Re: Alternatives to CABG and Stent???

In article
<not-to-here-williamwag-524ECA.15562223092006@xxxxxxxxxxxxxxxxxxxxxxxxxx
..net>,
William Wagner <not-to-here-williamwag@xxxxxxxxx> wrote:

In article <21uah255pvlmnurq82e48mm4jl51mva7hi@xxxxxxx>,
Don <don81846@xxxxxxxxxxxxxxxxxxxxx> wrote:

x-no-archive: yes

I've seen a little bit about angiogenesis drugs and other CABG
alternatives recently but my doc says that stuff is a long way in the
future. Is it???

Recent Lipid Panel:

LDL 174
HDL 26
Triglyceride 112
Glucose 109

I know my LDL is high and the HDL is low. I've had a lot of "skipped"
heart beats all my life but I've never had angina. My HDL is probably
low because I stopped riding 3,200 miles a year on my bike due to bad
back pain.

I probably do need some type of intervention but I'm concerned about
some of the problems associated with CABG. I've read that memory loss
and cognitive problems occur at a high rate with bypass surgery. I've
observed this in people that I've known.

I've read that those problems are caused by emboli and tiny gas
bubbles reaching the brain. The problems can be reduced by not using
the heart/lung machine and by not disturbing the aorta during surgery
but the reduction is only about 50%. That's still pretty bad odds in
my opinion.

I will appreciate your feedback.

Thank you.

Don


Hi Don!

Look at this sometime and play with the numbers.

http://www.yourdiseaserisk.harvard.edu/hccpquiz.pl?func=start&quiz=heart

Ask your doc about Niacin to get that HDL up. Look into Yoga or Tai
Chi or walk about but back pain that stopped a biker? Serious!
Anyway move ....consider dance too.

https://www.heartprofiler.nexcura.com/Secure/InterfaceSecure.asp?DB=1

There is some controversy concerning intervention for mild angina.
Last cardio meeting spoke about this but I can't find the info. Perhaps
someone can post it?

Best!


Bill

Found it Don.


Pack Rat Bill.


...............

2006 AHA/ACCF Syncope Statement stirs debate
Drs Carlos Morillo, David Benditt, and Adam Strickberger discuss the
recent AHA/ACCF Syncope Statement.

Studies linking drug-eluting stents to increased mortality/MI spark
impassioned pleas for reason and calls for calm

September 3, 2006

Shelley Wood






Barcelona, Spain - Many attendees of the World Congress of Cardiology
2006 had quit the conference center for sunshine and sangria by the time
Drs Edoardo Camenzind (University Hospital Geneva, Switzerland) and
Alain J Nordmann (University Hospital Basel, Switzerland) took the stage
Sunday evening with the final presentation of the hotline session,
stunning the remaining audience members with evidence of increased death
in patients randomized to drug-eluting stents (DES) within the trial
programs that secured approval for the devices in the first place.

Both of the meta-analyses combined all of the Cordis/J&J-sponsored
Cypher randomized trials, as well as the Boston Scientific-sponsored
Taxus program: one found an increased incidence of death and Q-wave MI
with the Cypher stent and a trend toward increased death/Q-wave-MI with
the Taxus, while the second found no differences in cardiac mortality
but an increase in noncardiac mortality, again with the Cypher stent.




Dr Edoardo Camenzind


The separate presentations, which shared a single hotline
slot?necessitating rushed synopses on the part of the presenters?spurred
discussant Dr Salim Yusuf (McMaster University, Hamilton, ON) to deliver
a thundering indictment of what he later described to the press as an
"epidemic of madness" over misuse of PCI for stable angina in general
and drug-eluting stents specifically.
"As clinicians we seem to have lost our clinical judgment, let alone our
ability to view data and evidence," Yusuf stated. "We therefore need a
thoughtful and selective approach to PCI, complementing full medical
therapy. . . . The whole field of angioplasty has been led astray by a
preoccupation with restenosis, for which study after study has shown has
no prognostic value. We're chasing problems that are iatrogenic that
naturally would not exist in people. We've had a perverse financial
incentive on the practice of cardiology. It is time to stop and
reevaluate."

