CPC COH2018 | Case 2 | Masked hypertension contributing to severe hypertensive HD

By Adem Lewis / in , , /

– A 73-year-old lady, a retired pediatrician, who had been followed up with, as Christian mentioned, and our client for a number of years, after being labeled with what we say, labeled essential hypertension in 1994. In terms of other aspects
of her background, also high cholesterol,
hypothyroidism, obesity and asthma. Her antihypertensive regimen had included a combination
of dihydropyridine, calcium-channel antagonists, fluctuating between amlodipine and lercanidipine over the years. We’ll look into that a
little bit more in a second as well as a thiazide. Also on a statin, some thyroxine replacements and inhalers. In the past, had been troubled by a cough, on an ACE inhibitor, so we avoided that. Looking over the course of
her trajectory over the years, so, yes, if we look at her trajectory over the early years from 2010 to 2013, we can see that both
in clinic and at home, she had genuinely
reasonable blood pressures and what is sort of key here
is to point out was that in 2012, on amlodipine,
developed some ankle swelling. So we converted to lercanidipine
by the GPs we mentioned. Then, in 2012, one slightly
elevated clinic reading which led to uptitration
of the lercanidipine. But overall, it had been relatively stable on this regimen and over the years. What I’d like to do over the
course of the presentation is take you on a journey from 2014 to 2018 and look at the trajectory
of changes over that period. If we focus first on 2014, we can see that she
declined in blood pressure, above target, 152 systolic. At home, had been troubled by fatigue, but with certainly
reasonable blood pressures. Her husband, you may have
seen in the previous slide, had previously suffered a stroke and unfortunately, passed away and that was maybe contributing
to some issues at home. But because of the fatigue
and the home readings, her GP had changed it from
lercanidipine to amlodipine. Based really on the clinic
blood pressure at that point, we proceeded to arrange an ECG as well as an ambulatory monitor. If you’ll look at her ECG, it demonstrates sinus rhythm, and some ectopics, but certainly nothing too much to write home about there. Moving onto look at her
ambulatory blood pressures. The same in 2014. We can see reasons that are,
you know probably reasonable, perhaps there’s a little
scope to be more aggressive, but definitely, there’s evidence of a loss of a nocturnal dip. So, generally, satisfactory readings but with loss of the nocturnal dip. When we followed her back up in clinic to review this result, we had the client reading, that was certainly satisfactory. So we continued on the current
measurement of that point, which was amlodipine at 10
milligrams and the thiazide. On this point, I just thought we might stop, just with that introduction of the case to get people’s thoughts
on the case to date and the management of that point, what people’s opinions were and if they would have
done anything different at that point. (man speaking faintly off mic) – [Woman] Can you come to the microphone? – John Floras from Toronto. At this point with the fatigue, which is in a woman of this age, who is obese, who is on medications that you described, plus the loss of nocturnal dip, my next step would be to organize a sleep study. – Yes, that is an excellent point and we heard discussions yesterday about the importance of sleep in hypertension and cardiovascular risk. Certainly, in Glasgow, we have much more of a focus now, especially with clinical ability to that and it would be an ideal
point to consider, yeah. – Yeah, perhaps for the U.S. aliens, we are not totally familiar with the dose of this diuretic. Is this a hydrochlorothiazide type? Because the dose of 2.5 would be totally homeopathic. Here, we use 12.5.
