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Archive for January, 2010

Ignorance based cardiology : As the CAD has become pandemic, we have little spare time to think about how human coronary arteries develop in the firstplace !

Posted in Cardiology -unresolved questions on January 15, 2010| Leave a Comment »

Many times , human coronary arteries are the sacred sites upon which  mankind’s history and destiny is written.We now have an pandemic of CAD in our hands. It has a  great impact not only on the cardiovascular  health but also the productivity of this world .

  • We  , work hard ,  day and night in cath labs  ,  to remove the blocks from the suffering CAD patients
  • Some  treat it medically.
  • Few others work in preventing CAD
  • Not even a handful  work on the anatomy of the problem !

How and why the human coronary arterial system behave so bizarrely ?

  1. From where does  coronary artery originates ?
  2. What determines the coronary collateral seeding and genesis ?
  3. Why some have only anatomical collateral without functional  use ?
  4. Why artificial  neoangiogenesis  has  not helped much in  CAD ?
  5. Why ,  one human being   lives  comfortably with a totally occluded coronary artery ,  while others suffer  with severe angina even with a 70% occlusion ?
  6. Why the COURAGE  and OAT study had the surprising  conclusion ?

Answers to  all these lingering questions   may be  clarified soon !

Read this  gem of an article   from Brazil in   a  less fancied   “Journal of morphology “

International Journal of Morphology – Origen y Desarrollo de las Arterias Coronarias

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ECG of an athlete : It’s different !

Posted in Cardiology - Clinical, cardiology -ECG, tagged , , , , , , , , on January 15, 2010| Leave a Comment »

ECG of an athlete is many times difficult to interpret. The influence of autonomic tone in  athlete’s heart is an complex one.Contrary to our expectations the parasympathetic tone is higher in well trained athletes. The resting heart rate can be as low as 30/mt which is 99.9 times pathological in non athletes.This happens due to a concept called accentuated antagonism.The athletes who have episodic surge of high catecholamines keep stimulating the para sympathetic neurones in a constant fashion.

LVH is the most common feature.Here there is simple myocyte hypertrophy, without pathological fibrosis.This differentiates athlete’s, heart from HOCM .

Many ECG abnormalities are reported in athletes.

Excerpts from the ACC recommendation

1. Electrocardiographic findings that are common and training-related and that do not require additional evaluation are sinus bradycardia, 1° atrioventricular block (AVB), incomplete right bundle branch block (BBB), early repolarization, and isolated voltage criteria for left ventricular hypertrophy (LVH).

2. Uncommon and training unrelated electrocardiographic findings that mandate further evaluation include T-wave inversion, ST-segment depression, pathological Q waves, atrial enlargement, a hemiblock, right ventricular hypertrophy, a BBB, or a Brugada-pattern of ST-segment elevation.

3. Training-related electrocardiographic findings are more common in men than women, athletes of African descent, and high-endurance athletes such as cyclists.

4. Sinus rates <30 bpm and sinus pauses >2 seconds are common in highly trained athletes, particularly during sleep.

5. A normal chronotropic response to exertion and the absence of bradycardia-related symptoms distinguishes training-related sinus bradycardia from sinus node dysfunction.

6. 1° AVB and Mobitz I 2° AVB are common, but Mobitz II 2° AVB or 3° AVB should not be assumed to be training-related and require evaluation.

7. Early repolarization in Caucasian athletes most commonly consists of upwardly concave ST-segments and tall and peaked T waves; in black athletes, there often is convex ST-segment elevation and negative T waves, mimicking a Brugada pattern.

8. In the presence of voltage criteria for LVH, pathological hypertrophy should be suspected if there is left atrial enlargement, left-axis deviation, repolarization abnormalities, or pathological Q waves.

9. T-wave inversion ≥2 mm in ≥2 adjacent leads should prompt evaluation for structural heart disease.

10. Electrophysiological testing for risk stratification with possible catheter ablation is appropriate in athletes with ventricular pre-excitation.

Source :  Fred Morady, M.D., F.A.C.C.

http://www.ncbi.nlm.nih.gov/pubmed/19933514?dopt=Abstract

For an excellent article on the topic click here

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How does magnesium acts as an antiarrhythmic drug ?

