Case of Refractory Hypertension Controlled After Surgical Intervention

Case of Refractory Hypertension Controlled After Surgical Intervention


Our next speaker is
Dr. Mohammed Siddiqui from UAB, mentored by
David Calhoun. And this is a case of
refractory hypertension that was miraculously
controlled after aortic and mitral valve replacement
and coronary bypass grafting. So acclaim for the
surgeons, I guess. And Siddiqui will
explain the pathogenesis. Good morning. Thank you for inviting
us for do this CBC. So we have a case of
refractory hypertension controlled after aortic and
mitral valve replacement and coronary artery
bypass grafting. So me, along with Dr. Calhoun,
will be presenting this case. So we had a 38-year old
African-American man who came to hypertension clinic at
University of Alabama at Birmingham for uncontrolled
blood pressure. And he was first
seen in August 2011. So his blood pressure
was always uncontrolled. So we have a timeline
of his blood pressure from 2011 to 2016. And his systolic blood
pressure was around 150, more than 150. Diastolic blood pressure
was around 80s, but systolic was high. So an average systolic blood
pressure over these years was around 167 and
diastolic was in 80s. So the mean arterial pressure
was high too, in hundreds. So this is a case of
refractory hypertension. Refractory hypertension is
recently been evaluated as a phenotype of antihypertensive
treatment failure. And we, along with
couple of other centers, have been working
on these studies. Dr. Calhoun is my mentor, who
does refractory hypertension, and if he would like
to talk about it. Yeah, I just wanna …
We are very interested in these cases of really
antihypertensive failure. And, so, we have ongoing
protocol where we are trying to characterize
these patients. So I just want to sort of give
you that context of what we’re thinking about in general
about these patients. So, obviously, patients
are referred to us for uncontrolled hypertension. We’ll try to confirm
their blood pressure, usually with out-of-office
blood pressures we can’t… don’t do ambulatory
monitoring on everybody, just out of convenience. But confirm their out-of-office
high blood pressures. Our treatment approach,
I think, like most of us, is gonna be- initially,
is a triple combination of: a RAS blocker, calcium channel
blocker (in our clinic is almost always Amlodipine) and
then patients are typically referred to us on
hydrochlorothiazide, and some of the earliest
changes we make is switching them from hydrochlorothiazide
to the Chlorthalidone. So, that’s, sort of, our
standard triple regimen. We do screen them
for secondary causes. In our clinic, we get –
patients with resistant hypertension – we’ll get a
24-hour urine on all of them, looking at sodium, protein,
cortisol and aldosterone. And, obviously, get an
aldosterone-renin ratio as well. If there’s a high
level of suspicion, we’ll screen them for renal
artery stenosis by doppler, and then easily screen them
for Pheo by metanephrines. As a fourth agent,
we’ll add Spironolactone. And then, after that,
it’s sort of individualized. Or we typically will add a
combined alpha-beta blocker. We typically use
Labetalol, mostly, as opposed to Carvedilol. At least, we prefer to because
of the wider dose range. We can get to
much higher doses, which I think is
more effective. We’re, sort of, forced into
using Carvedilol more often now because it’s
less expensive, so often preferred by
insurance companies. And after that, we may add
a centrally-acting agent. We do use Guanfacine,
doesn’t do a lot. At least it’s once a day. We’ll try to use a Clonidine
patch, but also expensive. Then, lastly, add a
vasodilator – hydralazine. Again, we confirm
out-of-office blood pressure. They spend a lot of time
teaching patients how to measure their blood pressure,
encourage them to obtain a home blood pressure monitor,
and if we can, do the inventory monitoring. And then, obviously,
trying to exclude white coat. And then, lastly, adherence
is going to be an important issue in all these cases,
in this patient as well. So we will, obviously, try
to get an assessment by self-report, pill
counts if we can. We do ask them to bring in
their pill bottles at each visit, and look at
refill rates online, now, more and more electronically. We do have an ongoing
collaboration measuring urinary metabolites,
but it takes a while, so that’s not
clinically available on a case-by-case basis. So, I’ll let Dr. Siddiqui
take over now in terms of the individual situation
of this patient. So, since 2011, the patient,
when he first showed up at our clinic, he was on three blood
pressure medications: an ARB, a calcium
channel blocker, and a thiazide
