Archive for February, 2014

Is “Non-flow limiting coronary  lesions  more prone for ACS ?

  • If  your  answer  is “No”, you can skip this article.
  • If your  answer is “Yes” , you need to read this article.

ACS is the commonest cardiac emergency .Thousands of patients are treated every day.Millions of dollars are spent.Bulk of the cardiologist’s life revolves around this entity.

Scattered atherosclerotic plaques in coronary artery lead to ACS either in a random fashion or in a predictable manner .

Still, we are  highly  uncertain about  which lesions are likely to result in ACS ! Some time in the beginning of  21st century, the main stream cardiology media were abuzz with the concept, that non obstructive , non-flow limiting lesions are more prone for ACS rather than more tight  stenosis.

atherosclerosis  flow limiting lesion  glagov  plaque rupture vulnerable erosion fissure vs dissection

I fail to understand how a tight lesion is less  prone for ACS. Tighter lesions are  bigger and must be  prone for more complications . Image courtesy :http://upload.wikimedia.org/wikipedia/commons/9/9a/Endo_dysfunction_Athero.PNG

This reasoning was based on few studies, that lacked  solid scientific proof . In fact the initial  observation was  not made in living coronary arteries rather by autopsy observations .(Later live virtual histological studies came ,  but didn’t confirm this !)

Surprisingly the degree of  anatomical narrowing was conferred  vulnerability  , when we know plaque compositions , morphology and hemo-rheological  factors are many fold important in precipitating ACS . (Lipid content , fibrin cap  thickness, eccentricity , etc)

So where is the truth hidden?

Is it really possible, lesser the stenosis more  is the propensity for rupture ?

 We need to introspect .

“In all probability,  it is a meager statistical illusion”

For every tight lesion there are as many minor lesions scattered around in a given a coronary artery. These can progress into ACS  later.

It is basically wrong to assume non-flow limiting lesions are more prone for ACS than non-flow limiting lesions.To believe so , seriously underestimates  the  culpability of big lesions .It appears a coronary mockery to me  !

At best , we can conclude  non-flow limiting lesions  are not benign and can be an important source of ACS.

An unscientific chain reaction !

If we start believing non flow limiting (say  30%  stenosis ) is more prone for ACS , why we are not stenting all  those lesions ?

If the above concept  is  is applied in cath lab  routinely , the principle of  FFR   which relies solely on hemodynamic impact  will  crash into the dustbin !

Some  more truths

However , It is indeed true  when a plaque is hardened by severe sclerotic process or calcification it is less prone for  rupture and clinical ACS  but can be a source for stable angina.

Is it  justified to assume , larger the plaque the harder  would be it’s content  that  resists ACS ?

Meanwhile , we also know there need not be any lesion at all to cause an ACS.( In a young  smoker ,  100 % thrombotic STEMI  is possible  over an area of coronary erosion caused by endothelial dysfunction ! So , where do we go from here !)

Let us be clear

Are you confused more !   . . . after  reading this article, let us clear it by two-line summary !

As on 2014 ,

  • Symptomatic flow limiting lesion   are tackled by stents.
  • All non-flow limiting lesions  are treated by  high dose Statins  and vigorous medical management.

Final message

Contrary to popular  perception, tight lesions are  more complex, eccentric , soft and are at immediate risk of ACS.

Non flow limiting lesions remain static in most,  regress in many , still  carries  distinct  risk of progression into full blown ACS , at any time if conditions are favorable.

Fixed concepts and ideas in medical science do not help us  taking medicine forward. Especially so, when these are based on assumptions and approximations. If only we redo these studies with the currently available technology (FFR/OCT/NIR the conclusions would be dramatically different !

Caution : There is no scientific proof  for the above discussion,  of course . . . we lack evidence against it as well !


2.Glagov S, Weisenberg E, Zarins C, Stankunavicius R, Kolletis G. Compensatory enlargement of human atherosclerotic coronary arteries. N Engl J Med. 1987; 316: 371–375.

3.Fuster V, Lewis A. Conner Memorial Lecture. Mechanisms leading to myocardial infarction: insights from studies of vascular biology. Circulation 1994;90:2126-2146.

4.Ambrose JA, Weinrauch M. Thrombosis in ischemic heart disease. Arch Int Med 1996;156:1382-1394

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Many decades ago Potts  shunt  (Central Aortic -PA shunt)was used to increase pulmonary blood flow for severe RVOT obstruction mostly for TOF  and tricuspid atresia .With the advent of  ICR and  Fontan role for central aorti shunts waned.

Now, read this

Chronic ,refractory pulmonary hypertension of any cause has dismal  outcome.In  patients with severe PAH  many patients  reach supra-systemic pressures . RV   a volume handling chamber faces a uphill task of overcoming huge RV after load. As cardiac physicians , we  struggle  to  perfuse the lungs in such situations.

The only option  seems to be  lung transplantation !

How to perfuse the lungs if the RV is failing ?

