ACE inhibitor cough
Peppermint Patootie
been on a beta blocker for a number of years. Neither medication is or
was for my blood pressure. The beta blocker was for migraine
prevention, and the ACE inhibitor is for kidney protection from the
effects of my diabetes.
I had heard about the ACE inhibitor cough side-effect, and now I'm
wondering if what I'm experiencing is it. I'd read "persistent dry
cough" and thought it would be a chronic thing. My cough comes on about
6-12 times a day, beginning as a tickle in the back of my throat. I can
occasionally (but rarely) deliberately calm it and avoid breaking into a
coughing spasm, but usually it escalates into full-throated coughing
spasms until I can pop a (sugar free) cough drop into my mouth. Some
times it wakes me up in the middle of the night, and I awake later with
the remains of a cough drop in my mouth.
This is a new cough to me. It's winter, which means that my sinuses are
busy, and I'm blowing my nose off and on most of the time. I can
usually identify my sinuses as fairly full when the cough happens, but
then they're usually full-ish. Sinuses draining down the back of my
throat would have been what I presumed was the cause of the cough if it
didn't feel like a new phenomenon.
Does my description match other people's experience of the ACE inhibitor
cough, or, if not, could someone please describe it?
Thanks!
Priscilla, T2
Peppermint Patootie
and found this:
"The history in ACE inhibitor cough is quite characteristic. The patient
feels that there is a tickle at the back of the throat which leads to
paroxysms of coughing. These may be extreme enough to lead to vomiting.
Between episodes the patient is asymptomatic..."
This is from http://www.issc.info/cough.html#Aceinhibitorcough
I'm going off the lisinopril now until I can get a different
prescription from my PCP. I'm taking only 5 mg, and it's not for BP
control, so I'm not worried about going off it for a while. The cough
has been making me crazy.
PP, T2
Bill who putters
<Peppermint_Patootie-...@news.individual.net>,
Peppermint Patootie <Peppermin...@yahoo.com> wrote:
Make your own decision. Stuff I follow.
Bill
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
heartwire: "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; p<0.0001), cardiovascular mortality
(r=-0.61; p<0.0001), MI (r=-0.85; p<0.0001), stroke (r=-0.20; p=0.06),
or heart failure (r=-0.64; p<0.0001).
"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 heartwire: "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 heartwire: "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.
Related links
� BEAUTIFUL for some: No overall advantage of ivabradine, but
high-heart-rate patients may benefit
[Clinical cardiology > Clinical cardiology; Aug 31, 2008]
� New review "beats the drum" for not using beta blockers in
uncomplicated hypertension
[Lipid/Metabolic > Lipid/Metabolic; Aug 08, 2007]
� Central aortic pressure readings seen as more prognostic than
standard brachial pressure
[Prevention > Prevention; Jun 18, 2007]
� Cochrane review: Beta blockers should not be first line for
hypertension
[HeartWire > News; Feb 02, 2007]
� New UK hypertension guidelines omit beta blockers for routine use
[HeartWire > News; Jul 06, 2006]
CAFE published: Amlodipine/perindopril combo reduces central aortic BP
[Hypertension > Hypertension; Feb 21, 2006]
......................
: J Am Coll Cardiol. 2008 Sep 23;52(13):1062-72.
Links
Beta-blockers for primary prevention of heart failure in patients with
hypertension insights from a meta-analysis.
Bangalore S, Wild D, Parkar S, Kukin M, Messerli FH.
Department of Medicine, Division of Cardiology, St Luke's Roosevelt
Hospital and Columbia University College of Physicians and Surgeons, New
York, New York 10019, USA.
