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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.

 

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.

Conference bulletins

dr-venkatesan-e-poster

E-PosterPresentationSat10thDec csi cohin 2016

Session – Preview 

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

Syncope and seizure are most dramatic symptoms that rarely fails to call the attention of the patient and family.Syncope is primarily evaluated at medical or cardiac units. However ,when syncope presents as convulsions (often It is ! ) the patient lands up in a Neuro unit as a case of epilepsy.Some how, many of them are prescribed anti convulsants without being evaluated for what triggered the seizure.

heart_and_mind

Cardiac seizure and Neural syncope : Require a balanced approach ! (Image courtesy http://3.bp.blogspot.com)

Real life experience now suggest, a bothering  number of patients in epilepsy clinic might harbor a primary cardiac disorder in the form of either brady or tachycardia which is often inherited due to defect in ion channels of cardiac cell.

The issue is two fold. 

  • Cardiac patients mis-diagnosed as seizure
  • Primary seizure patients suffer a cardiac death (as seizure induced arrhymias or acute pulmonary edema )

Incidence of sudden cardiac death in patients with seizure disorder though rare is being increasingly recognised. Mechanical problems like valvular Aortic stenosis can also result in syncope followed by seizure.

Final message

Cardiologists do have a major role these situations.It may be wise to advice basic cardiac work up in  every seizure disorder.  As we are beginning to understand the neurogenic triggers in sudden cardiac deaths , the need for Neuro-Cardiac units is real.(Some of big university hospitals do have such departments)

Reference 

1.Zaidi A1, Clough P, Cooper P, Misdiagnosis of epilepsy: many seizure-like attacks have a cardiovascular cause. J Am Coll Cardiol. 2000 Jul;36(1):181-4.

2.Leestma JE, Annegers JF, Brodie MJ, Brown S, Schraeder P, Siscovick D, et al. Sudden unexplained death in epilepsy: observations from a large clinical development program. Epilepsia. 1997 Jan. 38(1):47-55.

3.Kloster R, Engelskjøn T. Sudden unexpected death in epilepsy (SUDEP): a clinical perspective and a search for risk factors. J Neurol Neurosurg Psychiatry. 1999 Oct. 67(4):439-44

4.Leestma JE1, Walczak T, Hughes JR, K A prospective study on sudden unexpected death in epilepsy.Ann Neurol. 1989 Aug;26(2):195-203.

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 ?

Secondary collaterals in stroke

There is one more collateral system that connects extra cranial branches of carotid to intra cranial  circulation though Opthalmic artery and leptomeningeal collaterals .This could help prevent or mitigate cerebral Ischemia . A rare review about this important concept worth reading for both cardiologist and neurologists( David S. Liebeskind Collateral Circulation  Stroke. 2003;34:2279–2284)

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

How do you evaluate the success of thrombolysis or primary PCI  ?

If you say its coronary angiogram and the final snapshot  of  TIMI flow , you need to read further. If you thought its actually the quantum of ECG ST regression . . . great ,  you can exit this page  with credits.

CAG  may not be the gold standard in defining PCI success , it just tells you whether IRA is patent or not .Instead , the good old ECG tells you about whether  the myocardium is successfully reperfused or not .  TIMI flows are simply not good enough to identify  adequacy of  myocardial reperfusion .

By the way ,  who is telling this  ?

knowledge-2

It appears there is only a  narrow gap between Ignorance and Knowledge !

That’s what the simple message I got  from this landmark study  published in year the 2000 in JACC by Shah.A in the thrombolytic era.The Importance of this paper  has far reaching consequences (If and only if we are  willing to accept and  understand  the concept and apply  as a whole in PCI era )

While success of thrombolysis is faith fully subjected to  the acid tests  of myocardial perfusion , primary PCI is rarely ever assessed in terms of  ST segment regression.

What is the next logical step this study should lead  us to ?  