– No, no, no. – This is a U.K. specific thiazide. It is like hydrochlorothiazide and the 2.5 are like the 25 milligrams of hydrochlorothiazide. – [Daniel] Thank you. – Thank you very much. – I wonder if there is history of nocturnal urination, of frequent nocturnal urination which may explain her nocturnal
hypertension on a behavioral rather than on a physiological basis. – Yeah, again, that’s
an interesting point. That’s something that was brought up in the first discussion this morning. It’s perhaps a question we
don’t ask that much in clinic and perhaps, something that
we should probe more in to. So, an excellent point for discussion. These were some of the issues
that we had considered. We did wonder where that actually, you know the ambulatory monitor that we had arranged at that point, I know it gave useful information. We saw the loss of nocturnal dip. Was it necessary? Should we perhaps, on the basis of our client blood pressure, had made an adjustment to that point? We touched upon the thiazides, you know slightly unusual but it’s a common practice in the U.K. As bendroflumethiazide, although it’s predominantly a U.K. drug, the most appropriate thiazide we can use. There may be other agents that act better. Particularly, if someone’s stable, should we, therefore, change them or continue on the current regimen? A key issue that we wanted to discuss is in terms of follow-up for this lady at this point. We’ve seen that she’s, you know relatively stable, but with lots of nocturnal dip. How you frequently should do
the ambu following her up. Where would be the best
setting to do that? And what approach do
you say we should take? I’ll hand you over to Christian who’ll chat through that a little bit. – Oh, thanks very much Alan. So there’s really not much to this because you have actually mentioned some of these issues. That’s one of the reasons why we wanted to present this case. So this is back in 2014. This is a very stable patient who attended the clinic for quite a few years already. I think our clinic is as busy as many of the clinics that you do. So the question is really would the management
really change dramatically if you have 15, 20 patients on the list and some of them present with real issues? Then, you have this one here
that’s actually not too bad. Blood pressure, complaining of some fatigue, but no real red flag signs here. So I think it was a
perfectly fine management at this point in time to say we’re not making
any major changes here. If do the point, I take the point that maybe sleep studies and other things would be appropriate, especially now in 2018. What I wanted to show very briefly here is just from the new guidelines for this, recommended, actually, as follow-up. I think you’re all aware of this and we are all aware of this, that, of course, at the very beginning of the management of our hypertensive patients, we should be much more aggressive in terms of the follow-up and see patients much more frequently, about monthly intervals here. But later on, three to
six monthly intervals would be entirely appropriate. I would like to discuss also very briefly is that the focus of this
follow-up appointment should really be on adherence and the number of other
issues including side effects, but also the occasional screen
for any other conditions like target organ damage. Of course, we should also bear in mind that somebody who is labeled
as primary hypertensive, could, after many years, still develop a secondary
form of hypertension and we should always be alert of this. One of the issues that Alan
very kindly pointed out was the issue of the
loss of nocturnal dip. It’s probably something
we can discuss later on during the presentation
if this would be something that would really trigger the
search or the investigations into secondary forms of hypertension that could be associated
with this finding. This is just to remind us
that there may be a few issues why we should screen for
secondary hypertension and maybe loss of
nocturnal dip at this point in this patient could have
been one of the factors that could have triggered
for the investigations. But, let’s not discuss
too much at this point, because, I think, at this point, back in 2014, everybody was quite happy that she was so very controlled. – Exactly, thank you, Christian. Taking you now to 2015, her GP she had presented to complaining of predominantly
atypical chest discomfort with no other associated symptoms and was referred to a cardiology clinic at that point. As we can see here, blood pressure was elevated, 160/80, but the examination by the cardiologist was otherwise unremarkable. Proceedings with initially an ECG which was pretty much unchanged to prior, nothing too much to write
home about at all there. Also, an exercise tolerance test, probably due to her body habits, obesity. She only managed to
exercise for three minutes, short of a predicted six, but, overall, it was a relatively satisfactory exercise tolerance test. Combined with the atypical symptoms, the cardiologist were
reassured on this basis and felt, overall, her symptoms were not suggestive of ischemia. They had noticed that
elevated clinic blood pressure and contrasting that to what
had been noted previously, they proceeded to arrange
an ambulatory monitor, as well as an echocardiogram. We’ll look at the
echocardiogram images first and as we can see here, and this should work. It has worked up until now, but, I guess, we’ll see maybe when we go on to the future echocardiograms, hopefully, they were a
little bit more exciting. But, essentially, what we can
see from this echocardiogram is mild and concentric left
ventricular hypertrophy. If we have been able to show the images, we would see that the LV
function was satisfactory. So, overall, just a mild concentric LVH, perhaps nothing too concerning from this echocardiogram. As I’ve mentioned, they also arranged an ambulatory
