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In one of my  meetings , I told a small gathering  , that regular exercise can shrink atherosclerotic plaques and regress CAD. I also quoted , a recent  large  study which  has proven this fact convincingly !

I concluded, simple  exercise  and other life style changes,risk factor correction  may convert a 90% lesion to 70 or even 50 % . I stressed the importance of this study and asked my colleagues to avoid misuse of  Angioplasties .

When many  seemed to agree with me , one  angry  Interventional cardiologist questioned me, and  asked  the name of the  study, and in which journal  it came , What was quality of the paper ?

evidence based medicine ebm experince

I told him , It is an Imaginary study done  in my back yard . It never got published in print. You may call it as E-journal* , not exactly though.It is not available in any websites , but located in the  biological servers, and  neuronal circuits as digital imprints in learned brains !

*Journal of experience

You may call it , a scientific  forgery , to quote a non-existent study,

But this study  benefits whole lot of my  patients”.

He was amused , and became agitated !

He told over the mike , “You are making  foolish statement. . . don’t corrupt young minds” !

May be , he is true !

I asked him to be calm and  requested  to listen to another study which I was about  to quote  . . .

He couldn’t sit any more  and rushed  out of the hall !

Final message

We  are ready to believe all those  rubbish stories about a fourth  generation   self disappearing BVS that is  able to scaffold a coronary artery and maintain a MLD by 2.5mm  and TVR by 20 % and prevent near MAZE  at 30 days  by 9 % and improve long term survival  by 6 months at  the cost of 100, 000 Rs  per month  .Only to realise, it may be a farce  . . .  5 years down the lane !

How to cleanse the darkened face of science ?

When falsehoods come with evidence and harm people , Good deeds can  be preached without evidence to save our fellow human beings !

modern medicine ethics hippocrates

Every pacemaker has  a metallic “Reed switch” . Putting this switch on and  off is possible with an external magnet .The circuitry is such that , switching on  makes sensing function null and void.It functions as asynchronous mode.In other words  pacemaker converts to a mandatory  pacing mode .All  sensing  related issues are immediately removed.

magnet rate reed switchNote : This switch can be activated by any strong magnetic filed applied externally .And removing the magnet disconnects the circuit.

When a magnet is applied the pacemakers changes the mode in the following way.

  1. VVI  to VOO (Paces only ventricle  without sensing)
  2. AAI  to AOO (Paces only Atria)
  3. DDD to DOO  (Paces both ventricle and atrial with a fixed AV interval )

magnet application permanent pacemaker ecg 002

Purpose of magnet application .

Essentially it may be called as a safety mechanism to prevent external sensing in strong electrical fields in case the need arises.

Indirectly , it may aid us in detecting end of life  of  battery as well

During elctrocautery and related procedures  application of magnet will help.

What is magnet  rate* ?

  • The moment you apply the magnet the pacing rate  changes
  • This is variable with each make and preset.
  • End of life magnet rate will be different . It can be 65 to 85  fixed depend upon the make.
  • Some pace makers  fire initial magnet rates with 3-6 beat fast run and later revert  to steady baseline rate.(One should not be confused )

* Always check with the pacemaker manual for the exact response.

When I put a magnet over nothing happened .What is the inference ?

  • Magnet is not placed properly
  • Pacemaker battery  is totally dead.
  • Very rarely some pacemakers  have magnet function  turned off

What happens  during magnet application in ICD ?

  • There is no change in ICD mode.
  • All anti tachycardia functions are immediately suspended. (A major use in an unusual runaway inappropriate  ICD shock situation )

Is there any risk of applying magnet ?

Since magnet removes the sensing function , interfering a cardiac rhythm which  is dependent on sensing can be  problematic.Similar situation arises in MRI scans and other magnetic fields.

Hence , application of magnet in a patient  as a part of pacemaker trouble shooting who has no pacing spikes is rarely a problem While one should not do it without supervision of  a learned cardiologist.

What is smart magnet ?

Each pacemaker  and ICD  is interrogated with the respective programmer.As such , there is no cross brand  programmer  available.This makes it difficult for patient( as well as physicians)  to call for help in case of malfunction.

The solution is to make standard universal analyser and programmer .This requires  cooperation between various stake holders.Meanwhile as temporary relief a magnet which can community two way with  basic functional switches can be developed .

There is a need for universal smart magnet with constant interaction between device and magnet ..

Since , the generation next generation human  heart  is going to be wired and deviced in a complex manner,  we need to know the basics about these  issues.

Final message

Magnet application is akin to novice’s  pacemaker analyzer. Every cardiac care unit must have one in their shelf. It aids us to diagnose over-sensing as a cause for pacemaker  malfunction.(* please note , it has little  role in all other pacemaker issues !) .In an emergency it can help stop inappropriate ICD shocks.(More importatnly  It gives  time to call an expert ! )

Reference

role of magnet application on pacemkakers icd  oversensing magnet rate

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 expect LBBB in RV pacing . . .but if RBBB is recorded we are worried ! (Often times it may be neither  LBBB nor RBBB )

Is it really a panic situation ?

  • Not necessarily. The only issue is septal perforation .It is rare , can be recognised by echo or fluro .
  • In true RV apical pacing with tined leads , RBBB  is extremely uncommon .
  • If the lead  is fixed  in the septum and para hisian  area ,  there is  definite  possibility of  deviation from typical LBBB pattern . Screwing leads  that faces high septum  or outflow , RBBB  can be noted occasionally.
  • The commonest cause for RBBB pattern in RV pacing ,  is due to  screw tip going deeper into septal planes  and activating the fibers of left bundle early .
  • For LBBB pattern to occur right  bundle should be morphologically intact .In diffuse CHB  with bilateral bundle branch blocks  the relative contribution ( Impulse conduction ) will determine the QRS morphology . If right bundle is more damaged than left bundle ,RBBB pattern  may prevail  even in the midst of RV pacing !
  • In elderly men with sigmoid septum typical LBBBs are not observed.
  • Anther plausible mechanism would be , even though RV is paced , the pacemaker current’s  exit route may be from LV side .
  • Finally , always  think about coronary  sinus pacing .It is extremely common in blind temporary pacing.

What should we do if we encounter RBBB morphology after PPM ?

  • Analyse the ECG meticulosuly for capture or sensing failure .
  • Do an echocardiography in RV inflow view.
  • Screen the lead by fluroscopy
  • Check the pacing  parameters.
  • Do a holter if  you are really anxious .

If everything is fine , just forget the RBBB.Don’t split your hair for this apparent paradox. In medicine  impossibilities will always  galore !

This paper from Taiwan would vouch for this

RBBB during RV pacing safe ecg

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 ?