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Posts Tagged ‘thrombolysis’

Failed thrombolysis is an important clinical  issue  in STEMI   as  successful thrombolysis  occurs  only in  about 50-60%  of pateints . The typical criteria to define failed thrombolysis is  the  regression  of less than 50% of sum total( or maximum)  ST elevation in infarct leads.

So what do you do for these patients with failed thrombolysis ?

It depends upon the patient’s symptom, hemodynamic stability, LV dysfunction .

They  should  get one of the following .

  1. Conservative medical management  with /without CAG
  2. Repeat thrombolysis
  3. Rescue PCI
  4. CABG

Medical management is  thought to be  too inferior a  management,  many of the interventional cardiologists  do  not want to talk about . But  , there is  an important  group of patients (Not often addressed in cardiology literature)  who  technically fulfill the criteria  of failed thrombolysis  , but   still  very  comfortable , asymtomatic  and in  class 1. These patients ,  have  a strong option for continuing the conservative management .

Repeat thrombolysis does not have a consistent effect but can  be  tried in some  stable patients. CABG  can be a genuine option in few

Rescue PCI

This terminology  has become  the  glamorous one since the  catchy word  rescue is tagged in the title  itself. For most of the cardiac physicians ,  this has become the default treatment modality.This is an unfortunate perception . What  one should realise   here is  , we are  tying to rescue  the myocardium and  the patient ,   not the patient’s coronary artery !

Opening up a coronary obstruction is not synonymous with rescue .

For rescue PCI ,  to be effective it should be done within the same time window as that for thrombolysis (ie within 6 or at the most  12 hours) .This timing  is  of vital importance  for the simple reason , there will be nothing to rescue after 12 hours as most of the muscle  would be  dead. Reperfusing a dead myocardium has been shown to be hazardous in some ,  as it converts a simple  infarct into a hemorrhagic  infarct.This softens the core of the infarct and  carry a risk of rupture. Further,   doing a complex emergency  PCI  ,  in  a thrombotic milieu with   presumed  long term  benefit ,  is  a  perfect recipe for a potential  disaster.

While the above statement may be seen as pessimistic view , the optimistic cardiologist would vouch for the“Curious  open artery hypothesis” .This theory simply states , whatever be the status  of the distal myocardium ( dead or alive !)   opening an obstruction in the concerened coronary artery  will benefit the patient !

It is  huge surprise , this concept   continues to  be alive even after  repeatedly shot dead by number of very good clinical trials (TOAT, CTO limb of COURAGE etc ).

The REACT study (2004) concluded undisputed benefit of rescue PCI for failed thrombolysis  , only if the rescue was done  within  5-10 hours after the onset of symptoms.The mean time for  pain-to-rescue PCI was 414 minutes (6.5hours)

Final  message

It is fashionable to talk about time window for thrombolyis but not for PCI  .The time window for rescue PCI is an redundant issue  for many  cardiologists ! . But ,  the fact of the matter is ,  it is not . . .

The concept of time window in rescue PCI  , is as important as ,   that of  thrombolysis. Please , think twice or thrice !  if some body suggest you to do a rescue PCI in a stable patient  ,  12hours after the index event .

Important note : This rule   does not (  or need  not  ) apply for patients in cardiogenic shock  or patient ‘s with ongoing iscemia and angina.

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NSTEMI constitutes a very heterogeneous population .The cardiac risk can vary between very low to very high . In contrast , STEMI patients carry a high risk for electro mechanical complication including sudden death .They all need immediate treatment either with thrombolysis or PCI to open up the blood vessel and salvage the myocardium.

The above concept , may be true in many situations , but what we fail to recognize is that , STEMI also is a heterogeneous clinico pathological with varying risks and outcome !
Let us see briefly , why this is very important in the management of STEMI

Management of STEMI has undergone great change over the past 50 years and it is the standing example of evidence based coronary care in the modern era ! The mortality , in the early era was around 30-40% . The advent of coronary care units, defibrillators, reduced the mortality to around 10-15% in 1960 /70s . Early use of heparin , aspirin further improved the outcome .The inhospital mortality was greatly reduced to a level of 7-8% in the thrombolytic era. And , then came the interventional approach, namely primary PCI , which is now considered the best form of reperfusion when done early by an experienced team.

