http://www.theheart.org/viewArticle....l_id=tho22oct0
8


HYPERTENSION
Reducing heart rate in hypertension is harmful‹or is it just atenolol?
OCTOBER 22, 2008 | Lisa Nainggolan
New York, NY - Slowing the heart rate with beta blockers in people with
hypertension is associated with an increased risk of cardiovascular
events and death, a new systematic review shows [1]. Furthermore, the
slower the heart rate, the greater the risk, report Dr Sripal Bangalore
(St Luke's Roosevelt Hospital, New York) and colleagues in the October
28, 2008 issue of the Journal of the American College of Cardiology.

What we show is that in hypertension, when you slow down the heart rate
with a beta blocker, it actually shortens your life.
Senior author Dr Franz Messerli (St Luke's Roosevelt Hospital) told
heartwi "Slowing heart rate is known to prolong life expectancy, and
with beta blockers post-MI and in heart failure, the slower you can make
the heart rate, the better. But this new paper goes against the grain.
What we show is that in hypertension, when you slow down the heart rate
with a beta blocker, it actually shortens your life expectancy, it
causes more heart attacks, more heart failure, and more strokes."
Messerli says he and his team believe the likely explanation for this is
"that slowing the heart rate with beta blockers increases the central
pressure, and obviously the latter is one of the determinants of stroke
and heart attack."
Another hypertension expert sees things slightly differently, however.
Dr John Cockcroft (Wales Heart Institute, Cardiff, UK) argues that in
this review, the studies included almost exclusively used
atenolol‹something the authors do point out‹and that it is this drug per
se that is likely the culprit here.
What is vitally important to determine in this setting, he adds, "is
whether it's atenolol that's bad or whether it's reduction of heart rate
that's bad." This is crucial because there are other drugs that aren't
beta blockers that lower heart rate, he explained, such as the new agent
ivabradine (Procoralan, Servier). "This issue needs resolving because if
it's heart-rate reduction [that is the cause], then that's bad news, and
we need to know about it."

Bradycardia not synonymous with cardioprotection in hypertension

In the new review, Bangalore et al included nine randomized controlled
trials evaluating beta blockers for hypertension that also reported
heart-rate data, including 34*096 patients taking beta blockers, 30*139
taking other antihypertensives, and 3987 receiving placebo. Of the
patients in the beta-blocker arms, 78% received atenolol, 9% took
oxprenolol, 1% propranolol, and 12% received
atenolol/metoprolol/pindolol or hydrochlorothiazide.
Paradoxically, a lower heart rate (as attained in the beta-blocker group
at study end) was associated with a greater risk for the end points of
all-cause mortality (r=-0.51; p0.0001), cardiovascular mortality
(r=-0.61; p0.0001), MI (r=-0.85; p0.0001), stroke (r=-0.20; p=0.06),
or heart failure (r=-0.64; p0.0001).
"In contrast to patients with MI and heart failure,
beta-blocker-associated reduction in heart rate increased the risk of
cardiovascular events and death for hypertensive patients," the
researchers conclude.
Messerli told heartwi "In the past, the term cardioprotection was
synonymous with bradycardia. The more you had bradycardia, the better
the heart was protected. This is not the case in hypertension. This may
be okay post-MI and in heart failure, but it's not okay in hypertension."
In an editorial accompanying the review, Dr Norman M Kaplan (University
of Texas Southwestern Medical Center, Dallas) agrees [2]: "With this
addition to the evidence, beta blockers will surely remain as indicated
for heart failure, for after MI, and for tachyarrhythmias, but no longer
for hypertension in the absence of these compelling indications."

Difficult to extrapolate findings beyond atenolol

Messerli and his colleagues do state in their discussion, however:
"Further studies are needed to establish causation. It should also be
noted that the beta blocker used in the studies was mainly atenolol, and
hence, any meaningful extrapolation of these results to other beta
blockers, including the newer vasodilating beta blockers, should be done
with caution."

