Posts Tagged ‘oat study’

Coronary  atherosclerosis is the number one killer of mankind. Many would consider it as an  essential  process of aging .Modern  life styles and habits make this appear  very early in life . There is currently an endemic (or even  a pandemic ) of   CAD due to premature  atherosclerosis. We need to recognise CAD is not a  primary heart disease  .It is an irony, heart is an  innocent bystander  to the  biological derangement  of coronary  vascular system  when  it is infested with atherosclerotic plaques .

So , when we  are confronted  with  serious atherosclerotic lesions in a coronary artery   what shall we do ?

We have three options

  1. Take on the enemy in a direct confrontation (Like war on terror ) : This is  some times called as Interventional cardiology .Caution is required as the battle  is within the human coronary artery ,  cross fires and collateral  damage  are unavoidable.

2 .Next  method  is to  find the basic cause  of  terrorism , identify  the perpetuates, facilitators    and try to correct the   root cause of it (CAD ) .This approach  also refered to as medical management  in cardiology community*  . It  aims  at regression of plaque  by statins, and life style modification and preventive cardiology. This modality is most ridiculed and  insulted by the main stream cardiologists.

*Comparable to  bilateral peace talks for a political solution to terror

3. And third option is a  real  surprise !   This  neither  confronts   the lesion   nor does it  address the initiating factors . It   just ignores  the lesion and by pass it with a LIMA /SVG  fly over ,  as if  nothing has happened in this vital high way leaving the culprit scot-free  .This option is  executed by surgeons as  CABG surgery . . . and  for mysterious reasons  this is a  well accepted one .

CABG :Here the atherosclerotic  burden is untouched by surgery . The graft can get diseased  sooner or later , native vessel disease  shall  progress some times encroaching  the ostia of distal graft site . Incidence of acute coronary syndrome following CABG is not greatly reduced for the simple reason we are not doing anything primarily to the inflamed plaques .These issues  are left ,  to be  taken care by the  medical  management .

* This article  does not want to defame these great development in cardiology(PCI/CABG) . They have a  specific role to play. CABG AND PCI remain the only option for critical  lesions with limiting angina .But please remember without  proper  medical management  ( ie Targeting  the perpetuates of  crime )  both  PCI and CABG will be a big sham !

Final  message

Avoiding   the  lesion  or  attacking the lesion  is a  primitive  method to tackle CAD  . Passifying   the lesions  in a slow and gentle manner,   preventing  further progression  or regression  of lesions is the only  “sane” method for combating CAD   . PCI and by pass surgeries  can be termed  as  21st century’s   medical  adventure sports  which  has  limited role ,  in the overall control  of CAD  for the human kind .

And  now  answer this question . . .

Cardiologists attack the lesion and  surgeon avoids the lesion ?  Who is the winner in our fight against CAD  ?

Both of them are  clear losers .The winners are  all those  humble physicians and parmedical workers (or even the responsible lay public ) who  help recognise  the early forms  of  CAD  and  counsel properly to prevent it .

This is  what  Dean Ornish   in 1991  documented in  Lancet  which was never considered scientific   for the simple reason it has no commercial value !




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It is a well known fact  ,   CABG and PCI  provides immediate relief  for patients with angina ,  which is refractory to medical therapy. Of course , this happens only if a critical occlusion of  at least one epicardial coronary artery is  opened . It need to be realised ,  angina  due to  microvascular  disease can not be cured by maintaining  epicardial  patency .

While angina  relief is prompt ,  dyspnea is not ! . If we  believe,  opening  up a  coronary artery  in a patient with LV dysfunction will  restore the LV function  ,  it  is grossly mistaken !

Why is it so ?

