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Dual or triple preexcitation : Can type A WPW pattern convert into type B WPW in the same patient ?

Posted in cardiology -ECG, Cardiology -unresolved questions, cardiology congenital heart disese, Cardiology-Arrhythmias, pericardial disease, Uncategorized, tagged , , , , , , on April 15, 2011| Leave a Comment »

WPW syndrome remains as  a   fascinating ECG entity ,  ever since it was described by Wolf , Parkinson and White in the year 1930.It is  primarily a  disorder of cardiac embryology . Heart is an organ made up of  tissues from mesoderm and neuro ectoderm.The muscle which comes from mesenchyme has to be incorporated with specialized conducting system. This is a complex  process .It is determined by the bio-genetic forces. When errors happen in the embryonal  tissue  flow  congenital anomalies occur.

In  WPW this  error   happens  exclusively in the conduction  tissue movement  . Normally the specialized conducting system    pierces  the  entire  AV ring and connect atrium  and ventricle  .Later ,   it regresses in  all areas  except in the AV nodal zone  . When  It  fails  to regress ,  these  remnants of  conductive  tissue act as AV accessory tissue  and create electrical  short circuiting .This is the reason , all these pathways are located in the close vicinity of AV ring.

Accessory pathway shows   varying conduction velocity , but generally devoid of  decremental conduction properties .  The presence of such pathways make these individuals prone for variety of cardiac arrhythmias .It can range from  simple AVRT  to  malignant antidromic  AVRTs  that can end up in  VT /VF.

Resecting  these  pathways surgically was once popular.  Effective blocking  of  the pathways with  drugs  is a good option. Currently ,  it is possible to  locate and  ablate  most of these  pathways   successfully.

Even though there are many protocols to locate accessory pathway the one that is very popular is  simple   Type A and type B  WPW , which locates the pathway either in the  left  or  right  ventricle  respectively.

Huge data base  has been accumulated over the past 80 years  regarding WPW syndrome,  still   many questions are unanswered.  One of the important clinical issue is  multiple  accessory pathways , scattered  at  random  across the  tissue planes of atrium and ventricle  .

The other issue is intermittent pre-excitation and shuffling  of path ways during tachycardia  .

It is very rare to see a patient who manifests both Type A and type B pattern during sinus rhythm .Here is an  article from  unexpected  quarters  , Colombo Sri-Lanka in the year 1972  candidly  describes a patient with classical  combination  of  Type A and  B  WPW . It is great to see such an interesting  observation in the pre  EP/Echo era from a remote island nation.

Now , let us ponder over  these questions

    1. Can a pre-excitation  happen simultaneously in both right and left free wall pathway ?
    2. How will the ECG look like  when impulse travels over multiple pathway ?
    3. When dual pre-excitation combines   with  normal AV  conduction  ,     will  it not make  a  triple AV pathway ?
    4. How does a supra-ventricular impulse decide ,  which pathway it is going to travel  when confronted with a choice of  three or  four pathways ?
    5. How do you plan ablation for such a patient  ?

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A hurricane inside Left atrium !

Posted in Uncategorized on April 10, 2011| Leave a Comment »

Hurricanes  are ocean’s  reaction to the climate change  especially  in subtropics.  When low pressure  zones  form over the ocean surface  the nidus for hurricane is sown .It   gradually intensifies to form deadly cyclones.The maximum damage is done when it  encounters the land . The following image  depicts how the hurricane Katrina caused havoc in the southern US coastline .

Hurricane katrina .Click to view animation

 

When the human blood stream is interrupted  by any pathological hurdle  it  gets  agitated . It encounters both turbulence as well as  a  slow flow phenomenon . Virchow taught us centuries ago  , slow flow , a vessel wall defect and  an abnormal blood combine to create a  clot. This is what happens in mitral stenosis . What appears as a mild turbulence  gathers momentum  and becomes a storm .The eye of the storm has the  least velocity and it  forms  the core of the future clot.

Left atrial strom visualised by TEE

 

What is left atrial jelly ?

A  pre- clot stage with impending clot formation may be referred to as a jelly . The exact  duration for  a contrast to get converted to clot is not known.It depends host of factors from hemodynamic and rheological factors. It  is  believed every clot   must be preceded by at least a brief period of auto contrast.

Is there a intrinsic  defect in blood in those patients who have spontaneous contrast ?

