Archive for October, 2013

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.

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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  !

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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

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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 ?

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This post , is  probably not meant for cardiology professionals.

Few technologies are clear winners in modern medicine. ICDs play  games  that would rival the God !

What is an ICD ?

Here is a man , who  drops almost dead by a fatal cardiac arrhythmia . In few seconds  ICD  machine recognises this arrhythmia ,charges itself and  fires a shock  of about 30 joules direct current .The arrhythmia is reverted and the fellow gets up as if  nothing has happened !

Watch this video

This revolutionary devices are  to be used judiciously in individuals with high risk  for dangerous cardiac arrhythmia.

The current  indications  as on 2012

Post MI  ( Only after  4O days*)
LV dysfunction EF ≤ 35%   NYHA  II or III  ( Please note , If  ≤ 30%, even Class I  NYHA can be implanted an ICD) *Why 40 days ?  Residual ischemic, Irritable  focus  should settle down
Myocardial disease
  • Nonischemic DCM  EF ≤ 35% with documented VT
  • Rarely other structural heart disease with recurrent risk for VT ( Few HCMs)
Primary electrical disease
  • Survivors of cardiac arrest due to VF without any completely reversible causes (Includes Brugada )
  • Malignant forms of syncope  with   idiopathic recurrent VT /VF
  • Congenital Long QT syndromes not amenable to beta blockers


Guidelines ICD pacemaker 2012 ACC AHA

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This question always creeps in any coronary care unit.

Often times , there is a significant  histo-pathological overlap between severe degrees of  Ischemia* and  myocyte necrosis . (What is called micro infarcts, lacunar infarcts,  make us over diagnose MI). It is not yet clear , whether leaky myocyte cell membrane can release free cytoplasmic enzymes without actual cell necrosis.
Clinical Implication
Fortunately , there is not much .These bio markers are primarily used as prognostication tools .Many of these patients  need to  undergo early revascularisation. However , It is unwise ,to get alarmed by  just  Troponin positivity  in an other wise comfortable ACS patient.
* Some call severe degrees of Ischemia as Injury ! It is an old thought based entirely on ECG  .There is no specific cellular equivalent of electrical injury current !

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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






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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 .

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Few Innovations are real breakthroughs in cardiology . Here is an imminent technology waiting to explode in the  permanent pacing . Expected to hit market next year (2014 in Europe ) FDA approves clinical studies .


Click over for the animation video  of the procedure .

  • The wireless pacemaker has many advantages. (It’s devoid of all those pocket and wire related issues.)
  • The ability to change batteries is  a  going to be a  new paradigm shift in the filed of electro physiology. .
  • Down side would be,  right now it can be only VVI pacing . All that hype about    physiological pacing  will go to the background !

Future directions in Permanent pacing.

The only threat for this technology is the  concept of biological pacemaker Converting ordinary myocytes into  pacing cells by genetic engineering.This is expected to happen within few decades.

biological pacemaker

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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 !


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