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Oh , it’s a well recannalised IRA  and its flowing TIMI 3  as well.  Now, what shall we do sir” ?, An apparently worried senior resident queried after a second look at the images from a 8 hour old STMEI .Why you sound unhappy  man ?  As if recanalisation is an untoward event” ! I teased my resident !
and went on to ask . . .

What we mean by recannalised  IRA ? (Recan-IRA)

  • It is akin to natural or pharmacological angioplasty (or combination of the two )
  • It can be complete or incomplete from the IRA perspective.
  • It can either result in partial or fully salvaged myocardium.
  • It should be understood even a 30% recanlisation can result in TIMI 3 flow and result in near complete salvage
  • Even a 90% recannalisation may not accrue the same benefit if it has happened late. So its all in timing
  • Spontaneous recannalisation can some times even be  superior  to thrombus aspiration . However , some degree of residual thrombus would be present in most
  • Residual plaque burden is also an important factor that will decide the extent of angiographic recannalisation.
  • Some times the recannalisation  will make the vessel near normal with only luminal  irregularity
  • IVUS/OCT may provide accurate assessment of Recan-IRA , it’s is not logistically acceptable in STEMI setting.
  • After listening to my briefing on recannalised IRA , the fellow looked more confused than before. He bothered to ask again , what am I supposed to do once a well recannlised IRA is detected ?  Should I intervene or not ?

The term recanlised IRA generally convey a hemodynamic  meaning for a successful  early (natural plus or minus pharmacological ) reperfusion .If every parameter is fine , and the lesion is not significantly obstructing better to pause any further procedure ,  as consequences of deploying  stent in a well recannalised segment is not yet clear with a stro ng trend towards harm .The decision is to be taken on individual basis with reference to  symptoms, stability ,  residual ischemia and quantum of incomplete salvage and lesion morphology .

If you believe ,a spontaneously recannalised  IRA has provided a TIMI 3 flow , it is equivalent to well done job of natural thrombus aspiration by  a hidden hand and catheter . Consciously respect that .Most cardiologists would have  realised atleaset once ,  that any aggression on a God handled IRA can be counterproductive !

Is there a non academic angle to this issue ?

Undoubtedly yes , strangely  inspite of a positive phenomenon for the patient , recannalised IRA leads to a difficult debate  in cath lab .Suddenly , the  entire collective scientific wisdom of the cardiologist is put into a stress test. There is direct fight between reality , expectations .True patient benefits , obligations to hospitals , the parasitic  relations with device industry , do have a big say !

Final message

Practicing cardiology is simple , but when scientific and non scientific realities of life are in direct confrontation with patient welfare it becomes a huge struggle and only a determined few can win over this infinite fight against conscience !

Mohandas Karam Chand Gandhi ,  father of my country , India , made these observations in year 1925  about the  fundamental constituents of  violence in society . These words of monumental wisdom came when he was  addressing young Indians in a country- side rally .

mahatma gandhi quotes medical science humanity

Note, his finger points to , what  exactly is relevant to our profession ! He emphasized this  nearly  100 years ago, when medical science was at its infancy .One can only guess what would be Mahatma’s comment about our profession in it’s  current form !

Should we include moral, behavioral and ethical classes  right from the first year of medical  school along with Anatomy , physiology and bio chemistry.Medical council of India obviously need to burn more mid night oil , I wish it happens in my life time. !

 

The correct  answer could be any of the above , depending  upon the level of your knowledge.

Ever since Herrick reported coronary thrombosis as a cause for MI and Davies documented it by angiogram many decades later (1980) ,the fate of thrombus  and the mechanism of its dissolution is the key to our understanding of ACS.

Even though we are now able to take on this thrombus in a direct fight  by aspiration techniques ,still the hematological  aftermath  and the aberrant coronary behavior  can fool us at any time ! The major lesson learnt  in recent times  is the  success of pPCI  is not in clearing the thrombus but ensure it never accumulates again  at the site  in the future .This is why there is whole big industry working on post PCI anti coagulation and anti platelet strategies .

Clinical correlates of poor  perfusion in micro circulation.

Plugging of micro circulation is the most under-recognised  issue.This results in no reflow in acute fashion or LV  dysfunction and micro-vascular angina in long term . Late recovery of LV function is attributed to late clearance of thrombotic debri.

RCA vs LCA thrombus load.