Yes , there has been  excess  fibrinogen  in these  patients. http://www.ncbi.nlm.nih.gov/pubmed/11744141

Can we dissolve  spontaneous  contrast ?

It  may be  possible with intensive anti coagulation. Ultrasonic dessication may be a modality that could be developed in future.

Is  the presence of  spontaneous echo contrast a contraindication to do PTMC/CMC ?

Some centers do believe so. Currently intensive anticogulation ,   meticulous preparation   with  special  precautions  during procedure will reduce embolic  manifestation.

Reference


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How common is sudden brain death ?

Posted in cardiology -ECG, Infrequently asked questions in cardiology (iFAQs), Uncategorized, tagged , , , , , , on April 10, 2011| Leave a Comment »

Sudden cardiac death is the  most common cause of instant death.  We know , heart is  also  under massive neurological control . Still , heart can run for days even after brain dies ,   if respiration is supported.This implies ,  heart is independent  neurologically  !  what a paradox !  But this  independence of   brain  function after death makes the  human heart transplantation  possible.

Even  as we “wow” about this cardiac independence , we   witness  widespread deaths due to sudden neuro- cardiogenic  deaths .This makes medicine . . .  a wonderful puzzle  and  compels  us  to pursuit  the eternal    journey  of  knowledge !

When an area of brain fibrillates what will the heart do ?

When  the brain suddenly discharges  huge amount of electricity (Load shedding )  as in epilepsy or some other neurological  injury  , it  may  travel down  and make sure the heart also  shares  the electrical insult .Sudden deaths have been reported in many epileptic individuals and in  some forms of stroke .To distinguish   sudden brain deaths  from sudden cardiac death in such patients  is a very difficult task.

The message is ,  hypo-functioning  brain does not generally harm the heart (Men in coma live for years !) but , over -active brain can inflict major electrical damage to heart. This may  indirectly explain ,  how an  episode of  severe mental stress  could act  as a  trigger  for acute coronary  syndromes.

* We do not know , whether brain stem which has the cardiac high command  can fibrillate independent of cerebral  cortex .

Reference

Ictal asystole

Asystole during epilepsy could occur in significant numbers. As this  review   from France  reveals

 

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What is the role of “routine” oxygen in the coronary care unit during acute STEMI ?

Posted in cardiac drugs, Cardiology - Clinical, cardiology -Therapeutics, Uncategorized, tagged , on April 7, 2011| Leave a Comment »

Oxygen has an ubiquitous place in any  critical care unit. If some body is labeled as  critically ill , it becomes mandatory  for a tube to  be inserted per nasal. It is more of a conditioned  reflex and  sort of a socio- medical necessity .The futility of oxygen administration in critically ill is most evident in the management of STEMI.

Inconvenient  questions

  1. Does the oxygen  we  supply ,  ever reach the disputed  site   myocardium             (From  the port of entry . . . namely the nose  )
  2. Does it improve  the myocardial salvage ?

There is generally no hypoxia associated with STEMI . Even if it is there , the  ischemic myocyte can not be oxygenated by increasing the systemic saturation as the problem is with the   delivery of oxygen due to defective supply.

What does the guidelines say regarding o2  ?

Read  yourself    http://circ.ahajournals.org/cgi/content/full/110/5/588

Final message

Routine oxygen administration  is  required  to create  the intensive care ambiance .

Oxygen administration  by default has no scientific role.

However,   it is generally not harmful . As long  a drug is  not harming the patients , inappropriate  therapy is   forgiven by modern medicine.

When  is oxygen really indicated in STEMI ?

  • Significant persistent  Hypoxia
  • Associated LVF
  • Any arrhythmia
  • COPD

Forbidden discussions  in academic forums

Oxygen  administration has  become  mandatory to generate revenue  for the cash starved  corporates .It  is a standard practice to charge these patients on hourly  basis  of o2 usage  in many hospitals.

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A deadly cardiovascular complication of noise pollution !

Posted in Cardiology - Clinical, cardiology -Therapeutics, myocardial disease, Uncategorized, tagged , , , , , , , on April 6, 2011| Leave a Comment »

An  unwanted , unexpected , unpleasant sound  is  often referred to as  noise

Human ears , are  not meant to  hear  only the  pleasant  sound . We live in a noisy world. It is believed every cell in the body has ( Auditory ?) sense  receptors. But , the noise is perceived  only at brain .It is  incidental our ears  are located  right beside the brain , adjacent to  parieto  -temporal cortex . The auditory nerve  has   its  nucleus  located dangerously close to vasomotor centers of  brain stem .