Two meta-analyses draw on company-sponsored trials






As clinicians we seem to have lost our clinical judgment, let alone our
ability to view data and evidence.







Camenzind's meta-analysis was based on two separate analyses of the
sirolimus and paclitaxel data. In the first, the investigators examined
death and Q-wave MI in the published or presented papers, pooling them
by time of follow-up. From eight to nine months of follow-up, out to
one, two, and three years of follow-up, death/MI rates increased at
rates that ranged from 30% to 40% higher in the Cypher-treated patients
than those of the bare-metal-stent controls. A similar trend was seen,
over time, for the paclitaxel-eluting stent, but here the relative
difference between the Taxus and the bare-metal stent was only about 5%
difference over the three years of follow-up.
In the second analysis, all of the randomized trials within each stent's
program were stratified by last follow-up data. In this analysis,
serious adverse events in sirolimus were 6.3% compared with 3.9% in the
bare-metal-stent group (p=0.03) and in the paclitaxel trials were 2.6%
vs 2.3% (p=NS).
"We conclude that death and Q-wave MI [as the] clinical presentation of
stent thrombosis have a higher incidence in first-generation DES as
compared with bare-metal controls," Camenzind stated. "Excess events
appear to occur with both types of stents, although the magnitude seems
to be higher with sirolimus. A risk/benefit analysis of systematic use
of first-generation drug-eluting stents is warranted."




Dr Alain J Nordmann


Nordmann's findings, while raising the specter of increased deaths,
actually clashed somewhat with those of Camenzind. Nordmann et al
combined data from 17 randomized controlled trials of paclitaxel- or
sirolimus-eluting stents to evaluate total mortality, cardiac mortality,
and noncardiac mortality. While total mortality at one year trended
toward a benefit of DES, at two, three, and four years the investigators
saw a trend toward increased mortality with DES. For cardiac mortality,
however, there was no statistically significant difference between DES
and bare-metal stents or for either sirolimus- or paclitaxel-eluting
stent compared with bare-metal stents. Most striking, however, was the
data for noncardiac deaths, which at two and three years pointed to an
association between sirolimus stent implantation and increased
noncardiac mortality. Separate analyses identified these deaths as
cancer, stroke, or lung disease.
"DES for the treatment of coronary artery disease do not reduce
mortality when compared with bare-metal stents," Nordmann concluded.
"Preliminary evidence suggests that sirolimus but not paclitaxel may
lead to an increase in noncardiac mortality. Long-term follow-up and
assessment of cause-specific deaths in patients receiving DES are
mandatory to determine safety of patients receiving these devices."

Impassioned calls for a fresh look at DES, without industry involvement




Dr Salim Yusuf


To the press, Nordmann pointed out that obtaining raw data on mortality
from the stent manufacturers had been "extremely difficult,"
highlighting the need for non-company-sponsored, large randomized
clinical trials with ample follow-up.
At the very least, said Yusuf, large registries should be mandated to
track adverse events in DES recipients. But Yusuf also made a plea to
the major cardiovascular organizations to step up and revisit not only
the use of DES but the role of PCI in the treatment of stable,
non-drug-refractory angina. And to be clear, he added, PCI and
drug-eluting stents play a key role in the treatment of unstable angina
and acute coronary syndrome?it is as a treatment for stable angina to
treat non-life-threatening restenosis that Yusuf singles out as a "myth"
and a "man-made disease."






Long-term follow-up and assessment of cause-specific deaths in patients
receiving DES are mandatory to determine safety of patients receiving
these devices.