*One interesting observation is RCA thrombus clears more slowly as it has no well formed venous circuits .most RCA blood drains through thebesian veins which traverses  RV  myocardium .this can be hemodynamic hurdle unlike the LCA venous drainage

 

 

 

Here is a  video recipe  !

Please click here to  see more videos from my you tube site

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 . . .

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.

This paper was presented as a poster (Not good enough for  oral ! ) in the just concluded CSI 2016  (Cardiological society of India ) Annual conference at Kochi, India.

dr-venkatesan-e-poster

What constitutes successful  Primary PCI ?   A proposal to include “ LV dysfunction”  as an  essential  criteria !

A  series of breakthrough technologies  in drugs , devices, techniques has revolutionised the management of STEMI in modern times.This  includes various formats of heparin , antiplatelet agents thrombolytics  and coronary interventions.Of all these, primary PCI is considered to be the greatest thing to happen in STEMI care.

The success of primary PCI is currently defined as diameter stenosis less than 30% and TIMI 3 flow on final angiography without procedural complication. True success of reperfusion essentially lies  in the salvage of myocardium and in the prevention of LV dysfunction. In real world scenario we often find a paradox , ie Inspite of  successful pPCI by current definition a subset of patients suffer from significant  LV dysfunction. Surprisingly, LV dysfunction has  never been included in the definition of successful primary PCI .

success-of-primary-pci

In this context we did a reversed cohort  study  of patients with significant LV dysfunction (<40%) following primary PCI to find out possible factors contributing to LV dysfunction.10 patients who had LV dysfunction inspite of successful primary PCI were the subjects of the study. Patients with late PCI  beyond 12  hours were excluded .Echocardioraphy had been done at discharge and 2 weeks after the procedure to assess LV function.

TIMI  3  flow  has been  documented in all  patients at the time of primary PCI.6 patients had undergone pPCI within 6 hours.4 had it by 12 hours. 7 patients had a smooth , fast  pPCI as described by standard protocol.Of these,  2 patients had LV dysfunction inspite of TIMI 3 flow established early.7 patients 3 had complex angioplasty with no reflow managed subsequently.One had deferred stenting after 4 days for IRA.Non IRA lesion were also  tackled in two.

We also confirmed  there is no linear no correlation  between TIMI flow and  subsequent LV function .This becomes vital as time and again we are seeing PCI reports with successful TIMI 3 flow only to find  weeks later  thinned scarred ventricle. Time to reperfuse with anticipated and unanticipated procedural delay  was also  a critical  factor.

However, its clear the  incidence of significant LV dysfunction inspite of  timely, and apparently smooth  PCI is real .Why this happens is beyond the current reasoning. A scientific basis for  individual myocardial sensitivity to ischemic time is yet to be found. (Dynamic host dependent time window ?)

Meanwhile , It seems prudent , we should awake to a harsh reality of practicing coronary care  with a seemingly incomplete criteria for success of pPCI . Its proposed,  an  acceptable levels of  “LV dysfunction at discharge ” (It could be > 50 %) as an essential criteria  to define the success of pPCI  .Custodians of STEMI care should  immediately rectify this glaring omission. This will dramatically impact the current  outcome analysis of STEMI and help Improve the quality of care.

Medina classification  is the most popular angiographic classification  of bifurcation lesions based on the presence or absence lesions at the three levels  of branching  (0,0,0 ) to (1,1,1). The popularity of this scheme is essentially due to its simplicity.

It can further be subdivided according to angle and size .Though there are three angles possible it is the angle of LM with LCX that matters most.

T shaped  left main. Angle of LM-LCX is around 90 Degrees

Y shaped left main. Angle of LM- LCX is > 120 Degrees

Three types of Y according to size of branch vessel size.

Y1 Large left main divided two equal LAD, LCX.

Y2 Left main and one of its branches are equal

Y3 All three are equal diameter.

Here is a series of  lectures on left main (Probably the best I guess  !)  from Dr.Boris Varshisky ,Hadassah University hospital  Jeruselam.He critically discusses about the   nuances of left main disease from pathology, technical and therapeutic considerations.

Spend some time on these videos , you should be able to learn about

  • Distribution of left main disease
  • The complexities in defining the true shapes of of left main ostia .(Ostial sharing between LCX and LAD ?)
  • Lesion based strategy
  • Carinal shift vs plaque shift
  • Stent sizing in Y 3 left main

and much , much  more !

