Archive for March, 2011

Read with caution . This  may either injure or cure your patient !

Click on the ECG to view what happend !


How does  verapamil  terminate a  VT  ?

Physicians  often  debate  vigorously before   labeling  a cardiac arrhythmia as ventricular , atrial junctional  , abberant or not etc etc .  But  for  an arrhythmia   it matters little  from what  chamber it is going to to originate . After all ,  any cell in the heart if excited can generate an arrhythmia .  The ion channel abnormality and the influx and efflux of ions  that determines how a drug is going to terminate an arrhythmia.

In fact , way back  in 1989 the Sicilian Gambit stressed this concept when classifying anti-arrhythmic drugs .This classification taught us  , even though there is a  huge list of  clinical cardiac arrhythmias  , from the therapeutic point of view there are only a handful of receptors  (scattered  all around ) to target  !

When we look at this angle , we realise  , many of  ventricular action potentials  have  important slow  calcium currents  similarly  junctional action  potentials do have some  sodium currents.  Calcium current  is present in every  myocardial cell  more so in the vicinity of AV junction.  Further , at times of ischemic or hemodyanmic stress these ion channels  may  take a different avatar altogether.Slow sodium channels and fast calcium channels etc !  (A wild imagination or is it a fact ?) Other important targets are potassium channels

Heart is a complex structure both macro and microscopically  .  In the three dimensional  histopathologic   interface between atrium  and ventricle (Especially in the  basal areas , outflow tracts  , around the AV grooves ) there  are  lot of sharing  and overlap of  different morphology  of cells . A high septal VT can behave  exactly like an SVT  which  includes the  tendency to get terminated by calcium channel blockers.

Amiodarone is a most popular  drug for VT termination ? Are we clear about the mechanism of it’s  action in terminating VT ?

It is  more of a perception and belief  that  class 3 action   may be   responsible for termination of VT by Amiodarone . In reality it is very difficult   to prove this point.  As Amiodarone  has all the  4 classes  action that includes beta and calcium blocking properties.. In fact ,  now  there is evidence  to  suggest   beta or calcium blocking action  may be more important in terminating  VT when  it is administered  IV  . (While  the class 3 action predominates in long term oral therapy )

A verapamil sensitive   VT may  successfully  be terminated by  Amiodarone  not by its  unique  action  instead it   may simply represent  its  calcium blocking  property.

Final message

Many  of the  VTs terminated by Amiodarone   could  also be verapamil sensitive . Since verapamil is never tried first we will never ever know the incidence of such phenomenon that gives pseudo credit  to Amiodarone

It may not be big crime to try injection verapamil in some of  the  stable ventricular tachycardias( As my fellow did ) especially  when we we know there is an entity called verapamil sensitive VT !

Q for the readers :

How many deaths are reported in cardiology  literature  regarding    fatality  following   verapamil  in   VT ?

I am trying to find  the answer the  data is very hard to come by !

Critical comments welcome.


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Ever since Brugada found the unique pattern of ECG on right pre- cardial leads and its  association with  premature electrical death ,cardiac electro-physiology got a new impetus. Hundreds of articles(May be thousands !) on Brugada are  available . Many criterias  were proposed.  Brugada  and his colleagues should be credited for bringing  in such an interest in the  field of inherited ventricular arrhythmias.

On the down side ,  as we have a habit of  prematurely formulating criterias  ,  it brings  an artificial academic  barrier  Funnily , in medical  science  deviating   from a criteria (However hastily it  was  proposed  )   is a considered  big  offense Further . the hype surrounding  any new scientific  entity makes it difficult  for others  to overwrite  it .

Brugada recognized a ECG pattern with  a genetic predisposition for VT and VF  . Now , we know there are many etiologies  with a similar pattern  of ECG . What Brugada did was ,  he  exposed the tip of Iceberg called inherited ventricular arrhythmia . But the essential criteria –  Absence of structural heart disease ,  to diagnose Brugada   was  always questionable.