diuretic. And then he was added
a spironolactone. Then, eventually, he was
added on a hydralazine, a vasodilator. And then the sixth
agent was Clonidine. So, this patient was
uncontrolled on six blood pressure medications. So, this was his blood
pressures: systolic blood pressure is high, and this was
the gradual increase in blood pressure medication, so over
the years from 2011 to ’16. So, the GFR – the kidney
function was good, it was stable. GFR was around 55- more
than 60 over these years. The average of creatinine over
the years was around 1.35. So, we evaluated for
secondary causes of high blood pressure, and the other
conditions that might be related to high
blood pressure. So, here, the normal HbA1c,
so diabetes was excluded. The secondary causes of
hypertension were excluded by doing a renal doppler. He did not have any
renal artery stenosis. He had a normal aldosterone,
a normal plasma renin, so hyperaldosteronism primary
and secondary was excluded. And he had a normal
catecholamines and metanephrines,
so Pheochromocytoma was excluded, too. So, the other
co-morbidities he had, along with high
blood pressure, was he had a mitral
valve regurgitation. So, he had a
Myxomatous/thickened mitral valve, which was dilated. The annulus was dilated 5 cm. So, he had a moderate to
severe mitral regurgitation, and the jet was
posteriorly directed, which caused the systolic
retrograde flow in the right pulmonary vein. The E/A ratio was 1.5. I have a video of the echo,
I’m not sure how to play this. So, I’ll just skip
over to the next slide. So, along with the mitral
valve regurgitation, he had aortic valve
insufficiency. He had a thick aortic valve,
he had moderate to severe aortic insufficiency. The jet was eccentrically
directed towards the anterior mitral valve leaflet,
and these are the echo videos, which shows the
blood backflow. So, what is the interaction
of hypertension and aortic valve insufficiency? Systolic hypertension causes
increased wall stress, increasing left ventricular
volume to mass ratio. The left ventricle adapts to
the volume of the load with increasing end-diastolic
volume, increased compliance, and increased hypertrophy. Which causes the prolonged
asymptomatic stability in these patients. There’s an increase in
compensatory preload, and a decrease in pressure
volume relationship or elastance. When the limits of
compensation are reached, it increases the wall stress,
and causes myocardial dysfunction and
systolic failure. And simultaneously, there’s
left ventricular hypertrophy and fibrosis, causing
diastolic dysfunction. And these symptoms include
those of heart failure and angina. So, what is the management in
patients with hypertension and aortic valve insufficiency? According to the
AHA/ACC guidelines, the treatment of hypertensive
patients who have chronic aortic regurgitation, the
systolic blood pressure should be maintained above 140,
that’s stage B progressive AR and stage C
(asymptomatic severe AR). The medications used here
are Dihydropyridine calcium channel blockers, or
Angiotensin-converting enzyme inhibitor (ACE), or angiotensin
receptor blocker (ARB). This is 2014 guidelines. The echocardiographic
findings in this patient: This patient had a normal left
ventricular systolic function, but a severe left
ventricular dilation, and the ejection fraction was
around 50 to 55 over these years, stable, and he had
a tricuspid regurgitation, and pulmonary
regurgitation, too. So, here is the patient,
he had a stroke volume which was high, it was 97. So, besides the mitral
regurgitation and aortic insufficiency, he also had
a coronary artery disease. So, left and right
heart cath were done. The left main artery
had a 60% stenosis, the left anterior descending
artery had an 80% proximal stenosis and a 60%
distal stenosis. The left circumflex artery
had a 40% calcified stenosis. Besides that, right coronary
artery had 80% stenosis and posterior descending
artery had 60% stenosis. So, the left and
right cath were done. The right atrial pressure
was 12, which was high. The pulmonary artery
pressure was high, too. The mean pressure
gradient was high, and the pulmonary capillary
wedge pressure was high. So, again, a video. So, what would be the
management in patient with hypertension-coronary
artery disease? So, the blood pressure should
be targeted below 140/90mm, should be below. And the management for high
blood pressure and coronary artery disease is
either beta-blocker, calcium-channel
blocker, ACE and ARB, thiazide and nitrates. So, this is according
to the guidelines. So, to summarize, we had
refractory hypertension patient who was
uncontrolled blood pressure. We did automated
