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” 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

It is often said life is a cycle , time machine rolls without rest and reach  the same  point  again and again . This is  applicable for the  knowledge cycle as well .

We  live a life ,  which is infact a  “fraction of a time”(<100years) when we consider the evolution of life in our planet for over 4 million years.

Man has survived and succumbed to various natural and  self inflicted diseases &  disasters. Currently,  in this  brief phase of life  , CAD is the major epidemic , that confronts  modern  man.It determines the ultimate  life expectancy . The fact that ,  CAD is a new age  disease   and  it was  not  this rampant ,   in our ancestors  is well known .The disease has evolved with man’s pursuit for knowledge and wealth.

A simple example of how the management of CAD over 50 years will  help assess the importance of  “Time in medical therapeutics”

  • 1960s: Life style modification and Medical therapy  is  the standard of care in all stable chronic  CAD The fact is medical and lifestyle management remained the only choice in this period as   other options were not available. (Absence of choice was  a blessing as we subsequently realised  ! read further )
  • The medical  world started looking for options to manage CAD.
  • 1970s : CABG was  a major innovation for limiting angina .
  • 1980s: Plain balloon angioplasty a revolution in the management of CAD.
  • 1990s: Stent scaffolding of    the coronaries  was  a great add on .Stent  was too  dangerous  for routine use  was to be used only in bail out situations
  • Mid 1990s : Stents  reduced restenosis. Stents are  the greatest revolution for CAD management.Avoiding stent in a PCI  is unethical , stents  should be liberally used. Every PCI should be followed by stent.
  • Stents have potential complication so a good luminal dilatation with stent like result (SLR)  was  preferred so that we can avoid stent related complications.
  • 2000s: Simple  bare metal stents are not enough .It also has significant restenosis.
  • 2002: BMS are too notorius for restenosis and may be dangerous to use
  • 2004 : Drug eluting stents are god’s gift to mankind.It eliminates restenosis by 100% .
  • 2006:  Drug eluting stents not only eliminates restenosis it eliminates many patients suddenly by subacute stent thrombosis
  • 2007 : The drug is not  the culprit in DES it is the non bio erodable polymer that causes stent thrombosis. Polymer free DES  or   biodegradable stent , for temporary scaffolding  of the coronary artery  (Poly lactic acid )  are likely to  be the standard of care .
  • All stents  are  potentially dangerous for the simple reason any metal within the coronary artery  has a potential for acute occlusion.In chronic CAD it is not at all necessary to open the occluded coronary arteries , unless  CAD is severely symptomatic in spite of best  medical therapy.
  • 2007: Medical management is superior to PCI  in most of the situations in chronic CAD  .(COURAGE study ) .Avoid PCI whenever possible.
  • 2009 :The fundamental principle of CAD management  remain unaltered. Life style modification,  regular  exercise ,  risk factor reduction, optimal doses of anti anginal drug, statins and aspirin  is the time tested recipe for effective management of CAD .

So the CAD  therapeutic  journey  found  it’s  true  destination  ,  where it started in 1960s.

Final message

Every new option of therapy must be tested  against every past option .There are other reverse cycles  in cardiology  that includes the  role of diuretics  in SHT , beta blockers in CHF etc. It is ironical , we are in the era  of rediscovering common sense with sophisticated research methodology .What our ancestors know centuries ago , is perceived to be great scientific breakthroughs . It takes  a  pan continental , triple  blinded  randomised trial   to prove physical activity is good  for the heart .(INTERHEART , MONICA  studies etc) .

Medical profession is bound to experience hard times in the decades to come ,  unless we  look back in time and “constantly scrutinize”  the so called  scientific breakthroughs and  look  for genuine treasures for a great future !

Common sense protects more humans than modern science and  it comes free of cost  too . . .

I was recently asked to suggest a topic for debate on STEMI in  a major Indian cardiology conference. I wished , this is what we  should be mulling  over, with a set of  virtual  guest lectures and special invitees from heaven ! Plenary  session : State of the Art  STEMI care             Time :  11.AMSpeaker : Dr Hippocrates Topic : Aren’t  we erring   on either side of the  Noble profession ? Moderator:  Dr. William Osler Chairperson :  Dr .Harvey Cushings, Dr,Sir Thomas Lewis ,Dr Paul Wood , Excerpts : “While , vast number of  our country-men’s  culprit artery doesn’t even get that  mandatory  Aspirin on time . . . an urban rich  man’s  distal non-culprit artery  is decorated with a fancy  bio-vascular scaffold making  that innocuous lesion vulnerable in the process as well !  Aren’t  we erring   on either side  in the  Noble profession ?