blood pressure monitor and we can see a marked difference compared to the previous monitor, readings averaging up to
around 190/90, systolic and, again, a continuing, a loss of nocturnal dip and certainly more elevated,
the clinic blood pressure had been at that point
by the cardiologists. On the basis of that, I wondered what people’s thoughts are and if what you would do with it, with the next step in management that she was currently on amlodipine 10 and the 2.5 of bendroflumethiazide. Most people start with these and what would they do next? – Well, I was going to
say before this last part, that I think it was
probably not appropriate to ignore her ambulatory monitor and not add drug treatment when her, because her office reading was acceptable. So I think that you left the window open for ongoing target organ
damage by doing that. This is very different and her
pressures are quite high now. So, it’s appropriate, I think, to look for a secondary cause as well as assess target organ damage. I would say there is a
nocturnal fall in there, maybe not a full 20%, but, I think, that is not my big concern here, but more related to her
blood pressure control. – Exactly, and that’s one of
the points that we would hoped, we hoped would start to
tease out of this discussion. Was it a missed opportunity based upon the previous
ambulatory monitor? We were reassured by when she
came back to follow that up, a clinic blood pressure
she felt was satisfactory, but is it an ailment of
masked hypertension in there? We’ve discussed that over
the past couple of days at the conference that it’s something that we need to be much more aware of and more aggressive in
her management with. Was it a missed opportunity there? I think you touched on an excellent point and there certainly was, yeah. – I think, for me, you know as we’re putting, as we’re trying to treat the hypertension, we’re also trying to figure out what else is going on with this patient. The one thing that keeps coming up is the patient is fatigued. I
still don’t have a good idea what the etiology of that is just yet. I don’t think it’s because she’s not, you know sleeping well or whatnot. The issue is with the echo, what was the diastology there? Did you get any numbers in terms of, was there an elevated
left atrial pressure? What were the PA pressures? – I don’t have this, unfortunately, but certainly, cardio is reassured in terms of her systolic function, whether or not there was an element of diastolic dysfunction. You know I think that’s
certainly possible. Unfortunately, I don’t have the indices to discuss that with you, but I think it’s an
important area to consider, that, yes, there is an element of diastolic dysfunction there or even perhaps progressing to symptoms of HEPH path fibrillation a possibility and that it’s, yeah, one of the excellent points to pick up. – So that would lead me to
be a little more aggressive with my diuretics in this situation. Anything on an exam like a JVD, edema, anything that you’re seeing in terms of a signal there? – No. In terms of examination, it was unremarkable, but one of the points that we’ll come up as we go through the presentation, it’s actually, often, they’ll complain of ankle swelling, often attributed to her amlodipine, with switching. You know, perhaps, should
we be more inquisitive when patients present with
symptoms of ankle swelling? Did we, perhaps, inappropriately just attribute that to her amlodipine at that point? Or should we thought of more of HEPH path consider diuretic uptitration. – I think, if I recall
correctly, with her EKG and I may have been, I was sitting in the back, but you may have reached
the criteria for LVH by Cornell criteria on that EKG. Just a thought, I think she meets 20 with the V3 and aVL. – Sure, thank you. – So, with the nice documentation of the progression of hypertension, which is a very good topic, does hypertension really
progress in severity? Often, we just don’t know that, but here you have very nice documentation. I think the first thing on
the differential diagnosis, would be renal arterial stenosis. Obviously, you need to give us
information on urine protein because, often, this is the clue with unilateral arterial stenosis. And then, you have a lot of proteinuria. So can you share this information? – Sure, she didn’t have proteinuria. We didn’t go back to
reevaluate ultrasound imaging. As Christian touched upon earlier, when we see these patients, we note a change in time. Should we go back to the start? She had been followed up for many years in the hypertension clinic. Things have been felt to
be fairly stable really until we took a bit of a change in 2015. We noticed that should
we really go right back to the drawing board again and start evaluating her workup and, I think, you know we should. So, yeah, that is an important point. – So will you tell us? – We haven’t proceeded
to renal ultrasound, so I don’t have that information, but she doesn’t have proteinuria. – [Daniel] Very good, thank you. – I wonder about the, the decisions about
chronic drug management. Of course, I guess, certainly myself and everybody would sympathize with not changing a successful or apparently successful treatment. On the other hand, is the treating physician well aware that she has obstructive cardiomyopathy? I would say that generally speaking, dihydropyridines are
not exactly appropriate, neither are diuretics in this context because they may exacerbate obstruction. Therefore, I’m not all that surprised that she became symptomatic. If you have to be treating her with calcium-channel blockers, probably verapamil would have been, or a high-dose verapamil might have been more appropriate. The other thing is, what was her ACE inhibitor intolerance? How did it manifest? Was it the calf? Was it hypertension?