(Please realize , presence  or  absence of structural  heart disease depends , more  on  how advanced  our  imaging modalities are . If you can map a virtual histology of RV epicardium one may detect some  microscopic abnormality in every case of Brugada. In human biological system , God  usually bonds  structure and function too  closely  and hence  functional  abnormality rarely occur  in isolation )

Brugada is  not  a new disease ,   it is  a  recognition  of a  pattern of ECG  related  to sudden deaths . Subsequently , we  realized any dispersion in repolarisation in RV epicardial surface  , the   risk of sudden death  is increased. From the days of  Brugada  we  have  come  a long way.

What is new in Brugada syndrome  ?

(Not exactly new . . .  it is  known  for many years )

Brugada is no more an exclusive  functional disorder of  sodium channels of RV  epicardium .It can have structural defect (known & unknown ) .It may  have infective , degenerative etiology as well .

How does these structural changes appear ?

Chronic sodium channel malfunction  can result in cell membrane defects which can augment   Idio-osmole   inside  the cell and result in  apoptosis   etc .

Which comes first ,  electrical or structural abnormality ?

It is an  another  chicken- egg tale  waiting to be decoded   within the RV epicardial cells

Can wall motion defect occur in Brugada ?

Early observations done in out hospital (MMC Chennai ) has found anterior  RV free wall motion defects. Tissue Doppler studies are  being undertaken.

Final Message

The  following paper  wonderfully documents  the structural and histo-pathological  changes in RV epicardium .  This  implies ,  our belief   about this  unique electrical  disorder  is  bound to take a beating  and  we  expect a major perception makeover regarding Brugada  in the years to come .

Probably the most important paper on Brugada syndrome was published in circulation in 2005


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Acute STEMI is the numero uno of  all medical emergencies. Hundreds of life are lost every few hours in our planet.Significant  chunk of them  do not   even reach the hospital alive  . While the emergency crew has many vital responsibilities , the cardiologist job starts only after the patient reaches the hospital .  Hence  the ambulance  crew  need to act much more sharper. Please remember even the  skills   of the driver  will have a direct impact on the myocyte survival.

The symptom to first  medical ( or second  hospital ) contact could be as vital  as a primary PCI procedure itself . A 3 minute traffic jam can kill 3 thousand myocytes ! One could imagine the importance of  decision making process here.

Distance from  the point of contact to PCI lab , the anticipated delay ,   intensity of traffic  matters .

Is it not funny ,  to realise  when   we  have  a reperfusing agent on hand , within the ambulance and the vehicle stuck in  the traffic jam  waiting to reach a  reperfusion  room situated  50  km down the high way !

( One may wonder why can’t we thrombolyse every one  routinely  in the ambulance  and do  the PCI later in  . . . But surprisingly  this    concept  simply does  not work  !)

When we realise , even in  a well developed country like Netherlands ,  time to shift  to cath lab is a big issue (Read the following article )  we will never ever know , how much of myocardium  is consumed  by traffic jams  in  a  country like India  , where   the traffic   scenarios   can be  more chaotic  than a  VF  !

Events  that unfold following a STEMI  are crucial

It begins with chest pain recognition.

Call for first help Spouse/Family doctor /Neighbor

Call for 911/108 . Ambulance arrival time and boarding

Administration of  Aspirin + clopidogrel*

Meanwhile spontaneous thrombolysis will begin in most of them !

A promptly administered Aspirin and clopidogrel   a shot of heparin and a lytic agent within 30 minutes is distinctly possible and may be more  effective  at a fraction of cost.

Highway thrombolysis

Even though current studies still  . . .do not  favor primary PCI over thrombolyiss in the first hour ,  most of the cardiologist  do show some  favoritism  towards pPCI for some unknown reasons.

So by default ,  many of the   ill fated  STEMI patients    enter  an  unrealistic  hemodynamic   race  in the deadly highways and urban lanes our country !

For every minute  that goes by ,  the patient  not only loses  his  muscle but also the  golden opportunity to get salvaged by the thrombolytic agents .

Since ,  a delay  beyond  one hour eliminates the indication of thrombolysis  (if a cath lab is available in the vicinity  ) many times   traffic delays  convert a potential   hyperacute  thrombolysis  into a say . . .    3-6 hour old  PCI .(Should we feel happy about it ?)

