Archive for October, 2014

One of my patients with atrial fibrillation  recently developed a  fairly  moderate  sized right MCA stroke that resulted in dense left sided hemiplegia .He was on warfarin , but the stroke was confirmed to be ischemic,the etiology was fixed as cardio embolic .After a  smart  recovery he asked this question.

Why did the clot  from  my  heart preferred  to enter the  brain doctor ?  Is there no other place for it  to go ?

I  told him in simple terms , “It is  your destiny and  the clot’s wish”.  In fact , you are some what blessed as the clot did not enter  the left side of the brain .If it had gone, your speech would have severely affected and you may  not be asking this question to me ! It is true the clot do have other options to  embolise ,  however they are still  trouble some !

cardiac source of emboli embolus ischemic stroke animation embolic

What is the diameter of internal carotid artery , and cerebral artery ? The common size of LA appendage clot almost match with this !

It can go straight down to your leg , kidney , intestines or upper limbs .All are equally dangerous  and present dramatically . Very rarely  it can enter  coronary  arteries  bringing a heart attack rather than a brain attack .If it is going to the legs you are at risk of acute monoplegia instead of chronic hemiplegia .Peripheral embolism are very painful .Intestinal ischemia evokes a most excruciating pain one can  ever encounter !  Luckily  stroke is not painful.God is kind enough ,he foresaw  cerebral ischemia to be more common and hence  made it pain-free ! (There is no cerebral angina equivalent  !)

Having said that , I felt we should get a scientific answer to my patients query .

What determines  the destination  of these emboli in transit from heart ?


cardiac source of emboli embolus ischemic stroke animation embolic peripheral renal mesentric lerish syndrome 002

A large clot often fails to traverse the Aortic arch branches and invariably reach the periphery .

The dynamics of a cardiac emboli hitting the cerebral arteries can never be known in live human vascular tree. The following factors might play a role.

  • Clot size and morphology
  • Anatomy of aortic arch -Right MCA is in immediate capture  zone .
  • Arch type and curvature radius
  • Arch  branch ostial size , shape
  • Vertebral arterial embolism is rare because it  is a second order branch.
  • Dessication and disintegration of clot in  transit is possible leading to multiple destination.
  • Most shaggy looking large clots fail to enter carotid instead reach the peripheral circulation.
  • Vegetations, tumor debri behaves differently as the density and mass of emboli has a some effect on the transit velocity and momentum.

Variations in Aortic arch anatomy

aortic arch branching pattern A to Z

Image courtesy : Anatomy Atlases by Michael P. D’Alessandro, and Ronald A. Bergman, from university of Iowa. http://www.anatomyatlases.com

It is  surprising, human beings can have as many types of Aortic arch as  English  alphabets . Then,there are innumerable ways for cardiac clots to embolise too  !







Read Full Post »

We live in curious times .As we  advance in our intellect and wisdom ,bullet firings (either cross or straight !) have become an important cause  for sudden cardiac death.Sometimes a life is saved by unexpected way in extraordinary circumstances. Here is a man  from Florida , whose life was saved by  an ICD not by shocking a VF . . . but by blocking a bullet

ICD acts like a bullet proof jacket


A case report from Heart Rhythm


Bullet proof ICD jacket saves life

Complete Heart  Bullet Block : The Aftermath


It seems ICD is strong enough to stop a bullet !

Read Full Post »

Caring shall be an inbuilt character in the  Noble profession ,need not be a value added service or a separate medical specialty !


Read Full Post »

When  a life leaves the body  silently in CCU , an  undulating  flat line in the monitor has a hidden scientific tale  to tell !


A  56 year old obese women died a instant death immediately after engaging the Left main ostium  after first injection of 5cc dye. The monitor showed only  a short pause, few sinus beats , a long pause , asystole and death . In the last 2 minutes of survival she threw a random wave forms of suggesting EMD . At any point of time she never showed any evidence for ventricular fibrillation . 1o minutes of intense resuscitation failed that included temporary pacing , repeated shocks  and ventilation.(ECMO /LV assist excluded)


What is the mechanism of death ?

  • Is it electrical or mechanical ?
  • Acute mechanical stunning / the stone heart ?
  • Is it a primary electrical asystole ? (Acute sinus arrest or AV block )

Post hoc analysis of CAG did not show any significant clues except a tight distal left main.Apparently the catheter has triggered the event .( Or is it the  dye ? as some body suggested it as anaphylaxis  ?)

