AW: [HSF] The fallacy of surgical research
psimha
prasannasimha at gmail.com
Thu Aug 2 21:41:14 EDT 2007
Roberto , you forgot Theodore Kocher and Egaz Moniz .
Prasanna
Dr. Roberto Battellini wrote:
> Ani,
> Science in an art and science discipline (surgery) is very complicate, near
> the theory of caos. Tell the clinical academics to come to surgical
> services and do science. They are not going to make it better than we
> surgeons.
> Of course, we are not as good in biostatistics as they are. And the most
> important factor, the surgeon itself is never included in the studies!
>
> By the way, there are 2 Nobel Prize surgeons, Carrel and Forssmann (together
> with Cournand).
>
> Roberto
>
> -----Ursprüngliche Nachricht-----
> Von: openheart-l-bounces at lists.hsforum.com
> [mailto:openheart-l-bounces at lists.hsforum.com] Im Auftrag von Ani Anyanwu
> Gesendet: Mittwoch, 1. August 2007 22:14
> An: openheart-l at lists.hsforum.com
> Betreff: RE: [HSF] The fallacy of surgical research
>
> The other issue the discussions on myocardial protection brings up is the
> fallacy of surgical research and the poor understanding of research method
> by surgeons. This is what prompted the Lancet editor many years ago to
> describe surgical research as 'comic opera'. The reality is that few in
> academics or research takes us surgeons seriously. Look at the
> representation of surgeons in key research bodies, funding of surgical
> research by NIH or similar bodies, surgical influence in research groups,
> surgical publications in key journals, guidelines committees, involvement in
> key epidemiological efforts etc. The only Nobel prize received by a surgeon
> in the recent era wasn't even for surgical research. The problem is we as
> surgeons believe too much in our individual selves and individual methods
> that we become blinkered as to the requirements of the scientific method.
>
> Examples include
>
> - there is evidence that such and such an additive to cardioplegia is of
> benefit (this evidence comes from isolated animal hearts, animal experiments
> and at best clinical measures of surrogate markers - these do not mean the
> additive is benefit in the human, indeed it could be worse)
>
> - it has worked well in my cases so it is okay (but as Dr Salerno and
> Prasanna say the heart has great reserve - that nothing goes wrong does not
> mean all is okay)
>
> - i have had no deaths (the patient came to you alive; why is it an
> achievement that he remains alive after surgery? (unless the aim of surgery
> was to save life))
>
> - Kirklin and Buckberg or Cleveland clinic demonstrated...(i.e. eminence
> based medicine; but how many have ever read work of Kirklin or Buckberg? Do
> they stand up to the requirements of scientific proof? Indeed did either
> really show clinical benefit of the things we attribute to them? For example
> the 'seminal' Cleveland clinic NEJM paper purpurtedly showing benefit of IMA
> over SVG barely constitutes evidence of such)
>
> - There was no enzyme rise (has anyone cared to show any relationship
> between enzyme rise and any outcome of interest after surgery? Does the
> patient really care what his CK, troponin or coronary sinus lactate are? Why
> do we look at outcomes of no relevance to the patient?)
>
> - Ventricular fibrillation means bad protection ( but has anyone shown so
> scientifically? maybe fibrillation is intrinsic to some techniques and rare
> with others and is a reflection of the technique rather than the degree of
> protection; certainly a fibrillating heart in Salerno's beating heart
> technique has different implications to an Arch done by Martin on DHCA)
>
> - The patient was extubated the next day (and so what? Several times you go
> back to ask what happened to the patient 2 months later and you hear a
> different story. This outcome is of no relevance at all unless aim of
> surgery was to allow extubation in patient previously ventilator dependent)
>
> - My method of cold myocardial preservation works (but how do you know that
> that is what is working? As Salerno says if you don't know the myocardial
> temperature how do you know it is the hypothermia, and not some other
> factor, that is in play?)
>
> - Since I changed I use less inotropes (but you decide what you use- could
> you not be just biased towards the success of your change? Maybe you should
> compare two methos objectively)
>
> - Multiple defibrillation harms the heart and leads to bad outcome (maybe
> but could it be the condition requiring defibrillation that is resulting in
> the bad outcome rather than the shock?)
