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Hello, Card, and welcome. Welcome. Welcome. We are
in Rochester visiting University of Rochester Medical Center
and super stoked to be talking to Doctor
La, Doctor Sin O, Doctor Neil Gupta, and
we're gonna be talking about such an important
topic in cardiology. But before we start, team,
why don't we introduce ourselves. Go ahead. Hi
everyone. I'm La. I'm a Pg 4 first
year general cardiology fellow here at the University
of Rochester.
I grew up in the a great state
of New Jersey in stayed there at Rutgers,
Robert Wood Johnson for Medical School. I then
completed my controlled Medicine residency at Dartmouth Hitchcock
Medical Center. Now I'm super excited to be
here at the University of Rochester completing my
general cardiology fellowship. I'm interested in general and
interventional cardiology, and in my spare time I
enjoy running and cycling and I recently picked
up my guitar again after in long hiatus.
My name is Dion. And I'm the Chief
cardiology fellow here at the University of Rochester.
I actually grew up open Rochester and didn't
go too far for medical school at the
Jacobs School of Medicine at the University of
Buffalo. I did my residency in internal medicine
here at the university a Rochester, and I
stayed for fellowship. I'm interested in general cardiology
and echo. I'm happy to say that I'm
staying here as faculty for the next academic
year. In my time I enjoy exercising, cooking,
and hanging out with my family and friends.
Hi, everyone. My name Sin, I a third
year General cardiology fellow here at the University
overseer of Rochester.
I grew up in Toronto and went to
Med school at van University,
added my residency and internal medicine at Up
pm Pittsburgh. I will be sticking around with
the U of r for cardiology fellows hit
later this year, and this is also where
I was supposed to give a shout out
until the Cath out versus here below this
podcast, Dana and name.
In my spare time, I elected Cook and
listened to podcast, hope opioid more of the
true prime flavor than the medical kind.
Guys, That's awesome. Thank you and congratulations to
all the transitions that you guys are gonna
be having in your career right now. Super
exciting times and love the shout out. So
now let's get dirty and talk about some
cardiology, But before we do that, can you
take us to 1 of your favorite places
in the city? So we can settle down
and get ready to learn.
Well, absolutely. Well, seeing that it's almost the
summer, I think we should spend a nice
day out in the sun's sailing and pedal
boarding on Lake Ontario, followed by grabbing some
drinks and dinner by the waterfront.
Alright. Terrific. I've got my sunscreen ladder up.
And ready to go. So why don't we
dive into your case?
So we have a 63 year old man
with a past medical history of tension hyper,
and active tobacco use who presented overnight to
our emergency department, but a chic complaint of
sun onset schultz breath. The patient say that
he was in his usual state of health
when he suddenly felt short of breath earlier
this afternoon. He denied any chest pain or
pressure in hours to days prior to of
shortness of breath. But did notice some mild
chest pain described as mitt stern, non radiating
and non exert
that get shortly upped he'd be down feeling
disconnect. This history, Dad is always nov for
or would you take... I'm unloaded paint 5
milligrams
and hydro like 25 milligrams, hyper
for which she takes a to 20 milligrams
and ge for which she takes Ol
20 milligrams. He has never had any surgeries
as no allergies and no family history, of
coronary artery disease or sun cardiac.
Harmful charlie late, she does still smoked tobacco
but denies any other recreational substance abuse. What
would be your differential for some shortness of.
The differential for shortness of breath is quite
broad as you can imagine. I like to
distinguish however between a acute versus chronic causes
of shortness of breath. Fortunately, the differential for
acute shortness of breath is a bit more
narrow, and I like to break these down
into 2 buckets. Cardiac and pulmonary.
The big cardiac causes of sudden onset shortness
of breath include acute, coronary syndrome, heart failure,
and peri t.
Meanwhile, pulmonary causes of acute onset shortness of
breath include. Of course, pulmonary embolism as well
as pneumothorax,
Bro bass such as from Copd or asthma
and pneumonia.
Now, based on the patient's initial presentation, What
do you think the likelihood of a q
coronary syndrome miss? That's a great question, Neil.
I actually think a pulmonary embolism would be
higher on my differential just based on the
very limited information we have so far. A
acute coronary syndrome is certainly possible, but the
presentation of sudden onset shortness of breath. Followed
by somewhat mild chest pressures would be more
atypical of Ac acs. But now that we've
gone over his initial presentation, Let's refine our
differential diagnosis a little more. Sin, can you
tell us about the patient's vitals, physical exam,
and labs?
Sure. The patient has tachycardia at 01:30 beats
per minute with a blood pressure of 01:26
over 76.
He is a feb 95.9
fahrenheit.
His respiratory rate is 20, but he's already
a non breather mask with a flow rate
of 15 liter per minute and a hundred
percent oxygen. Sat 98 percent on this. He
later had to be placed on bi.
His exam shows a patient moderate distress without
nr rem mask on. And diffuse crackle.
His cardiac exam is limited by significant tachycardia
with no obvious memory appreciated. He has no
fetal edema and is warm.
