Thank you for attending my
05:41grand rounds,
05:42entitled updates, uniquities,
05:45special situations, and cardiogenic
05:47shock.
05:48I have no disclosures at
05:50this time.
05:52So today, I'd like to
05:53focus on these four learning
05:54objectives. At the end of
05:55my presentation, I'd like us
05:57to be able to properly
05:58and specifically stage our cardiogenic
06:00shock patients.
06:02I'd like us to rapidly
06:03recognize and mobilize resources and
06:05situations of cardiogenic shock,
06:07manage unique phenotypes of cardiogenic
06:09shock, and transition management to
06:11the acute care post acute
06:13care setting. You'll notice that
06:15the title and the objectives
06:16are intentionally vague,
06:17and that's because I wanna
06:19withhold the diagnosis for a
06:20little bit longer till we
06:21get into the case.
06:24Alright. Jumping right in. So
06:26day one, we have a
06:27seventy year old female patient
06:29who presented with lightheadedness, shortness
06:30of breath, and chest discomfort
06:32radiating to the throat.
06:35To give a little more
06:35detail, she says that she
06:37was in her usual state
06:38of health this morning, was
06:39feeling well the past few
06:40days. She was standing up
06:41at her retail job, working
06:43a later evening shift when
06:45her symptoms started, and she
06:47kinda remembers that, oh, she
06:48forgot to take her morning
06:49medications.
06:51She had persistent symptoms for
06:52one to two hours while
06:53en route to the ER
06:55and presented to the ER
06:56at an outside hospital at
06:57midnight. And just to orient
06:59you, you could see the
06:59time and the location of
07:01all the next steps in
07:02the bottom right hand corner.
07:05To give her a past
07:06medical history, she has a
07:07history of hypertension, anxiety, depression,
07:09and some other noncardiac diagnoses.
07:11She has a history of
07:12tobacco use.
07:14Her only medication at the
07:15time was venlafaxine
07:17thirty seven point five daily
07:18for anxiety.
07:20And of note, she has
07:21no family history of cardiovascular
07:23disease.
07:25Social history, so she had
07:26some prior tobacco use like
07:27I mentioned, and she,
07:29drinks three standard size alcoholic
07:31drinks per week, but no
07:32drugs.
07:34When she presented to the
07:35outside hospital, she was sick.
07:37Her physical exam was pretty
07:39obvious. Vitals, heart rate, one
07:41ten. Blood pressure, eighty five
07:43over sixty,
07:44with respiratory rate, sixteen.
07:46She was mildly distressed and
07:48anxious appearing, tachycardic
07:50with a grade two systolic
07:51murmur over apex,
07:53and her JVP was estimated
07:54at ten centimeters at that
07:55moment.
07:56She also had bibasilar,
07:58and her extremities were known
07:59to be cool and clammy,
08:01but interestingly, without a deep.
08:04On her labs, just to
08:05go quickly,
08:06of note, her,
08:08complete blood count and her,
08:10chem seven was pretty normal.
08:11Although, if you know her
08:12baseline creatinine is pretty low
08:14at point four
08:15two, and her presenting creatinine
08:17was one. Her ASC ALT
08:19from prior normals was one
08:20zero two and ninety nine.
08:22And
08:23of note, her NT proBNP
08:25was in the six thousand
08:26range, and her high sensitivity
08:27troponin was elevated but flat
08:29from ninety four to one
08:31fifteen over two, three hours.
08:32Her lactate was two point
08:34five at presentation.
08:36And just quickly, her AP
08:38portable,
08:39chest X-ray showed some mild
08:41interstitial pulmonary Amazing. Normal cardiac
08:43silhouette.
08:45And her EK was completed
08:47and displayed sinus tachycardia
08:49with a known chronic left
08:50on over in his block.
08:51And just for thoroughness sake,
08:52this is not the
08:54Scrubosa criteria for SC elevation.
08:56One piece. This is all
08:58occurring around one AM at
08:59the outside hospital. Do we
09:00need to test this on
09:01that? Care was Part of
09:03it just like this. Hospital,
09:04but unfortunately had some technically
09:06difficult
09:07poor windows.
09:08Although, they were able to
09:09find that there was a
09:10mild to moderate reduction in
09:12EF from in the range
09:13of thirty to forty, and
09:15she had had prior outpatient
09:16echoes in the past five
09:17years that showed a normal
09:18EF of sixty
09:21five. Her early management was
09:22as follows. She got a
09:23liter of fluids, but then
09:25after the point of care
09:26ultrasound, she got some Lasix
09:27forty milligram IV.
09:30Her repeat vitals at that
09:31time showed a heart rate
09:32one twenty one, blood pressure
09:34one zero one over eighty,
09:35and cardiogenic shock was considered
09:37high on the differential with
09:38the ER physician.
09:40And,
09:41expert opinion was sought at
09:43York Street with our CCU,
09:45colleagues.
09:46She was started on inotropy
09:47after some discussion, and dobutamine
09:49was chosen.
09:51It was started at two
09:51point five and rapidly uptitrated
09:53to five, and she was
09:55transferred to YNHCCU
09:57for concern for cardiogenic shock.
10:01On arrival to York Street,
10:02her vitals were largely the
10:04same on the five micrograms
10:06per k per minute of
10:07dobutamine,
10:08blood pressure one zero two
10:09over eighty four.
10:10She did have, some oxygen
10:12desaturation requiring three liters nasal
10:15cannula started by EMS.
10:17And her labs, interestingly, just
10:19one or two hours after
10:20her initial, were already showing,
10:23distinct signs of hyperperfusion, including
10:25creatinine increasing to one point
10:27five two,
10:28liver congestion, and a lactate
10:30of four point one.
10:33We tried to pocus again,
10:34but encountered
10:36some new findings, still that
10:38same low EF of thirty
10:39to forty, but some possibly
10:41new mitral regurgitation
10:42noted on color Doppler.
10:45And at that time, the
10:46patient was immediately given high
10:48dose diuretics.
10:49She was known to have
10:50poor urine output throughout transit
10:52at seventy five cc per
10:53hour,
10:54and a right IJ triple
10:56lumen and arterial line were
10:57placed for further hemodynamic
10:59information.
11:01And these yielded a central
11:03the triple lumen yielded a
11:04central venous sat of forty
11:06four percent and a bedside
11:07CVP of twelve.
11:10I'd like to kind of
11:11delve into our first learning
11:12point at this time. With
11:13this initial clinical information,
11:15how would we stage the
11:17shock?
11:18I think we're all pretty
11:19familiar with the twenty twenty
11:21one schema developed by Society
11:23of Cardiovascular
11:24Angiography and Intervention, Skye, wherein
11:26cardiogenic shock is described from
11:28an a to e scale,
11:30a being a hemodynamically
11:31stable patient who's at risk
11:33for cardiogenic
11:34shock, c being a patient
11:36with clinical evidence of hypoperfusion,
11:39with some hypotension possibly requiring
11:42pharmacologic or mechanical support,
11:44and e being patients with
11:45refractory shock and impending collapse.
11:48But in the years after
11:49the staging system was proposed,
11:51the cardiac critical care community,
11:54further detailed each stage and
11:55tried to elicit some nuances.
11:57Of note, the Kapoor group,
11:59and authors working with the
12:01cardiogenic shock working group, also
12:03known as CSWG,
12:05utilized a registry to describe
12:07cardiogenic shock due to myocardial
12:08infarction, heart failure, or, like,
12:10a combined
12:11neither cause bucket.
12:13And they provided this new
12:14schema for us to,
12:16use
12:18in place of or along
12:19with the pyramid.
12:21Their findings added the way
12:23that I understood, you know,
12:24these nuances is they fall
12:26into these three kind of
12:28central ideas.
12:30Firstly, they expanded on specific
12:32definitions of hypotension and hypoperfusion
12:35given, you know, strict blood
12:37pressure and lactate numbers as
12:39well as AST and pH.
12:41They introduced this idea of
12:42treatment intensity, which I will
12:44talk about.
12:45And three, how dynamic is
12:47the shock? Did the shock
12:48worsen, stay the same, or
12:50improve, and over what time
12:51course?
12:53Hypotension and hyperprofusion is probably
12:55the one we're most familiar
12:56with in our clinical practice.