We know,  classical Atrial flutter (Also referred to as typical /Common AF) records  saw toothed F waves  due to continuous atrial electrical activity across a macro- reentrant circuit within right atrium.

Though this  saw tooth pattern is easily recognised , it’s often difficult to say  whether the saw is facing upwards or downwards ?

ie  Is the flutter waves are inverted or upright ?

The general rule is the shallow stroke (one with a lesser slope) is to be termed  as antegrade  / initial deflection that will determine the direction of flutter waves.

mechanism-of-inverted-flutter-waves-in-atrial-flutter-saw-tooth

This is because , the forward limb traverses the slow path  of the circuit namely the cavo-tricuspid Isthmus, it then ascends up in the inter atrial septum (There by inscribing inverted F  waves  in leads  2,3,aVF .The return circuit  is relatively fast,  crossing the antero -lateral   free wall  right atrium and hence the later half saw tooth has a  sharp deflection )

In Reverse typical flutter  the flutter waves are upright (with a shallow slope ) in inferior leads but still uses the cavo- tricuspid Isthmus

* Note: In lead the polarity of F waves in V1 it will be opposite of that of inferior leads.

mechanism-of-flutter-wave-upright-or-inverted

Why should we bother about direction of flutter waves  ?

It may not be important for those hifi EP guys who can ablate complex arrhythmia with intra cardiac GPS catheters and accurate electro anatomic mapping system. Still , the  surface ECG always help us understand the basic circuits of flutter.

Reference

atrail-flutter-review-best

Reverse typical flutter should not be confused with atypical flutter where typical saw tooth waves are uncommon.The later group is termed as atypical atrial flutter that arises from various other focus including left atrium.

Critical multivessel CAD is commonly confronted by cardiologists .These patients either receive multivessel stenting, CABG, with or without optimal medical management(OMT) !

CABG is always done with intention of  complete revasularisation  for all significant lesions. Comprehensive  multivessel PCI though feasible is not practiced widely.Considering the diffuse nature of CAD no treatment is complete except probably intensive medical management.

As of now , addressing only one (or two ) critical lesions in a triple vessel disease by PCI though appear attractive and logical is considered unscientific.Guidelines are not clear in answering the issue.

multivessel-pci-ptca-courage-trial-syntax-cabg-freedom-bari-acc-aha-guidelines

In a triple vessel disease with a critical LAD lesion,  

Shall we do PCI for LAD and medical management for lesions in RCA or LCX  ?

How about this coronary wisdom  “While medical therapy can take care of less tighter lesions , only critical lesions need catheter based Intervention”

In fact, in STEMI setting we do apply this logic of  targeting one lesion (IRA) at a time. Why not in chronic coronary setting ? There are significant  pros and cons for this approach.While, most 0f us will go with the logical herd,an unique  paper by Mineok  asks us to think again(American Heart Journal, 2016-09-01, 157-165)

How do you define the completeness of revascularization? Is it not emprical ?

We know medical management has well documented advantages in chronic CAD. while multivessel stenting has its own hazards.Hence limiting the time spent within the coronary artery and reducing total stent length should be one of our important goals.

A mini quiz  . . .

How often you have left a fairly significant lesion (attending only the critical lesions )  in your practice ?

What do you think will happen to those non critical lesions  in the long run  ?

Do you believe earnestly drugs can take care of these lesions ?

Forget the science . Whats your experience and  gut feeling ? 

Do you agree , even surgeons do not always do a complete revascularisation either intentionally or for technical reasons ?

Finally ,why we are still  hesitant to call intensive medical therapy as a  “Revascularisation  equivalent”  inspite of valid proof for improved functional class, symptom relief , regression of atherosclerois , collateral preservation and improved microcirculaion.

Final message 

I would say , the science of coronary revascularisation in chronic CAD is stranded at a confused cross road even after three decades of aggressively grown interventional cardiology .At any given point of time medical  management can give a tough fight to catheter  based intervention in most stable IHD.

Hybrid therapy doesn’t always mean combination of PCI and CABG. Judicious mix of PCI and medical therapy is also  a hybrid modality that can bring CAD burden effectively in a meaningful fashion with less metal load.   If you can convert a critical triple vessel disease to non critical DVD or SVD with a single stent it should be welcomed without prejudice. 