Gi exams in soft non tender non abdomen,
and he has no focal findings on neurologic
examination. His D is fairly un remarkable aside
Cr Hong 0.1, which is at his baseline,
and his Cv is most notable for a
White Count of 13. His proponents are elevated
on dynamic at 5 70 to 08:01
nano per liter.
At our, 14 or stop thinking the bad.
An Nt prob B p is 09:48 kilograms
per ml, which is mildly elevated for our
assay
with 900 being the upper limit normal here.
D dime is Elevated 2.2.
Ab g on Nr shows ph 7.33,
Pc o 2 of 38,
Po 2 of 82,
of 19,
and an arterial lac of 2.2.
Upper normal b 0.8 mel per liter here.
La fawn, can you describe the patient's initial
chest x ray and Ekg?
Sure, Sin. So this chest x expert is
a frontal projection, and immediately we can see
diffuse bilateral
interstitial and aerospace capacities.
While there's also
civilization of the pulmonary veins, we do not
see enlargement of the cardiac silhouette.
Overall, this chest x clearly points to sense
of pulmonary edema. Now to go over the
patient's Ekg.
We can see the patient is in sinus
tachycardia at about a rate of 130 beats
per minute. There are T wave inversion in
lead 3 and Av f, as well as
about 0.5
to 1 millimeter S elevations in leaf 3.
And about 0.5 millimeter s elevation in the
lead Ad.
We can also see a deep qa win
lead 3, but it should be noted that
this can be a normal variant.
So certainly, we're worried about ischemia given this
dj, though it does not quite meet the
stem criteria.
Now, Sin enough, how do these initial labs
and diagnostics change your differential diagnosis and what
would be immediate next steps.
The chest x ran B along with his
d
or suggestive of congestive heart failure ideology of
his shortness breath. Although it's interesting that he
has no edema on exam,
which starts making us think about maybe an
acute el dysfunction process or left sided val
issue us the ideology.
The highly elevated dynamic conan raise a question
of an Mi as 1 possible cause. All
of the Ecg not fully consist with stem
as La pointed it out. Flash pulmonary edema
from hypertensive crisis can present similarly.
Although he's not hypertensive at this time. Pulmonary
embolism can't be begin considered as well given
the elevate d dime, but the level of
triple troponin elevation is a bit atypical for
those, and the level of
can be explained by the pulmonary edema
without invoking Pe.
The elevated latitude suggest hypo perfusion, which any
of these can lead to. In a case
like this where we up to separate information
and a presentation that is outside typical norms
or 1 pathology, a point of care ultrasound
can be helpful.
My threshold threshold for obtaining a Ct protocol
is also low these situations, which is what
the val team ended up doing.
Neil, can tell us will be saw in
Ct.
Our Ct,
chest did not show any evidence of pulmonary
embolism or aortic dissection. Is there anything else
you can do at bedside to help hone
your differential file? I think at this point,
we should get a point of care ultrasound
or focus on this patient as we worried
about d heart failure. This was done which
showed quite dramatically a hyper
L.
That's a great idea with the focus of
fan Good job. Obviously, as this modality becomes
more available and with handheld machines becoming more
advanced, We should really be incorporating this into
our daily practice. Do these findings help narrow
your differential fund?
Oh, absolutely, and that's a great point you
make meal As bedside Focus is incorporated more
and more and medical training, we all should
try to do at least a quick focus
on most of the patients with see in
cardiology.
When we see a piper dynamic L in
combination with evidence of ischemia on Ecg,
an el opponents
Our concern now is an acute myocardial infarction
resulting in possible mechanical
complication.
This is an amazing conversation, and I definitely
wanna just jump in and add to this
idea of Poke is that Poke is such
a valuable tool in this particular scenario where
you really wanna find out what's going on
under the hood And I think when you're
using point of care ultrasound or any echo
in general, you wanna have 2 kind of
philosophies. 1 is to be systematic and approach
a cardiac exam in a way that's thorough
and the same every time, and that will
allow you to capture all of the images
that you think are going to be helpful
for most patients. And not miss something by
jumping around in the exam and anchoring on
a particular diagnosis. But at the same time,
before you approach the patient focus, you should
ask yourself, well, what do I expect to
see from this patient's clinical presentation? Like, what
am I gonna be saying? So I have
a patient here who is not doing well,
they're in frank pulmonary edema, I may expect
to see really reduce left ventricular function. And
when you put that echo probe on them,
and you see this hyper dynamic function as
you guys described. Right? That is telling you
a very important piece of information. You're saying
this hyper contract left ventricle does not match
this patient's overall clinical presentation, something something is
going on here. And I may not have
captured all of the heart yet on the
echo imaging, but I'm now suspicious that while
the left ventricle is showing us an elevated
ejection fraction, much of that blood may be
going backwards. In fact, we know where it's
going. It's going back to the lungs resulting
in this crazy presentation of pulmonary edema, and
contributing to the patient's, primary symptoms, which is
respiratory
complaint and everything is starting to make sense.
