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Posts Tagged ‘rescue pci’

How early one can shift a patient for rescue PCI after failed thrombolysis ?

  1.  Wait for at-least 24  hours.
  2. A minimum  cool off period of 2 hours is required.
  3. It is never an issue . Rush the patient  immediately to cath lab
  4. The question does not arise  . Often times ,  rescue PCI is a dead concept  as  sufficient damage has happened !

Answer

The irony of  medical science  lies in our belief that every medical query  has a specific answer ! In reality it is rarely true.   In this instance , any of  the above can be a correct response.

A patient with  failed thrombolysis can belong to any of the  64 possible combinations*  based on  time of  thrombolysis , extent of  MI,  associated complications, co- morbid conditions , presence of symptoms . (For example there is  a sub groups of patient with  failed thrombolysis still  asymptomatic  and comfortable )

The issues for rescue PCI  do not  arise  in a   sinking STEMI (Cardiogenic shock ) , or  STEMI with persistent angina. There  is  no  management issues in  these patients  .They need to be rushed to cath lab. Unfortunately  in  impending  LVF or manifest LVF (But not in shock )  decision making is tough , as doing a PCI in patients  with basal crackles  and hypoxia is a real challenge .These are the patients who are likely  to hit hard  from the hazards of the procedure .Extreme caution is required.

I have seen  significant cohort  of  asymptomatic hypotensive patients getting converted into   drug resistant, IABP dependent refractory shock after PCI  ,  making every one look  pathetic  !  The  only solace for the interventionist  is  the gratification  of  stenting the  IRA !

This  happens  , in spite  of having  multi national trained  in house critical care anesthetics and  dual core processing IABP  . Realise  what we need is delicate decision making ,  So use extreme diligence in selecting patients with impeding shock .

Your medical management can  provide  more teeth to stabilise your patient than a PCI .If you are doubt discuss with your learned colleagues .  ( If you  do not  ask for evidence for  this statement , probably  it would confirm  you  as  an  experienced   cardiologist  !)

Real issues pushed to the sidelines ?

While the real issue  in the timing of rescue PCI  may be  different , the discussion traditionally  revolves around   hemo-rheological aspects . We know  the lytics and PCI do not combine well for two reasons.

  • Pro-coagulant nature of lytic state .
  • Excess bleeding risk at puncture site.

Now ,  we have evidence to say fibrin specific lytics  TPA, TNKTPA has less of this issue . ( NORDISTEMI)

Patients who receive  fibrin specific lytics  can  safely  be  taken for rescue PCI  in case it is needed without any increased risk .

Bleeding complication  has dramatically reduced as radial procedures are done often even in emergency setting.

Vascular occlusive devices  have added to our comfort.

* The definition of failed  thrombolysis by  itself is not standardized . Is it symptom guided ?  or ECG / enzyme / echo guided  ? A patient with  infarct  related chest pain (dull aching )  after thromolysis can be labeled as post infarct refractory angina and rushed for emergency angiogram .(This is due to our ignorance  about  the  residual pain signals  through  type c pain fibres  for up to 24 hours )

Final message

The indication and  timing of rescue PCI is  primarily  related   to the  overall   patient profile  rather than the bleeding or pro-coagulant issues .

Although   pro-coagulant  lytic state is based on weak scientific  foundation , it  is a blessing in disguise  as it  can  act  as a deterrent  in restricting  inappropriate rescue PCI !

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  • Acute myocardial  infarction is the number one cardiac emergency .
  • About a million papers and articles are available in  medical literature about STEMI.
  • Management of STEMI when they present early is addressed by every text book.
  • It is  really surprising to note there is no  simple and  specific guidelines  to manage STEMI when they present late to the ER .
  • Such a scheme is vital for physicians,  as experience suggest almost 40 % of all STEMI arrive late and are ineligible for specific reperfusion strategies.

The following  flow  chart is  exclusively meant for usage in STEMI when they  arrive late >12 hours .

This is a personalised version based on working in one of the oldest CCU in  Asia which handles  about  2000 acute coronary syndromes every year with a mortality rate of 6-7 %  Hope one can bear with it !

Please click on the chart for a high resolution Image

Comments are welcome

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Preamble

The much published TRANSFER -AMI study  has few important queries to ponder about.It was supposed to test the role of routine PCI following  thrombolysis. In other words it compared  rescue only strategy with routine strategy.The caveat is , even among  failed thrombolysis, the   rescue strategy has not convincingly proven superior to medical management  (if the time is lapsed ) as much of the damage is done .

In essence , Acute MI is  more about time management than drug or cath lab management

  1. Why the 67 % of  standard therapy cohort underwent PCI. Technically , you are supposed to transfer for rescue only if there is a  failed thrombolysis ?That is the standard approach , if  most of the cases are any way land up in cath lab , then you are trying to compare two similar groups .
  2. Why the rate of   failed thrombolyis with TNK-TPA in both arms not disclosed ?
  3. How can a 92% of study population be in class 1 Killip still considered to be high risk group ?
  4. Why the recurrent ischemia  was very vaguely  defined and still included and clubbed with primary end point along with deaths. If only recurrent ischemia was removed from primary end point . . .this study will straight away land in a regret bin.
  5. Why there were 6 additional deaths at 30 days  in routine early  PCI group ,  What was he cause of death ? Mind you these deaths have happened in a 92 %  Killip class  one cohort . Is it  not important ? The trend looks vitally   significant .We can not afford take refuge under a false  statistical roof .
  6. How many patients died or  developed MI  because of the early PCI in-spite of having  successful thrombolysis.This again could be vital . Complications during intervention  for a failed thrombolysis may be acceptable. While ,complications , when we try to  improve upon the already  successful thrombolysis is simply not acceptable .

