Challenges in the Management of Hypertension in a Patient of Angina
Friends, I was just going through some literature on
hypertension and I just saw one quote by Hay, “greatest danger to a man with
high BP lies in its discovery, because then some fool is certain to try and
reduce it,” and I just wanted to put “that some fool is there going to come and
give lecture today.” This was being said
because it was thought that hypertension as a matter of fact was a necessity,
that is why it was called as essential hypertension and Scott said, not very
long back in 1946, "may not the elevation of systemic blood pressure be
natural response to guarantee more normal circulation to heart, brain, and
kidneys" and that is why it was being called as essential hypertension but
today, we know that hypertension is a lethal disease and it is a lethal problem
that higher the blood pressure, higher the mortality, higher is the morbidity,
and especially involving the brain, the eyes, the heart, kidneys, peripheral
vessels, and so on and so forth. So
therefore, as the degree of hypertension goes on increasing and as you see from
the data that cardiovascular disease doubles with each 20 and 10 mmHg blood
pressure increments. So, it is really a
serious problem. Today, my talk is basically
how to manage a patient who has hypertension, has angina. The higher the blood pressure, higher is the
cardiovascular mortality so what my talk today is basically on how to manage
the patient who has angina, which may be of different types, which is
accompanied with hypertension. For
example, angina occurs because of the obstruction in the coronary arteries and
this can be nothing but like a chronic stable angina. Here is a patient who has got severe disease
in the circumflex vessel and there can be another patient who has an acute
coronary syndrome who also presents as an angina who has got an obstruction
into the left main artery and that can be presented as an acute coronary
syndrome. Angina manifestations are not
just plain and simple. Remember one
thing, do not take angina just an angina as a chronic stable angina with
hypertension, angina can manifest and can be accompanied with so many other
varied co-morbidities and co-conditions.
Say for example, a patient can have chronic stable angina which is
totally uncomplicated. The patient’s
ejection fraction is normal. He has no
diabetes and he has no albuminuria. On
the other spectrum, one can have angina which is unstable angina and acute
coronary syndrome. Angina can also
present as a post myocardial infarction.
It can be present in the patient who has left ventricular dysfunction
and heart failure. It can be accompanied
with arrhythmias like
atrial fibrillation, flutter, ventricular premature beats, or sometimes in some
patient more malignant arrhythmias like ventricular tachycardias. Associated comorbid conditions can be
diabetes, albuminuria, and very very important which many of the people do not
realize is the increase in the LV muscle mass.
This is very important because I will touch upon this and how to manage
all this. So, just managing and trying
to bring down the blood pressure and controlling his angina is not enough if
you have to manage a patient who has got angina. You must remember angina is a symptomatic
manifestation of co-existing or existing coronary artery disease which may be
from mild, as I showed you in circumflex vessel disease or can be very
malignant which can be like an unstable angina can lead to myocardial
infarction. So, you have to achieve not
only the relief of symptoms but you have to control hypertension to the target
level by reducing and also reducing the left ventricular muscle mass. We have to see that whatever drugs you use,
you will try to achieve the reduction in the death rate, improve the endothelial
function, reduce death rate, myocardial infarction, heart failure,
revascularization, and cerebrovascular disease and prevent chronic kidney
disease. So, whatever drugs you use,
single or combination, you must achieve these goals because you know that by
the time the patient has come to you with angina, he already has got
significant, along with hypertension, co-existing already a target vessel
damage to his heart. So to achieve all
these goals, these should be the goals whenever you want to pick up a drug or a
combination of the drug to manage a patient who has angina along with
hypertension. Say for example, here is a
patient who has angina. You can see
already the ECG showing a severe left ventricular hypertrophy and you see left
ventricular muscle mass, he has already developed a severe left ventricular
hypertrophy and there is lot of data available that if your left ventricular
muscle mass is more than 125 grams over the body surface area as compared to
the patient who have got less than 125 grams, the mortality is different. The mortality is much higher in the patients
whose left ventricular muscle mass is more than 125 grams. Also, when you institute a drug you must keep
on doing serial echocardiograms because you must know that if you could bring
down the left ventricular muscle mass significantly over the next one or two
years' time that is a drug which is helping the patient in controlling not only
his hypertension but also taking care of his cardiovascular morbidity or target
organ involvement. So, you have to see
that you give drugs which not only control his hypertension, control his
angina, at the same time by serial echocardiograms
we should try to estimate the left ventricular muscle mass to see and ensure
that the left ventricular muscle mass is reducing by the drugs that you are
giving.