>
> - I have done it this way for 10 years and never had problems (how do you
> know? Have you actually measured the outcomes on all your patients? Kocher
> said the same about his thyroidectomies and was shocked when he recalled his
> patients and found the majority had myxedema)
>
> etc
> The inability to critique within the scientific framework and a lack of
> understanding of, or refusal to apply the research method, is a major
> problem in surgery and is in part the reason why we are so diverse in
> opinion and yet so opinionated and firm in our belief that what we do is
> right (when yet examined there is often no evidence to support it). No
> internist or scientist or epidemiologist would approve a drug based on any
> of the criteria we list above yet we swear by what we do to the degree that
> we suggest alternative approaches are inferior.
>
> Until we start thinking in a scientific and epidemiological manner, we as
> surgeons will remain the laughing stock of academic medicine.
>
> Ani
>
>
>> Date: Thu, 2 Aug 2007 04:52:48 +1000> To: OpenHeart-L at lists.hsforum.com>
>>
> From: benjamin.bidstrup at bigpond.com> Subject: Re: [HSF] Inotropes,
> ventricular fibrillation and myocardial protection> CC: > > What this does
> is once again ask the question, how do we measure > myocardial
> preservation?> > We can look at the highly sensitive markers such as
> Troponin which > indicate some element of damage to components of the
> myofibrils. and > so on. Echo - RWMA ECG and the list goes on.> We need to
> look at use of inotropes, IABP, survival. Khuri published > on his
> intramyocardiall pH device stating that poor preservation as > reflected by
> pH changes resulted in altered long term survival.> > Much of the cocktails'
> components have been determined by isolated > rat heart experiments. They
> have translated well to the human, but it > is very hard to measure total
> water content of an intact heart or > regional blood flow distribution in a
> human model.> > Why is it that there is no universal cocktail. Put 100
> cardiac teams > in a room and you will have 120 different ways of preserving
> the > myocardium.> I review papers that look at different methods of
> preservation and > they use markers such as inotrope use to determine
> improvement. How > variable that is is a whole new debate.> > > > > >Tomas,>
>
>>>> A fibrillating heart is a dying heart? Is this an edict of some >
>>>>
>> sort? I've seen plenty of hearts that fibrillated during some part > >of
>>
> their open heart operation only to have a completely, and I mean >
>
>> completely, normal EF on remote echo. Speaking in absolutes serves > >no
>>
> purpose.> >> >> >> >Hal> >> >> >-----Original Message-----> >From: Salerno,
> Tomas <TSalerno at med.miami.edu>> >To: OpenHeart-L at lists.hsforum.com> >Sent:
> Wed, 1 Aug 2007 11:19 am> >Subject: Re: [HSF] Inotropes, ventricular
> fibrillation and > >myocardial protection> >> >> >> >> >A fibrillating heart
> is. "Dying" heart.> >The brain does not have seizure during CPB; neither
> should the heart > >fibrillate.> >Tomas> >> >----- Original Message ----->
>
>> rom: openheart-l-bounces at lists.hsforum.com >
>> <openheart-l-bounces at lists.hsforum.com>> >o: OpenHeart-L at lists.hsforum.com
>>
> <OpenHeart-L at lists.hsforum.com>> >ent: Wed Aug 01 10:45:53 2007> >ubject:
> Re: [HSF] Inotropes,ventricular fibrillation and myocardial > >rotection>
>
>> Ani,> >aving graduated from voodoo homemade cocktails to blood and its>
>> ariants, you would easily be able to see that the bad cardioplegia's> >id
>>
> have a higher (more accurately uniform) incidence of fibrillation> >hich
> came down with better modifications of cardioplegia's. That does> >ake us
> wary and anyway fibrillation is not something by any stretch>
>