Atrial fibrillation is the most  common arrhythmia we encounter in clinical cardiology .Ironically it is  uncommon during ACS and extremely rare in association with UA/NSTEMI. Surprisingly , an entity ” Ischemic AF” is not to be found in cardiology literature.

The incidence of AF in STEMI is less than 5%. Occurs more often due to factors other than primary ischemia of atrial musculature. Of-course , AF in association with Infero posterio MI and RVMI is an important trigger for AF.LCX disease is more often associated with AF as it gives up a consistent branch to left atrium.

Though it is tempting to implicate ischemia as a trigger for AF ,most often it occurs , in elderly ,associated COPD ,hypoxia preexisting atrial disease .Acute elevation of LVEDP and stretch of left atrium could be a more logical mechanism.

Hemodynamic impact

  • AF can bring down the blood pressure.
  • Worsen ischemia by increasing the MVO2
  • Could be very destabilising in RV infarction
  • Surprisingly it is well tolerated in many STEMI patients.

AF in STEMI- Is it an emergency  ?

It would appear so. But , if hemodyanmicaly stable one need not panic.Many times they are transient .Correcting  hypoxia, optimizing beta blocker would help.

Role of DC Shock  , Precautions before shocking  & Post shock events

  • DC shock is done only if there is hemodynamic instability  or ongoing ischemia .(Very difficult to rule out the later )
  • Mural LV clots can form even within 24 hours and DC shock embolic strokes may ensue .
  • Hence it is mandatory to do an echocardiogram prior to shocking.

Drug of choice

  • Betablocker
  • Class 1c -Flecanide.
  • Class 3 -Amiodarone./Ibutilide/

Role of Digoxin

There used to be a concern about usage of Digoxin in the setting of ACS as it pro-arrhythmic , but it remains useful in the management of AF .There is no other  anti-arrhymic drug available to control, the heart rate without depression of  the LV  function

Rate control vs rhythm control

Always aim for rhythm control in the setting  of ACS.Rate control is may not be a  logical concept in acute settings though Amiodarone does both.

Wide QRS Atrial fibrillation

As we know , AF in STEMI can conduct with aberrancy , and we have a traditional teaching all wide qrs tachycardia are VT in the setting of MI making our patients statistically vulnerable.

After all , both entities lack discernible p waves. At high rates it may be difficult  to identify irregularity  RR interval. However , one would shock such patients  and both AF and VT would respond .All is well that ends well.

Summary

AF during STEMI is a risky arrhythmia and needs urgent intervention , but one need  not be alarmed .There is a set of protocol . Only hemodynamically unstable AF require DC shock .Many times it is just transient.There has been instances of  physician panicky that has resulted in more adverse events .

Cardiologists do magic inside the human coronary artery , that too in a  live beating heart , unlike the surgeons.Blocks are removed , holes are closed, valves are inserted ,  scars are burnt, new electrical connections  are laid .They do this with relative blind vision with good degree of success. Still, as we aim for more precise interventions we require excellent imaging  modalities to assist us.

In  PCI of CTO(Chronic total occlusion)   the critical element to know  is  the morphology of the  tissue plane , what  exactly  we borough ?  as we navigate  through complex, often hard shapeless tortuous tissue tunnels  . Our patients will be  surprised to know we are currently doing this with our eyes shut. If only we have a camera guide in the tip of the wire it give us tremendous advantage .

CTO pathology

The CTO morphology .Image source : Kenichi Sakakura ,Eur Heart J. 2014 Jul 1;35(25):1683-93.

The exiting IVUS technology can only look sideways . Now a new vision is added by annular array of transducer at tip with CMOS sensor .The technology is just coming out it would be  use for us in the near future .