So therefore, what are the drugs that we can use in a
patient who has got angina with hypertension?
Now, we go to the JNC-7 algorithm because JNC-8 guidelines are still not
available to us. But just let take this
as a benchmark, and look at the benchmark, you come down to the initial drug
choices, divided into two with compelling indications and without compelling
indications. Now when the patient has
got angina, it is a compelling indication because he has already got a target
organ involvement. This is a compelling
indication therefore you have to look on the right side of the slide and see
the antihypertensive drugs that are indicated are the diuretics, ACE
inhibitors, angiotensin receptor blockers, beta-blockers, calcium channel
blockers as the need may be. So
therefore in this particular group of patients who have got angina,
hypertension, lets see out of these four or five groups of drugs which will be
the most ideal drug, either a single drug or combination of drugs for a given
patient. First of all, the principles of
management in angina concern number one is to increase the blood supply. To do either an angioplasty or do coronary
artery bypass graft surgery which will improve the left ventricular flow by
opening of the vessel or doing a bypass you will increase the coronary artery
flow so that will relieve his angina.
Now suppose the patient is either not willing or is not a suitable
candidate for either one of these two revascularization procedure or you feel
that the patient can still wait, the disease is not so extensive, the patient
can be managed with medical line of treatment then your effort has to be to
reduce the myocardial oxygen consumption.
To reduce the myocardial oxygen consumption, attempt to reduce the blood
pressure and afterload, reduce pulse rate, reduce platelet aggregation, reduce
contractility, achieve peripheral vasodilatation so that the blood pressure
falls down, improve left ventricular function.
Also you must which is not mentioned on the slide, which I will show in
the course of few slides give drugs which can improve the endothelial
function. Today, we have got drugs which
are antihypertensives, but at the same time also improve the endothelial
function.
Now let us look at what are our choices. The most important choice is group of drugs
are the beta blockers. As you know, beta
blocker have got all the salutary effects I have talked about. All of you know it reduces the heart rate and
reduces the blood pressure and it reduces the contractility of the heart. Many people do not realize that the
beta-blockers also have got an anti-platelet effect. They reduce the platelet aggregability. That depends upon the beta-blocker that you
use. Nebivolol has got the maximum
effect of reducing the platelet aggregability.
Now you have got heterogenicity with in the beta-blocker class. You have got some which have beta-1 and
beta-2 selectivity,
vasodilatation properties, and intrinsic sympathomimetic properties so therefore
you have to literally select which are the groups of beta-blockers or which
particular beta-blocker you would like to take in for your patient. As a mater of fact, there has been an
evolution right from the time of propranolol which came in 60s in the market
and basically we divide beta blockers into three generation. First generation are propranolol, then we
went to metoprolol, and now we have come to the third generation in which we
have either the carvedilol, we have nebivolol which are the drugs which are
many times used for some added advantage.
We will come to that in which particular subset of patients we would
prefer to use carvedilol if you have to use in a patient who has got angina and
hypertension. So therefore, if you look
at the BP reduction by beta-blockers, the mechanism are traditional that is a
first and second generation versus the third generation and the third
generation beta-blockers decrease blood pressure largely through reducing
systemic vascular resistance because they have got alpha-1 blocking properties
as well and if you look at the beta-blocker evidence over the period of last so
many years, this is a summary of secondary prevention trials of beta-blockers
when the patient who has already got angina you are using the beta-blockers to
prevent future events. It is a secondary
prevention; it is not a primary prevention.