Posted in Cardiology - Clinical, cardiology -Therapeutics, Infrequently asked questions in cardiology (iFAQs), Uncategorized, tagged on January 13, 2010| Leave a Comment »

Magnesium is a powerful cell membrane stabilizing agent. It is well recognized to act on the cerebral motor cortical cells and  suppress seizure , especially in eclampsia of pregnancy .

Mg SO4 is still the drug of choice for seizures of pregnancy. It  was soon realised  ,  the  molecular basis of  cellular excitability    is    similar  for  every cell  . And  thus , we got this  great antiarrhythmic drug !

  • Magnesium is a  cofactor in the enzyme Na /K ATPase in the myocyte cell membrane
  • Integrity of this enzyme is essential for proper maintenance of the intracellular potassium levels.
  • Many times hypokalemia can not be  fully corrected by administration of K + alone .
  • Co- administration of magnesium  increase the intracellular K +    and hyperpolarize the cells and make  it less excitable.
  • Further , magnesium competes with ca++  ions  to enter the cells and thus   it is a natural calcium blocker. This property also helps in controlling refractory calcium dependent  cardiac arrhythmia.

Indications for magnesium

  • Torsades de pointes . Note:  Magnesium does not shorten the QT interval significantly but still effective in torsades.
  • Any refractory VT especially , post MI.
  • Digoxin induced , hypokalemia dependent atrial tachycardias, MAT

It is administered 1-2mg boluses of 2-3 boluses.

Where we should not use magnesium ?

Routine Use of magnesium in recurrent non sustained VT following MI is not recommended .(Courtesy ISIS -4 trial )

Reference

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1368485/

Magnesium : Nature’s own calcium blocker

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1368485/

ISIS 4

Some think ISIS 4 was a delibrate attempt to defame magnesium !

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How do you manage a left main disease with good exercise capacity ?

Posted in Cardiology - Clinical, Uncategorized, tagged on January 11, 2010| Leave a Comment »

The term  left main disease (LMD)  invariably  creates  a  near  panic  reaction in   many of the   contemporary cardiologists . It may be acceptable   in  a broader sense, but it need to be realised , there  is a significant group of patients  with  isolated  non critical  LMD . Many times , these patients can be managed effectively with  intensive medical management.

However , the  following rules may be applied in the management of non critical isolated LMD

  • In patients  who present with unstable angina  ,there is nothing called non critical LMD .Any degree of lesion (Even a 20%)  is significant .
  • Lesions with irregular margins, hanging eccentric  plaques are always critical irrespective of obstruction.
  • LMD involving LAD /LCX ostium need to be tackled as an  emergency .

What are the safe left main disease ?

  • Isolated tapering  left  main artery .
  • LMD  with <  50% lesion.
  • A left main patient who is pain-free on a tread mill > 10 METS
  • Left main with stable angina responding well to medical therapy
  • New onset left main disease in a patient with functional LIMA to LAD /LCX *

*This is sometimes called protected  LMD.  Protects what ? Protects the LAD ,   in case of  complication occurring during LM stenting . If the  function of  LIMA graft is good enough to  protect LAD , why should we attempt to open  the diseased LM in the first place ?  It is an unanswered question !

Why is it riskier  to  stent an  insignificant  LMD or stable  LMD ?

A  left main artery ,  engulfed with a  50%   stable plaque is less riskier to develop an  ACS than an  artificially  normalised  left main lumen with a stent. This is especially true for the  drug eluting stents which need life long  dual antiplatelet therapy as the drug which is supposed  to  prevent  the  restenosis ,  interferes  with  the normal endothelialisation over the stent .

In effect,   PCI   especially  with a DES for a hemodynamically insignificant lesion is fraught with a risk of converting a stable  lesion into  potentially vulnerable lesion !

Final message

A discerning  reader may ask , is it possible at all ? . . .to  have a   patient  with LMD  & enjoying  good exercise capacity ?

Yes , it  may be  rare , but not “non existent” .  Remember ,  one of   the common cause  for  rarity in medicine is ” non recognition of a  fact” or   otherwise  called ” Ignorance”

It is an irony , LMD is considered  by many as a  homogenous  entity ,  even as we  acknowledge  there is a  huge spectrum of lesions among left main disease . There is a distinct (although small !  )  subset of LMD * where medical treatment could be ideal and PCI  may even carry greater hazard.