Is there any other alternative ?

Why not,use LV contractility  to perfuse lungs .

Great Idea isn’t ? After all , how can we allow left ventricle known for it’s  robust bumping function  sit idle and relax  when it’s counterpart is struggling with heavy load ?

How to use LV for increasing pulmonary blood flow ?

Create a central Aortic -Pulmonary shunt.

That’s resurgence of Potts shunt.

Dr Julie Blanc from France suggested this approach in in NEJM as a letter  (Potts Shunt in Patients with Pulmonary Hypertension N Engl J Med 2004; 350:623) .  It  was a great Idea.

Since then lots of patients  have a benefited from this vintage surgery.

potts shunt in severe pulmonary hypertension

Final message

A surgery blamed for early onset of pulmonary vascular damage due to potential Eisenmenger reaction is back .Indication for refractory Eisenmenger syndrome to perfuse lungs  at very high pressure Nothing is obsolete in medical science .Nothing is ironical as well !

Another Innovation : Now Transcatheter Potts Surgery

potts shunt for eisenmenger and severe pulmonary arterial  pht pah

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Cardiology as a filed has been the epitome of progress of medical science in the last century .Most research  in cardiac science  has grown and transformed with a definite clinical purpose.

The cardiac pharmacology has grown many fold and various drugs play a distinct role in relieving symptoms and prolonging life .

Which drug , do you think has  the maximum impact in the clinical outcome and overall cardiovascular health of our population  ?

My vote is for  the old warrior . . . yes the the drug ,  which is used atleast a  million times a month to unload the heart the meanly loop diuretic Frusemide ! Heparin came very close  second !

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Today , we  post cases for coronary angiogram , just like sending clients to breakfast table ! Close your eyes. Think for a moment. It is heartening to know how cardiac catheterization grew from a humble beginning . We know , Forssman , Cournand  and Richardson  who shared the Nobel price  for Inventing  cardiac catheterization in 1930s .

Soon after it’s  invention it was criticized by most, few ridiculed it outright , few others wondered about it . One man from the iconic  Grady memorial hospital  , attached to Emory silently  adopted this  procedure and almost single-handedly  did more than 1500 cardiac catheterization procedure. (Between 1940-50s)

How many of us know this man  from  Atlanta ,Georgia  ?

Some times history appears unkind. He is Dr Steads . . . to be precise Dr.Eugene Anson Stead Jr. ( 1908,  –  2005)


Born in a humble background in the suburbs of Atlanta , became a great medical teacher , researcher and educator . He is one of the founding  fathers  of cardiac catheterization . Defined it’s usage in  clinical cardiology . The other major  achievement was his strong conviction that  medical science is indeed simple  but made complicated by complex concepts .This  thought transformed  in him ,  as he found the concept of physician assistant . He believed focused medical knowledge in young and enthusiastic  mind can make huge  difference in the way medical knowledge  is disseminated, applied and consumed .What a stunning truth even today !


The legacy of Grady continues which is one of the largest public hospital in USA with special affinity to poor and low-income population.

The lab which Dr Stead worked was later taken over by Dr  Noble O Fowler* , another great cardiac physician continued the research and wrote the famous book on cardiac diagnosis and treatment.( * I think it should be in early 1950s when Dr Stead left for Dukes)

Final message

Invention of a concept is one thing . Accepting it , trying it ,  improving it ,  disseminating it , is an equally important  contribution to science. Dr Stead did exactly that .He remained  a positive force in  propagation of medical knowledge, made it  available for those  people who need it .

He passed away on June 12, 2005 at the age of 96 leaving behind a huge legacy .It will be  an  error if we don’t teach our  young students history of such great men , in medical  schools today  !

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Cullotte is a trouser worn by 18th century French aristocrats.Now,in 21st century French interventional  cardiologists  found a striking similarity  of cullotte with  two stent strategy in bifurcation lesion .

Though this technique is in vogue for more than a decade , it has not been popular due to  perceived complexity .

It is making a come back in recent years , as we begin to negotiate bifurcation lesions with better expertise and hardware.

7  steps  in Culotte technique (From NORDIC study )

  1. Wiring  both main and side branch .

  2. Pre-dilatation of  main branch  and/or side branch,( Optional)

  3. Stenting of main branch

  4. Rewiring  side branch  through main branch stent strut,

  5. Stenting of side branch  through  main branch stent,(Now main branch is jailed by side branch stent

  6. Recross main branch  through struts of SB.

  7. Procedure completed with  final kissing balloon dilatation

culotte technique  stenting ptca pci 004

culotte technique  stenting ptca pci

culotte technique  stenting ptca pci 002




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Note :This is a copy of  my earlier blog on coronary micro-circulation  published few years ago.Recently this got numerous hits .Hence I have just reposted it with slight modification.