As a secondary prevention, you can see the maximum effect comes when you
give it from the point of view of secondary prevention. For the acute treatment and acute myocardial
infarction or acute coronary syndrome perhaps they may not be as effective but
when you give it for secondary prevention particularly after myocardial
infarction if the patient has got hypertension you have got the maximum advantage
and if you see there has been overall advantage. If you look on the left side of the vertical
bar, if you give beta-blockers, the patient gets relief or gets improvement or
has an advantage. On the right hand
side, the patient has no advantage so you can see in all three indications that
is acute treatment, secondary prevention, and overall beta-blockers have got
salutary effect. Now, I thought I will
give you in form of case scenario. I
will show you two case scenarios which are totally divergent and see how you
would like to select your particular beta-blocker or any other drug to combine
along with the beta blocker.
CASE
#1: Here is a patient who is a male 54
years, obese built, increase abdominal girth.
He has got an angina on effort class II.
His blood pressure is 260/92. His
pulse rate is 92, slightly faster pulse rate.
His coronary angiogram shows obtuse marginal circumflex branch 70%
obstruction. His posterior descending is
100% with collateral recent angiogram which I showed you right in the
beginning. His ejection fraction is
normal at 55%. Since this patient’s
angina was only class II, he had circumflex lesion in the right coronary artery
lesion which was co-lateralized. Left
main was normal. LAD was normal. He opted the "let me try medical
treatment," so he becomes little low risk patient since angina is not
severe. So, we agreed that let him go on
a medical line of treatment but told that in case you do not get relief, we
will do either angioplasty with stents or incase we find that well by the time
the disease has progressed to the LAD or to the left main then he can go for
coronary artery bypass graft surgery also.
So now let us see what are the drugs which we can use in a patient like
this. For example, the best drug
combination for him would be #1 will be beta-blocker because beta-blockers will
control his angina. He is already
slightly tachycardiac. His blood
pressure is 92. You can select any of
the beta blocker because his ejection fraction is normal. Otherwise, if his ejection fraction is low,
carvedilol will be the drug of choice, so you can choose either propranolol but
of course propranolol now has gone out of fashion so you can give him
metoprolol, you can give him nebivolol, you can give carvedilol, whatever drug you
want to give him you can pick up and then give him a drug. There is an additional benefit of
beta-blockers. They decrease the
frequency of sudden cardiac death and VPCs. They improve exercise capacity. They have got favorable cardiac remodeling
and reduced risk of atrial fibrillation.
Same benefit in nonischemic patient also. Can be used in severe heart failure,
especially carvedilol, and equal benefit in males, females, blacks, diabetics,
and elderly. So this is the drug which
will be a drug of choice. Now do we add
any drug to this, look at the American Heart Association’s scientific
statement, the target for the patient who has got coronary artery disease,
stable angina, acute coronary syndrome or acute coronary syndrome following
STEMI target is pretty low, less than 130 and less than 80 mmHg, quite possible
and very likely. You perhaps may not be
able to achieve this target only with beta-blockers that is #1. #2 in a patient who has already got kind of
heart problem has, already got coronary artery problem; one would like to give
him additional drug which will prevent the future events. As I showed you in the first slide, the aim
is not only to control angina or control hypertension but also to prevent
future episodes of death, myocardial infarction, heart failure, or
revascularization. The target is also
stiff to achieve only with one drug so therefore it is always better in these
patients to combine with some another drug.
What are
drugs available to us to control angina and to control or prevent the future
events? The drugs which are available
today are either ACE inhibitors, ARBs, or calcium channel blockers. ARBs or the ACE inhibitors are basically
given for the cardioprotection to prevent future events. There are several trials available with
captopril, with ramipril, with trandolapril and you can see in the trials like
SAVE, AIRE, TRACE, and now the HOPE study have shown that when you give them
any one of these ACE inhibitors, there is a mortality reduction and this is
irrespective of the fall in blood pressure.