*The most important caveat in assessing a LMD  lies  in the   50% criteria. Calipers  we use ( often visual )are never going to estimate the lesion correctly considering the importance of  Glagovian  phenomenon . As of now ,  we have no simple means to  measure the vulnerability of a left main plaque .Thermography, OCR/Raman spectroscopy/ RF intravascular ultrasound would probable redefine the indications for intervention in LMD.

Legal issue in LMD

Can we  defend in the  court of law, if a patient loses  his life,  who was adviced  medical management for LMD ?

Any thing can be defended in this funny world of  judiciary . A person who kills in broad day light,  hundreds of  innocent lives can argue  he has never seen a gun ! and he may even,  be  acquitted  for want of evidence  !

How can we   prove  with evidence , the  death in question  occurred  “only because ” he was  adviced medical management ?

No court on the earth can prove it !

So , an occasional life lost due to an unintentional  judgment  error can  easily be argued in favor of the noble profession . Scientific  guidelines are only recommendations .If a person with a  significant LMD  due to  a smooth stable plaque , who has  little  symptoms , carry on with his daily activities comfortably  , his  cardiologist has every right to advice him  medical management.  The doctor , can not be penalised , provided  , he has explained  to the patient ,  that  he is deviating from the official guideline only  for the benefit of   the patient’s  health and  he   has  fully understood the issue.

Read further , for  more controversy !

Land mark  randomised control trials (RCTs) are generally  done in specialised centres with high degree of expertise . They rarely represent the real world patients  seen in  the remote towns (or even  cities ) of the  developing countries  .We can not equate a PCI  done in an  angiographic core laboratory , say in Cleveland or Mayo clinic  ,  with that of  cath labs  ,  that  works  with par time staff and non dedicated cardiologists . So , in these situations  intensive medical therapy (which do not have a geographical variation in efficacy! ) would score over complex procedures .

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Is verapamil and beta blockers really contraindicated in AV reentry tachycardias of WPW syndrome ?

Posted in Uncategorized, tagged on January 9, 2010| 2 Comments »

It is often said , old thoughts  die hard ! It is more so in medical science as we realise ,  perceived fears and  physician phobias  have a long shelf life . A  few  case reports of  verapamil induced acceleration of accessory pathway conduction  was enough , to create a   global  perception among physicians and cardiologists  that any drug which acts on AV node is dangerous in the management of AV nodal reëntry tachycardia (AVRT)

This is a gross perception problem due to dispropotinate importance given to a remote possibility  . Thus ,  a  great therapeutic concept was  put on the back burner.

AVRT is a macro reentrant tachycardia that traverses both AV node  , accessory  pathway  ventricle & atrium .This  tachycardia can be terminated by interuppting  the path way  any where in the circuit .

The most easy and simple option is  to block the   AV node ( Verapamil, beta blockers, even digoxin !)

These drugs have cured many thousands of AVRTs  in the past  .As our knowledge progressed , we  found  , it may not be safe to block the AV node in WPW as it could  divert incoming signals through accessory pathway and result in 1:1 conduction and  possibility of  VF

As soon as this concept was flashed all over the cardiology journals in early 1980s cardiologists  took it as sermon . At the same time, lots of new anti arrhythmic drugs were developed  and this concept came in handy to promote all these new class 1 c and class 3 drugs which are supposed  to act more on the accessory pathway and hence projected to eliminate the risk of  VF.  

It was never  minded ,  all these new group of drugs has it’s own pro arrhythmic  properties  like  prolonging   QT interval   and has a potential to precipitate dangerous ventricular arrhythmias 

So, by the turn of   millenium calcium blockers and beta blockers have been removed form the  cardiologist mind in the management of WPW/AVRT

What is the reality ?

Verapamil or betablocker induced sudden death in WPW is a grossly exaggerated concept in clinical cardiology .Treatments and procedures with many fold risks is being practiced in every walk of cardiac patients.

Complete heart block  and related morbidity  during RF ablation of WPW syndromes can easily exceed the   of verapamil induced  side effects  in WPW.

 How to  identify potential patients who are likely  to develop complications  with AV nodal blockers in WPW syndrome ?

