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Posts Tagged ‘non flow limiting lesions’

Fractional flow reserve is  a new coronary hemo-dynamic para meter used to assess physiological impact of border line lesions in coronary artery disease. The calculation is simple

FFR is  a terrible concept * for two reasons .

One ,  it never bothers about flow * across   a lesion. It simply  relies upon  pressure drop. We  know  there  is an intricate relationship   between pressure and flow . Simple pressure drop can never be  expected to translate into incremental flow in biological systems .

(FFR anology  in co-arctation of aorta . Can you take difference between upper limb  BP and lower  limb BP as a most accurate   Index of severity of co-arctation of aorta ?  )

How crude it would be   . . .  to  believe so ?

Two   it  ignores the  morphology of the lesion . We know an eccentric soft  lesion with a  good distal   FFR  is  live  coronary explosive .

The  FAME 1 and FAME 2 studies  glorified  FFR  !  I differ in many ways .

Some of  the  observations made about FFR.

  • FFR is to be  done only in discrete ,  safe looking  , intermediate lesions .(Do not ever attempt it in a eccentric lesion )
  • FFR wire is a  stiff ( stainless steel ) wire .  Careful maneuvering is necessary . Lesion crossing  and pull back  FFR wire require some expertise.
  • FFR / OCT  combo,   increase  not only the  fluroscopy time  ,  this procedure can be  more complex than  the intended   PCI .
  • My colleagues tell me FFR measurements are not often  reproducible .(I have little experience in this )
  • Adenosine induced vasodilatation  is not natural physiological model . Further it has  a potential for  a coronary steal if there is near critical lesion in contra lateral artery.
  • There are many occasions   FFR wire has caused  dissection  and  subsequent stenting was necessary  .(The very thing  the cardiologist wanted to avoid !)
  • Bifurcation lesion FFR measurement is prone for errors
  • FFR in two tandem lesions cannot be assessed   accurately
  • Post PCI FFR is not practiced routinely in may centers  the fear of  status quo of FFR.

Final message

This post is not to defame the FFR as a concept . Just to make you think  . . .  how often ,  we  are entrapped  in a  pseudo -intellectual  game in  the cath lab ! FFR  as a tool , can still  be valuable to assess coronary hemo-dynamics in a selected lesion population especially,  discrete,  single vessel ,  or left main disease  with around 70 % narrowing . But never go with FFR alone .Consider the morphology , location   of the lesion .

Finally do not forget  ,  the   good old  EST  can  give a stiff  fight  for supremacy over FFR  in terms of assessing physiological impact of a coronary stenosis (Especially in single vessel disease ) 

Reference

Fractional Flow Reserve versus Angiography for Guiding Percutaneous Coronary Intervention . http://www.nejm.org/doi/full/10.1056/NEJMoa0807611

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Atherosclerosis  probably ranks first among all  human diseases that cause maximum suffering  to  mankind.Since it is a disorder of blood vessel  it has an easy  access to every  vital organ  in our body to inflict the damages . Histo pathologically , atherosclerosis is an all in one disorder where inflammatory , degenerative and lipid injury  collectively  contribute to the disease progression. Diabetes and hypertension play a vital amplification role.

Atherosclerosis begins very early in life as fatty streaks in every individual and takes different avatars ( or remain indolent)   depending upon the risk factors and life style.

How to estimate plaque burden ?

It has  always been a difficult task to estimate the  atherosclerotic  plaque burden inside the  coronary  arteries.The fundamental flaw for many years is ,  we always thought  if there is a plaque it must  encroach  into the lumen.

Coronary angiogram  , has become the  default investigation  in clinical cardiology . Since it   can  visualize  only the coronary lumen ,  this  flaw  got further  curious  with skewed  interpretation as well.

When things were as it is . . .  Glagov suggested , what  could  possibly be   the  most important  concept in the interpretation of coronary  angiogram .

The concept  suggested  the  atherosclerotic  process  could  actually spread  within the  vessel wall  in a predictable manner .

What determines a plaque to either grow into the lumen or grow away from the lumen?

If we could decode the mechanism of direction of plaque growth we will probably conquer the atherosclerosis  at least by mechanical means . The implications are too many.

A stented coronary artery may be re-engineered to grow the atherosclerosis  towards  the adventia .This could grossly reduce  the incidence of restenosis.

Further , in post Glagov days we realised  mechanical factors like plaque stiffness, eccentricity , plaque mass effect, drifting , lipid core density, medial lysis , elasticity of elastic lamina all could determine the   plaque  movement.

Why compensatory lumen enlargement does not occur in some lesions ?

We do not know the exact reasons . We may call it a fate . . . shall we ?

Curious blessing  : Atherosclerosis  for  some unknown  reason  blesses a  few with coronary artery  dilatation rather than narrowing .

This is called coronary  ectasia . Medial necrosis , weakness of internal elastic lamina or  destruction paves way for plaque shift towards the adventia . It is estimated , if the medial necrosis occurs in at least  50 %  of  circumference of vessel wall   it will  result in ectasia .And  paradoxically if  the media  shows resistance   the plaque grows into the vessel wall.

Endoleak  and Glagovian phenomenon.

Endo leak is the Achilles heel of   endovascular intervention . In fact , many would  consider  it as  a dignified terminology  for graft failure . Endo Leak   occurs when  the artery outgrows the stent  graft and bllood starts  collecting  in the graft vessel -wall interface . When the  scaffold is  placed  within the lumen ,  one may wonder how it is going to prevent  the  artery  dilatation . (Which is basic defect in any aneurysm}In fact , the aneurysm does continue to grow  along with   centrifugal  atherosclerotic  forces ,  possibly by  Glagovian phenomenon .

This makes it obvious  endo- leak is a distinct threat in every vascular  intervention.


Final  message

Most cardiologists  think their ultimate  job  in this world is to  deploy  a stent deep inside a LAD  or RCA.  While a few others indulge in more exotic  adventure of  crushing a plaque ,  trap the debris and  catch it with a  with  a basket .

There  are bigger and bigger   blind areas  in the vessel wall ,  infiltrated with  deadly atherosclerosis which is conveniently ignored  .If only we realize   this fact  , we  can move forward in our war against coronary atherosclerosis.

Of course the good old   medical  interventions  . . .  exactly try  to address  these issues . Let us  think  straight , and  not succumb to glamor  in cardiology !

http://heart.bmj.com/content/84/5/461.extract

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