12:58We kind of intrinsically know
13:00through taking care of our
13:00patients that the cutoffs of
13:02systolic BP, like, greater than
13:04or less than sixty or
13:05lactate greater than two, greater
13:07than five, greater than ten.
13:10Of note in this kind
13:11of newer schema, they acknowledge
13:14a normal tensive cardiogenic shock,
13:16which shows, like, hypoperfusion,
13:18but normal tension, which you
13:20can kind of see in
13:21box b.
13:22And if we recall our
13:23patient details, we find that
13:24she falls into the c
13:26to d territory with presenting
13:28BP eighty over sixty and
13:30lactate two point five, increasing
13:32to four.
13:35The second nuance added to
13:36this sky shock staging
13:38is treatment intensity. So Kapoor
13:40and colleagues found that in
13:41patients with cardiogenic shock of
13:43any cause,
13:44including AMI, heart failure, as
13:46treatment intensity increased, meaning number
13:48of devices increased, number of
13:50drugs,
13:51hospital mortality increased significantly.
13:54Kind of makes sense.
13:55So where would we put
13:56our patient here in this
13:57moment? She was on dobutamine
13:59and no MCS,
14:01and comparable patients in this
14:02study had around an eleven
14:04percent mortality.
14:07And the third nuance is
14:09how dynamic is the cardiogenic
14:11shock. The critical care community
14:13has examined this in a
14:14few ways. The overall point
14:16to understand is that the
14:17first twenty four hours really
14:19defines the patient's trajectory.
14:21In this analysis by Ton
14:23et al using registry data
14:24from that same cardiogenic shock
14:26working group, they found that
14:27in the first twenty four
14:28hours,
14:29SKY staging mostly stays the
14:31same.
14:32Patients do not easily move
14:33between stages. And as you
14:35can see on this plot,
14:36the vast majority of patients
14:37who present in one stage
14:38persist in that stage at
14:40twenty four, forty eight, and
14:41seventy two hours.
14:44As part of this analysis,
14:46they found that in essence,
14:47if a patient is to
14:48deteriorate in the first twenty
14:50four hours, like from stage
14:51b to stage c indicated
14:53by the purple bar here,
14:54they have a higher mortality
14:55than if they came in
14:57sicker at stage c and
14:58just stayed in stage c,
15:00which is the green bar.
15:02Even larger deteriorations like seen
15:04in the orange bar here
15:05where a patient starts in
15:06b and goes to d,
15:08obviously, expectantly has increased mortality.
15:11And this really hammers home
15:12the point that deterioration in
15:14the first twenty four hours
15:15could matter more than severity
15:17of initial presentation.
15:20So this introduces a really
15:21important concept in a new
15:23concept in critical care cardiology
15:25called the golden day of
15:26shock.
15:28Main principles of this concept
15:29include early recognition and staging
15:32of shock in twenty four
15:33hours and early mobilization of
15:34resources
15:35and intervention within twenty four
15:37hours.
15:39What contributes to the golden
15:40day of shocks? We at
15:42Yale have hypothesized on this.
15:44Early diagnostic information in the
15:47form of pulmonary artery catheter,
15:50can be seen oops. Sorry.
15:51One second. Can be seen
15:53to have a significant,
15:54impact in the first twenty
15:55four hours to improve outcomes,
15:57and you'll see some familiar
15:59names on the screen.
16:01In this study by our
16:02team, patients in cardiogenic shock
16:04who received a pulmonary artery
16:06catheter on day one versus
16:07day two of admission had
16:09a lower risk of in
16:10hospital mortality,
16:11an effect seen in the
16:12overall cohort and then as
16:14you go down this plot,
16:15in the subgroup analysis.
16:17Additionally, patients who received a
16:19pulmonary catheter on day two
16:21showed higher lactate levels, greater
16:23use of vasoactive agents, and
16:25temporary MCS, and had more
16:27severe shock.
16:29Using the same cohort and
16:31hot off the presses, we
16:32have a brand new analysis
16:33by our team here
16:35showing that early use of
16:36mechanical circulatory support and cardiogenic
16:38shock may improve outcomes when
16:40deployed within that first day,
16:42that first golden twenty four
16:44hours.
16:45This forest plot displays that
16:46patients with IVP, Impella, and
16:48ECMO
16:49placed on day one versus
16:50day two had improved survival
16:52during their hospital stay.
16:55An important consideration during this
16:57golden day of shock is
16:59what's happening with the lactate.
17:01In the post hoc analysis
17:03of the DO RE MI
17:04trial, which I'm sure some
17:05of you are familiar with,
17:06investigators showed that rate of
17:08lactate clearance
17:09is actually a better indication
17:11of prognosis than absolute lactate
17:13value at presentation.
17:15And even more importantly, lactate
17:16clearance at eight hours was
17:18the strongest predictor of survival.
17:20And it's notable that the
17:21lactate on presentation between the
17:23two cohorts,
17:25survivors and non survivors, was
17:27the same at around three
17:28point seven.
17:30This ties into,
17:32like, kind of closing out
17:33our learning point, a really
17:34recent initiative by the president
17:36of Sky who introduced the
17:38concept of door to lactate
17:39clearance,
17:41wherein cardiogenic talk shock team
17:43should attempt to clear the
17:44lactate within twenty four hours,
17:46to improve outcomes and essentially
17:48really try to act during
17:50that golden day of shock.
17:52Alright. Now that we've really
17:54thoroughly specifically defined our patient's
17:56shock stage,
17:58let's return back to our
17:59case.
18:02Okay. So given this principle
18:04that our team you know,
18:05our cardio
18:06our cardiac critical care team
18:08knows,
18:09the team made the decision
18:11to pursue
18:12cardiac cath lab activation at
18:14four thirty AM after hours.
18:17It was a very planned
18:18approach. Operator chose femoral access
18:20in case mechanical circulatory support
18:23would be needed,
18:24and right heart catheterization
18:25was performed first to give
18:27her early hemodynamic information.
18:30The right heart cath displayed
18:32the following.
18:34The RA pressure was nine,
18:36r v sixty eight over
18:37sixteen,
18:38p a fifty one over
18:40thirty with the mean of
18:41thirty eight, and wedge twenty
18:43eight.
18:44Of note, the pocus, if
18:45you remember, showed some mitral
18:46regurgitation,
18:47but there were no b
18:48waves visualized.
18:51Cardiac output at that time
18:53was calculated to be two
18:54point six liters and
18:56liters per minute and cardiac
18:58index one point five.
19:00From the
19:01Left heart catheterization was then
19:03pursued.
19:04Here, we visualize and all
19:05goes fairly quickly through these.
19:07Okay.
19:08That the left main, proximal
19:10LED, and left circ are
19:12largely free of disease. Ryan's
19:14Minotaur is here
19:15today. Is that is that,
19:17like, this sponsor really I'll
19:18just go quickly through a
19:20little bit more interrogation of
19:21the LAD, conferring those significant
19:23proximal or distal CAE.
19:27And similarly, the right coronary
19:28artery was also significant Around
19:30the line, do you please
19:31mind muting? Stop myself.
19:34So things aren't really making
19:35sense. Right? We have pretty
19:37significant cardiogenic shock established.
19:39We have clean coronaries,
19:41and we have this possible
19:43mitral regurgitation, but no b.
19:44Wait.
19:46At that time, decision was
19:47made to cross into the
19:48LV
19:49for two purposes. One, ventricular
19:52ventriculogram,
19:53which I'll play a couple
19:54times so that everyone
19:56can make a little assessment.
19:57You're gonna have less than
19:58that. Yeah. Yeah. Yeah.
20:00To follow-up as, messaging.
20:03I think we're not talking
20:04about genetics, though. And then,
20:06additionally, the LV pressure
20:08was measured at one seventy
20:10five over thirty six
20:12with pullback to the aorta
20:13measuring at ninety eight.
20:17So I wanna close a
20:18question at the at this
20:19key moment in this case
20:20for you all to think
20:21about as we progress.
20:23What would you do in
20:24this moment? You know, I'm
20:25standing at the cap table.
20:26Would you add another inotrope,
20:28telomere nosy, or would
20:31you place a balloon pump?
20:33Would you lean off the
20:34beat of mean and get
20:35fluid?
20:36Or what time you're going
20:37to do the more aggressive
20:39fluid removal and
20:41for ultra filter.