Anatomy of the forward looking ultrasonic eye

ivus forward loooking cto intervention

Reference

In this era of synthesized evidence base,  one of my  intellectually aberrant  student asked  How can we indulge in  a popular coronary procedure   with  class 1 indication backed by level C evidence  ?   (As defined by  the seemingly invincible  guideline committee  of various  International cardiology organizations .)

medical ethics silence guidelines

I told him ,

  • Institutional protocols are to be followed
  • Guidelines are to be respected
  • Recommendations are to be considered
  • Please be reminded  all of the  above can be rejected  outright !

Finally , realise  Individual  decisions based on sound scientific understanding with zero non academic intrusions  will be revered forever !

*Caution : If you  think  you haven’t  yet reached that the level of  individuality , come what may ,  you are  expected follow these  advisories  which are primarily aimed at  providing quality care and  you will be pardoned of any adversaries as well  !

ecg pulse deficit biventricular bigeminy

 

Answer : Most probably  B .

What we feel in peripheral pulse ,  is one weak and the one strong beat in sequence .The later is due to post VPD potentiation. Since there is a compensatory pause , ECG rate (Number of QRS complexes /mt)  and pulse rate are same .

Ironically , heart rate and ECG rate are not same as VPDs impact mitral valve more than aortic valve  and cause additional  S 1 than S 2 making heart rate considerably more than pulse rate and logically it must be  double the pulse rate . This may be difficult to  appreciate by auscultation, but can be documented by phono-cardiogram or by M mode echocardiogram.

 

 

 

The gradient across coarctation  is not  simply (& solely ) determined by degree of obstruction , as one would believe.Understanding the hemodynamics and various factors that can influence the gradient is essential .Relieveing the  obstruction /gradient by stent or surgery  may not be synonymous with successful treatment as we understand now the entire aorta right from the root to abdomen can influence the gradient ,along with systemic factors.We also know , some of these patients harbor histological abnormalities in the entire stretch of  Aorta  what is  being  referred to as pan aortopathy  , that may influence the long-term outcome.

coarctation gradient collaterals002

A cardiologist  is  a physician who has  trained himself  in a special  way  to deal with any problem of heart.Ironically , it exists only on paper.The field has developed so vast  no one can master everything .There is no such  “Pan or global cardiology expert” .In fact it would be shortly become unethical to try to become one !

Pediatric cardiology  has developed into such a big field , doing a echo in newborn or  infant has become a comprehensive job and  requires  special talent .This unique  and excellent study from Narayana Institute , Bangalore published in the  prestigious Annals of pediatric cardiology   throws up interesting realities about the quality of echo report done by adult cardiologists in children .The error rate  appears  huge and stands at  prohibitive 38%. While many errors were minor , major  were also not insignificant (23%)

pediatric echocardiography by adults cardiologist

With bulk of the pediatric echo  involves  in the critical decision making  process of device closures and interventions the  data required  becomes vital .The commonest cause for  error is probably not due lack of  knowledge and but to due to lack of commitment and  continuous  exposure in doing echocardiograms in  those age group.

While this paper  decently skirts the issue of quality of pediatric echo done in medium sized hospitals without pediatric cardiology service ,I can say the error rates or inadequate reportage could be significant  in such hospitals  with apparently good ranking .

Final.message

Of course ,we have many  adult cardiologist who do  excellent  pediatric work , It looks like , as a general rule  performing pediatric echocardiograms  by non -institutionalized  adult cardiologist  may not be appropriate ! It may be wise for them to avoid doing echocardiogram in small infants with  truly complex disorders (even perceived  complex) till they gain the required expertise and confidence.

I recall an  adverse  issue happened years ago ,  when I had  missed an associated    PAPVC  in ASD that made my surgeon anxious on table .In a country like ours there is no one to audit our work , “our conscience remains the only option” to deliver the best for our patients  especially so, when they are tiny lives in distress.

After thought

Who am I to suggest  who should do echocardiogram ? , after all every cardiologist is licensed  to do that . One simple  suggestion  would be , if  not confident  they can at least mention in their report it is only  preliminary evaluation and need to be followed up with  an expert . I do that whenever its required  and gives me peace of mind as well !

More controversies* to come

Can adult cardiologist do pediatric intervention ?

* Controversy : One of the meaning for this word  is  “It is a thought  process  set into motion , that aids digging up hidden truths ”

Reference

 

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