Here , we need to know TIMI 2 flow achieved easily by thrombolytic  agents is  quiet effective in preventing myocyte death.

Fast  track   shift to PCI

Helicopter drop over cath lab -( Distant dream ?  or better to be in dreams )  It has been noticed even a helicopter was squarely beaten by the  thrombolysis  in terms of  early  and  timely  reperfusion.

Fast -Slow track PCI ?  (Like fast slow AVNRT !)

Unexpected delays on  road  , in  many countries  financial issues  /Insurance sanction etc  contribute to the time delay significantly . What starts as a fast track  protocol  peters out  into  slow race (Late primary PCI ) and may even  end  in a grinding halt.(No primary PCI )

Worse still  . . . some of these patients  are made   unsuitable  for  thrombolysis  as well !

Final message

Management of STEMI  is gradually becoming a team effort.  The emergency crew , the command , the destination hospital all need to be  alert  and proactive. When the  initial  anticipated delay  is getting prolonged , get the ground staff  in  cath lab  ready for  an  emergency landing .

A word of  advice  for  the ambulance crew .Involve them  more   in the decision making  as  they   are in a better position to calculate the  possible delay.  If delays  are anticipated  propose a thrombolytic order and get clearance from the command and administer the lytic agent as early as possible.

It is highly likely , restoration of   TIMI   2  flow  right in the middle of   national highways  is much  . . .   better than a   TIMI 3 flow  that  is going to come  later   . . .in  a distant  cath lab .

Finally use the common sense  liberally  before you  act   . . . unfortunately it has become  the most elusive  sense for man kind  !

References :

Here is a study that gives a fresh insight into this  enigmatic issue of pre-hospital thrombolysis vs primary PCI


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Interventional  cardiologists should revere  few  names for ever  . . .

They are

  1. Werner Forssman
  2. Masan Sones
  3. Andreas  Gruentzig
  4. Sven-Ivar   Seldinger

Sweden's Pride and cardiologist's ultimate Hero !

The  other men  in the  above  list  gave us insight  to enter the heart and do cardiac catheterization  and selective  angiograms

Ironically ,   the  man who  provided an easy access* to cardiovascular  system  from the  periphery is less often  remembered.  Still , it is because of him millions of procedure  are done every  year .

Every cardiologist should  read the life history of this great man.

*Previously all interventions are done in laborious  arterial or venous cut down

How the invention came about ?

“It is a  sudden attack of common sense”   That  is how seldinger described in his own words

Why not a Nobel prize for  Seldinger’s  sense which was so  uncommon to others  ?

If common sense has to be rewarded Nobel price ,  Seldinger’s    would probably will rank   first  among  all !


  1. http://ww.ajronline.org/cgi/reprint/142/1/8
  2. http://www.ajronline.org/cgi/reprint/142/1/8.pdf

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We  are at the mercy  of  the three major coronary arteries (LAD,LCX,RCA) that sustain our life . Their  job is clear cut  .It has to perfuse   about 300 Grams of   live bundle of energy  for  an average of 6-7 decades.

What are the hurdles it  faces ,  how it overcomes these obstacles  forms the fascinating story of   “survival  of  human heart”

When coronary blood supply is confronted with a sudden compromise  as in ACS  ,  often the heart has little  time to respond . Hence the damage  and risk of death is  more. Even here there are lots of safety mechanisms and natural lytic process that limit the loss of life to less than 30 %  of all STEMIs. This implies nature protects against the death in 70 % of individuals and help  them  to reach hospital.*

*Among those  who reach hospital , we  the cardiologists  try to reduce the  mortality to about 6-7 % (20% without treatment ) with all  those hi-tech gadgets .It is a  different story and will be addressed elsewhere .

When it comes to  chronic insults ,  the heart has a unique potential to  stage  long haul battles. It has many tricks  under its  sleeves when challenged in a slow fashion.