As for the meta-analyses themselves, Yusuf stated: "These new studies
raise concern. I do not believe these trials are convincing, but they
are disconcerting given that we have no data that this procedure is
useful. There is a significant excess in noncardiac deaths, and we need
to find out if this is real."
Pausing to assure a tittering audience that he was dead serious in his
comments, Yusuf added, "I call on the ESC to [convene] a balanced and
independent working group, and not just of interventionalists. Certainly
you can bring them in, but also noninterventionalists, health
economists, patient representatives, and government representatives, and
have a committee to find out what the real role of PCI is, of these
stents, and keep industry out of it."
Camenzind, for his part, stopped short of denying a role for
drug-eluting stents, insisting that his study, and his misgivings, apply
only to the two first-generation drug-eluting stents. "We need stents
that can control restenosis, that don't totally abolish the healing
process but that are able to control it."

Third study also sparks debate
Yet another study, presented earlier in the day by Dr Peter Wenaweser
(Thorax Center, Rotterdam, the Netherlands) also highlighted the stent
thrombosis risk with DES. In the study, Wenaweser and colleagues
examined rates of early and late stent thrombosis in patients enrolled
in the SIRTAX and Post-SIRTAX registries in Bern and the RESEARCH and
T-SEARCH registries in Rotterdam, between April 2002 and December 2005.
In Bern, patients received clopidogrel and aspirin for three to six
months, while in Rotterdam, patients received dual antiplatelet therapy
for three to 12 months. Only angiographically documented stent
thromboses were included in the analysis.






All of the presentations are pointing to the fact that stent thrombosis
is there and needs a solution. It exists, but it's not terrifying.







In all, 152 stent thromboses occurred in 8146 patients. The cumulative
incidence of stent thrombosis was 2.9%, yielding a rate of 1.3 per 100
patient-years. The rate of stent thrombosis was 1.2% at 30 days, 1.7 at
one year, 2.3 at two years, and 2.9% at three years, "an almost linear
increase of 0.6% per year between 30 days and three years," Wenaweser
commented.
In interviews with heartwire, experts tried to put the findings in
perspective, offering the oft-repeated calls for longer clopidogrel
duration. Dr Antonio Colombo's group (Columbus Hospital, Milan, Italy)
has a forthcoming paper examining rates of stent thrombosis in patients
who quit dual antiplatelet therapy at one year, compared with patients
who stayed on the drug out to three years.




Dr Peter Wenaweser


"I think all of the presentations are pointing to the fact that stent
thrombosis is there and needs a solution," Colombo told heartwire. "It
exists, but it's not terrifying. My problem with this issue is that we
did not use bare-metal stents in situations where we now use DES, so I
doubt we can do a fair comparison of stent thrombosis between DES and
bare-metal stents."
He also questions whether stent thrombosis rates continue to climb after
two years. "I'm not convinced that we have a continuous rate, I think it
probably grows up to two years, but from two years on, tends to level
off. . . . We should not forget that so many patients in the randomized
trials have been off antiplatelet therapy for a long time, and those
patients are not dying and having MIs all the time."
Also commenting on the Wenaweser study for heartwire, Dr Anthony
Gershlick (Nuffield Leicester Hospital, UK) insisted that it is
important to see published papers before jumping to conclusions. For one
thing, Wenaweser did not present data on percentage follow-up, making it
difficult to appreciate stent thrombosis rate increases over time. As
well, there are no studies tracking the "cumulative" stent thrombosis
rate for bare-metal stents. "The absolute difference between DES and
bare-metal stents will not be 2.9%, it will be 2.9% minus the cumulative
rate for bare-metal stents," he noted. "What we need to know is the
excess cumulative risk."
Copyright© 1999-2006 by WebMD. All rights reserved.
All material on this website is protected by copyright.

--
S Jersey USA Zone 5 Shade
This article is posted under fair use rules in accordance with
Title 17 U.S.C. Section 107, and is strictly for the educational
and informative purposes. This material is distributed without profit.
.