And so I love that you now pivot
it to say, well, is there a mechanical
complication going on here, such that we are
not having
adequate forward flow out of the L t
out of the aortic valve into the order
per perfusion the body, but rather going backwards
perhaps and this may lead us to the
diagnosis for this particular patient. So I just
love how you were able to recognize what
you were seeing on focus and pivot to
further the care of this patient 1 last
point about focuses is sometimes in the moment,
we are not able to capture everything because
we have to tend to the patient's clinical
needs. They're hem compromised But sometimes when the
dust settles, we can get in a formal
echo, and that kinda will fill in the
pieces and the gaps and help us recognize
what is going on with the patient and
the guy next step. So Did you end
up getting a formal echo after this point
of care ultrasound? Yeah.
Absolutely. Thank you for asking. And what I
would say is what we first notice there's
a hyper
of 80 percent, kinda like what La
notice on his focus
with a Pd distribution wall motion have morality.
There was normal Rv, size and function with
an estimated mildly elevated Rbc systolic pressure of
40 millimeters of mercury.
There was noticeable pap muscle rupture
with a fl anterior much leaflet with posterior
directed much of regurgitation. The reg tent volume
was 77.5
milliliters,
with a reg fraction of 64
percent. Based off of an L
and diastolic solid volume of a hundred and
60 milliliters
and an L and systolic volume of 39
millimeters.
Wow, a fl wet valve leaflet.
What a dramatic presentation?
It's important to remember that due to the
rapid
equalization of pressures
between the L and L.
Approximately 50 percent of patients with moderate to
severe acute
regurgitation have no audible murmur. Also, while mechanical
complications such as pap muscle rupture typically occur
in stem.
These complications can also occur, albeit much less
commonly in end semi.
Now, Sin, our patients of blood pressure starting
to fall too. What do you think should
be the immediate next step here.
The drop in mean arterial pressure reflects poor
forward flow given a severe
regurgitation.
Reduction is your friend here, but the hypo
is going to limit medical therapy.
As such, this patient needs mechanical circulatory
support with balloon of being to her modality
for many patients given the simultaneous
reduction and improved cardiac perfusion that this device
provides. Given that this is likely caused by
an Mi the patients should also have coronary
and geography have right for catheter characterization. To
guide next steps. The cardiac surgery team should
also be contacted sooner rather than later so
the patient can be evaluated for valve for
hair slash replacement.
And that's exactly what happened next. S, can
you describe for us what was seen on
cardiac catheter authorization, definitely.
So for initial stabilization, the Icu, the patient
had a balloon called place at that bedside
via the right frontal artery. He was then
sent down emergency to the cath lab. White
court capitalization there showed Cd of 9,
K pressure of 55 over 19
and wedge pressure of 17.
With the cardiac index of 1.4.
This was worth 1 1 balloon web support.
When the balloon pump was turned off temporarily
the white tracing showed large b waves to
40 millimeter
of mercury,
which again confer severe mitral regurgitation. Given that
the low Cardiac index, despite Iv p support
suggested that the Iv support was insufficient, the
patient was upgraded to imp Cp.
With subsequent juvenile cardiac index to 2.2.
Now that the patient was more stable,
we proceeded with coronary and geography.
We start out with views of the right
coronary artery.
There's an all plaque in the mid Rca,
which is not flow limiting.
It's about 60 percent stenosis severity. The patient
has a right dominant system. The left main
and left ci look pigment without obvious disease.
The mid Led, however,
has a very tight tubular lesion right after
to take off the first eye will Timmy
1 flow beyond it. Best shield in the
A cra view. We also see faint left
to red lateral.
So there might be a distal or obstruction
that will not
appreciate an year. The patient with then taken
for a t
meal. Can you describe what we saw?
Of course,
Rt T was performed at bedside in the
Cbs.
The L function was normal with basal to
mid infer wall motion at in.
The posterior media pap muscle was rupture served
with small segments of the 8 pure muscle
leaflet float of the 828
sc
leading to mitral valve non.
There was severe, posterior directed mitral
regurgitation with systolic flu reversal seen in the
pulmonary vein. The V contracted looked on the
color doppler measured at about 1.1 centimeters.
The imp was positioned approximately 3.2 centimeters from
the aortic valve and as well.
Neil, now that we have visualize our flow
mitral on both tint
and tu.
Can you describe for us what are the
echo
parameters of acute bi of regurgitation? Great question,
there's actually a lockdown down pack air, so
please bear with me.
Typically, patients with acute severe mitral
regurgitation are really really sick. So proper recognition
and diagnosis is absolutely.
Echo parameters used to diagnose a Qm mr,
opposed chronic Mr are actually pretty similar.
However, there are some ways to help differentiate
the premise of the.
For first, the clinical presentation is so so
controlled in these patients. As they usually have
some analysis h from pulmonary edema.
And they usually our hypo times, which is
a marker of cardio cell. Patients with chronic
mr typically have an insidious onset of symptoms
over time. Chronic Mr is also associated the
left ventricular
and left updates they'll dilation with a acute
mitral regurgitation The heart doesn't have time to
remodel, and these chamber sizes are usually more,
fairly often, patients with a Qm mr have
a hyper contract l.