Human coronary circulation stands unique among  others as it is a  life-sustaining circulation.It is indeed a great medical achievement  to visualise  the right and left coronary artery  system by coronary angiogram.  Actually,  what we see is  only a fraction  of  the surface area of coronary circulation .The surface area of  epicardial coronary arteries   constitutes  less than 5 % of entire coronary vascular tree .

And  . . .

An in vitro heart with special catheters showing the true extent of coronary circulation: Courtesy http://eurheartj.oxfordjournals.org/content/28/3/278.full.pdf+html

This  is the reason  normal coronary angiogram can never mean normal  coronary circulation !

This huge gap in our perception is the single important factor  that  explains the vagaries  of modern coronary care .

This also make any clinical coronary  scenario  a  reality .

“A patient with normal coronary angiogram getting a myocardial infarction , the next day and a severe triple vessel disease living comfortably  for  decades with medical management”

So , it is essentially a  false  sense of  scientific accomplishment  by the cardiac scientists  at  least in the  of coronary circulatory physiology.

What determines the extent of these invisible coronary micro circulation ?

There are innumerable channels of micro vessels traversing across the heart, sharing , bridging , branching, penetrating  and  perfusing the muscle mass.They can be anatomically patent , physiologically non patent .They can be recruited by hemodynamic stress .These are never visualized by current imaging modalities..It is also influenzed by  favorable growth milieu and hormonal and neural stimuli.

Ignorance based cardiology

What is the mechanism  of primary VF following acute STEMI ?

The quantum of  coronary micro circulation is like the vast  cerebral neuronal net work .We have every reasons to believe they are have unique genetic imprint.How else you can explain a man with full blown STEMI come 24 hours later comfortably to the OPD while another loses his life with a stormy primary VF before even boarding the ambulance !

Why many cardiologists   do not give due credit  the   coronary collateral  circulation  ?

Right from the days  of  Levine in 1970s( Who made a seminal contribution  about coronary collateral)  the  utility value of  coronary  collateral  circulation  was never able to convince the cardiology professionals .

It has been our traditional  teaching ( without much evidence of course  !) coronary collateral circulation  is not effective to support blood flow during exercise . This fact has been  disproved  many times . Coronary collateral circulation was indeed useful in limiting damage in ACS and  relieve symptoms in stable angina.It helps  in reverse remodeling and provided electrical stabilty as well in post MI population.

Still , the concept  was  alienated  and   made   totally irrelevant  in the interventional  era  . Many   cardiologists  found well-developed collateral’s as an interference to their expertise and ego since it has a potential to alter the indication of PCI.They  continue to have  strong  scientific conviction (Pseudo ?)   that man made collaterals must always been superior to God made collaterals !

Whenever  some credible  reports emerge about  collateral circulation   being   equivalent to  revascularisation procedure , these concepts were  prematurely buried for some reason.

In the last decade there was a concern  about  performing  PCI in patients with well-developed collaterals  .The argument was , they tend to develop early stent occlusion and restenosis . It  was a genuine  query  raised by few thought leaders in the field as  collateralised vessels  suffer from  low flow   after PCI ,   if the pre -existing collateral continue to function.

But  then , few  studies countered this , and PCI was shown to be safe and  in fact may  fare well   in  patients  with  extensive collaterals .

In these  studies  interventionist’s  argument looked  amusing !  as they  seem to  define a  successful  PCI  as  not only to open the occluded vessel  but also  make sure to close  all functioning  collaterals  .(What a  a pity for our natural biological  angiogenic forces which had  worked  and  grown meticulously for months!)

Cardiac science in the current format,  makes   the future look  bleak for coronary a collateral circulation .With  early PCI  becoming a norm we will never ever allow the natural collaterals to  grow  ,  and even the  established collaterals  will have to face a stiff   fight  for survival  with  sophisticated coronary interventions .

Competing interest in the filed of  coronary collateral   research

While the basic scientists want  to  grow collaterals with angiogenesis ,  stem cells etc  interventionists   continue to  indulge in rampant angioplasties which  will suppress  collateral growth.

This implies we will struggle to  establish  the true  importance of  coronary collateral circulation .

Final message

Can it be an  effective form of revascularisation  ? 

My personal  inference  is   coronary collateral  circulation  “would and should”  have  a definite role  in at- least  some of the subsets  with chronic coronary  syndromes. If we think otherwise . . .    it’s against the principle of  natural biological science .

A good  collateral   system with optimal medical management  can save not only our  patient’s  lives but also  their hard earned currencies !


Here is a rare article in European heart   journal that discuses coronary collateral circulation  . Let us welcome such wonderful  reviews which keep the interest alive on the filed.


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Left main ostial lesion remains a  challenging task .A new stent design is  proposed here.

The lesion

Left main  ostial  stenting lesion003

The hardware 

left main ostial coronary stent drsvenkatesan

The technique

Left main  ostial  stenting lesion002

Final message

This thought came  when I  recently encountered a patient with a left main ostial  stent which was projecting well into aortic root .It is an open access patency ,whoever is capable of converting this idea  to a clinically applicable technique is welcome to proceed !

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