.

When  excess noise enters our ears it vibrates  the brain stem as well . Noise travels in the nervous system as electrical  impulse , so it is natural  for  to expect a  spill over to the  nearby  adrenergic  centers  .

A sudden explosion or a thunder will skip a few heart beats is it not ?  Similarly , when   we experience  pleasant  sound /  melody**   it  soothes   the nerves ,  this forms the basis of musical  therapy.

So  it is logical to conclude   , when the  nice  music  has a capacity to heal ,  unwanted  noise  is expected   to injure  our biological system.

** A rock fan under the influence of  drug  may feel a every nonsense  as melody . . . is a different  story !

It is observed strokes and MI are more common in urban areas congested  with traffic chaos. Here is an article from European  Heart  journal   with  solid evidence on this topic.

Excess noise   could  result in  cerebral  or coronary arterial  spasm ,  thrombotic  occlusion or even a hemorrhage ?*

  • Noise  induced adrenergic trigger and spasm of blood vessel
  • Adrenergic  surge  and resultant hypertension

Associated  Phenomenon along with noise

  • Anger
  • Anxiety
  • Fear (A noise associated with a  missile attack  in the  war zone )
  • Relative  hypoxia , Air pollution in noisy  environment .

*A distinction must be made between   chronic noise  pollution  vs  Acute noise intoxication.

For  those who want  more depth in this  topic , I  was surprised to find  this  exclusive journal  that documents noise and human health .

Final message

Excessive noise  can have a detrimental effect in the nervous system . Since  cardiovascular system  is also under    neurological command  it  is  expected to  share the ill effects.

A comforting news for healthy men and women  . Noise per se  can not be termed  as a  coronary  risk factor . It can  (at worst ) be a  trigger  for an event  in individuals who have other major risk factors.

 

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Sino-Junctional rhythm : When a restless pacemaker goes for a walk down the lane !

Posted in cardiac drugs, Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, cardiology -Therapeutics, Cardiology-Arrhythmias, tagged , , , , , , , , , , on April 3, 2011| Leave a Comment »

SA node is  the ultimate   power  center  of heart located in the junction of SVC and right atrium .In normal physiology  it fires  at a rate of  60 -90 /minute   that  dictates  the  ventricular rate  .

SA node is a linear  spindle shaped structure with a length of  1.5cm . The P cells with unique mitochodria  are  responsible for pace making activity  . The ion responsible for pacemaker current is mainly  calcium  with the initial 25 % push given  by  sodium current as well .  These cells are predominately under vagal control.Even though  pace making activity  is normally restricted to the SA node  , the vagal innervation is such that  the pacemaker  has a  potential to shifts it’s activity  both functionally  geographically.

In fact , there is constant flux of pacemaker activity  with  the entire length of SA node.The  cranial   aspect  SA node has more fire  power than its caudal tip . It is possible Sinus tachycardia  and sinus  bradycardia could represent  minor changes in the firing focus in its cranio-caudal axis.Further the P cells of  sinus node can spill all over the atria and even up to AV node.

What is wandering  atrial pacemaker ?

This entity is poorly defined  in literature.  With pace making cells scattered all around  there is no surprise to note dynamic pacemaker  shifts  even in healthy people. This is  especially common in young athletes.

Wandering can occur

  • Within SA node ( Shift of focus of p cell firing .No visible changes in ECG )
  • Within SA node and atria
  • Between SA node and AV node. (Sino-Junctional rhythm )

Effect on ECG

  • Baseline bradycardia.
  • Changing P wave morphology
  • Change in PR intervals
  • Intermittent absent (Rather concealed  )  P wave if  is also possible
  • RR interval can also show minor variation.

Image Modifed from http://www.eheart.org

Clinical significance of  Wandering pacemaker(WAP )

  • A Benign condition generally has no clinical significance.
  • It is often an expression of  high vagal tone.
  • Usually transient.
  • Can be unmasked by beta or calcium blockers.
  • Severe forms of wandering  pace maker can be a marker of sinus node dysfunction  and  would need  further evaluation
  • In  the coronary care units it is  associated  with infero-posterior MI when the vagal fibers are  insulted.