As blood can now travel to a low
pressure left atrium opposed to the au. Also
a fill mental valve leaflet or pap muscle
rupture
is usually specific for acute much.
There are several quantitative
factors something we at with which to include
mitral pathology,
color doppler,
regurgitation flow as well as continuous wave out.
Echo parameters of severe mushroom
regurgitation
include a large
volume that greater than 6 see mode.
And a
regurgitation fraction of greater than or equal to
50 percent. The reg volume is the amount
of blood enters a left atrium
systole from the left function function. This is
obviously add. This is because
flow will follow the path to least system.
So prefer to enter a low catcher left
atrium,
poster a high pressure aorta. So considering a
normal stroke volumes 50 to a hundred milliliters
I reg volume of 60 milliliters is quite
a.
Reg it in fraction is simply the ratio
above that enters a left h atrium
divided by the total amount of log that
the L pumps out. So are there to
be severe much of regurgitation At least 50
percent of the blob that is pumped from
the left ventricle
is actually going backwards into your off trip.
This may be useful in their acute mi
and the L of not dilate, and volumes
actually are increased. Color doppler is another extremely
useful tool as it helps so the direction
motif the regurgitation. Whether it being posterior,
anterior or central. If there is a pathology
involving 1 of the leaflets, the color flow
is usually directed in the opposite traps.
Looks like our patient care who in a
fall anterior pulp. His jet direct posterior. Typically
severe Mr has a large colored boxer
which usually league encompasses at least 50 percent
of the lost train. Well this may not
be the case in patients with very eccentric
judge. Additionally, all doppler usually allows for
identification of slow,
which is typically referred to as proxima iso
velocity surface area. Or more simply put peace.
This can lead to the calculation of the
and vulnerable and measurement of law effective,
tent or area,
or the r pit. This is essentially a
measurement of the area that the soul travels
it. So the bigger the hole, the bigger
the leap. And ERA
greater than or equal to pump 4 centimeters
square is associated with severe much. Furthermore,
appease all of greater than Or to 1
centimeters
that Nike was limit of 30 to 40
centimeters meters a second. Is associated with severe
always well.
Lastly,
Avi contract a measurement of the smallest portion
of the mr set. And the value of
greater than 0.7 is a marker of severe
mr. Continuous way doppler also helps the diagnose
severity electric
vegetation. The C w can be traced and
use of to reg tint volume
cross the module valve will the quotation of
the continuity.
Assessment of the pulmonary veins is also so
shit. The Atrium are diastole during ventricular.
So blood flows in the pulmonary veins enters
a left atrium bearing system.
Severe mitral
regurgitation causes his blood to reverse and now
what leaves the left atrium and enters the
pulmonary vein dry.
This typically referred to as pulmonary veins the
solid soul aerosol and is usually path
for severe much phase.
Thanks for that incredible
explanation Neil. I know I definitely will have
to go back to listen to that segment
again, just to make sure I got everything.
Sin, can you tell us about lip path
of pap muscle rupture and how can this
be explained by the patients left heart catheter
characterization findings?
At the risk of overs simplifying things and
ob upsetting na compressors throughout a country, normal
left ventricle has 2 pap muscles. All the
lateral and the poster media
muscles given their locations. Each pap muscle has
chord connecting to both leaflets of the mitral
valve. On average around 62 of such chord
for pap muscle. The pap muscles actively contract
just before the rest of the ventricle eventual
and by cooling on the 4 day, prevent
the mitral valve of leaflets faint laps when
the left ventricle contracts. If the woods applied
to pap muscle is abruptly cut off, and
there is little no lateral lotus p as
is often in the case in a stem
The cells in the pap are muscle become
nec and in 2 7 days to structural
integrity of the pap muscle is reduced. If
the L function is preserved or even hyper,
the movement of the my
compounded with tension from the 4 day exert
eye shea stress onto dysfunction pap muscle. Leading
to a complete or
tear depending on situation. In fact, most cases
of pap muscle rupture or associated with a
small amount of ischemia and the left ventricle
overall. The post
pap muscle receives all of its blood supply
from the Pd in most people.
While the lateral pap muscle receives it from
the La, usually the first dia and the
left ci flex, usually the o 1. As
such, hosts media pap muscle tears are sister
12 times as common as unilateral. But again,
given how the chord connect to the leaflets,
This can sole affect both leaflets of the
mitral valve. Without the pap and muscle t
into leaflets, the lift of can pro during
ventricular systole.
Causing severe mitral
regurgitation. Additionally, given that many of these patients
also have Rb infarction from an Rca obstruction
that the R can become older overwhelmed by
the reg slow, leading to a death spiral.
In this particular patient, While we do not
see obvious or say obstruction, the presence are
left to right collateral as well as basal
to emit
and inferior walls hypo on goal suggests that
either a small vessel from the Rca was
obstructed at the time of the Mi and
no longer visible on geography.