Will the investigators share their experience ?

Finally

Why the title of the paper says it is about “Routine angioplasty” and  the conclusion emphasizes  it is indeed   “high risk subsets ofangioplasty” (While the study itself involves a 92 %  least risk Killip class 1 ) .  Why this double dose of confusion ?  (Is it deliberate  ! Which i think is unlikely )

NEJM please take note of this  . . .

All that glitters  are  not natural glitter . . .some are made to glitter !

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  1. Do 64slice MDCT  in all patients who has  a coronary event and follow it up with catheter based CAG.
  2. Use liberally the new biochemical marker ,  serum  B-naturetic peptide (BNP) to diagnose cardiac failure in lieu of basal auscultation.
  3. Advice  cardiac resynchronisation therapy in all patients  who are in class 4 cardiac failure with a wide qrs complex .
  4. As it is may be considered a  crime to administer empirical  heparin, do ventilation perfusion scan in all cases with suspected pulmonary embolism.
  5. Do serial CPK MB and troponin levels in all patients with well  established  STEMI .
  6. Open up all occluded coronary arteries irrespective  of symptoms and muscle viability.
  7. Consider  ablation of pulmonary veins as an  initial strategy in  patients with recurrent idiopathic AF. If it is not feasible  atleast occlude their left atrial appendage with watch man  device.
  8. Never tell  your patients   the  truths  about the  diet , exercise &  lifestyle modification (That can  cure most of the early hypertension) . Instead encourage the  use of  newest ARBs  or even  try direct renin antoagonists   to treat all those patients in  stage 1 hypertension.
  9. Avoid regular heparin in acute coronary syndromes   as  it  is a disgrace to use it  in today’s world. Replace all prescription of heparin with  enoxaparine  or  still better ,  fondaparinux  whenever  possible.
  10. Finally never discharge  a  heftily  insured patient   until  he completes all the  cardiology investigations  that are available in your hospital  .

Coming soon :  10 more ways to  increase cost of cardiology care . . .beyond common man’s reach

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Fundamental principle  of  human biological system is to live in harmony with nature and environment.Each cell  has a unique reaction  when it comes into contact with  external  material. This reaction can be acute or chronic  ,   local or systemic. The most severe form of allergy is called anaphylaxis  that can result in instantaneous loss of life. There  is a whole gamut of disorders  that  resulted  in a  separate  speciality called allergic medicine .

Further ,the transplantation  science have   taught us  an  organ or cell can be rejected at any point of time after implantation (Hyperacute -chronic) .With advancement of science we have started implanting a variety of devices  with complex metallurgy ,inside human body, metal clips, prosthesis, valves, wires, etc .How the body handles them .The consequences can be a mild reaction to major ones occasionally.

Consider ,a local allergy due to a orthopedic prosthesis  in one of the leg bones  is far less serious than a metal within a coronary artery  irritating the intima .

Remember hypersensitivity reactions can be severe . This lady reacted  like this to a sandal slipper -A  fiery red  infiltration

contact dermatits stent allergy pci coronary

Imagine  if a stented coronary artery react like this what would be the possible consequence ?

In susceptible  individuals  , can a metal cause

  • Intimal hyperemia
  • Intimal induration
  • Intimo-medial edema  following stent deployment

pci stent coronary angiogram thrombosis des

Why drug eluting stents are more prone for hypersensitivity ?

The answer is simple , while metal allergy is a comparatively rare phenomenon, the drugs we  coat and the polymers used are  many fold likely to result in hypersensitivity reaction.

While  the world is worried  more  about penicillin , sulpha allergy which occurs in 1 in 100000 ,  we tend to ignore the metal and drug  reactions within  the tender coronary arteries.

stent des rejection virmani  pci

What is  the clinical expression of  stent hypersensitivity ?

It is  often a coronary event in the acute phase and restenosis in chronic phase.

How much of acute stent thrombosis is related to stent allergy mediated reaction ?

The exact incidence  will  never be known. It could be high. Whenever a sudden unexpected early stent occlusion can be a suspect .

Is stent allergy a local reaction or systemic reaction ?

It is most often local .The drugs the stent elute can elicit a systemic reaction occasionally.

So what can be done to prevent this complication ?

Drug companies in it’s  package regularly  include the warning  message ! What does it imply to have a caution  on the covers ? .This warning simply represent about our ignorance in this issue. We presume it is a minor problem.

pci stent thrombosis stent allergy metal

Questions unanswered

  1. How does a cardiac patient knows whether he is hypersensitive to stainless steel or nickel ?
  2. Is it practical to have a stent allergic test in every patient before PCI ?
  3. Is routine administration of corticosteroids for few days after PCI an answer ?

Reference

R.Virmani , circulation 2004

http://circ.ahajournals.org/cgi/content/full/109/6/701?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=stent+%27allergy%22+&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT

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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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                                                    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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