Posts Tagged ‘coroanry angiogram’

Human coronary artery branching pattern is unique in every  individual . Left circumflex shows many variations.

The important ones are  a separate origin , variation in the angle of bifurcation, the number of OMs  .Further, the length of  mainstem  LCX  and its course in the AV groove are quiet unpredictable.The diameter of LCX vs are generally equal  (or LAD >LCX).

The division of  left main is such that circumflex  generally gets a lesser share  of blood flow . If  LCX is dominant this  ratio  may be little balanced. But if the LCX  is huge LAD definitely suffers !When left circumflex equals the size of left main  the pattern is distinctly  unusual.

This patient   we encountered recently had 4mm sized LCX   and  presented with a tight LAD lesion .

This man's LCX probably will never sufffer from atherosclerosis !

Other observations about large bored LCX

  • Narrow ostiums are prone for  atherosclerosis .A large mouthed  LCX rarely involves  in left main  bifurcation lesions.
  • Disproportionate size of LCX when compared to LAD  can  have hemodynamic implication of provoking LAD disease  .

The implication of  differential  sharing of left main blood flow is not fully understood .It needs further insights.

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Reporting a coronary  angiogram  may look like child’s play  for most cardiologists. Many do it in less than a minute. (It goes something like this  90 % LAD , 30 % ostial OM1, 50 % mid RCA etc etc ) The famous and meticulous  classification of Ellis and Ambrose proposed  two  decades ago appear largely redundant.

In this review we shall  briefly  debate an eccentric plaque or lesion .

Pathological definition

Pathologically  an eccentric lesion  will have a disease free arc  within an  atherosclerotic lesion.If we apply this criteria most of the plaques appear to be eccentric.

Angiographic definition

In simple terms  eccentricity is  said to be present when the plaque  volume is three times more on one side when compared  to opposite side .

The incidence of eccentric lesion is largely under estimated.  It can be up to 40 % of all lesions.

It has histological  as well as  hemodynamic  significance.

How to measure eccentricity index ?

Ratio between maximum plaque thickness and minimum plaque thickness (Including the media )

Image courtesy modified from Circulation. 1996;93:924-931

In the above figure : The eccentricity index is measured  as the ratio of the maximum  to minimum plaque plus media thicknesses. In the eccentric lesion  the maximum wall thickness measures 2.6 mm, minimum wall thickness measures 0.2 mm, and eccentricity index is calculated to be 5.2.  In the  concentric lesion  the maximum wall thickness measures 2.2 mm, minimum wall thickness measures 1.6 mm, and eccentricity index is calculated to be 1.4.

What are the associations of eccentric plaque ?

Calcification and hard plaques are more common in eccentrically placed plaques.The  most vulnerable point for plaque  rupture or disruption is  the shoulder region between normal and plaque segment.

A long eccentric lesion with over hanging plaque


Clinical implications

  • Acute recoil
  • Coronary spasm
  • Mechanical effects : Asymmetric expansion of stent
  • Drug eluting stents

An arc of normal plaque circumference predispose to acute recoil and spasm.this is logical as the normal  arc will have a fully functional  medial smooth muscle  which are prone for spasm.

Does stenting reverse  the eccentricity of plaque ?

It may not .  The drag effect of major plaque mass may either result in plaque prolapse or  asymmetric stent approximation  or even stent crushing effect.

How does the  the stents  elute in an eccentric lesion ?

Stents are not intelligent enough to  differentiate  the plaque surface and normal surface. We  also know these drugs are  toxic to  normal endothelium  and hence  are not welcome in the normal arcs of an eccentric lesion.

Since the drug secretion   is uniform throughout the circumference   it makes the   DES a perfect misfit in eccentric lesions  As  we  realise most of the lesions are pathologically eccentric one can guess the long term  consequences .

Final message

The more we think we know . . . the less  is understood .

The images we see daily in cath labs are too simplistic to make vital decisions .There are  constant innovations coming up but none seems succeed in  imparting  common sense to  majority  us.(Namely  direct plaque intervention can never succeed over a diffuse medical  disease called atherosclerosis  )

A good reference article


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Coronary artery lesions can be classified by many types . The popular ones are by Ambrose and Ellis  .They are adopted by ACC and SCAI  .While various  terms  are  used to   describe a lesion. (diffuse, discreet , eccentric , long , tubular  etc) A tandem lesion is the one which has special significance , but is not well discussed in the literature .

