Posts Tagged ‘fibrin cap’

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. !

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


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

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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