The fall in the blood pressure was very minimum, yet there was
cardioprotection indicating that they are basically cardioprotective drugs.
What about
the patient’s if angina does not get controlled, the blood pressure also does
not get controlled, what about the calcium channel blockers? Yes, calcium channel blockers are very
powerful coronary vasodilators as well as the peripheral vessel dilators. They have more effect on the peripheral
vessels and therefore can cause severe fall in blood pressure. That is why you must have read in the papers,
in the journals, that today short-acting nifedipine is not given for control of
angina. It is only for acute episode
that you can give because they are very powerful vasodilators. There can be sudden fall in blood pressure
precipitating a myocardial infarction in a patient who has got an acute
coronary syndrome. However, a
sustained-release calcium channel blocker like nifedipine can be very useful
added tool for controlling the patient’s angina and blood pressure in case he
is not getting control with the beta-blocker and the addition of the ACE
inhibitor or ARB. Also it has been found
that nifedipine is not only powerful vasodilator, but because it activates
nitric oxide synthase, it has got an endothelial protection effect. It reverses the endothelial dysfunction. So it is an added advantage in case you want
to use a calcium channel blocker, may be I think sustained release nifedipine
may be a good drug to combine in these patients.
Recently,
the fifth generation of the calcium channel blocker, cilnidipine which is being
used extensively in the patient with hypertension especially for the reno
protection, but one effect which I saw in the literature that there has been
reduction in the heart rate significantly greater in the cilnidipine group than
in the amlodipine group. Now any drug
which brings down the heart rate in the patient who has got angina, I will
postulate that will have salutary effect on the control of the angina, but I
think more trials, more data has to be available to see that this effect is
certainly available with the cilnidipine.
CASE
#2: This is a 65-year-old male. He had an anterior wall infarction six years
back. He had post myocardial infarction,
CABG five years back. He has got
shortness of breath class II with a low ejection fraction of 35%. He is nondiabetic; however, his creatinine is
1.4. Now, there are certain things in
this patient, if you want to prescribe any drug you have to be little cautious. First of all, he has an anterior wall
infarction. He has symptoms of shortness
of breath, i.e., LV dysfunction. His
ejection fraction is 35% and very important his creatinine is 1.4. If you were to calculate his GFR looking at
his age and body weight, you will find possibly GFR may be less than 60. So therefore, if that is so you have to be
very careful and choosy about the selection of your ARB or an ACE inhibitor to
ensure that the potassium does not go up and his creatinine does not go
up. Not that at 1.4, ARB or ACE
inhibitor is contraindicated but all that I am saying, you have to be little
cautious in these patients. There has
been risk reduction with all the beta blockers, especially in the subset of
patients like this who had a myocardial infarction and low ejection
fraction. All types of beta-blockers
especially carvedilol, metoprolol, and bisoprolol, these are three drugs which
have been used in the patients like this who have got a low ejection fraction,
LV dysfunction, myocardial infarction when these three drugs in the beta
blocker group will be very effective.
There have been several trials on the beta blocker mortality trials in
the patients who got heart failure, MERIT heart failure trial with metoprolol,
COPERNICUS trial on carvedilol and the CIBIS-II trial on bisoprolol. All three agents have been shown to have a
salutary effect on improving the left ventricular ejection fraction as well as
reducing the mortality. Now, which one
to chose, do you choose carvedilol or do you use metoprolol. There has been a trial called as COMET trial
in which there was a head-to-head comparison between the carvedilol and the
metoprolol and the patients were assigned to 2 arms and one found that carvedilol
proved to be superior to metoprolol. Though of course both of them did bring down
the mortality rate, they gave an advantage; however, the advantage was greater
with carvedilol. Only thing is that I
have seen and we all ourselves do not prescribe the optimum doses of
carvedilol. The optimum doses of
carvedilol is to go to 25 mg twice a day.