office blood pressure, which was more than 135/85. He was on six high blood
pressure medications, including an ARB,
calcium-channel blocker, thiazide, mineralocorticoid
antagonist, vasodilator and centrally
acting agent Clonidine. Secondary causes of
hypertension were excluded. There was no renal
artery stenosis, there was no
hyperaldosteronism, there was no pheochromocytoma. He was non-diabetic, had a
moderate to severe mitral regurgitation, moderate to
severe aortic insufficiency, and a coronary artery disease. So, I would, if any
audience wants to pitch in. They are all coming
to microphones, there is lots of
-(laughs) comments. -lots of speakers. This is a very
interesting case. And I’d like to go back to the
average systolic and diastolic blood pressures in the office. So, it looked to me like this
was predominantly systolic hypertension and there
was a relatively low diastolic pressure. And I’d like us all to reflect
that in this patient who has major coronary
atherosclerotic disease, this patient may be at risk
for a myocardial infarction when the diastolic pressure
drops below filling pressure. So, one has to be very careful
and walk a tight line here until definitive
therapy is achieved. Hi, Rob Phillips. So, with this
particular person, even though the guidelines
give the opportunity to use beta-blockers, I would
not do that in him. I wouldn’t give him all
that time for filling. I mean, you’re really giving
him time to raise his left ventricular and diastolic
pressure with all that aortic insufficiency and he’s already
demonstrating that he’s not able to tolerate that, with
regard to diastolic function. So, that’s one thing which
I just wanted to- I would operate on my- as a
cardiologist in a very surgical hospital,
Houston Methodist, the home of- still the
ghost of Michael DeBakey, I would’ve probably had him
in the OR a couple days ago. I would like to have a- I have
an issue with the need for some of the secondary
hypertension work-up. If someone takes an
ACE inhibitor or ARB, as this patient did, and
has severe hypertension, the likelihood that the
finding of [inaudible] atherostenosis will lead to
any helpful therapeutic action is nul, given that this
is the best prediction of renal [inaudible]. Pheochromocytoma is
extremely rare, in general, and in particular
at the age of 78, in someone whose hypertension
is somewhat justified and, I think, this is not helpful,
secondary [inaudible] is certainly something that is
important in this patient. I would like also to
have, if I may, a word, in terms of what are the
benefits of adding Hydralazine to a high dose of Amlodipine. Some, I think, 30 years
ago, when Nifedipine was an emerging product, my colleagues
and myself have found, as many others, that 30
mg of Nifedipine surpasses the anti-hypertensive efficacy
of 200 mg of Hydralazine. So, I think, in this
context, Minoxidil, and then eliminating
Amlodipine because, anyway, these drugs accumulate, might
have been a better choice, given that he is taking
beta-blocker anyway, and he’s taking the
diuretic anyway, so some of the expected
side effects of Minoxidil can be counteracted. Yeah, that’s exactly in
the hours- the reason for presenting the case
at this point, was, “How might we
have done better?” In terms of, obviously we
weren’t controlling his blood pressure at this point, in
spite of the six medications, so we were looking for
feedback in terms of what we might have done differently. I mean, just anecdotally,
we do see additional benefit adding Hydralazine to a
dihydropyridine calcium channel blocker, in
terms of blood pressure, so that’s routinely done,
certainly in our clinic. So, if the patient is
failing, dihydropyridine, though, in terms of blood
pressure and a vasodilator, so, again, our question was,
“What might we have done differently, at this point,
in terms of blood pressure management?” But, before we get to the
sort of abrupt resolution, if you will, I think Dom has
already told us last night what we should
have been doing. I think, echoing the comments,
I think one has to be quite careful with filling
pressures here. So, comment number
one would be, is, “How do you diurese a patient
in this current situation, and do you change filling
pressures too much with over-diuresis and, therefore,
worsen the situation?” I’m sure that went
through your mind there. Item two would have been
a trial of isosorbide mononitrate or dinitrate
while the patient’s in clinic, to see what the hemodynamic
changes were with the nitrate therapy. Nitrate therapy
may be unusable, it looks like there was
fixed coronary lesions here, calcific in nature, so you may
not have had a great response, but that is one of our hidden
sources of therapies in resistant hypertension,