Angina  relief requires  simple  restoration  of  oxygen supply and correction of local ischemia .  This happens without any issue as the blood  seeps in to the ischemic cells and soothes the ischemic nerve fibres that trigger the pain signals   . While  ,  for LV function to improve , the blood flow has to be converted to mechanical activity in the form of myocyte actin/myosin interaction. For this,   there need to be an intact  cellular contractile mechanism . The myocyte architecture should be appropriate .In post MI ventricles we know there is  zig zag  orientation of myofibrils due to myocyte slippage that interfere with mechanical recruitment . Further , integrity of  extracellular matrix  namely the collagen frame work is also vital . Note ,  angina relief  is not concerned with any of the above .

And now ,  we also realise  dyspnea  in failing ventricles  is vitally  dependent on diastolic function ,  which is also very much  impaired in ischemic DCM .There is little proof for  PCI/CABG  to correct the  molecular   mysteries in  diastolic dysfunction !

Dysfunctional LV means what ? (read the link )

It is a collection of  variety of myocardial tissues . Viz : Fully  necrosed , partially necrosed ,  ischemic viable, non ischemic viable, ischemic non viable, non ischemic non viable , Apart from this patchy necrosis, patchy ischemic, areas are common. Finally , necrosed segments   may  also be perfused normally by  spontaneous reopening of an IRA.

One can imagine the complexity  of events in these segments  once we do the  PCI /CABG . The response  is highly variable and unpredictable. The major concept we  , the physicians  believe or ( to be precise made to believe !) is  the  sanctity  devoted to  the viable myocardium .For  many us ,  it is considered a  holy  exercise  to identify viable myocardium in patients following MI and then revascularise them if  found to have significant viable myocardium (Atleast 20% of infarcted area )

A full 2 decades were lost or (shall  we   say wasted on this futile exercise !) as   we have since  realised most of the cardiologists do not follow this rule .

Now , even a scarred myocardium is revascularised in the hope of recovery .As such , we have reached a stage where  there is no contradiction for not doing a PCI /CABG   with reference to LV dysfunction.

Now every  patient  with post MI  LV dysfunction  is considered to  have  some amount of viable myocardium that is  fit   enough  for revascularization

Are we justified in doing  this ?

Many clinical  trials  have revealed  , the  recovery of LV function  in these segments  has not been consistent at all .

The most surprising discovery is  a viable myocardium need not  be ischemic   .It might get adequate blood supply either  from invisible collaterals or trickle of antegrade flow .  Hence an adequately  perfused myocardial segment can  still be   non contractile . This shatters the myth  that  revascularisation must have a dramatic effect on the recovery of contractility in all viable segments.

The other major finding is  ,  even ischemic   viable   myocardium ( documented by metabolic activities PET etc)  need not regain it’s original contractility  after the ischemia is fully corrected .

*reference for  both the above statements are available from variety of sources including real life experiences .(Type C evidence )

Final message

  • Do a PCI/CABG promptly for patients with refractory angina.
  • Never  advocate PCI/CABG  for  a primary relief of dyspnea .  (Never is a harsh word,  let it be  “use it  with caution ” ! and  the  patient  should be  revealed  the whole facts  about  what we know and what we do not know regarding the complex  hemodyanmic events  in  revascularisation   )

Counter point

If  the above statements are really true ,   How does PCI/CABG   help  relieving  dyspnea  and functional class  what is your answer for thousands of patients  with CAD and ischemic DCM who have greatly benefited from CABG ?

The answer could  be  simple , The revascularization  piggybacks  over the   medical management (which , these patients pursue vigorously)     like  ACEI,  statins, salt restriction, betablockers  , optimal diuretics and tend to hijack the credits from the poor  drugs !

Read a related blog

Revascularisation for ischemic DCM

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Medical profession has  evolved over centuries with humble discoveries by genuine researchers in the past . As we  pursued  science vigorously  , we  looked  for innovations , when innovation  work ( or many times shown to work !) we jump to sky , even as  some of these  innovations fail and crash down  to earth , many times  we continue to be in the clouds . This is the fundamental problem of modern medical science . When  our expectations reached  unrealistic proportions ,   we tend to lose the common sense . Prolonging life and reducing human suffering may be the ultimate aim of the medical  profession , but  If we try to fight the death with science and money without application of mind , our current  life may become  miserable ! Thats what is happening for the majority of the population of this planet . After all ,  death is an essential and final  component of life !