20:42And then doing air bloods
20:43go out. They just moving.
20:47They got the guts.
20:49Before I share what the
20:50team did next, I think
20:51it's important to go over
20:52the echo that was performed
20:53a little bit later in
20:54that morning if everyone Wait.
20:55Wait. Wait. Wait a second.
20:57I'll just
20:59Right at the bat Just
21:00like it. I'm going to
21:02go into our parasternal long
21:03axis view. We can already
21:05see that there's a decreased
21:06LVEF,
21:07and there's also some proximal
21:08thickening of the interventricular
21:10septum
21:11or sigmoid septum. We also
21:13get a preliminary notion that
21:14there's some wall motion abnormality
21:16in the mid interseptal
21:18and mid inferolateral
21:19segments.
21:20And the mitral valve appears
21:22structurally fairly normal, but we
21:24need to evaluate function a
21:25little more.
21:27In this color Doppler interrogation
21:29over the mitral valve and
21:30the LV outflow tract, we
21:31see some aliasing of color
21:33Doppler suggestive of possibly higher
21:35velocity flow in that area.
21:39For the sake of time,
21:40I'll just show some representative
21:41images for wall motion. So
21:43in our apical four chamber
21:44view, we see that RV
21:45function is preserved, but the
21:47LV mid interlateral
21:48and infraceptal segments as well
21:50as apical septal and lateral
21:51segments apical lateral segments are
21:53akinetic,
21:55and the basal segments appear
21:56normal to even possibly
21:58hyperkinetic
21:59in contrast.
22:01The LVEF by three d
22:02at this moment was noted
22:03to be forty four percent
22:05from her prior of sixty
22:06five.
22:08In this two chamber view,
22:09we further confirm mid to
22:11apical anterior and inferior hypokinesis
22:13with preserved or possibly even
22:15increased wall motion in the
22:16basal segments.
22:19And color Doppler over the
22:20mitral and LVOT
22:21in the,
22:23or five chamber view,
22:25displays MR with a posterior
22:27directed jet as well as,
22:28again, those velocities and aliasing
22:30in the LVOT.
22:32So our STU ECHO techs
22:34use, continuous wave Doppler to
22:36interrogate the mitral regurgitation
22:38jet as well as the
22:39LVOT.
22:40Focusing on the left hand
22:41side, the color Doppler and
22:43continuous wave are concerned for
22:45severe MR. But on the
22:46right hand side, if you
22:47notice where the point of
22:48focus is,
22:50and I've just highlighted that
22:51here,
22:52on the continuous wave Doppler
22:54line, you can see that
22:55when aimed in the region
22:56of the LVOT, we are
22:57able to find a very
22:58high gradient of sixty five
23:00at rest.
23:01And at this moment, I've
23:02talked a lot. I'll invite
23:04doctor Robert McNamara to give
23:05his preliminary thoughts on the
23:07findings and give us our
23:08diagnosis.
23:10You can do it, Sandra.
23:12K. Yeah. I think so.
23:16K. Can you hear me?
23:17Yeah. Thanks, Divya. You did
23:19a excellent job on the
23:20presentation as well as on
23:21the on the echo. I
23:22just have a few,
23:24comments,
23:25to make. I mean, this
23:26case is somewhat unique. We
23:28usually have the echo. We
23:29usually do not have the
23:31cap before we, have the
23:32echo.
23:34And many of the times
23:34we're trying to decide whether
23:36the patient should go,
23:38to cath because, you know,
23:39of course, they always say,
23:41I guess, am I allowed
23:42to give their diagnosis?
23:43Or,
23:46you know, for stress induced
23:47cardiomyopathy,
23:49you know, they say it's
23:50a diagnosis exclusion, so you
23:52wanna rule out coronary disease.
23:54But many times the patients
23:56are so sick that, the
23:57risk benefit ratio of that
23:59is, is difficult so you're
24:01trying to decide whether a
24:02cath is needed,
24:03or not. So a lot
24:05of it is, in terms
24:06of looking at the images
24:08to see what's the likelihood
24:10of this. And of course,
24:11if any patient can go
24:12to cath, they do,
24:13but many of the patients
24:15are so sick that you
24:16may not need to. But
24:18in any event, so
24:20the two d images are
24:21very important to kind of
24:22see and to kind of
24:23get that
24:24idea.
24:25You could see on here
24:26where it was the the
24:27typical apical,
24:31ballooning,
24:32cardiomyopathy
24:33that you have. But there
24:34are other ones we have
24:35mid,
24:36as well as basal that
24:37can make things more even
24:38more confusing.
24:41For this one, it's very
24:42interesting when the patients are
24:43so sick and you're you're
24:44worried about this gradient and,
24:47you know, particularly with the
24:48MR,
24:49it can be very difficult
24:51to differentiate the two and
24:52you can one of the
24:53things that we ask the
24:54synoders to to do is
24:55to give us this MR
24:57versus the LVOT.
24:59And on sometimes it can
25:00be very difficult because you
25:01look at this LVOT and
25:02this is very high. I
25:03mean, this looks like an
25:04MR,
25:05jet, in many ways and
25:07and could be very easily
25:08confused.
25:09But I asked if you
25:10could put this on next
25:11to each other because you
25:12can kind of see.
25:14It's subtle, but, if you
25:15look at where the jet
25:17starts,
25:18and compare it with the
25:19ECG, the jet is earlier
25:21on the left screen with
25:22the MR than it is
25:23on the right. And, you
25:24know, as we all know,
25:25the MR murmur is is,
25:28longer, starts earlier and ends
25:30later than,
25:32the,
25:32than an outflow jet. So
25:34that would be helpful. And
25:35it's and when it's this
25:36high, it's difficult to say,
25:37but the MR is always
25:38gonna have a higher velocity,
25:40than the LVOT. If you
25:42think about it, it's,
25:44it's a gradient across the
25:45into the aorta versus into
25:47the LA.
25:48So that's an important thing
25:49here,
25:51for for the jet because,
25:53you know, it can be
25:53confusing.
25:54Go to the next slide.
25:56And just very quickly, and
25:58I asked because I thought
25:58this was interesting.
26:00The data on strain and
26:02and stress induced cardiomyopathy is
26:04very mixed. Some have shown
26:05that you really can't differentiate
26:07it. But this case was
26:09very, interesting. If you look
26:10at the the bottom left
26:13one, you know,
26:15in general,
26:16strain,
26:17is very good. We do
26:18global strain and we use
26:19a lot in the cardiomyopathy
26:20and and global to try
26:22to see what what it
26:23is and a normal would
26:24be all red. That's,
26:26what we do for normal.
26:28And if you throw for
26:29amyloid, doctor Miller's looking over
26:31there and, you know, we
26:33have what's called cherry on
26:34top because the,
26:36the apex is preserved.
26:38But this one is, if
26:39you can think of it,
26:40it's exact opposite of that.
26:42It's the the pink,
26:44is, showing a a worse
26:46strain,
26:47than the red,
26:48which goes along with our
26:49clinical presentation. So,
26:51I can't say that this
26:52is,
26:53always this way and it's
26:54not, diagnostic. But in this
26:56case, it was, very,
26:58instructive.
26:59Thank you so much.
27:09I
27:10belong there. Yes. Please.
27:14Go back I don't know
27:15how to put it. Yeah.
27:19Okay. So go back to
27:20the mitral and the LVOT.
27:22So from the Cath Lab
27:24perspective,
27:25personally, I was struggling with
27:27the same based on hemodynamics.
27:28Is this MR
27:30or is an LVOT gradient?
27:32Right? So and that's why
27:33I asked you to put
27:33the wedge tracing because I
27:35I got fixated on that
27:37and had to rely on
27:38that. I don't see significant
27:39b waves. I don't think
27:41this is MR.
27:42And and that's when we
27:43crossed
27:44the the LV and noticed
27:46that significant gradient.
27:48It it was an invasive
27:50hypodynamic
27:50based diagnosis because as as
27:52Bob mentioned,
27:54we got the echo after
27:55the cath. So that's usually
27:56not the case. And and
27:58it's easier when you get
27:59the ballooning, apical ballooning, and
28:00then just cath them and
28:01see no coronary artery disease.
28:03But doing,
28:05just
28:06a hemodynamics
28:07based,
28:08diagnosis, I think it's one
28:10of the teaching points of
28:11this case.