Any meaningful extrapolation of these results to other beta blockers,
including the newer vasodilating beta blockers, should be done with
caution.
Cockcroft contends that because this new review contains studies almost
exclusively using atenolol, "this doesn't move the argument forward very
much." Atenolol, he says, "has been tried and found guilty, and yet
around 40% of prescriptions for beta blockers in the UK and in the US
are still for atenolol. Atenolol should not be given to anybody. Nobody
disagrees that atenolol is guilty, and yet we are still using it."
He says that people think lowering heart rate is good, "because it
reduces the amount of cyclical stress on the aorta, but if at the same
time you are putting the central aortic pressure up, these things may
cancel each other out." Atenolol has been compared in this respect with
one of the newer vasodilating beta blockers, nebivolol (Bystolic,
Forest/Mylan), and it was found that atenolol increases the central
aortic pressure but nebivolol does not [3], he notes.
"The newer vasodilating beta blockers may well not have any of these
detrimental effects. Because they are vasodilatory, they may well offset
the slowing of heart rate by decreasing wave reflection from the
periphery and, in the case of nebivolol, by releasing nitric oxide, an
endogenous vasodilator with antiatherogenic activity," he adds.

To beta block or not, that is the question

Regarding the role now of beta blockers in hypertension, Messerli
commented to heartwi "Beta blockers in hypertension are not very
useful, and you probably should use any other single drug first before
you add a beta blocker, and if you want to add a beta blocker, please
use a vasodilating one such as carvedilol or nebivolol."

Atenolol should not be given to anybody. Nobody disagrees that atenolol
is guilty, and yet we are still using it.
Cockcroft agrees with much of this, but maintains that beta blockade is
still very important. "Beta blockade is vital. A large number of
patients with hypertension have angina as well, so they've got to have a
beta blocker. Furthermore, there is now evidence that younger subjects
with hypertension (50 years of age) may well be better treated with a
beta blocker than older hypertensives, as they have a different
hemodynamic form of hypertension. It's what beta blocker you give them
that counts, and it shouldn't be atenolol."
He believes the continued obsession with atenolol is "partly due to
cheapness and habit, but also due to the failure of the people with good
beta blockers to disseminate information on the deleterious effects of
atenolol."

Most important issue still not resolved; central pressure should be the
focus

Cockcroft says the more vital issue "that still needs resolving is
whether it's atenolol that is bad or heart-rate reduction that is bad
news. If it's the latter, we need to know about it, because there are
other drugs that lower heart rate, such as ivabradine, and if you look
at the BEAUTIFUL trial with this new drug, it was very negative."
He believes a trial directly comparing ivabradine with atenolol in terms
of central aortic pressure is needed, "and then you look at the effects
on hemodynamics in terms of central pressure."
Another way of examining this issue could be to give atenolol to people
who have pacemakers in to slow their heart rate down and then switch the
pacemaker back on and bring the heart rate back up to the baseline
level‹still with them having atenolol on board‹and "if the detrimental
hemodynamics go away, then it's all heart rate, and if it doesn't, then
atenolol has some effect beyond heart-rate reduction that is bad.
"These are very, very important mechanistic experiments that need to be
done now that we have other drugs that lower heart rate that aren't beta
blockers, and we clearly need to be doing these studies," Cockcroft
stresses.
"I personally think that it's the atenolol that is bad and that it has
some effects beyond heart-rate reduction that are bad, but we don't know
from this Messerli review. If half [the trials they included] had used
another beta blocker, then you would know for sure."
"It's central pressure that the pharmaceutical industry should be
focusing on," he adds, "because different drugs, especially beta
blockers, have differential effects on central pressure, and we know
from the Strong Heart Study that central aortic pressure is a better
predictor of outcome than pressure in the arm."
Messerli is a member of the speakers' bureau for Abbott,
GlaxoSmithKline, Novartis, Pfizer, AstraZeneca, Bayer, Boehringer
Ingelheim, Bristol-Myers Squibb, Forest, Sankyo, and Sanofi and has
received research funding/grants from GlaxoSmithKline, Pfizer, Novartis
and CardioVascular Therapeutics. Cockcroft is on the advisory board of
Forest, which markets nebivolol, and has received research funding from
the company.

Sources
1. Bangalore S, Sawhney S, and Messerli FH. Relation of beta-blocker
induced heart rate lowering and cardioprotection in hypertension. J Am
Coll Cardiol 2008; 52: 1482-1489.
2. Kaplan NM. Beta-blockers in hypertension. Adding insult to injury.
J Am Coll Cardiol 2008; 52: 1490-1491.
3. Dhakam Z, Yasmin, McEniery CM, et al. A comparison of atenolol and
nebivolol in isolated systolic hypertension. J Hypertens 2008; 26:
351-356.