You start with smaller dose, but until and unless you give such high
doses you will not be able to achieve the hypotensive effect in patients whom
you decide to put on carvedilol. As a
mater of fact if you look at carvedilol its beta-1 blockade is 3+ and beta-2
blockade is 3+ and it has got an alpha-1 blockade of 3+. It can cause quite a good degree of fall in
blood pressure. As opposed to this
metoprolol has got only cardioselectivity, it has got beta-1 blockade
properties. Bisoprolol has only beta-1
blockade property. Out of all this when
the patient like this, what I showed you, the drug of choice should be
carvedilol in these patients. There has
been a drug which I am sure all of you have been using, nebivolol, and this is
one drug which also has been found to improve the endothelial function in
addition to controlling blood pressure and angina.
Now, what
about these data between the ACE inhibitors versus the ARBs in improving the LV
ejection fraction like the patient I have shown you. When it comes to ACE inhibitor, all trials
have been positive. None of the trial
have shown that the ACE inhibitors have negative benefit, they all have got
benefit. It depends upon whatever drug
you use. As a matter of fact it is
always said that the choice of ACE inhibitor is more by wits than by wisdom, so
whatever you want to use, you use. You
want to use more expensive, use more expensive like Cardace or ramipril. If you want to give cheapest one, you can use
the older one like enalapril, but all of them have been shown to have
beneficial effect. As opposed to this,
ARBs have been salutary, but there has been always some doubt in some trials.
Now, I will
come to last two or three slide to show certain things which we never bothered
to look at. When we treat the patient
like this angina, low ejection fraction, past myocardial infarction, now the
patient has got heart failure symptoms.
Couple of drugs which we have forgotten or we forget to write down are
the aldosterone antagonist. Remember
that they are very very important in managing a patient like what I showed you
and especially giving them a drug like spironolactone if you look at the trial
called, RALES trial, patients who are put on spironolactone had got reduced
mortality over 36 months period. It is a
very important drug and similarly another drug, like eplerenone, as you know,
which has been used or tried in EPHESUS trial when in the postmyocardial
infarction eplerenone has been showing to reduce mortality. So, any one of these two drugs can be used to
control hypertension and if you see when you give spironolactone to the patient
you have to wait and at the end of 6 months you will find that the systolic as
well as diastolic pressure comes down.
As a matter of fact, some patients who do not respond to your
conventional treatment, add sort of 50 mg or 25 mg of spironolactone a day, you
find their blood pressure comes down.
Only thing is that you have to be careful in a patient like this who has
creatinine of 1.4. Combining
spironolactone, combining ACE inhibitor or ARB you may inadvertently increase
the potassium level and the creatinine level, so be careful there is a word of
caution in this patient. One more thing
which many times we forget to look at, and this is not uncommon, is the Conn
syndrome. Primary aldosteronism is not
an uncommon condition. In various trial
and various literature articles, the incidence has been reported to anywhere
from 8% to 20% of all hypertension patient, it is not a small incidence. So, suppose you see a patient who has got
persistent hypokalemia, withdraw his diuretics, any thiazide or loop diuretics,
do his potassium after wash out period.
If you find the patient has persistent hypokalemia, suspect primary
aldosteronism. Simple test like doing
the aldosterone levels or doing an MRI.
In the MRI, you will see there is an arrow, a horn-shaped shadow there
which is a Conn’s tumor, you will pick up.
In such patient nothing else but to control the blood pressure,
spironolactone will be enough or eplerenone will be enough to control his
hypertension. Of course you will give
some other drug to control this, but you will be sure that you will not give
any thiazide diuretics.
Another
thing, very common, which is not recognized but we angioplasters recognize is
association of renal artery stenosis with coronary artery disease. These are the patients who have got
documented coronary artery disease, 8% to 15% patients who have got coronary
artery disease have significant renal artery stenosis and that may be the
reason for the uncontrol hypertension in these patients, so therefore do not
forget to get their duplex Doppler done to see if they have got an associated
renal artery stenosis and treatment is simple.