– It was a cough a number, – A cough of a number of years ago, and then, yet, you touched upon a very
interesting point with verapamil that we’ll come back to over
the course of the presentation. But, the ACE inhibitor intolerance had been labeled as a cough for many years previously. – So, obviously, the alternative might have been useful. – Exactly, yeah. – We don’t seem to have been, have demonstrated left ventricular outflow tract obstruction yet. So I think Dr. Burszytyn’s ahead of us. (many laughing) – Exactly, yeah, that’s right. – That’s why I thought I was looking at that echo and wondering. Just a couple of points from our clinica experience in research. In a woman like this with
a low pretest probability of coronary artery disease, we would do a treadmill stress echo and we would look at right
ventricular systolic pressure at the end of exercise. Because often, the chest pain these women describe is due to a high pulmonary artery pressure induced by exercise rather than by coronary artery disease. The other practical point is when you develop a gravitational edema with drugs like amlodipine, we demonstrated in research that that fluid will shift over the course of the night. It will shift to the chest. It will shift to the neck. It would lead to an
increase in neck diameter, a reduction in the airway, an increase in upper airway resistance. The amount of fluid that shifts
at night, we’ve quantified. The greater the fluid
that just sits at night with drugs like amlodipine, the greater the apnea-hypopnea index. So I think that plus nocturia, in a woman, nocturia, again, is a sign
of obstructive sleep apnea. – Yeah, a fantastic point. So it coming out in terms of, you know the exercise tolerance test. Perhaps, we should have proceeded to, you know stress imaging and yeah, we have already touched on sleep earlier in the morning. Exactly, the ideal points
that are coming out. I’ll move on just in interest of time. We’ve touched upon these issues. The overall impression,
masked hypertension. They told you there was
chest pain that should be, you know like with more detail there, investigations of that, not necessarily for the obstructive
coronary artery disease, but for other factors that
contribute to chest pain. In terms of the management of
that point, we did add an ARB. Losartan, 50 milligrams was commenced. We’ve touched upon, you know just if they
have masked hypertension, we’ve seen evidence of it all over, that, perhaps, wasn’t fully picked up and acted upon. Certainly more convincing from the ambulatory monitoring that we’ve seen at this point. It’s a topic that’s coming up over the course of the conference. It’s a common condition in our patients, prevalence of up to 30% and it’s a condition that’s
not a benign phenomenon. I present data here which
look at the instance of cardiovascular variance, comparing normotensive versus
masked hypertensive patients. There’s a two-fold increase. In terms of cardiovascular
mortality and risk of stroke, it’s compatible to that of patients with sustained hypertension. So it’s not a condition to ignore. It’s not a benign phenomenon. It’s something that we do
need to be more aware of and act more aggressively
with when we see. In terms of, you know detection and management of it, the 2017 guidelines
mentioned that patients who have an office blood
pressure which is the goal, but if we feel that there are
increased cardiovascular risks or we have some evidence
of target organ damage, then we should both be screening for it and if we detect it, intensify our treatment strategies. Moving on to 2016, she complains of further symptoms such as it were you know perhaps it could
be deemed as nebulous, or perhaps they may be more significant, postural, exertional light-headedness. Ankle swelling which is a recurring theme and clinic and home
blood pressure readings, 143, 135 systolic. But this ankle swelling
as we have touched upon perhaps, it was
inappropriately disregarded just as due to her dihydropyridine. Regardless, we reduced
that to five milligrams uptitrated to a losartan and continued her thiazide. Overall, her symptoms did improve slightly with that approach to blood
pressures around 140/90 and both at clinic and at home. Things did kind of fairly marked change when we followed her up in 2017. She had been seeing her GP for a couple of weeks with increasing dyspnea, fatigue and increasing peripheral edema. The GP, again, we’re
just having this switch. It’s all just due to her dihydropyridine converted to amlodipine
and to lercanidipine. She also had symptoms of a lower respiratory tract infection at that point. Cough, productive, a small
amount of green sputum. But blood pressure compared
to what we had seen before, was markedly lower, for her, 106 systolic. For her, I see a relative tachycardia, so heart rate at 90, having been much lower previously. She had a low systolic murmur audible across the precordium. At this point, there were good clinical signs, bibasilar crepitations and mild pedal edema. Her ECG had changed at that point. We touched upon whether the previous one had showed features suggesting of LVH. I think we can be convinced that when we do have LVH here on the ECG. Certainly, looking more tachycardic than previously. We arranged a chest x-ray really thinking about consolidation and a frank pulmonary edema. We can see that the