I think I am not provocating  , . . How to  get rid of the prevailing practice of jacking up the success rate of primary PCI  ? ( Conveniently,  Ignoring the echo detected significant LV dysfunction on follow up ) Mind you, this has resulted in  creating a new crop of patient sub group called  “Angiographic success and myocardial failure”

Reference.

Dear colleagues , please go thorough this article . Its from the thought leaders , Duke University ,North Carolina. I would argue the cardiology fellows to discuss this paper in detail in their  journal club as “classic paper”  till they  completely understand the conclusion .Though its  done with GUSTO 1 data  in primarily  lytic population,  its  conclusions are very much valid as an assessment tool  in reperfusion by any means.I am afraid, even 16  years after this paper  got published ,the truth has not penetrated to the targeted population within the cardiology community.

Prognostic implications of TIMI flow grade in the infarct related artery compared with continuous 12-lead ST-segment resolution analysis. Reexamining the “gold standard” for myocardial reperfusion assessment. Shah A1, Wagner GS, Granger CB, J Am Coll Cardiol. 2000 Mar 1;35(3):666-72.

Bedside wisdom

We have been  using unfractioned Heparin for long , and its  is better than any other anticoagulants  in ACS . . . 

Our observation shows that Streptokinase has distinct advanatge over Tenektepelase as it works longer duration  . . .

My experience  says Diuretic and beta blockers  are still good as first line therapy for Hypertension  . . .

Mind you , there are infinite  number of such wisdom in every sub specialty of medical field.

However , the typical response from any  modern scientific intellect would be . . .

Stop it . . . Its old  stuff folk  , What does the current data say ?

medical-data-ethics-futility

Common uttering  in scientific forums,

Is there data backing up your  treatment modality ?

Is there sufficient data ?

Come’on , grow up , don’t talk about experience in a scientific forum . . . come out with data man !

No one seem to care the quality of the data . Every one bothers  about the quality of the Author and Journal instead  .  if its X Y Z its ok If its A B C no its not acceptable data.

Probably , Data is most misused word in medical science.

In scientific world,  “unpublished sense” goes straightway to  dustbin ,while we have so many avenues for the  published nonsense to  be celebrated (Still, bulk of guidelines in cardiology is backed up by Level C evidence which means experience  of experts !)

By the way what do we mean by data ?

Its organised collection of genuine scientific information , that’s post processed ,  follow it up with sound inference and faithful questioning and debate that should ultimately end up as  “clinical  application” in patient domain for consumption.(No prizes for guessing , whats happening in real world !)

OMG, give us back that elusive Common sense . . . which  I  think we  lost some time  at the turn of this millennium  !

Wrong or useless data : Who will recall ?

Once applied to patient , these data is  to be scrutinized and monitored . If we find a study conclusion  and reality does not match , we  need to stall the data from adversely  exploding .Every stake holder should have the power to do it. There have been instances a treatment modality got banished in one country is legally permitted in other country knowing fully well the futility.

Final message 

Modern scientific Data* is not God sent. Its  created , synthesised and disseminated in various mind factories. All you require is , backing up with some pioneering journal publication with huge impact factor.It’s not really blasphemy to question things which doesn’t make sense .Unfortunately , wrong data can be tackled only with further data .(There is no other means I guess !)

When does “good common sense”  become hard data and evidence ?

Its the act of publication , so  please guys whenever you  find some contamination  in so-called scientific data  please post here.  To begin with I am registering a new Journal  “Commonsense journal in cardiology”

*Please note, data is not a bad word as this write-up  seem to suggest.Naturally occurring , epidemiological and  observational data about diseases are the foundations for medical science .The issue become murky when few motivated humans play brutal  games at the sensitive  interface between science and truth.

It should be acknowledged , there is a distinct risk  of  this fight against falsehood end up in blocking  true progress  of science . Still , Homo sapiens  are (believed to be !)  intelligent enough to differentiate good from bad , that’s the reason God gave us the sixth sense !

Link to Lown Institute (Started by Cardiologist and Nobel peace prize  Laurate Dr Lown who strives hard to pursue this goal)

Further reading :  Scientific Reversals in cardiology