Inspite of this wealth of evidence for the superiority of PCI , it is only a fraction of STEMI patients get primary PCI even in some of the well equipped centers ( Could be as low as 15 %)

Why ? this paradox

Primary PCI has struggled to establish itself as a global therapeutic concept for STEMI , even after 20 years of it’s introduction (PAMI trial) . If we attribute , lack of infrastructure , expertise are responsible for this low utility of primary PCI , we are mistaken ! There are so many institutions , at least in developing world , reluctant to do primary PCI for varied reasons.( Affordability , support system , odd hours ,and finally perceived fear of untoward complication !)

Primary PCI may be a great treatment modality , but it comes with a inherent risk related to the procedure.

In fact the early hazard could exceed the potential benefit in many of the low risk STEMI patients !

All STEMI’s are not same , so all does not require same treatment !

Common sense and logic would tell us any medical condition should be risk stratified before applying the management protocol. This will enable us to avoid applying “high risk – high benefit” treatments in low risk patients . It is a great surprise, the cardiology community has extensively researched to risk stratify NSTEMI/UA , it has rarely considered risk stratification of STEMI before starting the treatment.

In this context , it should be emphasized most of the clinical trails on primary PCI do not address the clinical relevance and the differential outcomes in various subsets of STEMI .

Consider the following two cases.

Two young men with STEMI , both present within 3 hours after onset of symptoms

  1. ST elevation in V1 -V6 , 1 , AVL , Low blood pressure , with severe chest pain.
  2. ST elevation in 2 ,3, AVF , hemodynamically stable , with minimal or no discomfort .

In the above example, a small inferior MI by a distal RCA occlusion , and a proximal LAD lesion jeopardising entire anterior wall , both are categorized as STEMI !
Do you want to advocate same treatment for both ? or Will you risk stratify the STEMI and treat individually ? (As we do in NSTEMI !)

Current guidelines , would suggest PCI for both situations. But , logistic , and real world experience would clearly favor thrombolysis for the second patient .
Does that mean, the second patient is getting an inferior modality of treatment ?

Not at all . In fact there is a strong case for PCI being inferior in these patients as the risk of the procedure may far outweigh the benefit especially if it is done on a random basis by not so well experienced cath lab team.
(Note : Streptokinase or TPA does not vary it’s action , whether given by an ambulance drive or a staff nurse or even a cardiologist ! .In contrast , the infrastructure and expertise have the greatest impact on the success and failure of PCI )
Final message

So , it is argued the world cardiology societies(ACC/ESC etc) need to risk stratify STEMI (Like we do in NSTEMI ) into low risk, intermediate risk and high risk categories and advice primary PCI only for high risk patients.

Reference

https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/226907

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Heparin was invented accidentally by a 26 year old  , Jay McLean, a  pre clinical  medical student  in 1916 .It was one of the greatest discovery  in  medicine .It helped us prevent blood from clotting.Frozen blood inside human circulatory system constituted one of important mechanisms  of  human  death.This ranged from acute myocardial infarction to cerebral thrombosis  .

heparin3

As we decoded the mechanism of action of heparin , it was clear it bound to the  naturally occurring molecule antithrombin 3 and effectively blocks the intrinsic coagulation mechanism and thus behaves as an important anticoagulation agent.

How heparin acts as a thrombolytic agent ?

We know , our hematological system has a powerful  natural  fibrinolytic mechanisms  to protect against unwarranted( pathological ) intravascular coagulation. This is mediated by  anti thrombin, protein C , protein S  ,  plasminogen  system etc  . Natural concentrations of tissue plasminogen activator (Tpa)  also  help in lysing intravascular clots.

There is a constant  , delicate balance between procoagulant , anticoagulant and antifibrinolytic molecules .Intra vascular  clots occur when a vascular  injury triggers  a clot formation and the clinical event occurs.

But,   once insulted ,   the  circulating blood   does not remain a silent spectator . It is  constantly  on the look out for a foe to attack the thrombus that is interfering  with its natural flow  . Antithrombin 3 is one such molecule. Success  of lysis depends on the power of natural forces. There are hundreds of episodes of microlysis that take place every day  (Which happen without our knowledge ) .In  patients with vascular  disease these episodes are likely to be further more.