Coming to the issue of CAD ,  in our country , a  rich gets a 4th generation drug eluting stent for a insignificant  asymptomatic PDA lesion , and poor fellow with left main dies without any intervention .This is  fairly acceptable   to this uneven world  , where a rich westerner  dies due to obesity related disease and a  poor African dies to malnutrition .

This article is in   response to  my  recent  experience  when  . . . I advised

Simple life style modification &   few drugs   for a patient with chronic multivessel   CAD  , I was  made to look   ordinary , inferior  and funny   by  many of the current generation cardiologists .

Further , the term optimal medical therapy(OMT)  for chronic stable angina has evoked laughter in one of the interventional cardiology  conferences  I  attended !

It is a sorry state of affairs  for the whole cardiology community , a  genuine scientific  fact , proven by  real life experience  as well,   is  being  ridiculed.

Richard  Conti tells in this excellent editorial in his journal   Clinical cardiology about the issue of medical management of CAD

“Respect in clinical trials”

Chronic stable angina pci vs cabg vs medical courage trial oat trial ethics in cardiology

Click here to reach the article  http://www3.interscience.wiley.com/cgi-bin/fulltext/122512853/PDFSTART

A similar study which  suggested  exercise  could be  better than PCI in the recent 2009 ESC is suffering the same fate !

What if regular exercise were as good as a stent for stable angina?


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Total coronary artery occlusion is a common finding in CAD  especially in chronic stable angina. Normal coronary blood flow is 5 % of cardiac output  that amounts to 250-300ml/mt.At an average  heart rate of  70/mt  , each  beat  injects  about 5cc blood into the coronary circulation.This is shared between two coronary arteries.  This means , only few CC (2-3cc) of blood enters  each coronary artery with each cardiac cycle .

When one of coronary artery is totally occluded what happens to the coronary

blood flow ?

A.Total coronary blood flow  can be be  maintained   normal  at rest  as it  forms  only about 5% of cardiac output  (or it is only  slightly reduced )

B. It is believed , the unobstructed coronary artery  could receive the blood meant for the contralateral coronary artery. This  possibly explains the increased coronary artery diameter in the non obstructed artery.

C. It’s nature’s wish ,  that the  contralateral  coronary artery  shall share  50% of  it’s  blood through  collaterals if available.

D.If collaterals are not formed it , the unobstructed coronary  artery  may be over perfused with double the amount  of blood flow.

E. Some times , the collaterals steal  much more than what  the  obstructed coronary artery  deserves and make the feeding coronary artery ischemic. This is many times observed in  total RCA occlusion with well formed  collaterals  from LAD/LCX.

F.The collateral flow  in CTO also depend on whether flow is directed from LAD system to RCA or from RCA -LAD system. The LAD is better placed to assist RCA than vice versa.This is for two reasons.1.LAD blood flow is higher than RCA so it can share it.2.The driving pressure is more  from LAD -RCA , as RCA can receive  blood flow even during diastole .

F.During exertion , the coronary hemodynamics become further complex.The collateral’s are traditionally thought to be less than adequate during times of exercise.But it is more of a perception than solid scientific data.This rule  may be applicable in only certain group of patients. We know CTO patients with very good exercise tolerance who have documented collateral’s.

G.Collaterals can be either  visible or invisible by CAG. The strength of collateral circulation is not in it’s visibility but it’s capacity to dilate and  respond to neuro humoral mediators at times of  demand.  Currently  , there is lot to be desired  regarding  our knowledge about  the physiology  of visible collaterals , no need to  mention about invisible collaterals !

Final message

The above statements  are based  on logics and observations .

Is it not a  irony  in cardiac literature ,  where  thousands of articles  are coming out every month  to tackle  totally occluded coronary artery(CTOs) ,  there is  very little data   regarding the coronary hemodynamics in chronic total occlusion .   How  does a patient with CTO can manage a active life with only one functioning  coronary artery ?

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