28:14I have a quick question.
28:16Since you brought up the
28:17question, the point, Carlos,
28:19just routinely, when you do
28:20have the echo first, it
28:22raises a concern of stress
28:23cardiomyopathy.
28:24How and so you do
28:25your left heart cath to
28:26rule out ischemic disease. How
28:28often do you consider to
28:29cross the valve to see
28:30if there's a gradient or
28:31not?
28:33Depends on the patient. It's
28:36stable.
28:37If the patient is stable,
28:38I don't think we need
28:39to document,
28:41an a gradient, which you
28:43can get by echo. But
28:44if the patient is very
28:45unstable like she was,
28:47I think it's important to
28:48know how bad the gradient
28:49is and what can we
28:50do to mitigate that.
28:59Just to show
29:02you don't see very often
29:04the distinction between the LVOT
29:06and the aorta
29:08aortic gradients that were measured
29:10simultaneously.
29:11Right?
29:13So
29:13yeah, this this one. Yeah.
29:15Oh, sorry. Comment on this
29:17because I think this is
29:18an important teaching moment. Okay.
29:19I don't think you see
29:21this so obviously
29:23obvious, this distinction
29:24between these two gradients. And
29:25and tell maybe tell the
29:27scientists in the room who
29:28may not see us every
29:28day why what what we're
29:30actually measuring here.
29:32I actually, I think I'm
29:34I don't wanna steal Carlos'
29:35center because he was actually
29:36gonna speak about this. So
29:37Oh, okay. I I can
29:38save it for Carlos to
29:39talk about when he speaks
29:40about it, when he's
29:42oh, then I'm happy to
29:44talk about it.
29:45So, I mean, I, this
29:47is where you're measuring your
29:47pressures inside the left ventricle.
29:49And so this is when
29:50they have the catheter in
29:51the LV. So you're measuring
29:52your pressures there and then
29:53you're the pigtail. And then
29:55you're, when you're pulling it
29:56out is where you're going
29:57to get the aortic pressures.
29:58And so you're trying to
29:59time this,
30:00close to each other, but
30:02that is where you're seeing
30:03this gradient that's here, notably.
30:08And then the reason as
30:09you know, so there there
30:11is apical ballooning, but your
30:12base is hyper
30:14active. Right? So this hyperactive
30:16base is what's gonna create
30:18creates your LVOT gradient
30:20a lot sometimes with, with
30:22the mitral activity,
30:23mitral valve, just like HCM.
30:26And so what we're doing
30:27here is we're comparing distal
30:29pressures with,
30:31pressures
30:32and see, you shouldn't get
30:33a gradient unless you have
30:34aortic stenosis and other problems
30:36that we deal with all
30:37the time. But if it's
30:39something dynamic about this patient,
30:41there is a there's a
30:43dynamic structure here. And remember,
30:45she came to the left
30:45of the mutiny point five.
30:47And so
30:49and,
30:50shortly. But go back to
30:51the options you presented there.
30:53The
30:56just to comment again.
31:00Why is there a question?
31:02I think, you you know,
31:03what we so somebody's in
31:05shock because they have a
31:06stress in the terrible stress
31:07induced cardiomyopathy,
31:09you expect the inhibitory pressures
31:11to be low. Right? You
31:13would expect to be able
31:14to generate that level of
31:16LV
31:17systolic pressure. So
31:19shot unintended
31:21when I when I saw
31:23first up there, and I
31:25understand
31:26septum, this sort of bulging
31:28septum is contributing to this,
31:30but that's still pretty surprising
31:32to me even with that
31:33explanation.
31:37Yeah. I think the aspurity
31:38of that.
31:41Yeah. I I I agree
31:43with that.
31:44So some of these options,
31:46I, you know, I started
31:47the whole video at five
31:48AM.
31:49I I got all those
31:50up by different providers. So
31:53so I basically that's
31:55that's why,
31:58for
31:59for this particular case, I
32:00think it's very important,
32:02at least the way I
32:03approach it is I stopped
32:05being an interventional cardiologist there,
32:07and then then I became
32:08a heart failure doctor. Right?
32:09So what how do you
32:10interpret those hemodynamics
32:12and
32:13what to do with those
32:14hemodynamics? Okay. I'm not sure
32:15we're gonna talk about it.
32:19Thank you, everyone.
32:23Okay. So at at this
32:24point,
32:25you know, like we've all
32:26discussed now together, we have
32:29our likely diagnosis, stress induced
32:31cardiomyopathy
32:31with LV outflow tract obstruction.
32:36You know, I wanted to
32:36do a quick review of
32:38kind of phenotypes of stress
32:40induced cardiomyopathy
32:41because I personally think this
32:43is an interesting phenotype that
32:44I've encountered
32:46a couple times especially late
32:47at night as a fellow
32:49evaluating a cardiogenic shock consult,
32:51SRC,
32:52York Street.
32:54Really quickly, you know, we
32:55remember that this is a
32:56condition that disproportionately
32:59affects postmenopausal
33:00women, carries a four to
33:01five percent risk of in
33:03hospital mortality related to cardiogenic
33:05shock and cardiac arrest.
33:07You know, I looked and
33:09tried to see how do
33:10people define these, like, phenotypes
33:12of stress induced cardiomyopathy and
33:14saw a good amount of
33:15work on these, like, four
33:17major wall motion abnormalities,
33:20identified with the majority of
33:21patients having, in the upper
33:22right hand corner, the apical
33:24type, smaller proportions displaying midventricular
33:27type, basal type, and focal
33:28type of wall motion.
33:30But, you know, I
33:32I suggest that we have
33:33a real phenotype here of
33:35stress induced cardiomyopathy,
33:36something different structurally than just
33:38wall motion, and it's this
33:40presence of LV outflow tract
33:41obstruction.
33:43We, like we said just
33:45now, you know, we
33:47established this via our catheterization
33:49first and then confirmed it
33:50by our echocardiography.
33:53How prevalent is this phenotype?
33:55Topic is very understudied.
33:58It's really not been fully
33:59described by what I reviewed
34:00in the literature.
34:02In the Takasubo International,
34:04Network Registry, they described about
34:06seven percent of patients with
34:08stress induced cardiomyopathy can have
34:10an LV outflow tract obstruction
34:12and ten percent in this,
34:14Spanish registry on Takasubo.
34:17But you know, I think,
34:18you know, in talking to
34:19doctor Davila, we thought it
34:20was probably even higher and
34:22really requires
34:23larger study.
34:26The proposed mechanism has been
34:28discussed by some authors and
34:29kind of borrows from similar
34:31discussion in the field of
34:33HOCAM, where some authors propose
34:34like a Venturi effect wherein
34:36pressure is lower after the
34:38obstruction leading to some kind
34:40of vacuum.
34:41Other authors propose like drag
34:43effect.
34:44In the distinct case of
34:45Takotsubo cardiomyopathy,
34:47something to think about is
34:49you have this LV outflow
34:50tract obstruction increasing your afterload
34:53and this actually is exacerbating
34:54your apical and mid myo,
34:56midventricular
34:57myocardial dysfunction,
34:59worsening the wall motion abnormalities
35:00and kind of working together,
35:03to cause this problem.
35:05Some authors have found that
35:07a small LV
35:08and presence of a hypertrophied
35:10interventricular
35:11septum is is associated with
35:12the development of LV alco
35:14tract obstruction and stress cardiomyopathy
35:16and if you'll remember,
35:17our patient does have a
35:18sigmoid septum, which we kind
35:20of look at further in
35:21the outpatient echo later on.
35:25Insights from that registry I
35:27talked about on Takasubo Syndrome
35:29gave some preliminary ideas on
35:30prognosis of this phenotype.
35:33Presence of LVL flow tract
35:35obstruction was associated with more
35:37acute kidney injury, more ventricular
35:39arrhythmias.
35:40There really wasn't an association
35:42with in hospital mortality, but
35:43of course the study was
35:45modest in number of patients.
35:48And we really don't know
35:49right now how does this
35:50affect mortality.
35:53Anecdotally and to connect back
35:54to some of the shock
35:56items that we talked about,
35:58it definitely caused some level
36:00of diagnostic uncertainty during that
36:02first twenty four hours, the
36:03golden day of shock. So
36:05I think that's an interesting
36:06thing to examine.
