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Distribution of Left main disease.

  1. Ostial
  2. Ostio-proximal (Within 1 cm of  origin )
  3. Shaft -Discrete  mid left main
  4. Shaft -Diffuse
  5. Isolated distal shaft( 1.0.0)
  6. Bifurcation ( Medina 1.1.0 -LAD)*
  7. Bifurcation (Median 1.1.0-LCX)
  8. Bifurcation ( Median 1.1.1)*
  9. Trifurcation ( With ramus )

* These three locations account for nearly 75% of all left main lesions.

left main disease coronary angiogram

We know atherosclerosis is  a branch point disease .Normal left main measures 1 mm to 20mm.The shorter the left main lesser is the the incidence of LMD. Short left main can not engage the atherosclerosis much (No left main = No left main disease ) However ,very short left mains  may increase ostial lesions .

  1. The commonest left main lesion is distal left main with one of the branch involvement (1.1.0.LAD is more common )
  2. Least common entity is discrete mid shaft lesion.

Simple strategy.

First dictum : All complex looking LMDs should be referred to a good  surgeon.

Final dictum : Remember medical management for left main disease is still an accepted strategy in stable , non flow limiting situations .

Interventional  Cardiologists  feel they have the exclusive rights   to indulge between these two  spectrum of LMD .May be true! But extreme caution is required as we are playing  our game in the most critical  coronary high way .

Some suggestions and thoughts.

  • 50 % diameter stenosis is significant. But significance does not mean we should tackle the lesion by aggression.
  • Symptomatic flow limiting lesion only to be intervened . (Flow limiting means both angiographic and a stress test .FFR <.8 is also an index for flow limiting .Symptom means Angina on exertion )
  • IVUS, OCT, FFR,NIR ,SYNTAX  are not path breaking tools .They essentially  add  more glamor  to left main disease than anything .
  • Most bifurcation LMDs are  managed by single stent with stent jailing the major side branch (Yes side branch can be LCX !)
  • However ,two stent strategies is not banished .It can be vastly  superior in some selected cases .(Especially with huge plaque load at carina )But needs expertise .
  • In very small vessels two stent strategies are risky .

Reference (2012 update)

left main disease  coroanry angiogram management  Fajadet

PRECOMBAT left main disease south korea everolimus
Link to related articles in this site

We know Nitroglycerine(NTG) as a most powerful epicardial coronary dilator  . We use it for instant relief during episodes of coronary arterial spasm in cath lab.

What will happen if we administer NTG over a stented segment ?

Does it dilate it with same vigor ? What will be the consequence  ?

A perfect setting for stent migration isn’t ?

Let us bust the myth around  NTG . NTG  rarely  show  visible coronary dilating effect except in the setting of coronary spasm .

NTG and coronary vasodilatation

Does a LAD with 3 mm diameter become 3.1 or 3.2  and so on with NTG ?

No .It won’t .It is my belief. It is well known , NTG’s action varies significantly in normal and diseased endothelium . Again , there is an irony .It seems , it can act only in normal endothelium , but  we need require it’s therapeutic action only in pathological segments.Further any stented segment would contain   clusters of  both normal and abnormal endothelium .

One more inference is that, stented segment exerts constant pressure on intima making any  pharmacological vasodilatation irrelevant .

Importance of  radial strength of a stent

This issue of vaso-dilator induced  stent migration may not arise in self expanding wall stent with high radial force.But we do not know how long these metals will carry this metallic property .Balloon delivered  stents ( currently used 99% of times ) do not have permanent radial strength .

Final message

I am yet to comprehend what nitrates are expected to do (and what it really does ?)  in a patient post PCI ? (By the way  . . . why we need to prescribe Nitrates it in the first place ? but  In real world most continue to take this for many reasons .)

We need to analyse the micro-vasomotion at the stent -coronary intimal interface.The dynamism in this  narrow space  can be critical  , and may make the difference between life and death !

After thought .

In the hind sight,  this post appears quixotic  for myself . But some one , some where , may generate a great idea  out of it , that will help our patients.

Today , November 2nd 2013 is Deepawali , Nearly 1 billion people  celebrate it

diwali-lamps

Wishing you all happy and Deepawali , Let goodness and wisdom prevail over evil and Ignorance !

Deepawali  is an ancient  festival of lights , millions  of Hindus celebrate It with sanctity.

It is a  war on darkness and ignorance .On this day goodness  prevailed  over evil (Asura)

Unfortunately , In the current versions , it would seem  Asura’s also join Deepawali celebrations and enjoy  it with more vigor !  which is supposed to eliminate them !

Please ensure , that doesn’t  happen . . . at least in your domain ! 

God is supreme  . . .  he will  never allow  the evil  to take over the world !  Be a soldier to God’s  Army !