What does  Intravenous heparin in high doses  do ?

Heparin immediately  blocks of powerful procaogualtion activity .One of the important heamatological principle  is “Thrombus begets thrombus “. It is  a vicious cycle. This is immediately  tackled by heparin .The powerful trigger of thrombus induced thrombus propogation is shut off .

This makes a  2 cm sized clot to remain  in  2cm . After  making sure of this , the blood in the immediate vicinity   start percolating the clot.  The heparinised blood   switches to  a pro- fibrinolytic mode as the balance of forces  is fully tilted in favor of fibrinolysis or thrombolysis.

Is there clinical evidence to call heparin as thrombolytic agent ?

Yes . Contrary to the popular scientific  principle we have only clinical evidence  . laboratory evidence is not convincing as heaprin lyses clot only in vivo . Since ,  evidnece based medicine requires  laboratory evidence  we hesitate to call this as  thrombolytic agent !

It has been a strong clinical observation ,   many  major intracardiac or  intravascular  clots  regress in size

(or totally dissolve )  with intensive heparin  regimen .The effect is seen in 48-72 hours.Some times in first 24 hours.

What are the clinical situations where heparin has successfully lysed the clots*?

  • Pulmonary embolism
  • LV clot
  • LA clot
  • Cortical venous thrombus
  • Deep vein thrombosis
  • Coronary thrombosis**
  • Portal vien thrombois
  • Renal vein thrombois

* Plenty of case reports available for each condition

** Sustained micro  thrombolysis  is the major mechanism of benefit in NSTEMI

If it is true ,  heparin dissolves thrombus , why  it is not called as thrombolytic agent ?

Why not ?  You decide yourself !

How does heparin compares with  the great thrombolytic agents*  like  Strepotiknase, Urokinase,Altepase, Retepalse , Teneckteplase (TNK TPA) ?

Many (Rather most . . .)  would consider it ,  as  foolish , to compare heparin with these agents .But the fact of the matter is except for streptokinase there is no comparison studies available. Attempting such a study  in humans will  be considered unethical. Without   a proper scientific  data  heparin  can not be ignored either.

But ,  some of the control groups in major  studies of thrombolysis  through some light !

In pulmonary embolism thrombolytic agents and heparin have similar effects on intrapulmonary thrombus

An important point to remember here is   , the powerful thrombolyic agents are administered  in as short duration (Bolus / 1  hour infusion ) .This is invariably  followed by heparin infusion . Why do we  do that ? because we know it is important . One may never know , how much of lysis is done  by the trhombolytic agent and how much by heparin .

if you analyse the  data  success rate of thrombolytic agents are infact attributable  to the follow up heparin

Thrombolytic agents  piggy packs on heparin and claims the  credit for thrombolysis *

In thrombolytic  therapy  , heparin  is considered  as an adjunct to streptokinsae but in reality  streptokinase  may an  adjunct to heparin

Importance of  heparin In Acute MI (HEAP Trial)

It should be realized  there is a time window for heparin too . . .  early administration  can have  great benefit

Early heparin prevents formation of  core  of the clot .The   importance of acute administration of  aspirin  in suspected STEMI  is well recognized  by paramedics  .  A bolus of heparin (10000 u)  immediately  could have great impact on the outcome as well  .Paradoxically we talk more  about emergency PCI,  on  transit TPA  etc . . . We have seen  number of patients  referred  with  STEMI   from   suburban areas traveling for hours with out any anticoagulants but promptly getting sorbitarate tablets ! Unfortunately prehospital heparin is rarely stressed in literature .

Watch the video : Heparin : The forgotten hero

Final message

  • Heparin is   an  under rated drug  as a thrombolytic agent.
  • Just because it has no direct action  on thrombus it is considered an inferior agent.( One other reason  for it to be  considered  inferior ,   it  is  very cheap  !)
  • Heparin too ,  has a time window effect in acute MI (Class 3 evidence ie   wide clinical experience)
  • It’s  usage should be early  and  liberal , especially  in out of hospital setting in vascular  emergency.
    Note of caution : This article is not meant  to  defame  the thrombolytic agents.It only stresses a point that , heparin has also a role , as a thrombolytic agent. *Whenever rapid thrombolysis is required in life threatening situations specific thrombolysis is indicated as per guidelines.

