Dr.S.Venkatesan MD

Erroneous concepts in Acute coronary syndromes !

February 25, 2014 by dr s venkatesan

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.

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. !

Waiting for someone to nullify such false concepts in a more scientific way !

Reference

1.Waxman S¹, Mittleman MA, Zarich SW, .Plaque disruption and thrombus in Ambrose’s angiographic coronary lesion types.

Am J Cardiol. 2003 Jul 1;92(1):16-20

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

Postamble 

This post was written in 2014. Happy to find a scientific proof to this concept in 2018.

Source :  PROSPECT study

Retrospective angiographic studies and the prospective PROSPECT (Providing Regional Observations to Study  Predictors of Events in the Coronary Tree) study have shown that plaques with severe stenosis carry a higher per-plaque risk for producing clinical events than plaques that cause no or non severe stenosis.

However, such lesions are few, and overall, most ACS are precipitated by plaques  without significant stenosis on an antecedent angiography
weeks or months before. This epidemiology is consistent with the distribution of TCFAs, as shown by a combined angiography and optical coherence tomographic imaging study of nonculprit lesions.

Lesions that caused severe stenosis were twice as likely to be
TCFAs than lesions with only non severe stenosis, but the total number of TCFAs with nonsevere stenosis was three times higher than those with severe stenosis. The mild pre-existent stenosis of most TCFAs and ruptured plaques is explained by expansive remodeling, because such lesions are, on average, large.

The long-held notion that mild to moderate obstructive coronary lesions are responsible for the majority of MIs has been challenged by studies that described significant narrowing in the days preceding MI. However, significant narrowing shortly before MI may be a result of (rather than a precursor) for rupture.

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Posted in Cardiology -Mechnisms of disease, Cardiology -unresolved questions, cardiology- coronary care, Pathology-Vulnerable plaque | Tagged acute coronary syndrome, fibrin cap, flow limiting vs non flow limiting lesions, ivus oct nir for plaques, lipid core, pathology of atherosclerosis, plaque erosion, plaque fissure, vulnerable plaque | Leave a Comment »

A tribute to a great cardiologist from Grady !

February 16, 2014 by dr s venkatesan

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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Posted in Cardiology classics, Cardiology-Land mark studies, cath lab tips and tricks, Great Men in cardiology, history of cardiology, Land mark articles in cardiology, Uncategorized | Tagged concept of physician assistant, dr stead eugene anson, father of physician assistant, grady memorial hospital atlanta georgia, history of cardiac cathetrisation, right heart catheterisation | 1 Comment »

Why 90 % of cardiologists suffer from coronary blindness ?

February 12, 2014 by dr s venkatesan

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 !

Reference

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.

http://eurheartj.oxfordjournals.org/content/28/3/278.full.pdf+html

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Posted in cardaic physiology, cardiac physiology, Cardiology -Coronary collateral circulation, Cardiology quotes | Tagged coronary angiogram, coronary blindness, coronary collateral circulation, coronary micro circulation | Leave a Comment »

How to measure and quantify epicardial fat ?

February 7, 2014 by dr s venkatesan

Epicardial fat is increasingly recognised to be a coronary risk factor.

Methods to measure and quantify epicardial fat has not been standardised.

Nomenclature issues

There is some confusion in the literature regarding  the definition epicardial, pericardial , paracardiac fat etc.

Epicardial fat is the true visceral fat located in proximity with myocardium .Epicardial fat shares the same blood supply as adjacent myocardium and also show  para-crine functions.This is the risky fat that is metabolically active.

Paracardiac fat  is  the fat deposited outside the parietal  pericardium .It is also referred to as  thoracic fat .They carry less risk and behave more like somatic non visceral fat.

Pericardial fat is a loose terminology .Many  use epicardial and pericardial fat interchangibly .It is to be realised , fat either deposit inside the visceral pericardium or outside the parietal pericardium. It almost never deposits  within the pericardial space.

* Currently it is better to use  only two terms .Epicardial fat and  thoracic fat .Other terminology should be avoided.

How to measure and quantify epicardial fat ?

Distribution of fat over heart is not uniform .Though it appears a random distribution there app eras to be a pattern to it .It is largely loaded anterior surface of the heart, over the AV grooves, invariably hugging the coronary arteries and great vessel origins.Fat deposition posterior to heart occurs in gross obesity.

There is no accurate way to quantify it . A rough estimate can be arrived . The following investigations are useful.

• Echo
• Multi-slice CT  Scan
• MRI

Epicardial fat pad thickness by M-Mode /2D  is simplest,  but considered crudest modality to quantify.  .Still , it is a useful screening test. In our experience , if there is distinct anterior fat pad > 5mm it is likely to be significant.

However, epicardial fat volume is ideal method to quantify it.(Read below)

Which part of cardiac cycle it is measured ?

Since epicardial  fat is a compressible structure , in diastole the myocardial mass encroaches the epicardium  any imaging modality the distinction between epicardial and para-cardiac fat  tends to attenuated.

Even MRI images obtained with  diastolic  gating ,  may  not be reliable .End systolic frames are now considered ideal.

(J Am Coll Cardiol. 2011 Oct 4;58(15):1640;Distinction of “fat around the heart”.Kaushik M, Reddy YM.)

What is the normal  epi-cardial  fat volume ?

There is no standard normal.In one large study from  Boston in people  with a BMI between 25-30 the  mean epi-cardial fat volume was 125 cubic cms

(*Intrathoraic fat  same as para-cardiac fat located outside parietal pericardium )

How to differentiate fat from pericardial fluid ?

It can be a very difficult issue especially  when you expect both as in hypothyroidism .It needs proper  gain settings and interpretation.

Here is case report of how epicardial fat was mistken for PE even in TEE

Can we measure  the  net mass of  cardiac  fat , does it compress the heart ?

When we say average heart weighs 300 grams it includes fat embedded in it. I don’t think it is possible to measure the fat mass ,but clinically it may be important.Read this .Can-epicardial-fat-constrict-the-heart-an-authentic-yes-from-ulsan-korea ?

Final message

Estimation of epicardial fat volume is largely a research tool.In grossly obese patients it may  have some clinical utility.Increased anterior fat pad in routine 2D echo is an useful  screening test. However, it requires MRI/CT imaging for accurate quantification.

References

2. Marwan J M, Achenbach .S  Cardiovasc Comput Tomogr. .Quantification of epicardial fat by computed tomography: why, when and how?2013 Jan-Feb;7(1):3-10

3. Sarin S, Wenger C, Marwaha A, Clinical significance of epicardial fat measured using cardiac multislice computed tomography. Am J Cardiol. 2008 Sep 15;102(6):767-71.

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Posted in Cardiac MRI, cardiac radiology | Tagged end systolic epicardial fat, Epicardial fat thickness, how to measure epicardial fat ?, para cardiac fat, paracardiac fat, pericardial fat, pericardial fat vs pleural effusion | Leave a Comment »

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