are nitrates. Third issue would be whether
or not the person had any vestige or hint
of sleep apnea, which may have explained some
of the right-sided pressures, although this certainly fit
with the left-sided phenomenon that are there. And the fourth
thing would be, “What would happen if we
switched the patient from a dihydropyridine to a
non-dihydropyridine and tried to use Diltiazem to see what
the hemodynamic change would be, starting with a low dose and
working upward from there?” The hemodynamics,
looking at it, I guess the EF was
between 50 and 55 percent, so you have a little bit of
margin for EF suppression, but the dynamics with
Dilt, for example, might be a little bit
different than the dynamics with Nifedipine. That being said, echoing
Dr. Phillips’ comments, if in Richmond, the patient
would’ve been in the OR yesterday. So, would you have considered
adding Diltiazem to the dihydropiridine instead
of substituting? Yeah, I think the only problem
with Dilt is when we run the medicine list and we look
for CYP3A4-metabolized drugs, it’s a potent
CYP3A4 inhibitor, so at a dose of 240 mg of
sustained-release Dilt, your AUC for
simvastatin, for example, or simvastatic acid
will go up three-fold. So, you almost have
to run the list, understanding that you
may upset the apple cart, so to speak, with the CYP3A4
inhibitor being put there. But the CYP3A4 inhibitor,
I guess the patient was on Nifedipine, is that correct? Was in Nifedipine
or Amlodipine? Amlodipine.
Amlodipine. Yeah, that’s
CYP3A4-metabolized, so you ramp up the blood
levels of Amlodipine, concurrent with having a
different calcium channel blocker type by
using the Diltiazem. But I think these are all just
measures where you’re trying to get the right fix or the
right amount of drug, but, unfortunately, until there’s
surgical intervention, you can’t quite figure
out what [inaudible] on. And the question is, “Why do
you get a derivative product of hypertension with this
kind of cardiac pathology?” Presuming it be either
modest cardiac ischemia, and/or changes
in contractility. So, you’ve got very
hyperdynamic precordium on physical exam, and
hyperdynamic set of values, so changing from hyperdynamic
to more isodynamic in nature sometimes can help
the blood pressure, but by no means are you ever
going to correct it in this type of patient
without surgery. Hi. Goldman, Philadelphia. David, I really appreciate
that you’re bringing attention to refractory hypertension. I actually had a poster at
the ASH meeting about three or four years ago, where we had
really reached this extreme level of not knowing how to-
my patient did not have the aortic valvular disease, but
we did notice that every time they would wind up in the CCU
with hypertensive urgency, they seemed to be controllable
with parenteral Nicardipine. So, we created the fairly
novel approach of sending her home on an IV Nicardipine
infusion just like- and you’d be surprised- just like
patients get home Milrinone. And I must tell you, it
was fairly successful. She ended up ultimately going
on dialysis and transferring to another facility, but it
was out of desperation we really did try that. Thank you very much
for sharing this case. I’m Vik Selva from Cambridge. Just two points:
one is pathophysiology. Can I just ask if you think
that the aortic regurgitation here is secondary to aortic
dilatation in the context of hypertension? This guy has a chronic
hypertentive resistant disease. Because in Cambridge, we see a
lot of resistant hypertension, and we see a number of
them with aortic regurg, and we think this is a
secondary phenomenon. We also notice this is more
common in people of black race. They have more cardiac
effects of hypertension. That’s my first question. Second is a bit
more practical. In terms of expanding therapy,
I know the licensed dose of Amlodipine, the
highest is 10 mg. What we do, and
may be considered, is switching them to
Nifedipine [inaudible] mg, which is the equivalent
dose, and up-titrating it in patients of black race. That seems to be something
that’s quite effective. Thanks. Yeah, in terms of
the second comment, I think I would agree. I think Nifedipine,
probably at the highest dose, is a superior antihypertensive
to Amlodipine. It’s just, again,
we’re restricted. Amlodipine is usually
preferred by most of our insurance companies in
terms of their tier system, whereas Nifedipine XL is
not, and so we can be limited because of that choice. I think, in terms of
the first question, there’s certainly-
we’re not, obviously, going to know for sure, but
it’s probably a combination of the high blood pressure in
the regurg as well as the underlying anatomic
abnormality, in terms of the aortic valve,