Or goes a transient occlusion of the mid
Lesion that has sims spontaneously
rec.
Is important to keep in mind that up
to 30 percent of stem have spontaneous re
rationalization. And the all appearance of the Rca
plaque could suggest that this was a culprit.
I think it is less likely that the
tight La lesion is solely responsible for what's
going on here, although given that the La
is speeding the collateral. Is certainly possible that
there was a multi fit event here. I
should add that other possible ideologies of pap
muscle rupture include 1 chest formal, although that's
classically near for the tri valves muscles, endo,
cocaine abuse, and of course,
ideologies. But it doesn't seem like any of
these were the case here.
That's a very interesting proposition for the mechanism
bleed to this patient's pap muscle rupture. Now
that we know what is going on with
our patient and also have an idea how
it happened. She, can you take us through
the management for a acute mr due to
pap muscle rupture?
Ultimately, this is a mechanical problem and requires
a mechanical solution. Pac muscle rupture is 1
of the indications for cardiac surgery in the
setting of stem. Given that has an 80
percent mortality in the first week if Treated
and performing con complement cabbage as a classroom
recommendation from the Acc and Aha.
However, the patient does need to be brought
out the shock state as much as possible,
and this is where mechanical circulatory support as
a role. This is a class 2a way
recommendation by the Acc.
While being optimized for surgery, the patients should
be on aspirin and an Iv anti clyde
such as heparin.
Invasive hem with swarm gan catheter, and arterial
line can also help with titration thrusters,
probes and diuretics, and until attempts.
And when it comes to surgery Scene, is
there a difference between repair or replacement of
the mitral valve?
It's an excellent question.
While in most primary, much regurgitation disorders
repair as preferable to replacement, calculated and muscle
rupture is rare enough that we have no
strong evidence based to guide us. The major
arguments against repair or that edema, tissue necrosis
and lack of tens cell strength in the
recently ischemic my and pap muscle,
mean that the repair might not hold, and
a patient will have recurrent severe much
regurgitation, requiring repeat surgery. As such, a coral
bearing Mitral Valve basement strategy might be superior.
According to 1 analysis of the Sc sds
database and 20 11 to 20 18, 79.8
percent of patients receiving mental valve surgery or
pap muscle rupture have mental valve replacement. And
the rest have repair. So in day day
practice, it does seem that replacement as preferred.
I should note that the database does not
have enough granularity to make conclusions on the
type of pap muscle
I. E. Was it partial or complete and
a type of surgery, but it does show
that the patients who received replacement
tended to be more in a cardio shock
state, higher of f
essentially be more sick overall.
Would suggest that these were likely the complete
terror patients were received replacement.
And how about Trans catheter interventions?
Given that most of these patients are very
sick, often requiring a academy support on pressures,
it would be great if there was a
trans
solution to offer this population. Either as a
destination therapy or as a bridge surgery when
the patient is more optimized, I e, no
longer in an acute shock or an acute
Mi state. Currently, around half of all patients
presenting with pap muscle rupture are not offered
surgery due the prohibitive of surgical risk. As
a result, there are several case reports of
6 success whole trans for edge to edge
repair for these patients. Well the largest price
series out of scripts showed that while the
procedural success is there with significant reduction of
severity of mitral regurgitation, 4 of the 5
patients who receive the therapy still died during
that hospitalization. This probably reflects the fact that
these are very sick patients and did not
have many other options. Of course, even if
the ball standard treatment of surgical repair slash
basement of the valve con incompetent bypass drafting
around 10 to 40 percent of patients with
pap muscle rupture do not survive during hospitalization,
which is a sobering reminder of just how
much work has to be done here.
La fawn, metal, we've talked extensively about the
acute much regurgitation for pap muscle rupture
Kain take us through a brief overview of
the other mechanical complications of acute core air
syndrome.
Of course,
So the 4 major mechanical complications of an
acute myocardial infarction are acute modular regarded regurgitation
from pap muscle rupture, ventricular sep defect ventricular
free wall rupture and pseudo aneurysms.
I think it's important to emphasize that all
of the combinations have relatively high mortality rates.
Babylon muscle rupture we have already talked extensively
about. The ventricular sep defects occur 3 to
5 days after a trans mural in fact.
The clinical presentation can vary from just an
isolated murmur typically described as a heart, loud
hollow systolic murder heard best at the left
lower stern border all the way to cardio
shock. Echo will show a left to right
shu across the septum, right heart
authorization will show a step up in oxygenation
between the Ra and a Pa, as well
as an elevated Q.
Anterior and api Vs are typically caused by
Led and forks, while posterior Vs are associated
with inferior in Spark. Ps are generally managed
by initiating after load reductions such as with
an intra aortic balloon pump followed by urgent
surgical or per subcutaneous repair. Next, we have
ventricular free wall rupture, which presents with elevated
Jb d, muffled heart sounds, and Pulse paradox.