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                                                    Drugs are poisons , whenever it is administered without valid purpose. it can enter human body  in many ways (Oral, intravenous, percutaneous etc ) And now we have another route namely intracoronary !

                                                   In quest for prevention of restenosis, many of the anti cancer drugs are now delivered directly inside the coronary arteries .These drugs are secreted  like a sustained release  tablet from the drug coated stents.These drugs are expected to prevent restenosis within the stented segment.But, after years of  intense debate and research  , we realised that ,  drugs  eluted from the stent  could damage the distal coronary vascular bed and coronary microcirculation.( And thus came the epidemic of acute stent thrombosis ! )

                                                The tender and sensitive coronary microvasculature  is constantly exposed to  these  powerful anticancer and immmunosuppresive  drugs .It is a great surprise , no body thought of  this dangerous drug -coronary artery interaction ! It required the genius of Renu virmani and others to point out this.

But still , the cardiology community by and large , fails to consider  this an important issue.This is proven by the fact, usage of DES is  still increasing  and used mainly as an off label indication.

Read this land mark article from circulation

picture1

http://circ.ahajournals.org/cgi/content/full/115/8/1051?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=1&author1=renu+virmani&andorexacttitle=and&andorexacttitleabs=and&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=relevance&fdate=1/1/2007&tdate=12/31/2007&resourcetype=HWCIT

 

Questions that need to be answered

  • What is the long term effects of drugging a coronary artery ?
  • Is no reflow or slow flow  more common after DES , because of the adverse drug reaction in the distal vascular bed ?
  • If a patient  with  DES  undergoes a CABG later what  would be  the impact of the  drug on the graft ? Will the functional vasodilatation   affected ?

Final message

                                  A drug , to get a legal clearance it has to undergo  hundreds of rigorous tests . Finally it is cleared for that  specific indication for which it is tested  .Just because a drug is cleared for one purpose ( Paclitaxel for malignancy ) it does not mean it is safe to use for any other  purpose for which it is deemed to be useful . Exactly the  opposite is happening   in the  the field of interventional cardiology . No body wondered to think what would be the effect of these drugs on the normal coronary endothelial cells and vasculature.Is it not a crime ,  without analysing this particular issue  , dozens of drug eluting stents have been released in the market . And now,  sounds of crying  foul is heard world wide !

Let us thank  , the so called negative forces in cardiology  for making this an  issue . In science ,  the watch dogs should bark  at  times of danger not wag the tail !

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Which is  the most important factor that determines thrombolysis failure in STEMI  ?

  1. Thrombus load .
  2. Drug efficiency
  3. Time delay
  4. Presence of a mechanical lesion
  5. Hemodynamic instability

Answer : 3 .(Though all 5 factors operate )

Failed thrmbolysis occur in about 40-50% after streptokinase and slightly less with TPA   and TNK-TPA . Delayed arrival and late thrombolysis are  most common cause of failed thrombolysis. As the time flies , the  myocardium gets damaged and the intra coronary  thrombus gets organised .Both these processes make delayed thrombolysis a futile exercise.

               Not all STEMI patients have large thrombus burden. There need to be a critical load of thrombus for thrombolytic to be effective

Some may have a major mechanical lesion in the form of plaque fissure, prolapse and it simply blocks the coronary artery mechanically like a boulder on the road  . The poor  streptokinse  or the rich Tenekteplace !  nothing can move this boulder .The only option here is emergency PCI .

How will you know when the patient  arrives in ER with STEMI whether his/ her coronary artery is blocked with soft thrombus or hard mechanical boulder ?

It is impossible to know.That’s why primary PCI has a huge advantage.  But still thrombolysis is useful as some amount of thrombus will be there in all patients with STEMI.Lysing this will provide at least a  trickle of  blood flow that will jeep the myocardium viable and enable us to take for early PCI.

Final message

The commonest cause for thrombolytic failure is the time of administration and the degree of underlying mechanical lesion  . So  it does not make sense  to blame  streptokinase always !