cardiac size has increased, probably no frank edema, though, and certainly no consolidation
in the chest x-ray. What I hoped will work at this point is a more interesting echocardiogram image which, thankfully, it does, we can see that there’s
much more impressive left ventricular hypertrophy here, severe left ventricular hypertrophy on this apical four-chamber view. If we move through to a
parasternal short axis, if this will play, then we can see much more marks in a left ventricular hypertrophy and concentric in nature. I’m just going back now
to the four-chamber. If I draw your attention into this left ventricular
outflow tract here to here, to focus on that, a key feature is the
motion of the mitral valve. There’s systolic anterior motion and combined with that
really chunky septum, that really now is a left
ventricular outflow tract and markedly impairs the cardiac output. So a real change in
echocardiogram findings, compared to what we had seen previously. So at this point, we noted severe left
ventricular hypertrophy. We said there was left ventricular outflow tract obstruction and importantly, systolic anterior motion of the mitral valve. We’ve touched upon, importantly, masked hypertension in this lady, perhaps in the background, of also essential hypertension with loss of nocturnal dip. I thought at that point, we will back up again for discussion to see on the basis of these
echocardiogram findings compared with our symptoms at this point, what people’s thoughts are. Would you agree with
our impressions so far? And what would you do moving forward? If anyone has any suggestions. – I guess, it’s now, it’s going up, I thought, I might as well kill some time. You know, obviously, with LV, you know sort of the
cavity being so small, and now you have true LVOT obstruction. I think now is the time where I would certainly
think about beta blockade in a situation like this to try to get that heart
to really slow down, give it some more filling time, and just try to relieve
that LVOT obstruction. Now, of course, with the GP, by increasing the amlodipine, what that GP did was, essentially, increase the gradient across the LVOT. So what he did, basically, was accentuate the LVOT obstruction. So at this time, we kind of
back off the dihydropyridine and really allow that
LVOT to really open up throughout the entire,
all phases of systole. This is the time, and you know this is a very (murmurs). If you don’t mind, can you just go over the BMI
of the patient one more time? – In the region of 30. – Okay, so a little bit
on the chunkier side. Is she a small woman? – About five foot seven. – Okay, that’s a larger woman, okay. Because, again, one of the
challenges that we have are smaller stature women who have small LVs to begin with, who, then, increase
their weight over time. So, essentially, what you have is a very small heart attached to a large body, which, obviously, accentuates the idea of a low output state. Those are patients that I
would certainly want to say, well, this is the time to really start you know dialing down the pounds as well. So that would be something
I would want to think about as we’re going forward because that would go a
long way here as well. – So we’ve had two suggestions,
a beta blocker or verapamil and where did you go? – In fact, that she got was
amlodipine and losartan. So I really agree with the discussion that the amlodipine was
not good for the gradient. The other drug that was
introduced, obviously, against the background of the
mild LVH was the losartan, but this would be exactly
the same effect here that it also further
increases the gradient. I think Alan will discuss
some of the details how really the clinical
decompensation in this patient was triggered by some of the
measures that we have taken, but maybe also by other
precipitating factors. – Exactly, yeah, thank you, Christian. Just, you know go over
what we do at that point, perhaps not ideally. However, we stopped her losartan with her bendroflumethiazide. We continued her dihydropyridine. On reflection, was that the
most appropriate approach? Probably not. But we’ll touch upon the left ventricular outflow tract obstruction often gives an impression of heart failure and traditional approaches to management can actually be deleterious in this. So when people initially manage someone who they may feel have heart failure, if they have left ventricular
outflow obstruction, some of those strategies
can be deleterious. We arranged the ambulatory monitor and referred her urgently to
our cardiology colleagues. I won’t dwell on the
ambulatory monitor too much, but it looks more
consistent than to previous, more reasonable readings. The key point is we’ve
touched upon is we then manage to start some calcium-channel antagonists. With verapamil, initially, 40 milligrams TID, then uptitrating to a more reasonable sustained release. We restarted her diuretic and discontinued her lercanidipine. Left ventricular outflow
tract obstruction we can see is one of the key points from this case. It’s being described in case reports from the mid- to late 1980s
as well as early 1990s as probably something that