As blood comes in contact with and irritates
to peri, the patient's Ekg can show nude
Elevations. As you can imagine, these cases of
very high mortality rates, and the management is
emergent surgery. Lastly, we have pseudo aneurysms, which
Unlike the others typically present weeks to years
after in fact. Pseudo aneurysms occur when a
cardiac rupture is contained by the peri adhesion
And a most commonly involves the inferior or
lateral walls, as anterior wall rupture are more
likely to cause massive hem peri and immediate
death. Patients usually present with shortness of breath
or chest pain, but can be asymptomatic. Diagnosis
involves the use of multiple imaging modalities such
as echo,
which can demonstrate pseudo aneurysms with a narrow
neck. Once diagnosed, pseudo aneurysms should be urgently
repaired due to a high risk for rupture.
So La, tell us, what about happening of
our patients?
I'd be happy to. It certainly scary managing
such a sick patient who was deteriorating
overnight. Ce presented with such significant pulmonary edema,
he was immediately started on wide pop with
positive pressure ventilation, hoping to reduce his L,
preload and after load. As if blood pressures
began to drop norepinephrine was started. Cardiac Surgery
was console consultant and an intra aortic balloon
was placed at bedside. A cardiac customization was
performed during which the intra aortic balloon pump
are removed and replaced by an imp. The
patient ultimately underwent a successful tissue mitral valve
replacement and cabbage with Lima to the Led
and diagonal.
He could occasionally to do well several months
out from surgery with no much regurgitation on
echo.
Man, I'm so glad this patient had a
good outcome, especially after Sin gave us all
the mortality with this complication of Mind.
Thanks for joining us through the case. Fun.
Thanks everybody.
La. Sin, and Neil, what a crazy case
and an amazing salvage, and I'm so glad
that you're patient is doing well. You took
us from a chief complain of D and
uncovered real bad within this heart, acute pap
rupture, which as you pointed out just generally
has an ab invisible prognosis, but it sounds
like with a rapid escalation of care. In
this case, mechanical circulatory support when a medical
therapy was failing, quick recognition of the pathology
and then a great treatment plan with multi
disciplinary team. Your patient actually had the outcome
we pray for when we have patients like
this. So thank you so much for walking
us through the case giving us an overview
of mechanical complications in Mi, and it's specifically
a deep dive in pap rupture with acute
mitral regurgitation. And I definitely appreciate that deep
dive into the echo findings these because that
can be very helpful. In this case, and
as well as in all cases of mitral
regurgitation. So thank you, team. You did a
stellar job, what a master class presentation. Thank
you so much for having us.
And now for the that's for cardio perspectives
and review segment for this episode, we're excited
to introduce doctor Jeff B. He is a
interventional cardiologist here at the U r that
we all love working with. He's also associate
program director of our interventional fellowship as well.
And we're excited to say that he won
the teacher of the year award this year,
so really excited to have him on our
podcast today.
Everyone. This is Jeff B. I'm 1 of
the interventional cardiologist from strong,
C Hospital, And I wanna say thank you
to our fellows for inviting me to participate
in this discussion of this great case. So
thanks everyone for having me.
So this gentleman had a relatively dramatic initial
presentation and This is a circumstance where he
need to be able to think on your
feet to sort of, quickly narrow down the
differential diagnosis
because some of the issues that could be
going on or potentially immediately life threatening. So
you really wanna focus on things that you
would need to identify an intervene on quickly.
I agree that based on the
description of the patient's symptoms,
pulmonary embolism would be a top of the
list in terms of concern
The 1 thing that you have going against
that is the significant amount of pulmonary edema
that the patient is exhibiting both on physical
exam as well as on his chest x
ray pulmonary edema is a relatively uncommon finding
and pulmonary embolism. And so
that's something that I would really you know,
sort of push me to look for alternate
diagnoses.
On similar lines, I wanted to make a
comment on the use of a d dime
in this clinical circumstance.
Which I think has limited clinical utility. D
dime is really useful in somebody,
who has low risk pulmonary embolism
you're looking to rule out pulmonary embolism,
finding of an elevated d dime in in
someone who
has multiple clinical signs or symptoms consistent or
potentially consistent with a pulmonary embolism.
The finding of a, negative d dime is
not gonna do much to sway you away
and the finding of positive d dime is
not really gonna change your clinical suspicion at
all. So,
you know, electing to obtain a d dime
in the circumstances,
really gonna be not a much clinical utility.
Based on the review of the patient's vital
signs, I think it's readily apparent that this
patient is in
in pretty bad shape,
the 1 thing that's
especially concerning is the patient's heart rate of
a hundred and 30 beats per minute in
sinus tachycardia.
Residents of sinus tachycardia and somebody who you're
evaluating for either pulmonary embolism or
an acute coronary syndrome
really carries with it a lot of pro
weight and can be used to identify patients
that are at higher risk for,
acute d compensation during the course of their
illness.
In this patient's particular
presentation,
the decision to get the Ct,
I'm not certain I would have
perform the diagnostic work up in that order.
As I mentioned before, the finding of pretty
significant pulmonary edema it's
severe enough to impact the patient's ability to
oxygen would really argue view against the thrust
of the Pe.