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                                     Hypertension is considered a major cardiovascular risk factor.Hypertension  can have multiple physiological and pathological effects on heart . The common response to  raised arterial pressure is the hypertrophy of the left ventricle ( LVH). This can increase the risk of heart failure in few ( Mainly diastolic failure)  It is a leading cause for stroke  and   less often a  coronary event.

What links Hypertension and  coronary artery disease

                                           Coronary artery disease is almost synonymous with atherosclerosis. There is no separate entity called hypertensive coronary artery disease. But HT can accelerate the process of atherosclerosis. It is widely understood, hypertension can cause  physical endothelial damage and functional impairment of endothelial function.The physical damage ie enothelial disruption , or erosion is a very uncommon phenomenon . So currently  there is sufficient clinical experience  HT is considered dangerous for coronary artery only if it is with the  company of diabetes and hyperlipidemia. (This will seem controversial as it is against the findings of iconic Framingham trial!)

What the medical community refers to hypertension , may not be really so inside  for the coronary arteries.

                                             The relationship between brachial cuff blood pressure and the intra coronary pressure has very little linear relationship. So one should recognise it is the intra coronary hypertension that has a immediate impact on the coronary events. Now only , we are beginning to understand the complexities  of the relationship between HT and CAD. If we analyse a series of individuals HT per se is not a very serious risk factor for CAD* , but it is a number one risk factor for stroke. 

Why HT in isolation  often result in stroke , rather than a MI ?

While HT  is notoriously common to result  intracerebral hemorrhage, the same HT  would not cause  intramyocardial bleeds . Why ?

What is protecting the myocardium against this complication ?

                                      The exact mechanism  is not clear.Acute surges of blood pressure can increase the risk of stroke many times  but  rarely precipitate  a coronary event(  But may cause a LVF) . The reasons could be the coronary endothelial shearing stress is less than the cerebral blood vessels.Both cerebral and coronary circulation has  auto regulatory mechanism . The coronary auto regulation is more robust in that it does not allow  intra coronary pressures to reach critical levels .There is no clinically relevant intra myocardial hemorrhage reported  even during malignant hypertension.

*But a  high intra coronary pressure can sometimes  result in spontaneous coronary dissection and plaque fissure .Lipid mediated injury is vey much facilitated in a high pressure environment.

Has Controlling blood pressure  to optimal levels  , reduced the overall CAD morbidity and mortality ?

                    The answer is yes, ( But not an emphatic yes ! ) Some studies had been equivocal. It is very difficult to say , how much benefit is attributable to BP reduction  per se  and   how much is attributable to indirect effect on atherosclerosis prevention.

Hypertension during ACS

                            High blood pressure during an episode of unstable angina or STEMI can increase the myocardial oxygen demand and worsen the ischemia. It requires optimal control with nitroglycerine ( Preferably ) or beta blocker and ACE inhibitors.Even though HT is commonly associated  with ACS,  one can not be sure the ACS is preciptated by HT. Many times the sympathetic surge during an ACS keeps the blood pressure high.It is a common experience the blood pressure suddenly dropping to normal or hypotensive levels once the pain and anxiety is controlled.

Hypertension during thrombolysis

                           High blood pressure is a relative contraindication for thrombolysis.It need to be emphasised here, It is the  the fear of stroke that make  it contraindicated .The heart can tolerate  thrombolytic agents delivered at high BP .In fact logically ,  hemodynamically and also  practically it is obseved , thrombolytic agents administered at relatively high blood pressure (140-160 systolic) has better thrombolysis than a patient who is lysed at 100mmhg.

                       The coronary pressure head which contain the thrombolytic agent (streptokinase and others ) need to have pressure jet effect on the thrombus.So the  mean coronary perfusion pressure becomes  a critical determinant of success of thrombolysis.

                            It is a paradox of sorts , very high blood pressures are a relative contraindication for thrombolysis and at the same time normal pressure patients fare less well to thrombolysis.