OBJECTIVES: This study sought to evaluate the efficacy of beta-blockers
(BBs) for primary prevention of heart failure (HF) in patients with
hypertension. BACKGROUND: The American College of Cardiology/American
Heart Association staging for HF classifies patients with hypertension
as stage A HF, for which BBs are a treatment option. However, the
evidence to support this is unknown. METHODS: We conducted a
MEDLINE/EMBASE/CENTRAL search of randomized controlled trials that
evaluated BB as first-line therapy for hypertension with follow-up for
at least 1 year and with data on new-onset HF. The primary outcome was
new-onset HF. Secondary outcomes were all-cause mortality,
cardiovascular mortality, myocardial infarction, and stroke. RESULTS:
Among the 12 randomized controlled trials, which evaluated 112,177
patients with hypertension, BBs reduced blood pressure by 12.6/6.1 mm Hg
when compared with placebo, resulting in a 23% (trend) reduction in HF
risk (p = 0.055). When compared with other agents, the antihypertensive
efficacy of BBs was comparable, which resulted in similar but no
incremental benefit for HF risk reduction in the overall cohort (risk
ratio: 1.00; 95% confidence interval: 0.92 to 1.08), in the elderly (>
or =60 years) or in the young (<60 years). Analyses of secondary
outcomes showed that BBs confirmed similar but no incremental benefit
for the outcomes of all-cause mortality, cardiovascular mortality, and
myocardial infarction but increased stroke risk by 19% in the elderly.
CONCLUSIONS: In hypertensive patients, primary prevention of HF is
strongly dependent on blood pressure reduction. When compared with other
antihypertensive agents, there was similar but no incremental benefit of
BBs for the prevention of HF. However, given the increased risk of
stroke in the elderly, BBs should not be considered as first-line agents
for prevention of HF.
PMID: 18848139 [PubMed - in process
............ Merck/Schering-Plough reach ezetimibe settlement
JULY 21, 2009 | Steve Stiles
Whitehouse Station and Kenilworth, NJ - The Merck/Schering-Plough joint
venture behind the cholesterol-lowering drug ezetimibe (Zetia; Vytorin
when paired with simvastatin) has announced it will pay $5.4 million to
35 US states and the District of Columbia, whose attorneys general have
been investigating whether the companies violated consumer-protection
laws in the way they marketed the drug after completion of the ENHANCE
trial [1,2]. The money is to reimburse the states for attorney's fees
and other costs related to the investigations.
The announcement is a coda to the tempestuous history of the drug,
which, as extensively covered by heartwire, pushed down LDL-cholesterol
levels significantly when combined with simvastatin in the 725-patient
trial, as it was intended to do, but failed to curtail disease
progression, as measured by changes in carotid intima-media thickness
over two years, compared with simvastatin alone. The population
consisted of patients with heterozygous familial hypercholesterolemia.
More controversial than the highly criticized design and conduct of the
trial was the nearly two-year interval between completion of ENHANCE and
any public disclosure of the results. Sketchy initial details emerged in
a January 2008 press release from the companies, and the final outcomes
were presented that March at the American College of Cardiology
Scientific Sessions.
The states alleged that the companies used direct-to-consumer
advertising to aggressively market Vytorin and Zetia during the long
"delay" in releasing the ENHANCE results, aware that they might cast an
unfavorable light on their products. Ezetimibe had been approved by the
FDA in 2004.
"Prior to the release of the study results, Vytorin had been heavily
promoted to consumers through TV commercials and print ads�.�.�.�that
suggest Vytorin is effective at treating high cholesterol caused both by
heredity and diet," observes a July 15 press release from the attorney
general's office of the State of Washington [2], which had participated
in the investigations of Merck/Schering-Plough. Washington will receive
$100�000 of the settlement money, it said.
"Today's agreement sets restrictions on how the companies market Zetia
and Vytorin in the future," the state announcement says. It also
includes a prohibition on ghostwritten articles, requirements that all
direct-to-consumer TV ads be vetted by the FDA before release and that
all other advertising adhere to the agency's regulations, and agreements
to appropriately register and report studies "and comply with detailed
rules prohibiting the deceptive use of clinical trials."