I suspect is a, sort of, a combination. Okay. We need to hear more. So, moving forward. So, this patient had acute
hospital admission on September 6th, 2016. The patient was admitted for
worsening shortness of breath, dyspnea on exertion,
orthopnea, PND, mild productive cough,
abdominal discomfort on distention, urinary frequency
and acute-on-chronic leg edema. So, the blood pressure
on admission was 224/77. Heart rate was 110. And BNP was elevated – 1899,
and the [inaudible] were elevated, too. So, he was admitted
and they did a cath, and they did echoes, and then
the patient agreed to have a surgery for mitral
valve replacement. So, he had a moderate to
severe mitral regurgitation, and he had a anterior mitral
vale leaflet prolapse, and the jet was
posteriorly directed. So, he had a procedure where
mitral valve was placed (a bioprosthetic valve)
and post-procedure, the valve was well seated,
it was functionally good, he did not have any
mitral regurgitation. Along with the mitral valve
replacement, he also- So, these are the
echocardiographic values before the surgery, taken. Mitral valve: severe- moderate
to severe mitral regurgitation. This is the echo four
days after surgery. He had a bioprosthetic
mitral valve. No regurgitation. His E/A was 1.5
before the surgery, but kind of increased to 1.9. But after the surgery, after
two weeks it came down. And this is the echo
after the surgery. So, along with the
mitral valve replacement, he also had aortic
valve replacement. So, he does have moderate to
severe aortic insufficiency. So, pre-procedural echo showed
jet of regurgitation directed towards the anterior
mitral valve leaflet. The procedure was aortic
valve replacement, a bioprosthetic valve, which was
placed in the aortic position. And after the procedure,
the post-procedural echo, the valve was well seated,
it was functionally good, and the patient did not have
any mitral insufficiency. So, the echo findings before and
after aortic valve replacement. So, thick aortic valve,
moderate to severe aortic regurgitation before surgery. This was the echo. And after the surgery,
echo after four days, he did not have
aortic regurgitation. And, similar echo
after two weeks. And did not have any aortic and
mitral valve regurgitation. So, the other echocardiographic
findings before and after surgery: so, here, the severe left ventricular
dilation that was obvious. And his systolic
function was normal, his ejection fraction
was around 50 to 55, that was before surgery. And after surgery, his LV
dilation was moderate – that was four days after surgery. And the left ventricular
systolic function kind of decreased after surgery. The ejection fraction was
30 to 35 but improved in two weeks and it was
again back to 55. But the LV dilation, which was
[inaudible] after the surgery, was borderline to minimum,
and the systolic function improved, too. And the other findings
with the right atrial size, the right ventricle function,
everything was normal. So, along with this
mitral valve replacement, aortic valve replacement, he
also had a coronary artery bypass grafting. So, as previously mentioned,
the pre-procedural cath showed a stenosis in
left main artery, left anterior
descending artery, left circumflex artery,
right coronary artery, posterior descending artery. So, the procedure was done,
coronary artery bypass grafting was done. Left internal thoracic artery
graft to LAD and [inaudible] vein graft to PDA. So, if anybody has comments. Rob Phillips again. The only thing I would
add to the case with the echocardiography is to
put in the values for the tissue doppler. Because, in the original echo,
it looks like he might have a pseudo-restrictive pattern. You would expect that to
go away with the surgery. But it’s very helpful to have
the tissue doppler values in there as well, so you can
follow those over time. Sure, will do. Thank you. So, the blood pressure
before and after the surgery. So, as we know, he had a
consistently higher systolic blood pressure above 150, and
diastolic blood pressure was normal, so if you can
see, after surgery, his systolic blood
pressure dropped to 120. Let me zoom in there. So, this is the blood
pressure before the surgery, and this is after surgery. So, the mean blood
pressure, before surgery, was in 160s and after surgery,
his systolic blood pressure dropped to 119. And this is the
average after surgery, and this is the
average of one year. And there was no change in
diastolic blood pressure. And it was in the 80s before
and after the surgery. [crosstalk] medicine. Medication? No medicine
[crosstalk]. Yeah, I’ll go over it. So, the mean arterial pressure
before and after the surgery was- mean arterial