36:09And comparing and contrasting our
36:11standard cardiogenic shock management to
36:13the special phenotype,
36:14we know that in standard
36:16CS, you know, we want
36:17to enhance contractility
36:19using inotropes, inopressors.
36:21We optimize our preload
36:23removing fluid with diuresis,
36:25and we optimize our afterload
36:27using medications and mechanical support
36:29devices.
36:31In the setting of LV
36:32outflow tract obstruction,
36:33we have to do the
36:34opposite, and we learn a
36:35lot of this from our
36:36patients with, HOCAM.
36:38We try to reduce contractility,
36:40avoid inotropes,
36:41give IV beta blockers in
36:43some cases,
36:44optimize preload by giving fluids,
36:46and do our best not
36:47to decrease afterload via medications.
36:50But really the question now
36:51comes to take to the
36:53next level is what do
36:54we do with mechanical circulatory
36:56support in these case, in
36:57this special case?
36:59With that question in mind,
37:00we can look at this
37:01study from our own colleagues
37:02again,
37:04which examined mechanical
37:05circulatory support usage and stress
37:07cardiomyopathy
37:08using a national database of
37:10nine zero two patients.
37:12This study found that use
37:13of mechanical circulatory support
37:16in this situation requires careful
37:18consideration
37:19especially with regard to device
37:21choice
37:22and whether or not to
37:23use MCS at all. Patients
37:25who received an Impella, for
37:26example, had a higher in
37:27hospital mortality renal replacement therapy
37:30and vascular complications than those
37:32who,
37:33received a balloon pump.
37:35And to delve a little
37:36bit more deeply into this
37:37topic of MCS and stress
37:39cardiomyopathy
37:40and specifically in patients with
37:42also an LV equal tract
37:43obstruction. I invite doctor Davila
37:45again to speak about this
37:46special phenotype
37:48and some of his thoughts
37:49around MCS.
37:51Yeah. So so this case
37:52prompted this analysis. Right? I
37:54finished the case, and
37:55we said,
37:57do we know how many
37:58of these patients
37:59have an LVOT obstruction and
38:02what's happening with them? So
38:03alongside with some of the
38:05fellows, we just asked the
38:06question, how many patients with
38:08diagnosed
38:09stress induced cardiomyopathy
38:11are getting devices and what
38:12type of device?
38:13So a lot of limitations.
38:15It's retrospective. It's based on
38:16administrative
38:17database. But as you saw,
38:19there is a significant group
38:20of patients that get balloon
38:21pumps.
38:22And even with this thought
38:24process of reducing afterload, it
38:26will be detrimental.
38:27And also patients who are
38:29collapsing,
38:30probably Sky Stage E, getting
38:32ECMO,
38:32and overall mortality relatively high
38:35for a relatively low prevalent
38:38condition.
38:39So the reviewers came back
38:40to us and asked, Okay,
38:42so why don't you try
38:43to provide an algorithm, a
38:44suggestive algorithm on how to
38:46deal with these patients?
38:49And this is all based
38:50on no data at all.
38:51Right?
38:52So this is all made
38:54up. But what we try
38:56to do is try to
38:57extrapolate some of the numbers
38:59that we use for hypertrophic
39:01cardiomyopathy,
39:02for example. So a significant
39:03LV to a gradient of
39:04more than thirty, that's what
39:06it's considered significant for hypertrophic
39:08cardiomyopathy
39:09at rest or after exercise.
39:11I think what we need
39:12to establish first is the
39:13def is you gotta establish
39:15the patients who are in
39:16cardiogenic shock. Right? And you've
39:17covered all the definition.
39:19And then further stratify them
39:21using the sky stages. I
39:23think we can we can
39:23all agree that that's very
39:25important
39:25because that will help you
39:28consider how sick these patients
39:29are, where
39:31do they need to go,
39:31and who do you need
39:33to wake up in the
39:33middle of the night. Right?
39:35And then once you further
39:36risk stratify them, are are
39:38you dealing with an LVOT
39:39obstruction? Yes or no? And
39:41if you're dealing with an
39:42LVOT obstruction, how do you
39:43deal with that? So as
39:44I said, that patient came
39:46on dobutamine two point five
39:47and had received a lot
39:49of diuretics.
39:50After getting those hemodynamics,
39:52we said stop the dobutamine,
39:54flood it with fluids, and
39:56and that's a that's a
39:58bold decision. Right? I didn't
40:00have the guts to put
40:01her on beta blockers, but
40:02we thought about it. Like,
40:03should we put her in
40:04s model and see if
40:05she gets better or not?
40:06But,
40:07I think, you know, understanding
40:09that and trying to restrutify
40:11these patients are very important.
40:13The the intent of this
40:14algorithm was not to say
40:16who should get a device
40:17and what type of device.
40:18I think it's
40:19identify shock, identify if there
40:21is a gradient or not,
40:22whether that's
40:23with with echo or cath
40:25invasive gradients, and then restratify
40:27them using your sky stages.
40:29In someone who is tremis,
40:31mine need early ECMO. I
40:32think that we should agree
40:34with that.
40:35And someone who doesn't have
40:36an LVOT gradient or even
40:38with an LVOT gradient, you
40:39have to understand this is
40:41a relatively contraindication for a
40:42balloon pump. I think that's
40:43that's what we can conclude.
40:45I don't think we should
40:46say who gets an impeller,
40:47who doesn't. And for that,
40:49I asked Diva to add
40:50this. So this is when
40:51Tarek and I were fellows.
40:53We were doing some PV
40:54loops.
40:56And this is what happens
40:57when you go on and
40:58off with the balloon pump.
40:59Right? So you can see,
41:01this is LV pressure and
41:02volume, and you can see
41:03a significant reduction in afterload
41:05once you go on on
41:06a balloon pump. And in
41:08someone who has a significant
41:09LV at the obstruction, that
41:10that's clearly detrimental. Right? So
41:12I think,
41:15I know you guys know
41:16that, but, I I think
41:17that's the ditching point of
41:18this.
41:20Thank you so much.
41:22Okay. So returning back to
41:23our case,
41:26let's, you know, doctor Dubila
41:28kinda hinted at what happened
41:29next, but,
41:31at this point, you know,
41:32during the left heart catheterization
41:34and the early recognition of
41:36Takotsubo or stress induced cardiomyopathy
41:38with a gradient on aortic
41:40pullback,
41:41no mechanical circulatory support was
41:43placed.
41:44Dobutamine stopped, IV fluids given,
41:47and patient was returned to
41:49CCU where that echo occurred.
41:51Patient was actually normal tensive
41:53though there was some discussion
41:54in the notes about starting
41:56phenylephrine
41:57and as doctor Dibila mentioned,
41:58considering Esmeral as needed.
42:01Continue some intermittent fluid boluses
42:03that day.
42:05And, you know, by the
42:08later in that day, two
42:09PM, patient was thoroughly headed
42:10in the right direction.
42:12Blood pressure was normalizing one
42:14twenty seven over eighty four,
42:15heart rate coming down to
42:16the late eighties.
42:18And in our labs, we
42:19can see a leveling off
42:20of our creatinine
42:21and a nice,
42:23leveling off of the AST
42:24ALT,
42:25and very importantly,
42:27lactate going from two point
42:28five to one point two
42:30over the course of that
42:32twelve hours. Our first set
42:33of labs was around one
42:34to
42:35AM.
42:37On day two,
42:38she was improving and warm
42:40and well profuse on exam.
42:42She recalled that on the
42:43day of presentation, she forgot
42:45to take her Venlafaxine,
42:46if you remember from the
42:47history, and was suffering from
42:49severe generalized anxiety during work,
42:51which could hint at a
42:52trigger for her stress cardiomyopathy.
42:54And on day two, there
42:56was early initiation of PO
42:58beta blockers with metoprolol succinate.
43:01And just to go quickly
43:02through, so
43:03she transferred to Cardiology four,
43:06heart rate was tolerating the
43:07Metoprolol,
43:08all her perfusion indices vitals
43:10tolerating, and she and it
43:12was increased, And she was
43:13started on guideline directed medical
43:15therapy for new heart failure
43:16including empagliflozin,
43:18Spiro,
43:19and ASR was considered and
43:21planned for outpatient but given
43:23her recovering creatinine,
43:25was planned for outpatient like
43:26I mentioned.