Differential diagnosis .

  • Some times it  need to  be differentiated form ectopic atrial rhythm /Low atrial/Coronary sinus rhythm etc .
  • Sinus  slowing  followed by a  functional escape and  reemergence of sinus beat   can be a termed as a form of wandering  pacemaker

Final message

WAP : This attractive and  descriptive ECG entity  is   largely insignificant in clinical cardiology .

It should not be confused with more dangerous cardiac arrhythmia  like sinus pauses and arrest .

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In diabetic nephropathy . . . Is there a proteinuria equivalent in heart ?

Posted in Cardiology - Clinical, cardiology -Therapeutics, Cardiology -unresolved questions, Infrequently asked questions in cardiology (iFAQs), myocardial disease, Uncategorized, tagged , , , , , on April 1, 2011| Leave a Comment »

Diabetes is a systemic disease affecting  almost every cell  that metabolises  glucose .What begins  as  a minor  functional impairment  ,   worsens gradually and ultimately   end up in severe  structural changes.The basement membrane of  cells  face  the brunt of the attack .  (In the strict sense every cell has a basement  but it is well  developed only in kidneys ) . We also  know , diabetes  is able to inflict universal damage by targeting the vascular endothelial cells.

In the kidneys DM makes the  glomerulus  more porous causing protein leak*  and ultimately damages the tubules and end up in CRF. In the retina it excretes the  proteinaceous  material into the vital layers  and result in  retinopathy and progressive visual loss.

* Micro/Macro albuminuria

In fact , there is  a very close link between eyes  and the kidneys  Nephrologists   hesitate to make a diagnosis  of diabetic nephropathy without ocular  changes. The peripheral vascular disease and diabetic foot are  another expression of this microvascular  dysfunction.

What is the impact on cardiac micro-circulation ?

Whenever significant diabetic nephropathy is present there must be a significant cardiac micro- angiopathy as well.This is now  a fact than an assumption. We are not recognizing it rather  ! (If only we have a cardiac  creatinine we can easily identify diabetic myocardial protein leak !)

When kidneys lose protein , cardiac capillaries  lose proteins to interstitial   space  and result  in progressive  fibrotic reaction . We know  extravasaation   of high osmolar  proteins   can play havoc  in cardiac interstitium  !

Proteins are the particles of life   . . . but in wrong places  it can  transform into deadly  molecules  in a fraction of time !

Hence ,  the cardiac protein leak in diabetes can cause  any of the following clinico -pathologic entities.

  • A mild left ventricular  hypertrophy .
  • Increase global  cardiac  mass (Similar to bulky kidneys  seen in early diabetic nephropathy )
  • Simple diastolic dysfunction.
  • Severe restrictive features
  • NDCM (Non dilated cardiomyopathy )
  • Finally a DCM  like  transformation

How to recognize cardiac protein leak ?

  • Clinically it presents either as  angina or early heart failure symptoms ( not both usually ) .Diastolic dysfunction  in echo,  positive stress test , patchy thallium uptake abnormality  often with  features  of   syndrome X  is also recognised.
  • Many of the low flow or slow flow phenomenon  in coronary angiograms  might reflect micro-circulatory dysfunction .
  • This is recognised by prolonged TIMI frame counts  and  prolonged  coronary sinus filling and emptying time .

What about macro-vascular  complications  in diabetes ?  How is it different from micro-vascular complications ?

Though we expect a direct  link between  micro and macro  vascular complication ,   the later  appears  to a  patho-genetically  independent  process . This will be addressed later.

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V for . . . ventricular tachycardia

Posted in cardiac drugs, Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, cardiology -Therapeutics, Cardiology -unresolved questions, cardiology- coronary care, Cardiology-Arrhythmias, tagged , , on March 31, 2011| 1 Comment »

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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Propably this is the most important paper on Brugada syndrome* !

Posted in Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology-Anatomy, Cardiology-Arrhythmias, tagged , , on March 29, 2011| Leave a Comment »

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

*http://circ.ahajournals.org/cgi/content/full/112/24/3680

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Traffic jams and TIMI blood flows in national highways !

Posted in Uncategorized, tagged , , , , , on March 27, 2011| Leave a Comment »

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

http://www.ncbi.nlm.nih.gov/pubmed/21315205

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