--
Garden in shade zone 5 S Jersey USA
http://www.youtube.com/watch?v=dBnniua6-oM deals with Sugars
Peppermint Patootie
Bill who putters <b2fore...@snip.net> wrote:
> In article
> <Peppermint_Patootie-...@news.individual.net>,
> Peppermint Patootie <Peppermin...@yahoo.com> wrote:
>
> > I may have found the answer. I finally googled it more intelligently
> > and found this:
> >
> > "The history in ACE inhibitor cough is quite characteristic. The patient
> > feels that there is a tickle at the back of the throat which leads to
> > paroxysms of coughing. These may be extreme enough to lead to vomiting.
> > Between episodes the patient is asymptomatic..."
> >
> > This is from http://www.issc.info/cough.html#Aceinhibitorcough
> >
> > I'm going off the lisinopril now until I can get a different
> > prescription from my PCP. I'm taking only 5 mg, and it's not for BP
> > control, so I'm not worried about going off it for a while. The cough
> > has been making me crazy.
> >
> > PP, T2
>
> Make your own decision. Stuff I follow.
I don't have hypertension, so I'm skipping all the stuff you cut and
pasted in.
PP
Kurt
Ask a qualified doctor about it, they may switch you to Ramipril or
Altace. A friend of mine had the same problem and switching to an
alternate fixed it.
For those who aren't on an ACE ask your doctor if it is something that
might be right for you. It has been proven (by accidnet from what I
remember) that an ACE inhibitor protects kidney problems for people
with diabetes. We're talking small dose (.5 mg daily). It is something
all diabetics should be taking, regardless if they are in good control
or not.
Kurt
Ozgirl
> I recently (a few months ago) started on an ACE inhibitor after having
> been on a beta blocker for a number of years. Neither medication is
> or was for my blood pressure. The beta blocker was for migraine
> prevention, and the ACE inhibitor is for kidney protection from the
> effects of my diabetes.
>
> I had heard about the ACE inhibitor cough side-effect, and now I'm
> wondering if what I'm experiencing is it. I'd read "persistent dry
> cough" and thought it would be a chronic thing. My cough comes on
> about 6-12 times a day, beginning as a tickle in the back of my
> throat. I can occasionally (but rarely) deliberately calm it and
> avoid breaking into a coughing spasm, but usually it escalates into
> full-throated coughing spasms until I can pop a (sugar free) cough
> drop into my mouth. Some times it wakes me up in the middle of the
> night, and I awake later with the remains of a cough drop in my mouth.
That would pretty much describe the 'pril cough. Go for an ARB. I take
Candesartan personally but there are many different ARB's.
vince
wrote:
> In article
> <Peppermint_Patootie-F27E1B.18553231122...@news.individual.net>,
> Peppermint Patootie <Peppermint_Patoo...@yahoo.com> wrote:
>
>
>
And the bad news for most beta blockers just keeps on coming...
http://www.eurekalert.org/pub_releases/2009-11/uoia-cst112009.php#
Carvedilol shown to have unique characteristics among beta blockers
CHAMPAIGN, Ill. — In a new study, researchers report that a class of
heart medications called beta-blockers can have a helpful, or harmful,
effect on the heart, depending on their molecular activity.
The study, which appears in the journal Circulation Research, found
that beta-blockers that target both the alpha- and beta-receptors on
the heart muscle offer the most benefit to cardiac patients, while
those that target only the beta-receptors can actually undermine the
structure and function of the heart.
Circulation Research is published by the American Heart Association.
Heart disease is the leading cause of death in the United States.
Patients with heart disease usually have higher levels of
catecholamines – hormones that activate the beta-adrenergic receptors
to stimulate cardiac muscle contraction. In this process, the heart
initially grows to become a more efficient pump. Unfortunately, the
researchers found, this growth also predisposes the heart to eventual
failure.
Traditionally, beta-blockers targeting the beta-adrenergic receptors
have been utilized as a long-term therapy for heart failure.