43:27She was discharged on DDMT
43:29in the coming days.
43:31One month later at outpatient
43:33follow-up, she was doing great.
43:35She was on DDMT,
43:36losartan was started, she was
43:39doing all her daily activities,
43:40no signs of Von's overload,
43:42and,
43:44repeat echo was planned, and
43:45just, to go very quickly
43:47through,
43:48we see that there really
43:49wasn't much of a significant
43:51gradient anymore. We still noted
43:53that septal hypertrophy with a
43:55thickness of one point five
43:56centimeters.
43:58She had mild to moderate
43:59MR compared to prior severe
44:01that we saw in a
44:02case, and her EF recovered
44:04to sixty four percent.
44:05So just in these last
44:06few minutes, I actually don't
44:07know what time it is.
44:10I just wanted to
44:11sorry? Eighteen minutes. Oh, okay.
44:12Great. Awesome.
44:15So medical management,
44:17in the post acute care
44:18setting, I just wanted to
44:19briefly touch on this,
44:21because a lot of these
44:22questions come up in my
44:23mind during fellows clinic.
44:26You know, a question that
44:27comes up, like I said
44:28in clinic, was, you know,
44:30depending on the etiology of
44:31heart failure and the presence
44:33or absence of cardiogenic shock,
44:35should we continue GDMT
44:37indefinitely
44:38on all of our patients?
44:40Is there nuance to, you
44:42know, whether the etiology matters,
44:44whether the presence of cardiogenic
44:45shock like I mentioned?
44:47Bart Filiar Community is in
44:48agreement, this paper from twenty
44:50twenty four,
44:51which looked at the French
44:53Observatory of Management of Cardiogenic
44:55Shock, the French Shock Registry,
44:56showed that patients who have
44:57an improvement of EF and
44:59stay on triple GDMT as
45:01opposed to double or single
45:02or none,
45:03have better survival.
45:06But how about specifically in
45:07heart failure or cardiogenic shock
45:09due to stress cardiomyopathy?
45:13From my review, there's really
45:14a lack of clarity around
45:15this specific situation.
45:18There's some modest data from
45:19meta analyses
45:21such as this one, but
45:22no inclusive
45:23large scale observational or clinical
45:25trial data.
45:26This study from Italy showed
45:28that there really wasn't any
45:29conclusive evidence, and of note
45:31this is, you know, back
45:32in twenty fourteen,
45:33no conclusive evidence to support
45:35that beta blockers or ACE
45:37inhibitors,
45:39prevented recurrence of Takotsubo. And
45:41for what it's worth, the
45:42risk of recurrence of Takotsubo
45:43itself is just five to
45:45twenty two percent in five
45:46years. So not really clear
45:48what the effect of GDMT
45:50would be there.
45:51And unfortunately, like I said,
45:53no large care evaluation of
45:55the usual things we look
45:56for in heart failure, repeat
45:57hospitalization,
45:58adverse cardiac events, heart failure
46:00symptoms.
46:01Even less evidence,
46:03exists for,
46:04you know, these special phenotypes
46:06of Takasubo like our patient
46:07with LV outflow tract obstruction.
46:10And to that effect, I
46:11would like to have my
46:12last speaker today, doctor Nikhil
46:14Sikan,
46:16comment on,
46:17in this patient, would you
46:19continue guideline directed medical therapy?
46:22What further
46:23sort of diagnostic investigations would
46:25you recommend, and what would
46:26you,
46:28do with your fluid management?
46:30Thanks, Divya. I I think
46:31this is a great case
46:32that you put together.
46:34I mean, asking a heart
46:36failure cardiologist if they're gonna
46:37continue GDMT is a I
46:39don't know. Like question. Yeah.
46:41Clearly, I'm gonna have an
46:42answer on that, which is
46:43yes. But I I think,
46:45like, is this data is,
46:47I think, interesting, maybe hypothesis
46:49generating in that sense that
46:51we need to, you know,
46:52bring a lot of these
46:53patients together and study how
46:54they do long term. But
46:55I think I tend to
46:57apply
46:58the data that looks at
47:00how do patients with heart
47:01failure with improved EF do
47:04overall
47:05as a group, because that's
47:06the group that we have
47:07the most data for. And
47:08I think the overwhelming evidence
47:10is that withdrawal of GDMT
47:12in those patients carries a
47:14risk of,
47:15relapse of heart failure, whether
47:17or not it's, you know,
47:18a new Takotsubo or just
47:20a relapse of heart failure
47:21with worsening injection fraction or
47:22with clinical heart failure. So
47:24I I think
47:26my practice based on that
47:27would be to,
47:29obviously, have a patient centered
47:30discussion because these medications may
47:32be continued for long periods
47:33of time, if not the
47:34rest of their lives. But
47:35if they're tolerating these medications,
47:37I think it makes sense
47:38to continue them at some
47:40doses,
47:42because the risk of
47:43of relapse in improved ejection
47:45fraction is a third, maybe,
47:47you know, more than that
47:49of patients.
47:50As far as other, like,
47:51diagnostic workups, I think maybe
47:53what you're getting at is
47:54that,
47:55the patient did have,
47:58septal hypertrophy here and LVOT
48:00obstruction, which sort of brings
48:02up the question of whether
48:04they have some sort of
48:05subtype of
48:07hypertrophic
48:07cardiomyopathy
48:09or another cardiomyopathy.
48:12It would be a bit
48:12unusual to have that kind
48:14of presentation where you have
48:16a stress myopathy in the
48:17setting of an underlying HCM.
48:19Although, HCM, as we know,
48:20is very common. Probably one
48:22in two hundred fifty people,
48:24to one in five hundred
48:25people have some form of
48:26it. So, it's possible. What
48:28I would say with these
48:29patients who have,
48:31these kind of borderline
48:33findings like this is I,
48:35especially in our institution, often
48:37will get a cardiac MRI
48:38in them
48:39to better understand,
48:42the exact measurements,
48:43as well as,
48:45late gadolinium enhancement, and some
48:47of the other findings that
48:48may be helpful
48:49to suggest. And then, obviously,
48:50take a good history understanding
48:51if they have a family
48:52history or comorbidities. I believe
48:54this patient had hypertension, so
48:56it's entirely possible that the
48:58basal septal
48:59hypertrophy is from that,
49:02and that, you know, I
49:03I think could probably explain
49:05what we're talking about here.
49:06But if you had a
49:07suspicion, it's not unreasonable to
49:08obtain genetic testing in an
49:10MRI given the, how common
49:12HCM is.
49:14I have a question.
49:16So, Nikhil, this patient, Divya,
49:18this patient was discharged on
49:19what day? Hospital day? Hospital
49:21day three. To hospital day
49:23three or Yeah. Three or
49:25four.
49:26So
49:27taking the chart trying to
49:28find it. So, Nikhil, if,
49:30you know, our mantra is
49:32to get all of our
49:32patients on TDMT before discharge.
49:34This patient just recovered from
49:37LVOT obstruction.
49:39Do
49:39I hesitate not from a
49:41renal perspective like this team
49:42did, but from a blood
49:43pressure lowering perspective of starting
49:45an ACE and AR? Do
49:47I still maximize it to
49:48the to the maximum tolerated
49:50per the studies? Do I
49:52does is there any change
49:53of how I think about
49:54the timing of this?
49:56Or, how would you have
49:57approached it if you were
49:58in the primary? Would you
49:59have delayed or would you
50:00said, nope? You know, studies
50:02show put the patient on
50:03all four GDMT before discharge.
50:05Let's add the r before
50:06on day four, or would
50:07you have waited a little
50:08bit?
50:10So I I think those
50:11studies that we're talking about
50:13really look
50:14at adherence, and, certainly, patients
50:16that are on,
50:17all four pillars of GDMT
50:19prior to discharge are are
50:21more likely to take those
50:22medications long term, and then
50:24because of that are more
50:24likely to have a better
50:25outcome.
50:26But, I think we kind
50:27of need to individualize
50:29patient decisions. And I think
50:31more important with a patient
50:32like this is arranging for
50:33close
50:34follow-up in the outpatient setting,
50:36not so much that we
50:36need to necessarily have them
50:38on all four pillars.