As a matter of fact the first line of treatment is to try to manage them
medically. If they cannot control their
hypertension then of course the option to the renal angioplasty is always
available. One more thing and the last
thing, I want to sort of highlight that several of these patients in your
clinics will come back and ask you a question.
Because all of them are older group, senior citizens, and they are on
the antihypertensive drugs you have given them and majority of the
antihypertensive drugs will lead to erectile dysfunction. This is not an uncommon complaint the patient
will come back to you. This is one of
the challenge you have to accept and advise the patient what to do. Many of them will come to you back with
erectile dysfunction and beta-blockers, calcium channel blockers, and ACE
inhibitors. All three of them along with
diuretics of course, diuretic is not the drug which I was advising but all
these three drugs can combine lead to erectile dysfunction, so what should we
advice to them. Do you all allow them to
take sildenafil or not. Let me show you some data on this. If you look at the patients who had no
antihypertensive drugs versus who had antihypertensive drugs and when you give
them sildenafil, you will find that the difference was not significant. There was fall in the blood pressure with
sildenafil and no antihypertensive
group, slightly more drop in the systolic and diastolic blood pressure in the
sildenafil group. So if your patient is
on beta blocker or a calcium channel blocker and not very large doses as we
call it complex combination, you can certainly advise them to go ahead and take
sildenafil. So, this is one of the
challenge, you have to see, what has to be done or advice to the patient like
this. Only thing is that you have to be
sure that your patient has no concurrent use of nitrates because you are going
to advice him, the patient has got angina, he has hypertension so you are going
to advice him nitrates. So ensure that
the patient is not on nitrates. If you
want to use sildenafil tell him to take nitrate free period of 48 hours. Let him have a washout of nitrates from body
for 48 hours then you can use the sildenafil.
But patient being on simple drug regime like some small dose of
beta-blockers, small dose of calcium channel blocker, no problem you can advice
them, but suppose if he is on a very complex, like very large dose of
beta-blocker and large doses of calcium blockers and very large dose of ACE
inhibitors or ARBs, perhaps in such a patient you have to be very
cautious. Of course, you have to see
that the patient is not in left ventricular failure, he has no creps, he has no
S3 gallop, and little bit careful about advising him sildenafil in such a
situation.
Every
lecture must end, I always say with a CME question. So, I have got CME question to you and I
would like you to answer this questions.
Which one is the more hypertensive during this exercise test, doctor,
patient, none, or both. Who says doctor,
who says patient, and who says both, and who says none. I say none because both of them are
happy. Happiness does not bring
hypertension. Thank you very much.
QUESTION AND ANSWER
QUESTION FROM AUDIENCE:
Sir, using beta-blocker and getting an heart block on an ECG,
particularly a trifascicular block, do you have to be externally cautious when
you initiate beta-blocker, particularly in ischemic heart disease and how do
you follow them up?
Dr D B Pahalajani:
See first of all beta-blockers do not cause a trifascicular block
because, the effect of beta blocker as with the proximal conduction system at
the sinus nodal level and the AV nodal level it does not cause any distal
blocks. So it does not cause bundle
branch block, it does not cause a trifascicular block, and does not cause any
intra-atrium block, so whatever blocks occur, they occurred proximally that is
#1. You are certainly right that even if
it is a proximal block it is mater of concern because you do not want to reduce
the pulse rate to such a level that the patient get symptoms, because
ultimately when the pulse rate goes down below 50, 55, 40 and if he is not use
to it like athletes are used to pulse rate of 35 and 40, but he is not an
athlete, so he may feel asthenia and may feel weak so then you have to reduce
the dose of beta-blockers in these patients.
Though it may not be even AV block, it may be sinus nodal block, so the
patient may develop a sinus bradycardia.
In such a patient you have to reduce the dose of beta-blockers and may
be increase the dose of calcium channel blockers or increase the dose of ACE
inhibitors or ARBs certainly you have to be careful about these patients.