I think, you know,
a quick, point of care ultrasound as the
team ended up doing,
would be 1 way to really,
really sort of narrow down the diagnostic
picture to either right or a left side
and issues without the need for obtaining a
Ct scan of the chest, which is gonna
carry with it. Pretty significant contrast load that
you may want to utilize doing something else
like potentially looking at his coronary arteries.
Point of care Ultrasound can definitely be a
great bedside diagnostic tool. Point occur Ultrasound machines
on the market are continuing to improve. And
becoming more widely available.
The quality of the machines and some circumstances
can vary pretty widely. So the older machines
did not have the ability to measure doppler
waveforms or get good color doppler.
So in some circumstances that can really limit
your ability to evaluate for some processes.
In this case, for example, would have been
very useful to have, the ability to have
color doppler over the mitral valve that would
have major diagnosis
immediately and showing you this if you're mitral
regurgitation, whereas, you, you know, without collar doppler.
You're really left with trying to make some
determinations based on the hyper day ami y.
Who would definitely agree that using point of
her ultrasound just like any ultrasound, more modality
and formal echo cardio really need to be
very simple
systematic and thorough and do your same exam
the same way every time.
The other thing that's really important to keep
in mind is that
point of care Ultrasound is gonna be very
good at finding findings that are there. I
think it's less useful,
you know, for ruling things out. You know,
I think you need to be careful about
completely excluding
certain diagnoses just on the presence or absence
of the findings based that point of your
ultrasound due to some of the limitations quality
of the device. 1 thing that I would
add about this patient's, treatment course is that
you know, some patients like this
useful to have a low threshold for invasive
assessment of hem thermodynamics, you know, taking the
patient like this to the Cath lab might
allow you to make a more rapid diagnosis
of this problem.
Especially with the used of ventricular
you could pretty quickly see that there's severe
mitral regurgitation. And,
the ability to obtain a rate heart count
authorization allow you to measure the cardiac output
and another hem parameters would get you a
way to risk strat him and and to
help you decide
which kind of mechanical support strategy would be
best for this patient or if he needs
mechanical support and all. I think this is
time to bring up the idea of a
balloon pump super responder. So a balloon pump
although, in most patients does not provide additional
cardiac output that would be sufficient to resolve
shock states,
in certain subgroups of patients,
there been identified groups of of cases where,
patients may have a an exaggerated hem
response to balloon pump and, keep mitral shoulder
regurgitation is 1 of those circumstances
where,
simply by, you know, improving the patient's after
load, you can result in the and the
substantial improvement in patients for cardiac output. The
other group of patients that tend to be
building from super responders or sort of normal
intensive cardio gen shock patients,
that you see with
advanced cardiomyopathy my is to
wind up having a high map, so those
patients that have not yet gone into a
phase of dial state.
Those patients also tend to respond very well.
To pump counter polarization via the same mechanism
of vaginal load reduction. So you would anticipate
that this patient should have a pretty good
response to balloon therapy.
Although it turns out that he he didn't
actually have a complete response to the belief
And therefore was upgrading to more aggressive mechanical
support strategy.
And really in this circumstance,
pretty much any of the available mechanical circulatory
support. Et ideologies should make us substantial difference
in in terms of, improving an organ function
for this group of patients, either mechanical support
with an imp device as we ended up
doing for this patient versus using Va ecm,
if the patient is in especially bad shape
would would both allow for, adequate improvement patients
cardiac output. And some of that is gonna
vary, from institution to institution on availability of
particular support devices and practice patterns but really
any of the available mechanical support strategies would
would work for him. So the An in
this patient's is very interesting,
and that it does show had of an
ol plaque in the mid Rc, which looks
like it definitely could be culprit. Although has
kind of a torn up appearance with maybe
s t on top of it. The interesting
part is that the the vessel has,
Timmy 3 flow, and there's no abrupt vessel
cutoff off in any of the runoff territory
which you would expect for someone a completed
Mi. But I think the most likely scenario
is that he rupture to plaque either of
that that area or a a chunk of
t down dis into 1 of the board
distal coronary branches and far that territory, which
is now subsequently rec
clearly, based on the clinical scenario, you would
not attempt to rev
this already even though it's the pulp vessel,
because you are planning on likely managing this
patient surgical as the team will go into
in a little bit.
I would also disagree a little bit with
sin
characterization of flow in the Led, there's definitely
80 or 90 percent,
lesion following the take off a major diagonal
branch, but I'd characterize the flow as maybe,
T 2.
The flow does reach the end of the
vessel and it's
slower than normal. Although, not not
not totally normal. You know. I think it's
greeting Timmy flow is something that's very subjective
and you know, matters based on what's your
contrast flow rate and how long you stand
in the puddle. You know, in this case,
I I do think it's probably a little
better than taking 1. And then, you know,
again, the decision about whether or not we
re is that hurry is gonna depend a
lot on
what the anticipated surgical management is gonna be
hun leave alone for now.