A tandem lesion is  diagnosed when  two lesions  closely abut  each other one behind the other  with an  intervening normal segment. (Like the bullets loaded in a  tandem fashion  in a  gun )

Generally there will be at least  few millimeters of normal intervening  coronary segment.This is  referred to  as  connecting segment.

Clinical importance of tandem lesion

Tandem lesions  carry  the  same significance  like  any other lesion. But ,the primary aim is to tackle the two lesions with a single stent. We know stent edges are rheological culprits.  Two stents  have   4 edges. It is better to cover  the tandem lesions with one long stent* even if we have a sufficient  connecting segment.Geographical miss is less likely with a long stent.  In the strict sense one wold require an IVUS (Intra vascular  ultra sound ) to confirm the normality of the connecting segment. Tandem lesion is  a  marker  of diffuse atherosclerosis  and  the connecting segments often   show ectatic changes.

* This is a ironical as  the conventional wisdom would  tell us , lesser the  metal load it is better for our coronary arteries.But once we embark on a complex  intervention we just can’t restrict the use of stents. The more you put the more it will demand.There are some interventional cardiologists who convert the entire coronary artery in to a metal tube (With or without realising the consequences !)

Illusions of  tandem lesion.

Many  times ,  spiral folds  from a single  atherosclerotic   lesion mimics  a double lesion .This need to be differentiated from true tandem lesion.

What is the hemodynamic significance of  tandem lesions ?

Rules of hemodynamics  would  dictate ,  in a linear and laminar flow  model across a tube ,   immediately after an obstruction there will be a significant  drop in resistance.

This  forms the fundamental   phenomenon  within the coronary artery  . This explains the biggest mystery in cardiology . . .  How  the  TIMI flow is  maintained till 90 % of the  lumen is narrowed. This  also  explains the concept of flow limiting lesion .(Why  a coronary lesion do not obstruct the flow  till late stages  ?)

Does this rule on  hemodynamics  apply in tandem lesions ?

When a lesion is followed  by a lesion with little normal segment in between what happens ?

The blood gets a double jolt every time it traverses a tandem lesion. There  may not be sufficient time and anatomy for the mandatory pressure drop to occur. So for a  given degree of obstruction ,  tandem lesions  is likely to be   more thermodynamically significant than a single lesion.

Pressure recovery after  an obstruction is also incomplete , as the forward head of blood column encounters another hurdle even before it recovers from the initial turbulence.

Which lesion is more important   in tandem proximal  or  distal  ?

The distal lesion determines the thermodynamics of proximal lesion while the distal lesion as  such is  less influenced by proximal.

Long lesion vs tandem lesions

Some times it may appear ,  it is better to have a long lesion than  a two lesion  in tandem. This is because the stent will approximate more evenly .Further there is less likely hood of in -stent restenosis in long lesions as the   edge effect can occur  right in the middle of  the stent in tandem lesions .

Now it is increasingly realised, many of the sub acute thrombosis  are due to po0r stent approximation in tandem lesions or long lesion.



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In any field  , errors and mistakes  transform into   experience in retrospect. (Of course only  if we  realize  our mistakes !) . Many would argue prevention of such errors is the  only way to move  forward in science  , but ,the opposite could also be true.

In Medicine ,

  • Most errors are mild ,
  • Some errors  can   be fatal but it helps us prevent further fatalities.
  • Some errors create history  and  re-define the science.

That’s   what  happened on 1958 , to be precise on  October  3oth , 1958  in a lonely laboratory of Henry  Ford hospital/Cleveland clinic *

*A correction -This  invention actually happened in Cleveland.  ( Sones learnt  all his techniques in Henry ford)

When  Sones along  with his assistant were trying  to do an  Aortogram in a patient with RHD,  the entire dye meant for aorta went straight  into  the right coronary artery.When every one was stunned ,the  patient happily  survived the injection  with a few skipped beats.

The man behind  this horrendous medical mistake was   Mr . Sones . He   was guilty for many days ,  spent many sleepless nights  ( In spite of  the patient surviving  the episode ). In fact , he was much amused  about the patient’s  survival . At that point of time,  even a spill over of dye into coronary artery was considered forbidden.  He pondered over the incident for months  .

Had  two queries  lingering in his mind .