The key determinant is the accessory pathway refractory pathway . If it is < 250ms  the chances of accelerated conduction is considered high. EP study is needed to measure accessory path refractory period.If it is > 300ms the accessory pathway is unlikely to condcut fast .

Is there a  non invasive bedside method  to estimate  accessory pathway refractory period?

NO, It is not possible , but some clinical clues are available .

  • All concealed accessory pathway have very high RP *thats why they are concealed .Since they can not conduct antegradely   resting  baseline ECG do not show any evidence for preexcitation . They  are  safe .
  • These patients can develop only orthodromic tachycardias as the accessory pathways allow only a retrograde conduction  and AV nodal blockers are ideal in them as there is no purpose to use Amiodarone and  related drugs as antegrade  condction thorough accessory pathway is naturally blocked .
  • Intermittent WPW syndromes  have negligible risk of fast antitrade conduction. As episodes of  disappearance of delta wave indicate the antitrade conduction has a tendency to get blocked so no great worries.This is especially important if the WPW disappears at higher heart rates .

This clearly tells us  , many times  accessory pathway  shares some of the decremental properties of AV node (Applying automatic  electrical  breaks at higher  heart rates ) and it is a safety mechanism .The exact incidence of such property is not known . So , it may be a good idea  to subject patients with WPW on a treadmill and look for it’s  influence on delta waves and degree of pre excitation  .Even a few normalised beats  or prolonged PR intervals can give us assurance  against  rapid rates at times of  AF .

*One should  also remember , if a concealed WPW , manifest only during excercise it is the most dangerous group of patients in whom AV nodal blockers are absolutely contraindicated . They are immediate candidates for ablation . The above phenomenon  tells  us  , during excercise  the  AV node expresses the decremental conduction properties while accessory pathway  does not !

 Final message

Verapamil and betablockers are not  the  drugs to fear upon in WPW syndrome.In fact ,  even in this era of  hi tech cardiac care , it has a  useful role to  play  in the chronic management of WPW .

May be ,  it need to be  used with  caution . Atleast  , some  efforts  must be taken to estimate the refractory period of accessory  pathway before prescribing these drugs.

Using with caution is not synonymous with contraindication   

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What is the simplest way to differentiate pseudo normal mitral infow doppler from normal ?

Posted in Uncategorized, tagged on January 8, 2010| Leave a Comment »

Diastolic dysfunction  as concept  has  come a  long way after  initial hiccups . Now,  it is a well established  left ventricular pathology  , and has   a  sound physiological and molecular basis. Even though there are variety of methods available to quantify  LV diastolic function,  echocardiogram is the simple method to identify and grade diastolic dysfunction.

There are 4 grades of diastolic dysfunction

1.Impaired relaxation  (without elevated filling pressure)

Some  describe another grade  1 a  with elevated filling pressure

2.Pseudonormal mitral inflow

3.Restrictive -Reversible

4.Restrictive -irreversible

What is pseudo normal pattern ?

The grade 1 is the  most common type  diagnosed  . It is diagnosed when the  A  velocity is more  than E velocity . This  simply implies ,  ventricular filling needs greater assistance from atrial contraction than in resting conditions. It is so common , especially in elderly ,  many thought it should not be considered a pathology . In youngsters it is definitely pathological especially if it is persistent.

The issue that  really concerns  us  is  this  : When the diastolic dysfunction  progress  from grade 1  to grade 2  ,  the mitral the inflow  doppler pattern ,  instead of showing any  new changes simply nullifies the changes that occurred in grade 1 and  records a normal E : A velocity .

So , a person with grade 2 diastolic dysfunction will have a near normal pattern .Of course  deceleration time, and IVRT is shorter than in grade 1 but it is not very useful in differentiating it from normal .

Pseduonormal is  actually  equivalent to moderate diastolic dysfunction , but the abnormality is masked  as near normal  filling is restored with atrial assistance . So,  technically it a  assisted LV filling . A  superficial  look at the doppler pattern may exactly mimic normal . But there will be a  2 D echo  abnormality  that makes the patient  pathological . Our eyes need to look  beyond  doppler  ( in coherence with  2 D ) to differentiating  normal or pseudo normal.