Interestingly, blocking adrenergic receptors has been widely used
clinically for nearly 50 years without a full understanding of the
molecular consequences of these drugs, said co-author and graduate
student David Cervantes. Kevin Xiang, a professor of molecular and
integrative physiology at the University of Illinois led the study.
The research team also included researcher Catherine Crosby.
A previous study in 2003 showed that the beta-blocker carvedilol
produced a greater survival benefit than another drug, metoprolol
tartrate. Carvedilol targets both the beta- and alpha-adrenergic
receptors.
The new study unveiled an elegant intracellular signaling system in
which beta-receptor activation modulates alpha-adrenergic signaling.
It showed that blocking the beta-receptor alone promotes cardiac
remodeling via growth of cardiac fibroblasts induced by alpha-
adrenergic receptor signaling. The growth of fibroblasts in the heart
further damages the integrity and function of the heart.
This observation suggests that the use of carvedilol in combination
with inhibitors of angiotensin-converting enzyme (ACE inhibitors) may
be of the greatest benefit to cardiac patients, and has significant
clinical implications on which beta-blockers patients should take.
"I think this is really good stuff," Xiang says. "It's a surprise
project. It's not what we initially intended looking into. But it's a
very nice, elegant study and a very beautiful cellular mechanism. It
definitely will help people along the way to understand how to further
manipulate this system. Beta blockers are still the most commonly used
drug for heart disease."....
Interestingly most beta blockers including the most widely
prescribed atenolol are of type that appear to cause heart damage.
Loretta Eisenberg
reason as you for protection of the kidneys. I went for my three month
visit to the endo and he heard me coughing and asked how long I had the
cough I told him a couple of months. He immediately took me off of it
and put me on a pill called diovan which didnt not cause any side
effects and my kidneys are perfect. Now my insurance company refuses to
pay for it. It is 300 a month. I am waiting for my doctor to come up
with a substitute.
Loretta
--
I
Andrew B. Chung, MD/PhD
It is likely that your PCP will switch you to an ARB (Angiotensin
Receptor Blocker) because of your not tolerating the ACEi
(lisinopril).
Love in the truth,
Andrew <><
--
Andrew B. Chung, MD/PhD
Board-certified Cardiologist
and Author of the 2PD-OMER Approach:
http://groups.google.com/group/sci.med.cardiology/msg/9ad0c19df5ffc2f7?
Jacquie
blocker with it and the cough went away. My Internist had just read an
article that the two drugs taken together seemed to have stopped the side
effects...it did...however, once they took me off the calcium channel
blocker the cough came back...they then put me on ARB's...I got shortness of
Breath big time...they said it could be a sign of allergy...so took me off
of it and tried another Ace Inhibitor...and I ended up with a serum rash
all over my body....come to find out years before when I was on it I did get
a rash on my ankles but thought is was a rash from the sun...it turned brown
and lasted quite a while. I no longer can take Ace Inhibitors because they
are afraid the allergy will get worse.
"Peppermint Patootie" <Peppermin...@yahoo.com> wrote in message
news:Peppermint_Patootie-...@news.individual.net...
Peppermint Patootie
"Jacquie" <happi...@earthlink.net> wrote:
> I had that cough with Ace Inhibitors.....they gave me a Calcium Channel
> blocker with it and the cough went away. My Internist had just read an
> article that the two drugs taken together seemed to have stopped the side
> effects...it did...however, once they took me off the calcium channel
> blocker the cough came back...they then put me on ARB's...I got shortness of
> Breath big time...they said it could be a sign of allergy...so took me off
> of it and tried another Ace Inhibitor...and I ended up with a serum rash
> all over my body....come to find out years before when I was on it I did get
> a rash on my ankles but thought is was a rash from the sun...it turned brown
> and lasted quite a while. I no longer can take Ace Inhibitors because they
> are afraid the allergy will get worse.
Thanks, Jacquie. That's helpful.
I've been off lisinopril for a couple of days now, and today (so far) I
haven't had one coughing fit. :-)
Priscilla