50:40Obviously, this patient was in
50:42shock, I guess, seventy two
50:43hours before discharge. And so,
50:45in my mind,
50:48you know, the beta blocker
50:49makes a lot of sense
50:50given all the physiology that
50:51we've talked about. But some
50:53of the other GDMT, I
50:54think, would be important to
50:55get on board. I mean,
50:56personally, I would have, you
50:57know, had considered some kind
50:59of RAS inhibition
51:01at very low dose prior
51:02to discharge. But,
51:04you know, I don't see
51:06it as a requirement. But
51:08I I do see it
51:08as a requirement that this
51:10patient be seen very close
51:12follow-up, and then have those
51:13medications titrated in that setting.
51:15Awesome.
51:17So maybe we can open
51:18up for questions.
51:19And I'm gonna make a
51:20few comments and then give
51:21it to Stefania, who I
51:22was gonna ask you to
51:23comment on, actually. So,
51:26so first of all, phenomenal
51:28job.
51:33And, and really,
51:35I I wanna highlight a
51:36couple of things. One is,
51:39I hope you realize this
51:41patient
51:41could have easily died
51:44in the out in an
51:45outside hospital, and in many
51:46cases, would
51:48not do well.
51:49And so this really highlights
51:50the power
51:52of our health system,
51:53of our expertise
51:55across
51:56we have four different subspecialties
51:57identified here in this front
51:59row
52:00and,
52:00and and the command of,
52:03of of this,
52:04of their knowledge. And I
52:05think it's just really wonderful
52:07to see. So, really, just
52:08a comment in general.
52:09You know, when I I
52:10had the,
52:12you know and John might
52:14add some comments after this
52:15after Stefania's question, but and
52:17and, Jeff. So I think
52:18this brings us back to
52:20trying to understand first principles
52:21and mechanisms a little bit
52:23because,
52:24you know, the there was
52:25a couple elements that I
52:26recognized, and I'm, you know,
52:27no expert here, but was
52:29probably there's some baseline microaggressation
52:31that's increasing LV out to
52:34LV pressures.
52:36That changes our the the
52:38limit
52:39the wall stress in general.
52:41And what was happening likely
52:43was that this person was
52:45getting increasingly ischemic even though
52:47they had epicardial
52:48normal coronary arteries
52:50because of the fact that
52:51wall stress was increasing and
52:54endocardial
52:55perfusion was decreasing.
52:57And troponins were elevated, BMPs
52:59were high,
53:00and
53:01some of the natural instincts
53:03of how we approach these
53:04patients could have only made
53:06that worse. Right? And so
53:07you had to, you know,
53:08kind of modify it. So
53:10in six years sitting on
53:11the myocardial sphemia and metabolism,
53:15study section,
53:17and I inherited that seat
53:18from Larry Young, who I
53:19didn't know really well before,
53:22I would say that
53:23pretty much on every
53:25meeting there were several
53:27outstanding,
53:28and smart
53:30submissions
53:31on the role of catecholamine
53:34excess,
53:35as a mechanism
53:36for stress carboxy. But to
53:38my knowledge,
53:39we still don't know exactly
53:42the the mechanism
53:43for stress carboxy.
53:45And so I'm curious, you
53:46know,
53:49since this case really demonstrates
53:50this ability to use multiple
53:52subspecialties and get through challenges,
53:55in the ideal world, and
53:56this is to maybe to
53:57you guys, Lou,
54:00what kind of, if you
54:01were able to sample
54:03in real time to try
54:05to understand
54:06mechanistically what was happening for
54:07this patient,
54:08and then that might drive
54:10decisions around beta blockade or
54:12other things,
54:13what would we have done?
54:14And so that's kinda just
54:15let's throw it out there.
54:16But maybe I'll give this
54:17to Stefani to ask your
54:18question and maybe John and
54:19Jeff's and maybe Jeff and
54:21others, Rachel,
54:22answer.
54:24Thank you very much. It
54:25was an amazing presentation,
54:27very digestible
54:28also for non clinician.
54:30Yeah. So, actually, related to
54:31that particular question, at least
54:33in in
54:34in mammalian
54:35model is being shown that
54:37aging,
54:38create denervation of the heart
54:40via a mechanism by which
54:42the vascular cell produce
54:44this narrow repellent molecule, semaphorent
54:47three, and then kick the
54:49neuron away. And we don't
54:51know why
54:52that happened in a natural
54:54aging environment, but I was
54:55wondering if patients
54:57that are subject to this
54:59stress induced might be indeed
55:00have a different mechanism
55:02by which
55:03they actually maintain a lot
55:05of innervation.
55:06And, therefore,
55:07when they're under stress, these
55:09nerves start to act in
55:11a bizarre way. So
55:13one way could test again,
55:16measure blood
55:17of this type of molecule
55:19that are important for regulating
55:21neuron. Science fiction, but maybe
55:23some idea. Yeah.
55:26I wonder too if,
55:28that could be connected at
55:29all to sort of the
55:31hormonal and biochemical milieu of
55:34postmenopause
55:35as well since we aging
55:36and postmenopause
55:37are together in
55:39in those patients present with
55:41stress cardiomyopathy.
55:42So
55:44Wonderful presentation. Thank you. You
55:47had mentioned that there was
55:48an old left bundle branch
55:49block. And I was wondering
55:51about your thoughts on the
55:52etiology
55:53and then whether it contributed
55:55to the the current acute
55:56picture.
55:58Yes.
55:59So, I think it
56:01if you wanna say something?
56:02I was so I I
56:03had his first
56:44Right. So if someone's sick
56:46with a love bundle,
56:47you gotta come in. And
56:48and for what it's worth,
56:49the the change that we
56:50made was also informed by
56:52my experiences as a fellow,
56:53and I know you guys
56:55have had the same
56:56experience where the patient comes
56:58in and you're trying to
56:59do the right thing, and
57:00you know how to manage
57:01cardiogenic shock, and you're trying
57:03your focus, and you're like,
57:04am I looking at a
57:05MR gradient? What am I
57:07looking at?
57:08I just simply remember second
57:09year calling one of my
57:11attendings and being like, no,
57:12no, that's the MR gradient.
57:13Stop doing what you're doing.
57:14So,
57:15you know, that's that's why
57:16we added that piece of
57:19struggling a little bit more
57:20Thank you. In
57:21the lab. Yeah. That was
57:23great, Divya.
57:24So the patient was started
57:26on metoprolol
57:27because we all use metoprolol.
57:30So
57:31any thoughts about using
57:33those beta blockers that may
57:35reduce
57:36beta adrenergic receptors,
57:38I. E. Those with intrinsic
57:40sympatomeimetic
57:41activity?
57:42And is there any data
57:43about that? Is this something
57:44that should be studied?
57:48I certainly think it would
57:49be interesting to study that,
57:51especially given what doctor Velasquez
57:53was hinting at with the
57:54catamaranergic
57:56surge that happens in Takacsudocardiography
57:58as one of the proposed
57:59mechanisms.
58:01I will say that I
58:02think that decision was more
58:04informed just by, you know,
58:05the evidence we have for
58:06guideline directed medical therapy, metoprolol
58:09succinate being one of those,
58:11but I think that would
58:11be very interesting to explore.
58:17So,
58:18that was an awesome presentation,
58:20and,
58:21again, congratulations
58:23on managing the case. I
58:24would never
58:26suggest that
58:28the
58:29positive
58:29outcome was luck. I would
58:32not wanna say that.
58:34But maybe a little bit
58:36you know, we've all seen
58:38a range of stress induced
58:39cardiomyopathy.
58:40Some people
58:41recover quickly,
58:43which I would
58:44suggest that this person
58:46recovered quickly from their stress
58:48induced cardiomyopathy.
58:50Some, it takes much longer.
58:51We've seen I've seen people
58:52in the neuro ICU
58:54that have had extremely low
58:56cardiac outputs for
58:58weeks, actually.
59:00And the problem here was
59:03that that this patient had
59:04a a fixed cardiac output,
59:06right,
59:07because of the outflow obstruction.
59:09It's like taking somebody with
59:11really critical AS and thinking,
59:13what can I do to
59:14help their cardiac output? And
59:15you have to relieve the
59:16obstruction.