With a section of cardiac scientists are in hot pursuit for a completely  bi0reabsorbable stents , let us adopt this “Minimalistic PCI approach” in multivessel CAD, till the time  we reach the “dream the end point” of modern coronary care , ie to  get rid of stent altogether by biological cure for atherosclerosis.

Reference

1.Mineok chang, Jung MinAhn, Nayoung  complete versus incomplete revascularization in patients with multivessel coronary artery disease treated with drug-eluting stents Kim,American Heart Journal, 2016-09-01, 157-165,

 2.Tamburino C, Angiolillo DJ, Capranzano P, et al: Complete versus incomplete revascularization in patients with multivessel disease undergoing percutaneous coronary intervention with drug-eluting stents. Catheter Cardiovasc Interv 2008; 72: pp. 448-456

3.Wu C, Dyer AM, King SB, et al: Impact of incomplete revascularization on long-term mortality after coronary stenting. Circ Cardiovasc Interv 2011; 4: pp. 413-421

4.Gao Z, Xu B, Yang YJ, et al: Long-term outcomes of complete versus incomplete revascularization after drug-eluting stent implantation in patients with multivessel coronary disease. Catheter Cardiovasc Interv 2013; 82: pp. 343-349

5.Ong ATL,Serruys PW. Complete revascularization: coronary artery bypass graft surgery versus percutaneous coronary intervention. Circulation. 2006; 114: 249255

If you think , the  various appropriate use guidelines for cardiology practice are collection of great scientiifc truths , beware . . .many  of them hide behind semantics.  (After all , English is an unique language one can play  with it !)

Is it not funny , to note a  recommendation  that goes with a caption “may be appropriate” conveys exactly the same meaning as “may not be appropriate” as well .

Here is a rare article which tries to expose the importance of  linguistic Interventions in cath lab that can Impact the patient outcome for good or bad.

http://www.invasivecardiology.com/articles/%E2%80%9Cmay-be-appropriate%E2%80%9D-pci-ambiguities-appropriate-use-classification?inter_email=alNyWXNEY3VFR3RzZEM2b3hHRjVseDIzWjlCdkN1Snp2MDlNbnR5RkVacz0%3D

In early days of  medical school we were taught there is an important vascular grade separator in the base of  brain .God  would not have created this circle (of Willis ) without any purpose  , he must have designed it for a reason.

circle of willisHow good is the circle of  Willis to prevent a stroke ?

Unfortunately , we have not answered  this in detailed manner . Obviously  it can’t prevent all strokes however , it is strongly  believed it can  abort  many of  them .My guess would be but for its presence many of episodes of TIA, syncope ,near syncope would end up in stroke with various degree of deficit.

The other factor that tests the efficiency of circle  of Willis is the acuteness of the vascular insufficiency.Chronic carotid occlusion  as expected are well  tolerated . We failed to respect  this natural hemodynamic  sharing  and indulged in so many  unilateral carotid interventions with dubious results .

Here is a paper  with fresh  knowledge from Dr  Seemant Chaturvedi ,  Miamai , Florida .Hats off to the authors.

Are the Current Risks of Asymptomatic Carotid Stenosis Exaggerated?Further Evidence Supporting the CREST 2 Trial  Seemant Chaturvedi,  Ralph L. Sacco,JAMA Neurol. Published online September 21, 2015.

Internal carotid artery (ICA) occlusion when occurring in a chronic fashion  could be as benign as a small peripheral vessel occlusion .(Of course they can be symptomatic)

For all those patients with unilateral total carotid disease , let us thank the “circle of Hope” which if regulated by God whom should we fear ?

Further reading

carotid stenting crest 1 crest 2 ACAST ACSE CEA

cartoid stenosis current management stenting

http://www.amazon.com/Carotid-Artery-Stenosis-Treatments-Neurological/dp/0824754174

DAPT -Dual anti-platelet therapy has become  a standard in many clinical situations of CAD.There has been significant confusion about ,Indications, best combination, duration of DAPT, withholding of DAPT, conversion to MAPT (mono) etc.The  JACC september 2016 issue  brings much needed clarity  on this issue.

Link to key summary from NEJM journal watch.

http://www.jwatch.org/na42407/2016/09/28/update-dual-antiplatelet-therapy-patients-with-coronary?

Full text guideline