I wanted to take a little bit of
a deeper dive into the idea of Pis,
which I find to be 1 of them
most fascinating concepts and echo
and
very creative use of what you normally think
of as an artifact.
So Pis is entirely based on color doppler
assessment.
Which is a variant of Pulse doppler. And
1 of the issues with Pulse doppler is
that there is a maximal
velocity that pulse wave doppler is able to
measure. And after that velocity,
the doppler will start to alias, which means
that instead of reading out a high velocity
it'll then become low again. The idea is
sort of similar to looking at a wagon
wheel on an old film. So if you're
watching,
you know, like, a covered Wagon go across
the desert covered Wagon wheels might actually look
like they're going backwards, and that's because of
the difference between the frame rate of the
film. And the speed of the wheel. And
so it's catching at just the right time
so that it looks like it's going backwards.
So color doppler because it's based on Pulse
wave doppler, you actually are able to measure
the alias thing velocity, and it's given to
you something called a ny quiz limit, which
is shown on a scale, usually at the
upper rates corner and the screen during your
cup computer color doppler assessment. And you can
draw out the limit
of where that velocity line
flips from
from 1 direction to the other.
The advantage of that is essentially you're now
able to calculate the velocity of blood in
all areas along the sphere as the flow
converge to go through the whole. So as
blood sort of lines up and gets lined
pass through the opening.
There's a period of
lam flow, and then the flow will become
turbulent.
And so in that region of lam flow,
the alias velocity will happen, you can calculate
the overall flow of blood in the dome
of blood that's made up by that. By
that Pis dom.
1 thing that I think is really important
to highlight about this case is the,
overall epidemiology of mechanical complications of Mi, which
are very
incredibly widely from institution to institution.
A lot of it is driven by patient
populations and abilities to access care, and we
actually saw an uptick in in the number
of mechanical complications that we were seeing during
the course of the Covid pandemic as patients
waited at home with heart attacks rather than
seek care immediately like they would have before
So it can be a marker of places
where there is,
more limited to access to care or more
difficulties than obtaining timely care for Mi.
We've also seen a number of mechanical complications
in younger patients who
ordinarily you wouldn't think of as being as
especially higher risk for,
like acute coronary syndromes, but
because that perceive risk is low, patients, you
know, don't
don't think that they're having a heart attack
and might wait to seek care. So we've
seen all kinds of mechanical complications and younger
patients as well, which is, you know, can
be very unfortunate very difficult for patients to
deal with.
The bottom line for dealing with all of
these mechanical complications is to have a high
index of suspicion for them as you bring
patients over to the cath lab. You know.
This goes back to this overall fundamentals,
you know, good physical exam, good clinical suspicion
can help you, more rapidly
identify these problems and that definitely changes your
management strategy
in the Cath lab or, you know, ideally,
for most circumstances, you'd be focused more on
rep reproducing the muscle. Whereas for someone who's
experienced a mechanical complication, the idea shifts more
towards institution or evaluation from mechanical support and
keeping them stable until they're able to have
a definitive repair for surgery. So, for cardiology
follows that are listening,
definitely, every single patient that comes to the
cath lab, you should be listening for murmur
very carefully. I know that's really difficult. The
emergency room work can be loud and there's
a lot of people around, but incredibly important,
particularly for things like ventricular simple rupture, which
are gonna be really, really challenging to pick
up on focus.
Without a careful color doppler
examination. Oh, thanks for our fellows for such
a great presentation, and thanks for inviting me
to lend my 2 cents to this conversation.
Thanks everybody. Bye
And finally, to close out this great episode,
let us introduce our cardiovascular
disease fellowship program director of Doctor Be Holmes.
So he can share his thoughts on our
program. He is an electro epidemiologist
and a great metric for every 1 of
us He's such a strong advocate for our
daily education, and we just love working with
them every single day.
Hi, everyone. I have Be hall, the program
director for the Cardiovascular
disease fellowship program here at the University in
Rochester.
Thank you, La sin and N for the
excellent presentation on a patient with acute pap
muscle rupture.
This patient was fortunate to receive such outstanding
care from all of you.
I learned a lot during this case presentation,
including the La placed that could tar, which
I did not know.
Our fellowship program at the University of Rochester
is truly Soc.
We see a wide variety of clinical cases
serving a catch area that extends down to
the Pennsylvania border.
With 6 fellows per class, our graduates pursue
advanced fellowship as well as academic and private
practice careers.
We have a very busy heart transplant center
and El program, and we offer extensive training
and critical care, including a 1 year cardiac
critical care fellowship.
Additionally, we provide significant research opportunities with 2
full time research faculty members.
Our location in Central New York gives fellows
the opportunity to care for patients in both
urban and rural communities.
We are excited about the upcoming fellow applicant
interview season this fall. And if you decide
to apply to a program, we really look
forward to meeting you.
Thanks again, and great job with the presentation.
Thank you for 20 n to this card
unit episode. The audio and editing for this
episode was performed by me Ot fe h,
I an in intern card Academy House in
Poland. And a research follow at the mayo
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