...........

Bill who is drug free.

--
Garden in shade zone 5 S Jersey USA

Bill

--
Garden in shade zone 5 S Jersey USA

Bill

On Oct 22, 5:00*pm, Bill wrote:
http://www.theheart.org/viewArticle....l_id=tho22oct0
8

HYPERTENSION
Reducing heart rate in hypertension is harmful‹or is it just atenolol?
OCTOBER 22, 2008 | Lisa Nainggolan
New York, NY - Slowing the heart rate with beta blockers in people with
hypertension is associated with an increased risk of cardiovascular
events and death, a new systematic review shows [1]. Furthermore, the
slower the heart rate, the greater the risk, report Dr Sripal Bangalore
(St Luke's Roosevelt Hospital, New York) and colleagues in the October
28, 2008 issue of the Journal of the American College of Cardiology.

What we show is that in hypertension, when you slow down the heart rate
with a beta blocker, it actually shortens your life.
Senior author Dr Franz Messerli (St Luke's Roosevelt Hospital) told
heartwi "Slowing heart rate is known to prolong life expectancy, and
with beta blockers post-MI and in heart failure, the slower you can make
the heart rate, the better. But this new paper goes against the grain.
What we show is that in hypertension, when you slow down the heart rate
with a beta blocker, it actually shortens your life expectancy, it
causes more heart attacks, more heart failure, and more strokes."
Messerli says he and his team believe the likely explanation for this is
"that slowing the heart rate with beta blockers increases the central
pressure, and obviously the latter is one of the determinants of stroke
and heart attack."
Another hypertension expert sees things slightly differently, however.
Dr John Cockcroft (Wales Heart Institute, Cardiff, UK) argues that in
this review, the studies included almost exclusively used
atenolol‹something the authors do point out‹and that it is this drug per
se that is likely the culprit here.
What is vitally important to determine in this setting, he adds, "is
whether it's atenolol that's bad or whether it's reduction of heart rate
that's bad." This is crucial because there are other drugs that aren't
beta blockers that lower heart rate, he explained, such as the new agent
ivabradine (Procoralan, Servier). "This issue needs resolving because if
it's heart-rate reduction [that is the cause], then that's bad news, and
we need to know about it."

Bradycardia not synonymous with cardioprotection in hypertension

In the new review, Bangalore et al included nine randomized controlled
trials evaluating beta blockers for hypertension that also reported
heart-rate data, including 34*096 patients taking beta blockers, 30*139
taking other antihypertensives, and 3987 receiving placebo. Of the
patients in the beta-blocker arms, 78% received atenolol, 9% took
oxprenolol, 1% propranolol, and 12% received
atenolol/metoprolol/pindolol or hydrochlorothiazide.
Paradoxically, a lower heart rate (as attained in the beta-blocker group
at study end) was associated with a greater risk for the end points of
all-cause mortality (r=-0.51; p0.0001), cardiovascular mortality
(r=-0.61; p0.0001), MI (r=-0.85; p0.0001), stroke (r=-0.20; p=0..06),
or heart failure (r=-0.64; p0.0001).
"In contrast to patients with MI and heart failure,
beta-blocker-associated reduction in heart rate increased the risk of
cardiovascular events and death for hypertensive patients," the
researchers conclude.
Messerli told heartwi "In the past, the term cardioprotection was
synonymous with bradycardia. The more you had bradycardia, the better
the heart was protected. This is not the case in hypertension. This may
be okay post-MI and in heart failure, but it's not okay in hypertension."
In an editorial accompanying the review, Dr Norman M Kaplan (University
of Texas Southwestern Medical Center, Dallas) agrees [2]: "With this
addition to the evidence, beta blockers will surely remain as indicated
for heart failure, for after MI, and for tachyarrhythmias, but no longer
for hypertension in the absence of these compelling indications."

Difficult to extrapolate findings beyond atenolol

Messerli and his colleagues do state in their discussion, however:
"Further studies are needed to establish causation. It should also be
noted that the beta blocker used in the studies was mainly atenolol, and
hence, any meaningful extrapolation of these results to other beta
blockers, including the newer vasodilating beta blockers, should be done
with caution."