 
*For more about this great Hindu festival click on the Link here Deepawali

CAD is growing as an epidemic in most  parts of the globe. It  is  a major determinant of health status of any country .Great strides in diagnostic, treatment modalities of CAD  have been made in the last few decades. Still , the core principle of management of CAD resides in simple things like  risk factor reduction / optimization , life style changes and few essential cardio-protective medications  Aspirin, beta blockers and statins.

However , modern scientists have made a  firm statement that  knowing the coronary anatomy before starting the treatment is the only scientific approach . It is a huge assumption !

Is it practical ? or is it really required ?

CAD can be managed  by  means of medicines  ,  interventions or surgery. Revascularisation is required  only for  those , who have  critical , symptomatic lesions.

It is estimated , in only  a fraction of CAD patients ,  we would require to know the anatomy . We have set criteria to choose  patients  for CAG , who are  likely to have critical lesions.Physicians  are trained for that elusive wisdom to choose  such patients .Standard text books do mention clear-cut Indications for doing  CAGs. Unfortunately , it is  least respected and followed .

Cardiac physicians who  would boast  they  can’t treat a CAD without knowing  the coronary anatomy  are clinically handicapped  or poorly trained.

I am afraid such a class of  cardiologists are rapidly breeding in the country side. They are  encouraged to attend  CME on clinical  cardiology and basic principles of  clinical decision-making  .

We can’t  keep  on doing CAGs like ECG for every episode of  angina . In fact treating CAD without knowing  the anatomy remains (And it should  be ) the dominant theme contemporary  clinical practice . CAG is multi -edged sword

The most important side effect of routine  coronary angiogram  is , it  ends up in infinite number of inappropriate interventions ! 

I think , we should pray in Hippocratic  temples for sufficient wisdom  to choose our patients. We can also learn it from Neurologists , they  somehow  manage most  forms of cerebrovascular  diseases (scientifically too ! )  without asking  for angiogram of  circle of Willis !  Mind you. . . brain is equally a vital organ !

Final message

It needn’t be a crime to treat  CAD*  without knowing the coronary anatomy. Rather  . . . it would be so  , to ask for CAG indiscriminately  , in every episode of chest pain , without applying clinical sense !

* Emergencies included.

News : In any developed nation , 90 % of  total  health expenditure is  exhausted in prolonging  final few days of  human  life !

When cost of dying   . . .  exceeds cost of living   . . . this world will go nuts !

The current real world  experience  from India’s  five star  hospitals  indicate,  many elderly rich men and women  spend their  last few days  before being buried or burnt  .They spent an average of 15 lakh Rs per death . This amounts to the entire  “life time” cost of living   of  majority of Indians .

modern medicine art living and dying

Image courtesy from Flicker/ Rachel sian photostream

When   human organ donation is considered  a greatest philanthropic act, there is one more excellent alternative for those who can’t do it .If only every super rich translate  their cost of dying  into  cost of  others living !   many new lives  will bloom .

The exorbitant rise in  cost of  dying  in India ,  is a recent development and reflects the affluence , honor , pride and of course lots of prejudice lack of wisdom ! Instead of filling the  deep  pockets of greedy  corporates why not the rich add new  lives   ?  !

Final message

Let all elders  with irreversible conditions , who have finished their life , shall  die peacefully at home .Why don’t we ( Affluent  .  . . would  be cadavers !)  cross sponsor their dying cost to a  public  health , nutrition or medical fund .

After thought

Oh America ,  . . .  Am I right  ,?  Obama thought it and implementing it too !  I would believe , his health care policy is  a  small first step in this  direction  !

We know LVH and SHT go together . Mind you , this is not an Intimate relationship.

Widespread utilisation  of echocardiography  has revealed  , definite  LVH occurs only in about 20% (A guess !) of  HT . (Do you know in the Famingham study the incidence of LVH  after 12 year follow up was a paltry 3 % .Will you agree with that ? Mind you , It was in 1969 when Echo was not there )

What determines LVH ?  The clear answer is elusive. It is easy to escape  from the issue by calling it  multi factorial !

Why don’t you try this question .

My guess would be ,  magnitude ( or  even duration of HT !)  is  less important than genetic predisposition  or  associated diabetes ,  renal involvement.Our analysis from  hypertension clinic reveals LVH is many fold common in secondary HT  when compared to primary HT !

I often used to provoke the students by saying if the LVH is gross in HT it can not be primary , 9/10 times  ! Invariably  we find some  other  association or reason for the HT !

Link to related topic in this site

Why-lvh-does-not-occur-in-all-patients-with-systemic-hypertension ?

How-diabetes-modifies-lvh-due-to-hypertension ?

incidence of lV left ventricular hypertrophy framingham study

Next  . . .

How does LVH regress with treatment ?

The current  fad called EBM has lots of lacunae. Though evidence based approach is  considered  the ultimate  journey  towards  truth  ,lot of non academic factors contaminate it .In it’s  current form , it is difficult to comprehend it.