It is learnt  ,  2D abnormality of LV or LA occurs in nearly 90 % of grade 2 diastolic dysfunction .(There can be a pure functional grade 2 diastolic dysfunction  without structural changes in LA/LVH in minority -This is poorly understood form of silent sub clinical CAD manifesting only as diastolic dysfunction  )

Traditionally  there are few methods taught  in echocardiaographic schools  all over the world to differentiate normal from pseudonormal

1.Pulmonary vein  doppler

2.Response to valsalva maneuver

3.Tissue doppler etc

One simple echo feature  that is   often forgotten , that can be really useful in differentiation of  normal from pseudo normal is    left atrial dimension

While patient with pseudonormal who  have  progressed   into  stage 2  will show a  definite left atrial abnormality .

When does a left atrium begins to enlarge in diastolic dysfunction?

  • It depends  on LA thickness  and  LA afterload (LVEDP is the afterload for LA)
  • It is generally believed  LAE  will be there in almost all cases of grade 3  diastolic dysfunction.
  • It is present in  majority of patients  with grade 2 as well . But the degree  of LAE may be less  ( 4-4.5cm)

It is yet unclear ,  the onset of LA enlargement in diastolic dysfunction .This is potentially a research topic for the fellows !

It is not uncommon  to find   LA enlarge  like a balloon even in stage 2  of diastolic dysfunction. So , in patients who are suspected to have  pseduonormal  doppler profile , look for the presence of LAE  , (however mild it may be !)  , there is no business for LA to enlarge in normal persons.

Ofcourse , if  you are a echo expert one can measure A reversal in PV doppler, tissue doppler echo etc .But remember a simple 2D echo feature like a LA dimension / LVH   may score over the sophisticated (Also read complex  . . .) parameters  in the grading of diastolic dysfunction

Final message

While  we  immerse  ourself  in   sophisticated doppler methods  to differentiate normal from psedunormal pattern, the fact that  , normal persons will  have normal hearts  is often forgotten , and    presence of left  atrial enlargement (Which is all too common in pseudonormal !)  straightaway   settles the issue . Detailed diastolic function studies are warrented only if the LA size is normal .

*Correction: in table A reversal in normal is less than 35cm/sec

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What is the therapeutic approach for failed primary PCI ?

Posted in Cardiology-Coronary artery disese, tagged on January 5, 2010| Leave a Comment »

” This is post is 5 years old , Newer developments should be given considerations”

STEMI is the “Numero Uno” of  cardiovascular emergency .The  treatment has evolved over decades,  right from   the primitive  arm chair approach to the  air dropping of  patients  over the cath  lab  roofs  for primary PCI ! We realise by now ,both are extreme forms of treatment and  may  have unique  hazards. What we forget is the , the natural history of STEMI is too  much dependent on the degree of initial damage to the myocardium , and it is very difficult to alter this,  however good is the therapeutic strategy .  We are yet to find an answer regarding the mechanism of primary VF and modes of preventing it. We also have no answer for  ,  why  some  develop myocardial damage  very fast and  the  cardiogenic shock occur in an  accelerated fashion. (Fate ?)

Many would consider  ” non availability of   infrastructure and expertise ”  is the major issue  for  primary PCI . But the real problem is much more than that .When an  illusion of knowledge is  created by constant bombardment of data  , it is natural for human beings to believe whatever is told or printed in books and journals. We cardiologists are made to believe thrombolysis is a far . . .  far  inferior treatment than primary PCI in STEMI .  It is not so in any stretch of imagination !

The fact that,there is no entity called ” Failed primary PCI ” in cardiology literature  , would  suggest how biased we are against thrombolysis. Every cardiology  resident will  recognise  thrombolysis fails  at least 40% of time .Yes , it is  a  fact  , but the irony is , this   is  often  used   to convey a surrogate  meaning , that  is , primary PCI is  near 100% successful !

How  do you assess success of primary PCI ?

Unlike elective PCI where the criteria is too liberal, we can not afford to adopt the same in an emergency PCI. Here the aim of the procedure is entirely different (Salvaging dying myocardium vs pain relief  ).

It’s still a  mystery ,  while  thrombolysis is vigorously assessed  for it’s  effectiveness   primary  PCI is rarely  subjected to the same scrutiny  . A check angiogram  after the procedure ,  is all that is done . . . and every one  leaves the cath lab happily. The  effect of primary PCI on ST segment ECG resolution must be documented immediately after PCI. While ,  It is mandatory to take ECG after 60 -90 mts after thrombolysis , this sort of protocol is rarely  followed after PCI.