Well some
of these patients who may have had sinus node disease say for example
preexisting sinus node disease, in these patients even a small dose of beta
blocker you give them, suppose you started with metoprolol 25 mg b.i.d., or you
gave him an extended release of metoprolol XL preparation, you found that after
seven days his pulse rate has further fallen down. It is quite possible you go back on his old
ECG, you find that he has sinus bradycardia and may be he has a sick sinus
syndrome. In such a patient you probably
should not give beta-blocker and fall back on calcium blockers and combine with
the ACE inhibitor or ARB.
QUESTION FROM AUDIENCE:
Doctor, you just made a passing mention about superiority of nifedipine
in terms of endothelium, now does that affect is not there for amlodipine.
Dr D B Pahalajani:
No, that is what the nifedipine people are saying that is the basic
difference between nifedipine and amlodipine.
While nifedipine, equally brings down the pressure, but it has got
salutary effect on the endothelial function whereas amlodipine has no such
function. So, that is the basic
difference between the two.
QUESTION FROM AUDIENCE:
I am sure that most of us, if you see the combination, you will have
atenolol with nifedipine plenty of combination, amlodipine with atenolol
combination. there is no combination of nifedipine with metoprolol. I think Eris can make a note of it.
Dr D B Pahalajani:
You see I will tell you nifedipine went into very big disrepute for
about five or six years back when the data came out, there was an adverse
reaction of precipitating acute myocardial infarction because in those days we
ourselves also use to write down short-acting nifedipine and may be some time
we would write nifedipine retard, but many time we write down nifedipine say 10
mg three times a day or 5 mg three times a day, it was short acting 6 hourly
working acting nifedipine, but when the data came out that when you give such
acting nifedipine in some patient where you were not very careful about
eliciting the history of the patient, some of them were acute coronary syndrome
and unstable angina, in these patients when you give nifedipine sudden precipitous
fall in blood pressure precipitated myocardial infarction. So that is where headlines came that
“nifedipine precipitates heart attacks” and that was for particular type of
nifedipine. But when you give sustained
release nifedipine, it has no such effect.
There has been actually GITS trial and so many trial have been, ENCORE
trial, INSIGHT. Actually largest trial
has been ACTION trial, and they have found that there has been no such effect
with the sustained release nifedipine.
But since the fear is there in our mind and now the other drugs are
available, like cilnidipine is going to be available large scale in market, the
amlodipine is available, but no body is now going back into looking at the
endothelial function aspect of the nifedipine because now you have got ACE
inhibitor and ARBs, which improve the endothelial function. You have got statins which are been used so
you have got another salutary effect on the endothelial function, so people
have forgotten that particular function of nifedipine. They say why unnecessarily write on a
prescription where we are not sure.
QUESTION FROM AUDIENCE:
I would just take a take on role of beta blocker in a patient who is
also an asthmatic. You did this display the kind of beta-blockers that we have
hypertensive, CAD patient who is extremely asthmatic would you be happy enough
to use beta-blocker in such a patient or any subset of beta-blockers that would
be safe?
Dr D B Pahalajani:
Very good, excellent question, and as a matter of fact, there is a slide
on which they have shown that tolerance of the patient to the traditional
contraindications to beta-blockers and one of them was COPD and in all this
traditional contraindication 85% of patient could tolerate beta-blockers, only
15% patient who could not tolerate. Now
question comes for the patient who have got bronchial asthma. Very good question. In these patients you should try, if you want
to give a beta-blocker, should try cardio-selective may be something like
metoprolol which you can try. But again
the selectivity is purely dose related.
Literature says 200 mg, but I would say in Indian population were body
surface area is small, body mass index is small, I would feel that 100 mg
should be considered as the cut-off dose beyond which we should not go, but up
to 100 mg cardioselectivity is preserved, so you can try, but still even up to
100 mg when you keep on giving them for longer time some patient will develop
bronchospasm, so then you have to switch over from say beta-blockers to either
calcium channel blocker or ACE inhibitor or ARB, but you can still try
cardioselective beta-blocker, remember it
is dose related.