The main weapons are two

1. Coronary collateral circulation.

2. Ischemic preconditioning.

Here is a patient who fights his life even after all his  three coronary arteries   totally blocked and surviving with one of the branches of left main -Ramus intermedius .

If you have thought his RCA was the savior  you are  mistaken  .

To every one’s   surprise  his  RCA was awful  as well !

He had angina which was  troublesome  but manageable .Was able to live a life with acceptable standards (Indian standard )  After the angiogram he  received  CABG.  A turbulent post operative course ensued  due to various reasons . He  struggled but   fully recovered  . . .  and  ultimately  reached the  previous  standard  of life !

Final message

Modern cardiology is all about not trusting  powers of nature .

But youngsters should realise the enormous potential of those invisible powers.It may sound philosophical , but please  remember  . . .after all . . .  philosophy  is nothing but  search for truths. Atleast believe in them  once in a while !

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Newtons third law of motion  says for every  action  there is  an equal and opposite  reaction .

In vascular hemodynamics  whenever there is a an obstruction , there tend to be a dilatation of   the same blood vessel  somewhere distally.

It may not be linked to newtons law but it is  observed in many .It is more common in large vessels than small ones.

Here is a patient with a tight LAD lesion with a significantly  dilated segment located immediately beyond the  obstruction.This can be considered as a post stenotic dilatation. Coronary ectasia is  also a  possibility but since it is related to site of obstruction the former is likely .

What determines the post stenotic dilatation ?

The exact mechanism is not clear. There is  a definite ,sudden  pressure drop distal to  the  obstruction. This  pressure drop  recovers beyond a certain distance . At this point ,  the rate of increment in  velocity of   peaks .This somehow has an effect on the  distending  pressure  and the adjacent vessel wall gets radially stressed and begins to dilate. (Opposite of what is expected in Bernoulli effect ?)

Is there a anatomical defect in  post stenotic dilatation ?

Not every  one goes for post stenotic dilatation.There is a possibility it occurs only in genetically susceptible individuals .

Significance in  interventional cardiology

The post stenotic segment has a potential to misbehave in the period following  PCI . If the distal instent stenosis  occur (even if it is minor ! ) it can induce a cycle of post stenotic eversion of normal segment and risk of edge effect or stent thrombosis is more.

Read also Glagovian phenomenon – A form of  intra stenotic coronary artery dilatation

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Non invasive imaging of inflamed macrophages  within athersclerosis

The medical  imaging science is  reaching new heights. With most of the  research so far within the anatomical arena we are moving into the  physiologic  and metabolic  imaging. Identifying vulnerable  plaques  within the coronary  artery is a separate field. Most of them are catheter based and invasive investigations.

We  have ben  searching for an  ideal PET scan based metabolic imaging of atherosclerosis. Macrophages are the key elements in an inflamed plaque.

Image Source : Circulation. 2008;117:379-387 .Note the Acttive Macrophages in the Aortic arch area and Coronary ostia

Can we take a photograph of these  inflamed zones   within  the  atherosclerotic plaque  ?

  • It seems we are approaching  that possibility. Every time we screen a person for CAD we can risk stratify on the basis of  percentage inflammation of their coronary artery or aorta .
  • This will complement the CT  or conventional angiogram .
  • If this technology is perfected it can be useful in the evaluation of response to medical interventions .
  • It  could also tel us  the  significance of  raised CRP /cytokines in other wise asymptomatic individuals

PET scan with newer tracers are constantly evolving . One such tracer is  based on copper molecule   64cu-TNP.





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When LV fails the  lung gets congested and flooded with blood . Similarly when coronary sinus  ,  the major draining outlet of coronary  circulation resists  the incoming blood  flow . . .  myocardium  will  get congested !

This is  the concept  of  retrograde perfusion  in treating refractory CAD with angina . It is a double-edged concept. If the coronary  sinus  pressure is  excessive it may interrupt even  the normal  flow .It should be optimal so that it prolongs coronary micro-circulation time without compromising ante-grade flow. .

Picture courtesy : http://www.dartmouth.edu

Clinical example

We know cardiac failure patients rarely complain of  angina .