we should be more aware of and certainly screened for more. It’s a condition that requires an anatomical substrate as well as a physiological trigger. So often hypertension or aortic stenosis leads to increased afterload, perhaps with this lady, a masked hypertension because of the non-benign phenomena. But regardless, this leads to
left ventricular hypertrophy, and that can lead to ailment
of diastolic dysfunction, but particularly with left ventricular outflow tract obstruction, as well as that anatomical substrate, there’s then some form
of physical trigger. That can either be a
physiological response, perhaps to sepsis with relative
hypotension, in this case or if we have agents
which act as vasodilators, often starting perhaps
because of a management going to another strategies. These, then, accentuate this problem leading to increasingly
impaired diastolic filling, the left ventricular
outflow tract obstruction and almost obliteration,
at times, of the LV cavity and a systolic anterior
motion of the mitral valve that then occurs really not as though in that LV outflow tract. At least the triad of symptoms that are they are typical in terms of chest pain, breathlessness and syncope. In terms of how we would best manage that, the things to really point out is that we need to avoid
things like vasodilators or positive inotropes
that may be commenced if you go down the wrong strategy and don’t really screen for
LV outflow tract obstruction and consider that it might be there. We need to think about beta blockers or calcium-channel blockers, which have both come
out from the discussion. We went for a calcium-channel blocker, verapamil with subsequent uptitration. What these agents are able to then do is to improve the diastolic filling while slowing down the heart rate. That, then, allows some reduction in the LV outflow tract, reduction of the systolic anterior motion and, then, subsequently
improvement of symptoms. That’s the approach that
we took with this lady. If we, then, fast-forward to 2018, her exercise tolerance had improved, blood pressures perhaps
still not at ideal target, but maintained on verapamil. We felt, at that point, because of her symptoms that improved, she had developed and
improved exercise tolerance, we could re-add an ARB, continue her bendroflumethiazide and led to more satisfactory
blood pressure readings, both at home and in clinic. We’ve updated her ambulatory monitor just around a week or so ago and we can see much more
satisfactory readings, but, again, with the ongoing
loss of the nocturnal dip. If we now contrast the echocardiogram after that period of management with verapamil placed here, we can see marked improvement in the left ventricular hypertrophy and a much more open left
ventricular outflow tract, that’s contributing to the
marked improvement in symptoms that we’re seeing further. Let me just flip back to the presentation. Well, we’ve taken you
through a journey from 2014 is a lady who had been
relatively stable at that point, but who, then, started to
develop masked hypertension as well as a loss of a nocturnal dip. She probably, due to
the masked hypertension, started to develop severe
left ventricular hypertrophy. We, perhaps, weren’t as aggressive in our management strategies
as we could have been, when we detected the masked hypertension. Had we done so, perhaps, we
could have prevented that and progression to what I mentioned, is the anatomic substrate that then combined with
the physiological trigger, both from the relative hypertension, perhaps in the context of infection, combined with some of our
other management strategies led to the left ventricular
outflow tract obstruction. As a condition to be aware of, because the implications for management really are important if you adopt some of the strategies that may be managed for heart failure with diuretics in the first instance. If you don’t think about beta blockade or appropriate calcium-channel blockade, then you would go down the wrong avenue, you would accentuate the symptoms and make the situation worse. There have been reports of that from the case presentations presented from the late 1980s. Fortunately, for this
lady, we were able to, you know identify it and relatively, promptly treat her successfully
with a negative inotrope that led to marked
improvement in her symptoms as well as the echocardiogram findings. I hope to have, along with Christian, you know on your self, discussed over the course of the morning, there’s some key features
that we need to be aware of in terms of masked hypertension, not being the benign phenomenon. We’ve talked about the importance of considering nocturnal uresis at night, probing into that as well as the aspect from sleep studies. We touched upon whether
we could think about more appropriate imaging when we had the symptoms of chest pain, perhaps with some functional imaging. Then, the management of left ventricular outflow tract obstruction to lead to improvement in symptoms. I’d like to, you know thank everyone for their attention and contributions over the course of the past 45 minutes. We still, I think, have
a short while for time. So we can, you know open up
again for some more discussion. – Thank you. I have a comment and a question. Firstly, I would have
expected her to improve with the treatment that you’ve given her. But, the response, especially
with the echo, is miraculous. That’s my comment. Secondly, lots of people have