59:18So in this case, I
59:18think the obstruction got better
59:20because
59:21the wall stress has improved
59:23and the stress induced cardiomyopathy,
59:27got better. I'm I'm wondering
59:29this is long winded, but
59:30I'm wondering
59:32if this was a big
59:33enough
59:34phenotypic subtype
59:36and some of these people
59:37actually didn't do well, did
59:39very poorly. Because as you
59:41as as you and Carlos
59:42correctly pointed out, there are
59:44very few of the usual
59:45maneuvers are gonna be helpful
59:47in this setting.
59:48Is I wonder if you'd
59:50even have to think about
59:52acute measures to
59:53relieve the obstruction somehow, and
59:55I have no idea what
59:56those would be. I mean,
59:58I don't think you're gonna
59:58do septal ethanol ablation in
01:00:01a patient in shock. You
01:00:02know? But but something to
01:00:04relieve the obstruction. Any any
01:00:05thoughts from the structuralist
01:00:07about that? Yeah. I think
01:00:08from from from the pharmacologic
01:00:10perspective. So the first thing
01:00:12we did was stop the
01:00:13debutamine. Right? So you're stopping
01:00:15the inotropic.
01:00:16And,
01:00:17we gave, I if I
01:00:18remember correctly, two liters of
01:00:20saline,
01:00:21wide open.
01:00:22And,
01:00:23we were ready to go
01:00:24on NEO, which is just
01:00:26pure alpha.
01:00:27So you're you're you're
01:00:29applying HCM principles
01:00:31into into this. In terms
01:00:33of mechanical relieving of the
01:00:35LVOT,
01:00:36unless you have something across
01:00:38the aortic valve into, like,
01:00:40an and and that's where
01:00:42that's where
01:00:43the non provoking LVOT gradient
01:00:45MCS comes into play, I
01:00:47e, the transvalvular
01:00:48pump.
01:00:49I I don't see any
01:00:51quick fix other than that.
01:00:53But I just wanted to
01:00:54ask Nikhil, from the advanced
01:00:56therapies perspective,
01:00:58you know, so this patient
01:00:59recovered relatively quickly, but how
01:01:01long do you wait
01:01:03on
01:01:03to pull the trigger on
01:01:05advanced therapies, and how do
01:01:07you list these patients? I
01:01:08mean, there is no special
01:01:09consideration
01:01:09for
01:01:11for,
01:01:13Takatsubo,
01:01:13or do you list them
01:01:15based on what devices they're
01:01:17on, if they're on any?
01:01:18Yeah. I guess you're referring
01:01:20if the patient doesn't make
01:01:21it out of the hospital
01:01:22or if they do.
01:01:24Yeah. I mean, I I
01:01:25think we would treat them,
01:01:28I guess, two points. One
01:01:29one was, you know, if
01:01:30if this patient is in
01:01:31some kind of shock spiral,
01:01:33and we're unable to get
01:01:34them out of it with
01:01:35medical or MCS interventions,
01:01:38you know, I I think
01:01:39that would become apparent relatively
01:01:41quickly. You know, it may
01:01:43be that a patient like
01:01:44this, you know, in that
01:01:46algorithm that you had nicely
01:01:47created gets escalated to like
01:01:49a VA ECMO.
01:01:50At that point, we usually
01:01:52do start the evaluation process
01:01:53if we think that they
01:01:55are
01:01:56a reasonable candidate for advanced
01:01:58therapies,
01:01:59based on other factors, including
01:02:01their age and and things
01:02:02like that, and and other
01:02:04disease.
01:02:06But I guess and the
01:02:07other point is, you know,
01:02:08we'll we'll talk as an
01:02:09interdisciplinary
01:02:10team. I mean, there are,
01:02:11I guess, to Jeff's point,
01:02:13potential surgical interventions
01:02:15that can relieve,
01:02:18mechanical obstruction. The Mayo Group
01:02:20has published on this in
01:02:21mid cavitary obstruction.
01:02:23There's a subset of HCM
01:02:25patients that have severe mid
01:02:27cavitary obstruction, and using an
01:02:29apical approach, they've been able
01:02:31to surgically relieve that.
01:02:33So if we believe that
01:02:34the single driving force is
01:02:35that ongoing obstruction,
01:02:37in the right, you know,
01:02:38surgical team's hands, there may
01:02:40be an intervention that we
01:02:41could do. But I guess,
01:02:42in answer to your question,
01:02:43you know, it we would
01:02:44probably list them like anybody
01:02:46else. And if they needed
01:02:47MCS, that would mean, you
01:02:48know, status two or status
01:02:49one.
01:02:51I just wanna,
01:02:52clarify.
01:02:53I would say it's not
01:02:54necessarily an apples to apples
01:02:56of saying a fixed obstruction
01:02:57like an AS.
01:02:59So at the time that
01:03:00Carlos did this cath, the
01:03:01patient was on five o
01:03:02debutamine. And so there is
01:03:03definitely, you know, as we
01:03:05see in the top left
01:03:06corner, this is where we're
01:03:07having the obstructions from the
01:03:09hyperdynamic
01:03:10base. And so we were
01:03:12definitely exacerbating it with the
01:03:14dobutamine increase. And that is
01:03:16the that is why we
01:03:17were getting the contradictory, you
01:03:17know, lab results. And that
01:03:17is why we were getting
01:03:18the contradictory, you know, lab
01:03:18results. And that's
01:03:19lab results.
01:03:20And that's why we saw
01:03:21those findings on this cath
01:03:22numbers was on five o
01:03:23two b. So a lot
01:03:24of it was androgenic and
01:03:26was us exacerbating the problem.
01:03:28And that's where Carlos has
01:03:29thought of doing the LV
01:03:30gram
01:03:32and getting that and getting
01:03:33those gradients across the valve
01:03:35showing that this is an
01:03:36obstruction
01:03:37is where it really revealed
01:03:38what we need to do
01:03:39and we need to reverse
01:03:40course, which is what he
01:03:41did.
01:03:42So maybe one last question
01:03:43from Aria, and then we
01:03:45can, close it up. And
01:03:47I mean, I have, actually
01:03:48question here, regarding your dumetamine
01:03:51because initially, actually, improved the
01:03:52blood pressure.
01:03:54When you put the patient
01:03:55up between, it it didn't
01:03:56improve it. And it's very
01:03:57in contrast with IP HCM
01:03:59because HCM patient don't have,
01:04:01you know,
01:04:02gargleone
01:04:03and hypercontractor.
01:04:05So maybe kind of my
01:04:08a little titering
01:04:09may actually help in this
01:04:10case. The second thing is
01:04:12that, Kay, what what Mehran
01:04:13actually mentioned, there are anecdotal
01:04:15report that beta adrenergic receptor
01:04:18are actually much more
01:04:20present in these patients in
01:04:21the apical region. So the
01:04:23catecholamine is not different. So
01:04:24if you look at the
01:04:25cases where people have been
01:04:27given by mistake adrenaline in
01:04:29by dentist or somebody, there's
01:04:30no basal,
01:04:33kind of preservation of the
01:04:34contraction. They have global. Everything
01:04:36is down. So this is
01:04:38not catecholamine itself, but actually
01:04:40responds to catecholamine.
01:04:41Oh, thank you.
01:04:43Well, I since the hour
01:04:45is at the end,
01:04:46I just wanna end with
01:04:48just a comment about our
01:04:49Wednesday education day and what
01:04:51a phenomenal capstone this is
01:04:52to the educational opportunities for
01:04:54the fellows. I'd like to
01:04:55congratulate the organizing team for
01:04:57putting together this great conference,
01:04:59the mentors
01:05:00for clearly being able to
01:05:02develop this really great discussion,
01:05:05and to Divya. I think
01:05:06there are two divergent audiences
01:05:08here. You have the ninety
01:05:10percent of the audience who
01:05:11thought this was a fantastic
01:05:12and unbelievable presentation and so
01:05:14well presented. And then you
01:05:15have your third year co
01:05:17fellows who are now,
01:05:18a little bit,
01:05:20upset because they have to
01:05:22live up to this bar,
01:05:23but I'm sure they will.
01:05:24So congratulations. We'll see you
01:05:25all.
01:05:26Thank
01:05:31you.
01:05:32Thank
01:05:35you. Thank you. Thank you.
01:05:36Thank you. Thank you. Thank
01:05:37you. Thank you.
01:05:39Thank you.
01:05:44Thank you. Thank you. Thank
01:05:46you so much. I really
01:05:47appreciate it.