 Final  message

                        Hypertension continues to be a major cardiovascular risk factor.It has direct and indirect effects on the heart.Generally HT is more of a risk factor for stroke than CAD.A slightly high BP ( Just around the  upper limits of normal or just above it ) has a hemodynamic advantage during thrombolysis.(Class C evidence )

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 Rescue thrombolysis in acute   myocardial   Infarction  

 *Venkatesan sangareddi ,Madras medical college,Chennai.India

 

 

   Back ground  Failed thrombolysisin acute myocardial infarction occurs in 30-40% of patients. The incidence of progressive pathological remodelling and cardiac failure is high in these patients. The approach to the patient with failed thrombolysis is generally considered to be catheter based and the outcome is not clear. Bleeding can be troublesome in patients, taken for interventional procedures in the immediate post thrombolytic state. The option of repeat thrombolysis has not been studied widely and is not popular among cardiologists.

Methods:We present our experience with six patients (Age 42-56, M-6, F-0) who were thrombolysed for failed first thrombolysis. All had anterior MI and had received either urokinse or streptokinase (between four to nine hours) after the onset of chest pain. All of them had persistent ST elevation, angina not responsive to maximal doses of IV NTG and beta blockers. The initial thrombolysis was deemed to have failed. Repeat thrombolysis with streptokinase (15 lakhs) was given between 16 and 24 th hour. The clinical outcome following the second thrombolysis was rewarding. It relieved the angina, ST segment elevation came down by 50% and coronary angiogram done at 2-4 weeks showed complete IRA patency in four out of six patients. The factors responsible for failed thrombolysis is complex and multifactorial. A logical explanation from the fundamentals of clinical pharmacology would suggest that a common cause of failure of any drug is due to a inadequate first dose.

Conclusion :We conclude that repeat (Rescue) thrombolysis can be an effective medical intervention for failed thrombolysis in AMI.

Personal perspective                  

                             Repeat  thrombolysis for failed ( initial ) thrombolysis  is still   considered  a  fantasy treatment  by most of the cardiologists !  The utility and efficacy of this modality of  treatment (Rescue thrombolyis ) , will never be known to humanity , as planning  such a  study , in a large population  would  promptly be  called unethical by the modern day cardiologists.

                     While a cathlab based cardiologist  take on the lesion head on with multiple attempts  , it is an irony , poor  thrombolytic agents are given only one shot  and if failed in the first attempt,  it is doomed to be a  failure for ever.Currently,  the incidence of  failed thromolysis could be up to a whooping 50 %  .There has not been much scientific initiative  to enhance the efficacy of these drugs.

                            Common sense and logic would suggest it  is the  inadequate first dose ,  improper delivery , pharmacokinetics is   the major cause of failure of action of  a drug in clinical therapeutics.

If the first  dose is not working ,  always think about another  incremental dose if found safe to administer.

Can we increase the dose of thrombolytic agents  as we like ? Will it not increase the bleeding risk to dangerous levels ?

This is a clinical trial  question.

  • In patients with prosthetic valve thrombosis and acute pulmonary embolism we have safety data of administering of  1 lakh units for an hour for up to 48 hours.

Can  the same regimen be tried in STEMI if the initial thrombolysis has  failed  and emergency intervention is not possible  ?

Logic would say yes . Unfortunately we can’t go with logic alone in medicine .We need scientific data ( with or without logic ! ).But now ,  as we realise common sense is also a integral part of therapeutics  It is called as level 3 evidence / expert consensus by AHA/ACC .

Applying  mind , to all relevant issues ,  continuous streptokinase infusion 1 lakh/hour for 24-48 hours in patients with failed thrombolysis can indeed be an option,  especially when the patient is sinking and  no immediate catheter based intervention  possible .This study question is open to all researchers , and may be tested in a scientific setting if feasible.

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Answer: Do  coronary angiogram  for all patients  who had suffered from an acute myocardial infarction* ( Forget about all those mulitpage ACC/AHA  guidelines !).

For an  interventional cardiologist ,  it is often  considered a crime to  follow a conservative  approach !

*Caution This one line guideline is not based on scientific fact  but reality based . Ideally one should identify  high risk subsets among the patients who had an AMI .Patients who had complications during the MI get immediate CAG. Others need  a focused LV function asessment ,  pre discharge  sub maximal excercise stress test or perfusion studies .But this concept has been  virtually replaced by pre discharge coronary angiogram for all ,  in many  of the centres in the world.

