Posts Tagged ‘flow limiting lesion’

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 !


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Scientifically ,  the  indication for coronary revascularisation   should be  based on following

  1. Patient’s  symptom ( more specifically angina , dyspnea is less important !)
  2. Prov0kable  ischemia  ( A significantly positive stress test )
  3. Signifcant LV dysfunction with  documented  viable myocardium &  residual ischemia
  4. A revascularisation eligible coronary anatomy * TVD/Left main/Proximal LAD etc ( *Either 1, 2 or 3 should be  present  in addition )
  5. All emergency PCI during STEMI /High risk NSTEMI

Practically ,

A CAD  patient  may fulfill  “Any of the above 5 or  “None of the above 5” ,  but ,  if   a coronary obstruction  was  revealed  by coronary angiogram  and if he  fulfils The 6th criteria , he becomes  eligible for  revascualrisation

6th criteria

If the patient has  enough monetary   resources (by self  ) or by  an  insurance company  to take care of PCI /CABG *

*The sixth  criteria overrides all other criteria in many of the cath labs .Of course , there are few genuine ones still  fighting hard , to keep the commerce out ,  from contaminating cardiology !

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Left main coronary artery disease (LMCAD) often evokes  a panic reaction  among cardiologists .Not every LMD deserve that re. To  label  it as  significant, we have a criteria ,  that is 50% diameter stenosis.  So what you do , for a tapering  or narrowed left main with 40% stenosis. Isolated insignificant left main is rare *, but real incidence is not known.  LMCAD  is  most often due to  , atherosclerosis of left main coronary artery without limiting the flow.

What are the options ?

  • Leave it alone, with intensive medical management assisted by high dose statin(80mg)
  • Elective PCI with stenting , even though the lesion is not significant.

*If associated LAD  or LCX is there decision making is easier .

How  significant is a coronary stenosis ?

The significance of a coronary lesion with reference to “lumen diameter obstruction” is basically flawed. The significance of a coronary stenosis, by tradition is  based on it’s hemodynamic impact ,right from the  CASS days in early seventies.Unfortunately our mind set has not changed even after realising    non obstructive – sub critical lesion is more prone for acute coronary syndrome.  Is it not ironical to call a  40% lesion a non significant one !

So, the  significance of coronary stenosis is two fold.

  1. Hemodynamic  significance
  2. Clinical and  pathologic significance

The former predisposes to often chronic stable angina, later likely to result in ACS.

How will you approach a apparently insignificant left main disease ?

A 40 % lesion in left main is hemodynamically not significant , but pathologically very significant.It needs intensive treatment. Plaque passification with medical approach is first choice.If the lesion morphology is eccentric,  has irregular margins or involves  LAD  or LCX ostium doing a PCI or even a CABG is to be considered in spite of the lesion is  hemodynamically insignificant .

Why , PCI is   considered  “not appropriate”  for   less tighter lesions , even though these lesions  have great clinical significance ?

The answer is simple, The risks  and the  potential cost are more than the benefit !

And further ,  stents are  not innocuous devices  either  , they  always carry a risk of sudden occlusion as like  a sub critical lesion  !

Answer to the title question

True incidence is not known . Our experince (Class 1 c evidence) would suggest Left main disease constitutes up to 10 % of CAD.Among this one third would be hemodynamically insignificant

Suggested reading

Handbook of Left Main Stem Disease

edited by Seung-Jung Park



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