pressure was high, and after surgery was-
so, just to zoom in, and was reduced to 85. So, what happened to these
medications after surgery? So, as we know, he was on six
blood pressure medications over the years, so
he was on a ARB, a calcium channel blocker,
a thiazide, a spironolactone, hydralazine, and clonidine. That was before surgery. So, after surgery,
for a month or two, he was on no medications. He was on zero medications,
his blood pressure was in 120s. And, eventually, he was
added Amlodipine 5 mg by the cardiologist, and then later on
he was added the spironolactone. So, the blood
pressure response, along with the medications, so
the timeline, if you can see, there was no change in the
blood pressure when all these medications were added,
but after the surgery, he was not on any blood
pressure medication, but eventually he got on one,
and then on the spironolactone, second blood pressure
medication. So, what would be the
possible mechanism? I mean, the first possible
mechanism we want to look into is medication adherence. Maybe was he not taking
all his blood pressure medications, and
after surgery, well, he had a change of heart, and
then he started taking blood pressure medications. Well, if we think that he was,
we checked his blood pressure medication adherence,
we see them verbally, he said he was taking all his
blood pressure medications, we checked- they bring the
pill bottles, we checked that. And we checked the refill
authorization at the pharmacy, and he was actually
refilling all his blood pressure medication. It was a few years back,
and we did not do any urine testing for drug
metabolites in this patient. So, the medication adherence
probably would not have played a role here, because,
I mean, maybe, let’s say if he was on zero
blood pressure medications, he was not taking any
medication and his blood pressure was in 160s, and
even after the surgery, for a few months, he was not
on any medication and his blood pressure was in 120s, so
probably that might rule out any medication non-compliance
in this patient. So, what happened
to the weight, BMI. So, the weight was stable
during those years, even after surgery he
did not lose any weight. So, blood pressure does go
down with weight reduction. So, there was no
change in weight, and there was no change
in the BMI before and after the surgery. So, we rule out any mechanism
that weight reduction may have played any role in blood
pressure reduction in this patient. So, GFR, serum creatinine
before and after the surgery. GFR was stable, and after the
surgery, it went down and, again, improved in a month. Creatinine was stable in
1.35 and after the surgery, creatinine went up to 2.5. He had a AKI. We have to exclude out if it
was acute tubular necrosis, but he did have an AKI. And then the creatinine
came back to normal. So, this is the zoom in
where his GFR went down and improved, and this
was the creatinine. And before the surgery,
his creatinine was stable, and after the surgery,
excluding the high creatinine, it was similar, but
I’ve included here, so it looks a little
bit more than the pre-procedural creatinine. So, kidney function: so,
there was decrease in systolic blood pressure around 40mm-
48mm reduction in systolic blood pressure. So, there was decreased kidney
perfusion after surgery, and that decreased
the kidney function. And, obviously, the kidney
function improved back to normal in a month. So, he had the
open heart surgery, and what about
cardiac anesthesia? So, these are the medications,
the cocktail of medications, given in cardiac anesthesia. So, does cardiac anesthesia
reduce blood pressure? Well, it does, but
not for a year. So, there is short-term blood
pressure reduction after anesthesia, and it’s a
prolonged effect of anesthetic and pain medications they
are given after the surgery. And there might be blood loss,
there might be dehydration, heart problems,
allergic reactions, and acute infection that might
cause blood pressure reduction after surgery. But that’s not
prolonged for a year. And he had a coronary
bypass grafting, too. So, CABG was done,
and after CABG, there are multiple reasons why
blood pressure goes up – due to pain, stress. And a few of the blood
pressure medications after surgery will be discontinued,
and then eventually, blood pressure goes up,
and they are prescribed medications back again. But according to literature,
blood pressure progressively increases in 24-hour and
daytime systolic and diastolic pressures go up, up to
14 weeks after CABG. And nocturnal blood pressure
dipping gets restored progressively, but in complete
restoration after 14 weeks. And, parallelly, there is