Any meaningful extrapolation of these results to other beta blockers,
including the newer vasodilating beta blockers, should be done with
caution.
Cockcroft contends that because this new review contains studies almost
exclusively using atenolol, "this doesn't move the argument forward very
much." Atenolol, he says, "has been tried and found guilty, and yet
around 40% of prescriptions for beta blockers in the UK and in the US
are still for atenolol. Atenolol should not be given to anybody. Nobody
disagrees that atenolol is guilty, and yet we are still using it."
He says that people think lowering heart rate is good, "because it
reduces the amount of cyclical stress on the aorta, but if at the same
time you are putting the central aortic pressure up, these things may
cancel each other out." Atenolol has been compared in this respect with
one of the newer vasodilating beta blockers, nebivolol (Bystolic,
Forest/Mylan), and it was found that atenolol increases the central
aortic pressure but nebivolol does not [3], he notes.
"The newer vasodilating beta blockers may well not have any of these
detrimental effects. Because they are vasodilatory, they may well offset
the slowing of heart rate by decreasing wave reflection from the
periphery and, in the case of nebivolol, by releasing nitric oxide, an
endogenous vasodilator with antiatherogenic activity," he adds.

To beta block or not, that is the question

Regarding the role now of beta blockers in hypertension, Messerli
commented to heartwi "Beta blockers in hypertension are not very
useful, and you probably should use any other single drug first before
you add a beta blocker, and if you want to add a beta blocker, please
use a vasodilating one such as carvedilol or nebivolol."

Atenolol should not be given to anybody. Nobody disagrees that atenolol
is guilty, and yet we are still using it.
Cockcroft agrees with much of this, but maintains that beta blockade is
still very important. "Beta blockade is vital. A large number of
patients with hypertension have angina as well, so they've got to have a
beta blocker. Furthermore, there is now evidence that younger subjects
with hypertension (50 years of age) may well be better treated with a
beta blocker than older hypertensives, as they have a different
hemodynamic form of hypertension. It's what beta blocker you give them
that counts, and it shouldn't be atenolol."
He believes the continued obsession with atenolol is "partly due to
cheapness and habit, but also due to the failure of the people with good
beta blockers to disseminate information on the deleterious effects of
atenolol."

Most important issue still not resolved; central pressure should be the
focus

Cockcroft says the more vital issue "that still needs resolving is
whether it's atenolol that is bad or heart-rate reduction that is bad
news. If it's the latter, we need to know about it, because there are
other drugs that lower heart rate, such as ivabradine, and if you look
at the BEAUTIFUL trial with this new drug, it was very negative."
He believes a trial directly comparing ivabradine with atenolol in terms
of central aortic pressure is needed, "and then you look at the effects
on hemodynamics in terms of central pressure."
Another way of examining this issue could be to give atenolol to people
who have pacemakers in to slow their heart rate down and then switch the
pacemaker back on and bring the heart rate back up to the baseline
level‹still with them having atenolol on board‹and "if the detrimental
hemodynamics go away, then it's all heart rate, and if it doesn't, then
atenolol has some effect beyond heart-rate reduction that is bad.
"These are very, very important mechanistic experiments that need to be
done now that we have other drugs that lower heart rate that aren't beta
blockers, and we clearly need to be doing these studies," Cockcroft
stresses.
"I personally think that it's the atenolol that is bad and that it has
some effects beyond heart-rate reduction that are bad, but we don't know
from this Messerli review. If half [the trials they included] had used
another beta blocker, then you would know for sure."
"It's central pressure that the pharmaceutical industry should be
focusing on," he adds, "because different drugs, especially beta
blockers, have differential effects on central pressure, and we know
from the Strong Heart Study that central aortic pressure is a better
predictor of outcome than pressure in the arm."
Messerli is a member of the speakers' bureau for Abbott,
GlaxoSmithKline, Novartis, Pfizer, AstraZeneca, Bayer, Boehringer
Ingelheim, Bristol-Myers Squibb, Forest, Sankyo, and Sanofi and has
received research funding/grants from GlaxoSmithKline, Pfizer, Novartis
and CardioVascular Therapeutics. Cockcroft is on the advisory board of
Forest, which markets nebivolol, and has received research funding from
the company.

Sources
* *1. Bangalore S, Sawhney S, and Messerli FH. Relation of beta-blocker
induced heart rate lowering and cardioprotection in hypertension. J Am
Coll Cardiol 2008; 52: 1482-1489.
* *2. Kaplan NM. Beta-blockers in hypertension. Adding insult to injury.
J Am Coll Cardiol 2008; 52: 1490-1491.
* *3. Dhakam Z, Yasmin, McEniery CM, et al. A comparison of atenolol and
nebivolol in isolated systolic hypertension. J Hypertens 2008; 26:
351-356.