If the ST segment  fails to retract  > 50% immediately  following PCI  the procedure  should be  deemed to have failed . Further , unlike thrombolysis  in primary PCI , the ST segment has to regress within 10  mts , as IRA patency occur instantly .If we apply this criteria , the success rate of primary PCI would be far less than what we believe*

* Not withstanding the official lesion , hardware, related failure. If we encounter a severe triple vessel disease , with a bifurcation lesion and thrombus it’s  a tough exercise as we are racing against time .

Primary PCI  Camouflaging  in semantics

  • A successful but  delayed   primary PCI  is actually a failed PCI
  • A  complicated  primary PCI  often  reach the equivalence  of   failed PCI
  • No  reflow is almost synonymous with failed primary PCI as successful correction of no reflow occur in minority.
  • Not all TIMI 3 flow is converted into myocardial flow.
  • Renal dysfunction following excess dye has a  high  morbidity
  • If patient  develops significant  LV dysfunction following primary PCI it is a failed PCI.
  • Finally if the cost of primary PCI exceeds the insurance limit it is  economically a  failed primary PCI as the patient  has to spend double or triple  the amount of sum insured .This stress has resulted in many recurrent coronary events .

Why is it important to recognise failed primary PCI ?

For failed thrombolysis we have a strategy . Unfortunately , even in this modern era  we have  no useful  strategy for failed primary PCI . Handing over a patient to a surgeon in a such a situation is considered by many as a great rescue strategy but in real world it does no good in most of the patient.

Doing an emergency CABG in a sinking patient with a battered coronary artery is no easy job /Many times it only rescues the cardiologists from the embarrassing situation of facing the relatives who ask for explanation.

So , what can be done at best , in failed primary PCI ?

  • CABG can be an option but still questionable !
  • Most times  there is  no other option except to fall back on the medical management.
  • Intensive anticoagulation and one need to consider even a rescue thrombolytic treatment !
  • Some times we can only prey !  Failed primary PCI for a patient in cardiogenic shock with IABP support is near death sentence !

Final message

  • Remember ,  success of primary PCI   is  not in  wheeling out a  patient  alive out of cath lab   , with a TIMI 3 flow  in the IRA ,  but in  garnering significant   myocardial salvage   which  should have an impact on   intermediate and long term  outcome .
  • Do not ever think primary PCI is a sacred treatment modality in STEMI  and the job of the cardiologists ends there. It is vested with  lots of important complications – defined, undefined , recognised,  unrecognised, reported, and unreported ,  concealed ,denied, poorly understood, etc etc.
  • There are  equally  effective, less dangerous treatment modality available .
  • Decision  to do primary PCI  must not be based   only on the  “affordability and  availability”  of  cath lab and expertise !
  • In  clinical cardiology practice,  no  procedure  is  great   & nothing is inferior either  !  Every thing has to be used judiciously , appropriately  and  intelligently (Intelligence is synonymous with common sense many times!)

Coming soon

Surgeon’s real time experience of operating  on a failed primary PCI. To our surprise , only a handful of surgeons  have this experience

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How common is persistent ST elevation in inferior leads following STEMI ?

Posted in cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , on January 5, 2010| Leave a Comment »

Persistent ST elevation is the  general technical term for  failed thrombolysis.Regression of 50%  of admission ST elevation is the required criteria for susccesful thrombolysis .

Thrmobolysis fails in about 40-50% .

Main determinant is the timing of thrombolysis – not the thrombolytic agent ! do not get carried away with all those curent hoopla  about Tenecteplase stuff

If we take 100 patients with persistent ST elavation 90-95 will be in anterior LAD territory .

This is a stunning a cardiology secret no book of cardiology address . . . Implication of which could be very significant . Primary PCI  will always struggle to  prove it’s superiority over thrombolysis  in the right coronary artery .(Note LCX STEMI is different , infact it is more tricky than even even LAD .This issue will be addressed seperately in my blog.)

Read the following link  for  answer to the title question .

How common is persistent ST elevation in inferior leads following STEMI ? https://drsvenkatesan.wordpress.com/2008/09/22/why-thrombolysis-rarely-fails-in-right-coronary-artery/

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