long-standing hypertension and don’t go down this way. I wonder whether this lady has late-onset hypertrophic cardiomyopathy and whether you have looked
at her sarcomeric genes, particularly, mast and binding protein C, which is commonly behind that. – Sure, that’s a key point. It’s just, you know a simple LV either due to hypertension or could there be a, you know more familiar component? If was felt because of the
more concentric nature, although, that doesn’t, you know exclude your whole picture, that it was more likely to be hypertensive in nature. I guess with the improvement in the echocardiogram findings along with their symptoms, we’ve continued doing that route but it’d be something to be aware of, certainly, had she not
continued to improve. Should we look at more of these proteins? Should we think of MR imaging for more detailed evaluation? So, yeah, it’s important to be aware that we just don’t fully attribute this to hypertensive LVH. We keep in the back of our heads that the possibility of
a familiar component. – But both in athletes
and in hypertension, there’s a hemodynamic stress, but it’s on the background of the underlying genetic makeup or constitutional makeup. Clearly, this lady is much more prone to get hypertrophy the most. Please. – I would like to comment
exactly on this point. My cardiology associates, would you probably have said that this is hypertrophic cardiomyopathy with hypertension on the side? At the same time, I would think, especially in the context of, I think that having hypertension or severe hypertension and below that, familial hypertrophic cardiomyopathy is a bit, I would say, obscene. (some laughing) I would like also add to it a sort of a clinical perspective. As clinicians, we ought to
seek treatable diseases. Since hypertrophic cardiomyopathy is maybe improved symptomatically
as demonstrated here and this could have been false, as I said before. Hypertensive, how the disease is preventable and at least to a certain extent, reversible and therefore, should be given higher consideration, again, than my cardiologist associates would have given it. – Yeah, thank you. – We take that as a comment. – Was there much discussion
about the dose of verapamil? You jumped to the other
drugs fairly readily. What about using higher doses as high as 540 milligrams? Which some people use in this kind of situation. You sort of half treated, in my view. I mean, you treated the
blood pressure beautifully, but if you’re looking
at what the problem was, why not use more verapamil? I guess, is a question. – Yes, that’s an interesting point. I guess we started, perhaps,
a little too cautious and perhaps, caution is a bit of a theme that’s recurring through this case. You know higher doses would, there could have been certainly
something to consider. We didn’t in this instance, but it would be an important thing– – Was it the fact that you had crackles or something like that? – [Alan] No, I mean the
verapamil was primarily– – I don’t think that would
bother me, particularly, in this. – It was primarily guided
by our cardiology colleagues and rather than ourselves. So, I don’t have the full background as to why this doctor added that dose, but it’s a theme that we could, perhaps, be more aggressive throughout the case. – At the same time, the other vasodilators were stopped, so she did not, she did get some kind of treatment by removing some of the drugs that would negatively
influence the gradient and she would get some
verapamil on top of this. So, at least she has two
therapeutic principles here at the same time. But, I agree that those
could have been higher. – Hi, the loss of nocturnal dip initially is an important trigger,
particularly, in females. There’s been a study many years ago which showed lack of nocturnal dip. It wasn’t called masked
hypertension in those days. In females, it led to hypertrophy. So we need to be aware that
an initial ambulatory is key. The other factor is
that masked hypertension can only be diagnosed by ambulatory, no other way. So we have a lot of discussion
at this meeting and others, lack of reimbursement,
particularly, in America, is a hindrance to ambulatory. So, maybe that’s something to take up with the associations, that we do need to identify, because this condition isn’t benign. – I couldn’t agree more. So what this lady probably had was three or four ambulatory readings over the times, so I think that’s not too bad. But the confusion that was here is certainly that we have some discrepancy between clinic readings
that were mostly fine. On some occasions, they were high and then, usually they would share that would say there’s some stress at home or other factors that caused this. We have the ambulatory readings as proper 24-hour readings, but we also have home
blood pressure readings. Now, think about what we all do. I think this is what this
case particularly features is that we just pick the best ones. If you take the ones that we like most and we say, well,
despite absence of a dip, most of her home readings are fine. So let’s not increase the treatment and you pointed out very rightly, that this absence of dip and the slightly borderline blood pressure that we’ve already seen back in 2014, should possibly have triggered
a more aggressive treatment– – She still got lack of nocturnal dip. So what are you doing?