  1. How the  right coronary artery  was able to withstand the 40cc dye  injected with  force .
  2. If 40 m l was tolerated ,  well what about routinely injecting  3-5 ml for visualizing the coronary  tree   by intentionally  seeking the coronary ostium .

That was the moment , the concept of diagnostic coronary  angiogram  was born . He published his observation as an  abstract in Circulation journal. Later he did many experiments  with video  engineering at Kodak labs , X  ray  technology to improve the cine imaging .By 1964 , he devised a perfect protocol  for doing  selective coronary angiogram. Then along with Rene Favaloro he pioneered CABG surgery in USA.

Final message

Cardiac  catheterisation was invented by  Forssman , Cournand , and Richards ,(Nobel prize 1956 ). It was  Sones who took it into the coronary arteries  and thus it was  made possible  for a whole new specialty  of coronary  diagnostics  and therapeutic PCI  which was  conceptualized by another extraordinary human life called   Gruentzig. Sones along with Gruentzig definitely deserve a Nobel in medicine which i think will happen soon ! They lived a great life constantly thinking, innovating  putting  patients interest in the fore front .

Mean while , I argue our youngsters  to  portray  the images of  these giants in  every   cath lab they  work   .You may get their blessings from heaven  , provided you do your interventions with integrity and honesty without any conflict of interest in the patient care.

Do not cry foul when some genuine errors happen in cath lab.Few among us (like Sones ) may innovate those mistakes into glory !




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Atherosclerosis   remains the number one cause for all vascular disease of human beings. It probably  kills more  patients than all other causes put together .

Modern medicine has never conquered the disease. How  the vascular system ages and why some develop premature atherosclerosis remains largely speculative. While it is true , we have identified some major risk factor for development and progression of the atherosclerosis  , patients with out any of those risk factors do develop severe atherosclerosis !So researchers sought to look for some other risk factors . There lies the difficulty  and irony .

We always tend to the research with the affected population .When we know millions of people with the so called risk factors live comfortably , there lies an opportunity  to  analyse why they are protected against the onslaught of atherosclerosis .It is always convenient to blame it or bless it on the genetic predisposition .But we need to look beyond that .Of course  . every genetic expression has to  manifest phenotypically .

While the search for all those hidden secrets has to continue , we should also realize in pursuit of breakthrough we some times waste our energy in false targets  for too many decades !

The reality as on today is ,  there is no reliable  &  undisputed drug available to arrest atherosclerosis  (Some would love to call statin so . . . )

While  our basic science colleagues struggle  in molecular  factories and biological models in pursuit of answer against  atherosclerosis , our elite  cardiac physicians   carry on with the cosmetic touches over this   progressive disease  in  sophisticated cath labs.

Let us hope  man prevails over nature . . .

A cartoon , Just for laughs . . .

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cardiologist Is he a person who puts  a   metal coil  coated with a synthetic fungus   in  a   incidentally  detected  block  inside a  small coronary artery and sends the bill to the Insurance company ?

Is he a person in a  cosmopolitan  hospital  who opens up a    chronically   closed  coronary artery , in an asymptomatic patient  and  live telecasts  his achievement trans continentally ?

Is he a person who   checks in by  the early morning flight and  puts multiple wires in  an  aged   patient   with  class 3 heart failure and  make  him walk  20 meters extra at a cost of  1000$ / Meter ?

Is he a person living in   Wall   street  ,   who   looks  for variety of holes In  the heart and trying to occlude  it  with   exotic   devicespci ptca stent

Is he the unknown   physician   who Intervenes in the natural history of Rheumatic heart disease   and arrests   immune mediated   valve damage by giving the  monthly injections  penicillin in remote parts of our country ?

Is he the person   who   Intervenes to prevent young   persons   from  smoking and help maintain  their  coronary endothelium  enriched with nitric oxide  & arrest  the coronary epidemic ?

cardiologist 2

Is he the small town doctor  who  Intervenes  to treat a breathless cardiac failure patient  with  digoxin and frusemide  and  dramatically alleviate the  symptoms and  prolong the  life of our poor country men?

Is she the village health nurse from an inaccessible health  centre  located in a  hilly terrain ,  Intervening  successfully, by   pulling out  live babies  from  severely anemic pregnant  mothers with failing hearts ?

pci ptca cardiologist coronary angiograms

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