>> ormal.Transient defibrillation may appear innocuous but then it has> >een
>>
> shown that such hearts have indeed been improperly preserved (from> >orks of
> Buckberg and Kirklin).Remember that sometimes speed etc etc may> >ompensate
> but this may become an issue in longer case.> >rasanna> >ni Anyanwu wrote:>
>
>> I still do not understand why we are alarmed about transient ventricular>
>> ibrillation on reperfusion and why using drugs to suppress it will have
>>
> any> >mpact on outcome.> >> > Ani> >> >> >> > > >> Date: Wed, 1 Aug 2007
> 11:51:47 +0530> From: prasannasimha at gmail.com> To:>
>
>> penHeart-L at lists.hsforum.com> Subject: Re: [HSF] Inotropes, ventricular>
>> ibrillation and myocardial protection> CC: > > I am not saying that the>
>> rocaine or lignocaine is still acting. What I> meant is that since the>
>> ibrillation is occurring with the hotshot delivery> with high local
>>
> lignocaine> >hanging the drug class may be beneficial.> Prasanna> > On
> 8/1/07, Ben Bidstrup> >benjamin.bidstrup at bigpond.com> wrote:> >> > I beg
> respectfully to differ. The> >idocaine (a fast Na channel> > blocker) is all
> but gone after a short while in> >he cardioplegia> > scenario. Getting a
> suitable level back into the > >circulation> >nd thus> > the heart at
> release of the clamp is what is > >needed.> >> > Perhaps a> >andomised study
> is in the offing.> >> > >
>
>> http://circ.ahajournals.org/cgi/content/abstract/79/5/1106>> >> > This
>>
> reference relates to defib energy levels but i think you will> > see> >here
> I am coming from.> >> > At James Cook, I was involved in the development> >f
> a non> > depolarising cardioplegia solution, which is slowly > >working its
> way>> > up the development path. The main components are lidocaine and> >
> adenosine.>> >> >> >> >> > >Ben,> > >I use Amiadorone in the pump for all
> emazes > >>(and postop)> >nd> > >Amiadorone in the pump for all aortic
> valves. Since the St Thomas> >> >Cardioplegia (which we mix in blood)
> already has procaine > >adding> > >Lignocaine> >ould be
> redundant.(Incidentally Amiadorone is very cheap> > >in India !!)> >>
>
>> Prasanna> > >Ben Bidstrup wrote:> > >>Why the amiodarone. Surely with some>
>> erfusion, the electrolyte> > >>imbalances within the myocardium would
>>
> correct> >nd SR ensue. If> > >>anything use lidocaine. Less toxic and
> cheaper, not a> >egative> > >>inotrope. It is what Yacoub taught me many
> years ago, and I have>> > >>used it to good effect (infrequently I might >
>
>> add).> > >>> > >>>Tohru,> > >>>> > did an AVR on an 87 yo man as a 2nd case
>>
> just a couple of> > >>>hours ago.> >gain, no LV vent, only a sump. While
> closing the> > >>>aortotomy, I began the>> > >>>continuous warm retrograde
> blood. The heart began fibrillating> > >>>after> > couple of> > >>>minutes.
> I gave amio and then cardioverted. The > >heart had a> >> >>>slow
> junctional> > >>>rhythm until the clamp was released. A sinus rhythm>
>
>> eveloped shortly> > >>>afterwards. He came off with no inotropes. It's
>>
> much> >asier on> > >>>the heart and> > >>>your nerves to cardiovert a >
>
>> clamped, flaccid> >eart rather than> > >>>trying to do it> > >>>after the
>>
> clamp has been> >eleased.> > >>> I look forward to your visit at the STS. As
> I said before,> >'ll> > try to> > >>>have a couple of interesting cases for
> you and other> >nterested> > >>>members of HSF> > >>>to watch and criticize
> to your heart's> >ontent.> > >>>> > >>>Hal> > >>>> > >>>> > >>>> >
>
>>>> **************************************> >et a sneak peek of the> >
>>>> all-new AOL > >at> > >>>http://discover.aol.com/memed/aolcom30tour>> >
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> FRCSEd FEBCTS> Consultant Cardiothoracic Surgeon> > Two things are infinite;
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