..........

Bill who is drug free.

--
Garden in shade zone 5 S Jersey USA

*Bill

--
Garden in shade zone 5 S Jersey USA

*Bill

Personal experience, I take a small amount of metoprolol after getting
stents for a nearly blocked coronary artery. This study has no
opinion on metoprolol . Never had hypertension in the usual sense but
now it is lower than normal along with tough time to get heart rate
above 100. To measure interior artery pressure you probably need a
heart cath. I had for high pulmonary artery pressure from a PE
resolved by surgery. Echo cardiogram can monitor pulmonary pressure,
but you're looking at a $1,000 test - heart cath considerably more.

Don't brag about being drug free. I was so until about age 60 but no
longer.

In article ,
Bill wrote:

http://www.theheart.org/viewArticle....l_id=tho22oct0
8


HYPERTENSION
Reducing heart rate in hypertension is harmful‹or is it just atenolol?
OCTOBER 22, 2008 | Lisa Nainggolan
New York, NY - Slowing the heart rate with beta blockers in people with
hypertension is associated with an increased risk of cardiovascular
events and death, a new systematic review shows [1]. Furthermore, the
slower the heart rate, the greater the risk, report Dr Sripal Bangalore
(St Luke's Roosevelt Hospital, New York) and colleagues in the October
28, 2008 issue of the Journal of the American College of Cardiology.

Good article, Bill. Thanks.
--

Billy
Republican and Democratic "Leadership" Behind Bars
http://electronicintifada.net/v2/article1248.shtml
http://www.youtube.com/watch?v=9KVTf...ef=patrick.net

In article
,
Billy wrote:

In article ,
Bill wrote:

http://www.theheart.org/viewArticle....l_id=tho22oct0
8


HYPERTENSION
Reducing heart rate in hypertension is harmful‹or is it just atenolol?
OCTOBER 22, 2008 | Lisa Nainggolan
New York, NY - Slowing the heart rate with beta blockers in people with
hypertension is associated with an increased risk of cardiovascular
events and death, a new systematic review shows [1]. Furthermore, the
slower the heart rate, the greater the risk, report Dr Sripal Bangalore
(St Luke's Roosevelt Hospital, New York) and colleagues in the October
28, 2008 issue of the Journal of the American College of Cardiology.

Good article, Bill. Thanks.

I wish this is not true. Something like BP not too invasive as a tool
to get a idea what our well being is in a mechanical way. Simple to
use with many drugs and active life style changes like sodium intake
reduction to get the desired end point. So it seemed and is widely
taken as a given .

http://www.americanheart.org/presenter.jhtml?identifier=3027275


Years ago normal BP was your age over 100. Perhaps it still is.

Bill

PS Billy thanks for the positive reinforcement !

--
Garden in shade zone 5 S Jersey USA

Bill

In article ,
Bill wrote:

In article
,
Billy wrote:

In article ,
Bill wrote:

http://www.theheart.org/viewArticle....l_id=tho22oct0
8


HYPERTENSION
Reducing heart rate in hypertension is harmful‹or is it just atenolol?
OCTOBER 22, 2008 | Lisa Nainggolan
New York, NY - Slowing the heart rate with beta blockers in people with
hypertension is associated with an increased risk of cardiovascular
events and death, a new systematic review shows [1]. Furthermore, the
slower the heart rate, the greater the risk, report Dr Sripal Bangalore
(St Luke's Roosevelt Hospital, New York) and colleagues in the October
28, 2008 issue of the Journal of the American College of Cardiology.

Good article, Bill. Thanks.

I wish this is not true. Something like BP not too invasive as a tool
to get a idea what our well being is in a mechanical way. Simple to
use with many drugs and active life style changes like sodium intake
reduction to get the desired end point. So it seemed and is widely
taken as a given .

http://www.americanheart.org/presenter.jhtml?identifier=3027275


Years ago normal BP was your age over 100. Perhaps it still is.

Bill

PS Billy thanks for the positive reinforcement !

Mistake Your age plus 100 over 100.


Duh

Bill

--
Garden in shade zone 5 S Jersey USA

Bill