Even though we conveyed the message to the relatives,  it’s was an unexpected massive heart attack , obviously we were not convinced with our  uttering  ! Mind you , she had  normal LV function but had recurrent angina prior.

asystole ecg 004

Image courtesy modified from http://www.ijaweb.org 2012 for representation purpose only.

We know if cardiac arrest is due to VF, it tends to give us  at-least some time and sense. Further,the VF protocols are more clear and success rate is more .

There is always an issue of  fine VF vs  asystole.If the flat line is indeed VF , there is more chance of revival as we try to pump adrenaline to make the fine VF  into coarse one  and shock again .The sequence can continue few times.

It is well known  asystole has a  dismal outcome .Even among the asystole there is some hope* if asystole is purely   electrical . (Like Stokes Adams in CHB or electrolytic asystole like hyperkalemia etc ) .But if asystole is due  mechanical cause , death ensues in spite of prompt temporary pacing .

* Important note : We have this  common  form of  treatable  mechanical asystole .It is called cardiac tamponade .It always present  with extreme bardycardia and asystole. It is extremely  rare to see a tamponade to present with VF. A prompt needle tap will do the job .It is vital  to recognise this in cath lab as our efforts are rewarding .

I would recommend a hand held echo machine , to hang like a catheter in every cath lab , ready to screen unexplained cardiac arrests with zero delay !

Why some hearts respond with VF  , while others go for asystole  with acute coronary insult ?

  • A million Rupee question ! We are yet to find a legible answer .What is probable is  the the heart doesn’t  even have energy to fibrillate !
  • The underlying disease need to be so intense .In this case it was left main stenosis supplying a truncated LAD and LCX. We could also see it supplying twigs to RCA  suggesting it to be a total occlusion .
  • So ,when a  “physiologically single” coronary artery that precariously  supply the entire heart is suddenly insulted the heart behaves violently with runs of VT/VF. Our ignorance is complete when we realise  the heart  can do the opposite as well .It does not react at all , goes for a deep slumber and result in electro-mechanical sudden death.
  • It is expected , in acute mechanical  deaths one may encounter flash pulmonary edema if the LV alone gets stunned. However , if both right and Left ventricle come to standstill in a synchronised sudden fashion , lungs will be as silent as deep sea . We believe this is what happened in our patient and it can be logically correlated  as  the critically narrowed left main was supporting the  RCA  as well.

Final message

Sudden cardiac deaths  9 out of 10 times is electrical . Majority  of them is  due to fibrillation. Next comes the electrical asystole ,Rarely (is that really rare ?) an ultra fast  sudden death due to mechanical asystole (Non -Tamponade ) is  possible , as experienced in our patient .

These mechanical asystole  are yet to be decoded.Whether it is a form  of Acute stunning , electro -mechanical uncoupling or mechano electrical standstill is not clear.



Read Full Post »

Inserting an ICD  for  DCM  may a be great therapeutic success  for the physician  as well as the patient . But there is one big truth hidden behind the statistical screen.

Following  study  provides dramatic data from Maanhiem in Germany in about 561 patients who had ICD .The long term patient outcome after appropriate shocks were much worse  than those without    shocks .This was more pronounced in Ischemic DCM .

appropriate and inappropriate shocks ICD

Source : Streitner et al ,University Medical Centre Mannheim, Mannheim, Germany PLoS One. 2013 May 10;8(5):e6391

The fact that these patients continue to throw VT , some thing is wrong in the cellular  milieu or a fresh scar / fibrosis / ischemia is progressing .Further , the VTs and the  subsequent  shocks  set in temporary  hemodynamic instability .We have evidence , EF can be depressed for days  worsening the long-term out come.

While it is easy  to blame it on natural course of DCM , there are  solid reasons to believe  , shock induced myocardial damage is definitely contributing to this  excess mortality.

One important  clinical tip is to screen  all  these so called Idiopathic DCM  patients  who  had appropriate shocks.  They should be monitored for fresh signs of any systemic illness  , like a  connective tissue disorder , chronic granulomatous lesions  like sarcoid etc .To our surprise  some specific  myocardial disease may unmask themselves in the natural history. Identifying them may offer a dramatic cure .