– That’s quite right. – That’s quite right. So we’re, we’re happy to take your advice. (chuckling) – So, along these lines, I think this case can
be better characterized as a case of severe
hypertension, progressive. I mean, masked hypertension is a term that we want to be pure in the definition, is better reserved for someone that, in the office, is perfectly normal. And then, surprise, surprise, the blood pressure is much higher at home with target damage. So, I think, in your case
when you write it down, I don’t know the title, but, I think, this is a case of progressive severe hypertension. Set along these lines, the lack of dip in this
hypertensive patient is another point for severe hypertension. That’s about the definition. You never told us the followup. Was the blood pressure markedly
improved after verapamil? Or you improved the symptoms and the blood pressure is still not fully controlled? Because I suspect this
is severe hypertension and you need to add a spironolactone, something else to control
the blood pressure. So what happened to the
blood pressure at the end? – So the last BPM reading
that Alan had shown just from a week ago, showed much better blood pressure control. It’s still not quite at the optimal range. There’s still loss of nocturnal dip. So she may benefit from some
changes in her treatment. The spironolactone that you mentioned, there’s actually quite
an interesting idea, especially, given the history of the left ventricular hypertrophy that she clearly have. – So my comment is, I think you got three sequential comments related to that. You have a wealth of information about where her nocturnal pressure is, but limited things were done, both from an investigative standpoint and management standpoint. I would argue that spironolactone not only would have value in terms of overall blood
pressure management, but along with what had been talked before about rostral shifts, fluid shifts. If she’s still obese, if she has a little aldosterone excess, we know that if she has sleep apnea, which I echo what others have said, should be investigated. The use of spironolactone
may have a favorable effect. Now, that her LVOT obstruction is gone or significantly improved, there, it could be safely used. Any diuretics could be safely used and if we believe in the value of spironolactone in HEPH path, it could be a double effect. – So I was gonna ask about
the role for spironolactone. So thank you. But I did want to just ask one thing about keeping the term masked hypertension because, well, I agree that it should be defined as normal in clinic, to remove it. Part of the problem in this
case was that we didn’t highlight the home blood pressures enough and to remove it from the diagnosis or to remove it from the label. We don’t want this person
going back to only office, so I think it’s important
to continue to highlight, that we need to rely on out
of office blood pressures for this patient. So, I don’t know if
there’s any thought about, how it balances. – I think that’s one of the
key points that we really need to look at the ambulatory
profile in this patient. Just to come back to this term, masked hypertension, you will have seen a very bold statement in the title of the presentation, but you may have seen
Alan’s small question mark in one of the slides where he asks, is this actually masked hypertension. I think the discussion has just shown us, is this masked hypertension? Because we picked the one time point that there was this clear discrepancy between clinic blood pressure and ambulatory readings. Or is this really a case of discord? And blood pressure readings
that we have over time as we have it in many patients and we have just missed
a natural progression of hypertension that was indicated by a number of readings over the time. – So in defend of, in defense of cardiologists, I will tell you that we would not have necessarily, sort of
called this patient HOCM simply because it comes with
such a terrible association with sudden cardiac death. Before we start telling patients
that they are at high risk for certain cardiac death, we’d want to do a little
bit of investigation. But, I guess, this is
sort of a shameless plug for cardiac MRI because
it’s sort of my specialty, but in the sense it would
be that in a situation where you do see a precipitous
increase in the LV masked as we saw in this case, a cardiac MRI would not only be helpful from a diagnostic standpoint to see if this patient had
laid down and said HOCM, but also from a prognostic standpoint. I mean, if you see a lot of
fibrosis in the LV myocardium, then you know that there is a higher risk for ventricular arrhythmias. So that, how you treat that patient is gonna be different than if you saw a low burden of fibrosis. Fibrosis can happen not only in HOCM, but also in hypertrophic
remodeling from hypertension, aortic stenosis, a myriad of clinical issues. The last question or the last point that I would have with this patient, if you noticed, she already has left atrial
enlargement on the echo, so she is knocking on the
door of atrial fibrillation. So if she does have some palpitations, you know what it is, okay. (many chuckling) – [Alan] Lovely, thank you. We know what to do when that comes. – [Christian] Okay, just one
other point that I’ve seen and obviously, we stressed
this during the discussion. This is a patient, who, initially didn’t look too bad when we go back to 2014. We have a lot of pressure in the clinics, obviously, to discharge patients from specialty followup. So if you have done this at this time and the patient would have seen by the GP, we may have missed even
more opportunities. Now, unfortunately, what we have done was probably not so much better in this case. So I think at the chest, this is one of the reasons why we have picked this case, that even with specialist management that we put into this patient, we probably were not
quite on the right track. You really have to make sure that all specialists’ services deliver what they promise and that we take these patients and their symptoms very, very seriously. The discussion has
shown a number of points where we could have gone down
a slightly different route which we may have missed. Now, in hindsight, I see some of these features, of course. – I think this goes back
to guidelines and targets. You know the higher we set the target, the more cases will pass through. If, you know as they are
primary care people use 150, this lady was controlled and yet, she developed
hypertensive heart disease. If we use the European guidelines, even, I think, this lady
was almost controlled. There’s a creep there, where she’s close to the target, I don’t want to hurt her. I don’t want her to fall down or pass out. So, we will undertreat people and this is an adherent woman who is educated, who, I believe, takes her medication and yet, in front of our eyes, your eyes, she developed
hypertensive heart disease, she should not have developed that. So, for many reasons, I think, when we start ratcheting up that target because we’re worried, I think we poorly serve the patient. – I think, at this point, we will stop. We’ve had a wonderful discussion, I think, and there’s much to reflect on. It’s interesting that
this rather unusual case has implications for the general run of hypertensives that we treat. Thank you both, Alan and Christian.
(many applauding)

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