This is an attempt to decode the mystery of EBM  expressed in a simplified  lay person’s term .They are the ones  from whom we learn  medicine. They are our teachers in the true sense.

evidence based cardiology guidelines evidecne levelBy the way ,it  is also my approach  to   EBM .Sorry , if  this post  sounds  arrogant ! It is not the intention .Truths often times appear brutal .

And   . . . the  Genius  approach to EBM  for comparison

 

2011_AHA_Classification

 

 

 

In one of my classes , this ECG  was presented .  Controversy  erupted.It was about the  basics .

What is the QRS axis  of this ECG  ?

ecg north west qrs axis  indeterminate

Not surprisingly there were  handful of answers .

  1. North west Axis
  2. Indeterminate QRS
  3. +150
  4. +180
  5. 0 degrees
  6. Extreme Right axis

Which is correct ? My guess  is ,  it should be  closer  to + 180 .  Lead 2 is equiphasic and perpendicular lead is negative limb of AVL ie + 150 .If you  plot Lead 1 and  AVF in graph and calculate  we get + 135 . (In the strict sense , we are not  supposed to take one standard lead and an augmented lead for plotting ). Finally, the strongest argument was ,  since  AVR shows  only positive forces  it  would make  north west axis more likely .

ecg qrs axis north west indeterminate

Causes of North west  QRS axis

  1. Denova North west axis
  2. Extreme Left becoming NWA*
  3. Extreme Right  becoming NWA

*Left becoming NWA is much more common than other types.

Chamber enlargement alone is not sufficient to shift the axis to NW corridor. There must be anatomical distortion of  his bundle and it’s branches to shift the axis dramatically .This usually occur in complex congenital heart disease. In acquired heart disease the  an apical VT is probably  an important cause for NWA.

One word about indeterminate qrs axis .

By the way , Indeterminate QRS axis  is not synonymous with north west axis. This term should ideally be used  if qrs complex is equiphasic  in all limb leads , when  qrs  axis  can not be truly determined .This situation commonly occurs when we encounter very very low voltage qrs  as in cardiac tamponade and severe hypothyroidism , constrictive pericardits, etc

If  the QRS is in north west  corrodor , How  to differentiate ,  whether it came from  extreme left axis  or  right axis ?

I am yet to find a correct answer for this.

  1. Pre-cardial pattern will help.
  2. A  q in V5/V6 would suggest  extreme left axis.
  3. May be we have to look the initial qrs vector in AVR lead for more clues

Traditionally , we talk about net qrs axis . We should realise net qrs axis is a combination of initial and late vectors .It can be dramatically different in different leads . QRS axis is  a two dimensional representation of three or more  (omni) dimensional electrical forces .That is the source for confusion. So,  do not unduly worry about the complexity .Blame it on the limitations of surface ECG !

Expecting some comments .

It is estimated nearly half a  million PCIs are done all over the globe every year .Evaluating diagnostic angiogram is a critical  vital step, but  often times it is given less time and left to fellows .This is done mostly offline by Image  processing software. Curiously , lesion assessment  becomes a causality to the   visual acuity .It ends up  with lot  of whims , intuition and bloated egos of senior cardiologists !

Technical issues

The fundamental flaw in the  lesion assessment is ,there is  a dissociation in choosing the  “best view”  for lesion morphology  and  length  . Size need not be well  assessed in  the same view as morphology . For example , LAD is fore shortened  in LAO caudal view  ,  length measurement would be  erroneous  ,  still morphology may be well delineated .(Vice versa in RAO caudal view )

PTCA guidewire calibratedcalibrated ptca guidewire

Other source of errors

Reference catheter may be far  away in the Aorta , and confer a  magnification error . This becomes important especially in ostial lesions and associated  major branch lesions. The computer uses the edge detection algorithm  which carries an   inherent error .

Advantage of guide wire as a scale

  • Instant online measurement
  • Always on . Repeatedly used in multiple views .
  • You can’t ask for more accuracy .The scale is within the coronary artery  hugging the lesion
  • The end on view is effectively nullified .
  • Magnification  factor do not operate.
  • Finally , and most importantly in complex  tortuous , tandem lesions few mm errors can be disastrous .These calibrated guide wires will make our life lot easier.

Final message

Measuring  a coronary lesion remains a delicate issue . If only we have radio opaque  rings every 1mm or so in the distal end of the guide wire , we can measure the lesion  instantly and most accurately.

This will  definitely make our life  not only simple but help our patients with accurate stent sizing and avoid costly geographical miss (or inappropriately  long stent  that increase  metal load .)

After thought

I do not know whether  any of the existing  guide wires have this facility .(I guess it is not   . . .then , let this idea  be patented in my name !)  After all , It is a mean  task for all those mighty coronary hardware companies to add  few radio opaque rings to all  PTCA guide wires!

Medtronic, Abbot, Boston  are you listening ?

And . . . your opinion please !