Why ? . . The myocardial congestion due to coronary sinus pressure is the most likely explanation.This goes well with the back flow concept in treating refractory angina.

While surgeons tried to link artery to vein  , Interventional cardiologists were smart enough to occlude the coronary sinus partially , that will result in stasis of blood in coronary micro-circulation and hence facilitates oxygen extraction .

Final message

God is a master craftsman. Do not think  there is only  one access to coronary micro circulation.Apart form LCA and RCA there is  a vast network of coronary  veins  traversing  the delicate surfaces and grooves of the heart .

Remember ,they also reach the same micro vascular  bed but in a different direction !

If we  can exploit  them  for myocardial arterial  perfusion we have a real breakthrough   in our hands. . After all , why should we take a vein  from a far way from legs (saphenous veins )  for by-pass surgery  when venous channels are  simply there beside  every branch of a  coronary  artery !

Let us be quixotic , we shall attempt to   congest the myocardium with blood for refractory angina by whatever means ! Mean while let us also remember  what happened to  TMR (Trans myocardial laser  revascularisation ) the biggest technology failure in cardiology in recent times !


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This term is quiet often used in the  main stream cardiology journals  ,  in work places , conferences  , hospitals and even among lay persons . No body bothers to define this terminology.   What exactly this term means ?

It  may  not mean anything  . . . to most  of us  even  as the percentage of inappropriate angioplasty is steadily  increasing over the years .

Picture courtesey : Jupeter Images

What does the term  Inappropriate angioplasty  mean ?

(Choose the correct answer  . . . one or more  may be  true )

A.It simply  means doing  unnecessary angioplasties and has no major implication  to  any one.

B.A form of medical ignorance  or  an unethical act and should be strongly condemned.

C. An acceptable cardiology practice ,  need not be discouraged , as  it improves the quality of life of physicians !

D. A  sure act  of  “error by  commission”   that amounts to   medical negligence .

E.It is a decent term for a major  guideline violation

E. It can be  termed  as medical malpractice as it amounts to harming the patient with or without intention.

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Heart has three layers

  • Epicardium
  • Myocardium
  • Endocardium
  • Epicardium is same as visceral pericardium . If pericardial inflammation dissusely occurs ,  it is bound to injure  the epicardium and subepicardium .

    Does  the  troponins  located deep inside the  myocardium  ?

No .It  can  even be present just few microns below the visceral pericardium  . Hence  severe forms of pericarditis can elevate the troponin levels without any issues .

Is troponin  release related to ST elevation ?

 Ideally  most forms of  pericarditis can be termed as epicarditis. The mechanism of ST elvation in pericarditis is actually a sign of  epicardial injury.In fact ,  there is no easy way to  differentiate  a  slice of epicardial infarct from an   inflammatory pericarditis accurately .

Is there any form of pericarditis which invlove only parietal pericardium ?

We do not know as yet ,  about  existance of such  an entity. It is distinctly possible. However , if present it is unlikely to result in significant  ST elevation in ECG.

In pericarditis ,  troponin release is due to inflammation  or necrosis  ?

Both are possible .Even transient wall motion defects are reported in isolated pericarditis.

What is myopericarditis ?

It is  a general term used  to indicate the above situation . In practical terms Pericarditis + Troponin positivity can be termed as myopericardits. It is well known pericardits can extend to endo- myocardium but it is rare other way  around( ie endocarditis extending to pericardium )

What is pancarditis ?

It is the carditis  involving all three layers of heart ,Cassically occura in rheumatic fever. Fulminant carditis is known to raise the troponin to significant levels.

Does troponin elevation  in pericarditis  occur in all  ?

We are yet to collect adequate data about this .  Diffuse , extensive pericarditis ,gross ST elevation ,  and associated pericardial effusion  correlate with troponin.

Crazy questions in pericardiology

What is the pericardial blood supply ? Is there  an entity called ischemic pericarditis ?

Final message

Do not ever underestimate the  importance of  pericardium  whenever you encounter unexplained ST elevation in ECG.


Here is an article which has   meticulously studied this issue

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