a complete restoration of sympathovagal balance. So, in certain patients,
blood pressure do go down after CABG, but it
does come back, I mean, they are back to the same
blood pressure levels, pre-operatively, and then the
blood pressure medications are introduced. So, aortic valve replacement,
he had an aortic valve replacement. So, blood pressure changes are
not predicted by the type of the valve inserted
nor its size. Diastolic hypertension
is prevalent, I mean, there’s diastolic blood
pressure increases after aortic valve replacement in
aortic regurgitation patient. And there is a study on
hypertension prevalence, and it showed that there is
a decrease in blood pressure prevalence of 57% from 65%
after aortic valve replacement in AI. But after a few weeks, they
were hypertensive again. So, what we think would be
the mechanism here is, well, everybody probably went
through this equation when they were in the
medical school. Mean arterial pressure is
cardiac output and systemic vascular resistance,
plus central venous pressures, which are minimum and they are
normally not incorporated into the equation. So, cardiac output is stroke
volume into heart rate. So, what happened to his
heart rate after surgery? So, heart rate before surgery
was stable, but after surgery, he did have intermittent AFib,
but he was good on discharge. And there was no significant
difference in heart rate before and after surgery. So, there was no drop in heart
rate or increase in heart rate. And there was no
change in heart rate, and heart rate would not have
influenced the cardiac output, hence blood pressure here. Stroke volume,
the other thing. So, his stroke volume
was 97 before surgery, and after surgery, he had a
massive reduction in stroke volume, to 47. So, there was no
change in heart rate, the stroke volume decreased
from 97 to 47 (a reduction in half) so that increased
the cardiac output. The systemic vascular
resistance does compensate, but it takes time,
it’s not a rapid process. So, this is before surgery. And after surgery,
his stroke volume decreased, his cardiac output decreased,
no change in heart rate. And that’s the reason we
think his blood pressure might have reduced. To summarize, we have a
refractory hypertensive patient on six blood
pressure medications. Systolic blood
pressure is in 160s, he had a mitral
valve replacement, an aortic valve
replacement, and a CABG. And possible mechanisms
we excluded was medication adherence, weight reduction,
kidney aspects, cardiac anesthesia,
mitral valve replacement, aortic valve
replacement, and CABG. I mean, it was the aortic and
mitral valve replacement that did the stroke volume, so,
possibly the mechanism was the decrease in stroke volume. But we think it would not have
been just the stroke volume, but a combination of things
might have influenced the reduction in blood pressure
from 167 to around 119. The stroke volume decreased,
the cardiac output, no change in heart rate
might have decreased the blood pressure. So, it’s been a
year since surgery. His blood pressure
is still in 120s. He’s on two blood
pressure medications, and he’s doing well. [crosstalk] So, Rob
Phillips one more time. So, I know you have
great surgery in Alabama. It’s not impossible
that he could have a late paravalvular leak
– He did not. Okay. I would say that the reduction
in stroke volume isn’t all that relevant because
before surgery, much of the stroke
volume was wasted, so… it can’t fully explain. Although it reminds somewhat
what in the old days was called decapitation of blood
pressure after myocardial infarction, and subsequent
reduction of stroke volume. [crosstalk] So, just wanted to
say that he was hyperdynamic before surgery, and there
was normal hemodynamics after the surgery. Not uncommon clinical
circumstances. The poorly treated, difficult
to manage hypertensive on five-drug therapy who
gradually develops systolic heart failure and the
blood pressures normalize. That’s what you saw here. Yeah. And the prediction would
be as the EF goes up gradually over time, you’re
going to need Amlodipine and two or three other
drugs to come in board, so it’s just the
hyperdynamic nature of it. But you have a clinical
corollary that no doubt you see in Alabama
in the same way. So, when someone comes in all
of a sudden well-controlled, you get asked the question of,
“What happened to their EF?” Yeah. So, [inaudible]
we need to wrap up. Okay. Thank you and wrap up. Alright. Do you want to? It’s okay. Well, that was really a tour
de force in both of these cases. I think all of us, despite
our vast experience, learned a lot from
the two of you today, and hope you enjoy the
rest of the meeting.

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