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Differential response of thrombolysis between left and right coronary system

  • Thrombolysis is the specific treatment for acute myocardial infarction. ( Privileged few , get primary PCI))
  • Failed thrombolysis occurs in significant number of patients ( 30-40%).
  • Persistent ST elevation  120 minutes after thrombolysis is best indicator of failed thrombolysis.
  • It has been a consistent observation  failed  thromolysis  is more frequent in anterior   or LAD myocardial infarction.

In a simple study we have documented  patients  with inferior MI  rarely had persistent ST elevation and thrombolysis  was   successful in vast majority  of  patients  ( Except in few patients associated lateral MI)

 

The mechanism of better thrombolysis in right coronary artery  is simple.The success of thrombolysis , apart from early time window , is directly correlated with pressure head  and the duration of contact between the thrombolytic agent and the thrombus. In right coronary circulation the  blood flow is continuous ,  occurs  both in systole and diastole that facilitates the maximum delivery of the thrombolytic agent . Further there is a favorable  pressure gradient  across RV myocardium  as the transmural occluding pressure across RV is considerably less then LV myocardium.

This paper was presented in the  “Annual cardiological society of India scientific sessions”

at Chennai, Tamil Nadu.India December 2000

Click to down load PPT full presentation

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                                  Indication for thrombolysis in ST elevation MI  is mainly determined by clinical and ECG features. ST elevation of more than 1mm in two consecutive leads with a clinical suspicion of acute coronary event demands immediate thrombolysis.

                                 Early repolarisation syndrome(ERS) is a  is typical mimicker of STEMI . In ERS , ST segment elevation occurs in many leads especially precardial .This entity is estimated to occur in nearly 3-5% of population where a genetic variation in the potassium channel activation is reported.

                              If they  land in ER with some sort of chest pain , chances are high for labelling  them as ACS . It is not uncommon for  CCU physicians  to  witness  an  ERS being lysed . Even in many of the land mark trials (ISIS ) there has been many inappropriate thrombolysis , recognised later on.

What can really happen if you thromolyse them inadvertently ?

Generally nothing happens . But they are exposed to the risk of thromolysis. The ECG changes persist. And troponin will be negative and  echocardiogram will not reveal any wall motion defect.

Are we legally liable if a patient  with ERS was thrombolysed and he ends up with a bleeding complication like stroke ?

                        While the physician may feel guilty , there is no reasons for him to feel so.The guidelines are kept little lineant  for  the indication for thromolysis. When we are promoting  a strategy of early  thrombolyis  on a population based approach  in STEMI ,  there is bound to have a overlap with normality .The benefits out of early thrombolysis for eligible  patients for outweigh the few inappropriate thromolysis.

When you want to catch  a   real criminal  it is unavoidable,  one gets hold of all suspected criminals before letting them free . Unfortunately  in this exercise , some of the innocent  might experience   intimidation or even a injury  at the hands of law enforcers.

                               Similarly if a patient with ERS develop a severe esophageal spasm and typical  angina like chest pain he is absolutely certain to receive thrombolysis. (Troponin, CPK come later , and the results never veto the clinical and ECG criteria ,except probably in LBBB) .Many times critical  time dependent decisions are prone for errors in CCU.   So it may be  unscientific to ask why an ERS was  thrombolysed !

 How can one prevent inadvertent thrombolysis in ERS ?

                            Always ask for the previously recorded ECGs .If it is available and  look exactly similar to the current ECG  chances are unlikely  for ACS. In ERS ST segment is generally concavity upwards . ACC/AHA  guideline for STEMI  ,is  aware of this fact , but still  advices thrombolysis for all ST elevation irrespective of the morphology of ST segment elevation. This is propably intentional,   not  to incorporate morphology cirteria of ST elevation  for thromolysis .It would potentially  make many true STEMIs  diagnosed falsely  as ERS and deny thrombolysis.

 

What is the latest news about ERS ?

                       Now data are coming up, ERS is not entirely benign condition.Some of them ( Even a fraction of ERS population could be a significant number) can have a overlap between Brugada syndrome and they  could be prone for dangerous ventricular arrhythmia when challanged with ischemic or other stress.

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