Final message

Some where along our EP mind-set  we are conditioned to think  , as along as there is an ICD in situ and it appropriately  shocks, every thing is bliss ! Blame it  on semantics . The  word “appropriate”  inappropriately  soothes  our nerves.

The fact of the mater is , every appropriate shock is a  grim reminder  that the heart  in question  is restless electrically and VT continue to emanate  from diseased  myocardium  . It could  mean either the LV   is destabilising  , or the original  disease  is   progressing  or a new disease  is evolving .

Mean while, paradoxically , inappropriate shocks give us a quixotic comfort , since the  heart is not really  throwing any dangerous arrhythmia, after all it is  the device related  false alarm   that  could be easily  reprogrammed!


ICD appropriate and inappropriate shocks

Read Full Post »

Your clock starts  now !


clock gif  dr s venkatesan002

Chronic stable angina : Most can be effectively managed  by  optimal /intensive medicines and life style Interventions .About 10% will require PCI/CABG.

ACS – STEMI:  Primarily  managed  with  rapid and competent  pre-hospital care with prompt thrombolysis in or out of hospital .Patients  with  large STEMI who develop complications (Again about 10 %)   require PCI and few additional  lives can be saved.

ACS-NSTEMI : This is  the group that demand  an  important role for PCI . All true high risk UA/NSTEMI patients  should receive urgent coronary  angiogram and critical lesions  should either be stented or  sent for CABG  (If the lesions are multiple and complex ) The field of interventional  cardiology  is  expected  to play a major  role in  this category of  patients for the simple reason , we  not only give dramatic  relief from angina and also prevent a  potentially a huge MI that is waiting to happen !

* It is vital to emphasise  the “Aim and  objective” in  NSTEMI  management  is critically different from other two. We know ,  in CSA   the aim is to give relief  symptoms  and improve excercise capacity . Both PCI/CABG  are  unlikely  to prevent a future MI in CSA..In STEMI it has already occurred .The aim is to salvage myocardium  and prevent  future events. While PCI can do the former , it can’t do the later . In STEMI scenerio ,we have very good  alternate  modality called thrombolysis which can easily beat the  pPCI  in , cost , availability and time  (and  hence efficiency as well  in  most  countries !)

Counter thought

The above suggestion  is too simplified ,generalized , misleading , and  unscientific, should   strongly be disagreed. For those people who disagree , I provide an alternate scheme  .It is ultra short ,comes in  5 lines .Very practical  and  scientific too  !

In any  patient , who is  suspected to have either  acute or chronic  coronary syndromes ,take them to the cath lab in an  urgent or semi urgent fashion .Do an angiogram and stent all lesions  that you feel important . If  stenting is not possible  manage  with optimal medicines and /or send them to the surgeons.

Final message

The essence of catheter based coronary care is simple.We complicate it. To understand this concept  100’s of cardiology  journals  and as many conferences and infinite  number of books are churned out every year !





Read Full Post »

Current guidelines advice us to wait for 40 days following STEMI to implant ICD in most high risk patients.

Why this  cool off period.? *

  • Essentially  we are waiting for the Infarct healing process to be completed.
  • By this time electrical stability may be restored. The  risk of VT/VF  declines per naturalis.
  • LV function recovery  is possible. As stunned and hibernating myocardium resumes its mechanical function and patient might  jump out of the MADIT-2  cutoff point. (EF< 30%)
  • Introducing  ICD very early  after STEMI may be a myocardial irritant and that it self can generate  arrhythmias.
  • There is a possible interference by the leads in the physiological remodeling  process.

Final message

So the cool off period is  not only to reduce  the unnecessary  ICD implantation  but also to  avoid lead related issues .

*  This 40 day rule is based on one  large study from Germany. (DINAMIT, 2004  ) . However  few believe  the rule is not absolute. There can be individual   exceptions in high risk patients with critical LV dysfunction .

Other  wise   . . . How do you digest  a death occurring on  35th day  in a patient  who is waiting for an ICD scheduled one week later ?


DINAMIT trial ICD nejm

Link to  ACC/AHA  Guidelines for ICD Implantation 2013

New development

How to bridge the 40 day gap in really high risk post MI patient ?

We can’t keep him in CCU. Here comes the role of WCD (Wearable cardiovertor defibrillator.) Life vest is  from Zoll . WCD can act like a bridge till the 40 days when the patient becomes eligible for ICD.



Read Full Post »