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Archive for the ‘Cardiology -Therapeutic dilemma’ Category

It was 1912 , Titanic had just sank off the Atlantic . When the world attention was elsewhere , An unassuming young Dr.Herrick J.B silently working in his Michigan lab inquisitively proposed thrombus occluding the coronary artery is the chief culprit in acute myocardial Infarction.It took seven more decades when Davis et all from Glasgow .UK. proved it by doing dramatic angiographic studies soon after STEMI in year 1979.

Now, even after 100 years , we, the confused cardiologists debate endlessly in glamorous global conclaves in exotic locales whether to aspirate these humble looking thrombus, threatening to damage the myocardium with every passing moment !

Why is this controversy ?

My answer

I am failing to understand the concept and the answer is elusive .While every one agrees that thrombus is true culprit, in bulk of the STEMI , still we are not authorised (In an assertive fashion ) either to lyse as first choice or to aspirate as second choice.

It seems vital, thrombus must be tackled vigorously by any means. Drugs,lytics,(Intravenous or Intra-coronary.) by micro and rheolytic catheters .Only documented, flow limiting complex mechanical lesions must be stented. If we are convinced tackling thrombus by mechanical means is problematic (As studies would suggest ) lysis should prevail over aspiration as a routine measure by default isn’t ?

*It’s a been quite a while , the world cardiology community has made it appear thrombolysing a patient who is otherwise eligible for primary PCI ! a “coronary crime*” Ofcourse , I must say , I proudly commit that crime with rewarding results in many MI patients.

*In fact , I would think not promoting or delaying prompt lysis should qualify for the definition.

In the management of STEMI, prehospital lysis followed by a Intensive care in a good coronary care center is best modality.

This doesn’t mean in-hospital lysis is banished. Yes, STEMI is a cardiac emergency , but triaging STEMI patients must be done by scientific means (STEMI risk score) as well with accumulated wisdom .Rush only true emergencies into cath lab. (A best estimate is about 20 % of all STEMI) If we are not able to decide which STEMI will require prompt PCI , it would Imply we need to go back and do once more the basics postings in coronary care of resident days !

An angry counter from a young Interventionist

Only God can tell whether a given patient with STEMI will (or will not) derive maximum benefit from pPCI. We are not yet trained to make that decision by looking at patient and his ECG.So my logic is all STEMIs are equal. I will continue to do emergency angioplasty in all STEMI patients . I expect them blindly to accept all the potential complications arising out of poking the thrombotic milieu in those low risk patients who might have done well with thrombolysis.

Never afraid of challenges. It is like going to war. Casualties are bound to happen.We have enough technology , Imaging , expertise, to tackle all those complex lesions we encounter during primary PCI especially in elderly comorbid patients. We can even do a triple vessel angioplasty , left main etc. Only Yesterday I posted in my nonstop whatsapp group , where I did a dramatic acute angled bifurcation angioplasty for a stable STEMI patient that required a iFR guided jailed side branch assessment and 3d OCT transmitting stunning snaps of fresh thrombus, ending with a semi culotte procedure.The patient is doing well with a Impella 2.5 device and a high frequency ventilator support and my anesthetist has promised me to wean him soon ! I must actually thank his Glo-Health plus Insurance company for clearing the procedure.

An Important tip for complex lesions during STEMI

We need to know there is always a saving grace , if for some reason we couldn’t accomplish PCI due to complexities of the lesion with multiple IRA mimickers. We can always sheepishly thrombolyse these patients inside cath lab . . . a modality just few minutes ago would have been ridiculed with all our vigor to convince the anxious family for a costly Invasive procedure !

Reference

3. Herrick Original paper . https://jamanetwork.com/

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 When half a dozen guidelines from extremely evidence based “Esteemed cardiac societies”  decide to confront an Incomprehensive cardiologist , there is no other way , but to create  a personalised i-Guidelines on STEMI !

*(i-Idiotic)

 

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Cardiologists at confused cross roads !

Perils of  limited Intellect & Infinite greed  

When not so appropriately trained cardiologists  do Inappropriate things “use becomes misuse” . . . then, it won’t take much time for science to become total abuse. That’s what happened with the murky world of coronary stents .No surprise, it’s time to firefight the healers instead of the disease !

Now ,Comes the ORBITA study . Yes , it looks like a God sent path breaking trial that spits some harsh truths not only in cardiology, but also in behavioral ethics .Let us not work over time and hunt for any non-existing loop holes in ORBITA. Even if it has few, it can be condoned for sure as we have essentially lived out of flawed science  for too long  Injuring many Innocent hearts !

ORBITA pci vs medical mangement drsvenkatesan courage bari2d ethics in stenting auc criteria inappropriate coronary stenting placebo effect of stenting acc aha esc guidelines chronic st

Yes , its enforced premature funeral  times for a wonderful technology !

GIF Image courtesy http://www.tenor.com

Meanwhile, let us pray for a selective resurrection of  stenting in chronic coronary syndromes  and stop behaving like lesser professionals !

Postample

Extremely  sorry . . . to  all those discerning academic folks , who are looking for a true scientific review of ORBITA , please look elsewhere !

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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

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Less than a century ago an easy chair  was enough to manage this most important medical emergency of mankind. Of course, at that time mortality of STEMI was estimated to be around 30%.We have since pushed the in-hospital death rate down to less than 10 %  and its around 5-8% currently.(*The lifeless chairs were able to save 70 lives is a different story!)

Heparin , thrombolytic agents, critical coronary care has helped us to achieve this , of course It must be admitted primary PCI also played a small role (at best 1 % ) in our fight against this number one killer.

Now, why not combine  both lysis and PCI ?

The concept of PIA (Pharmaco Invasive approach) came into vogue  primarily for two reasons.

1.If thrombolysis and  pPCI are powerful strategies by individual merits why not combine both and achieve double the benefit ?

2. Since pPCI is going to be a logistical nightmare in most points of care and we can’t afford to lose time . So, let us lyse first and consider PCI later !

Unfortunately medical science is not math .One plus one in medicine is rarely two !

Though , it looks attractive , Pharmaco invasive approach  has its own troubles.Fortunately , most of them are man-made, few are beyond our knowledge though.

Following general rules  may help us

  • STEMI  should ideally managed by early thrombolysis (or PCI) in all deserving patients.
  • Don’t wait for PCI if you think , there will be delay or reduced expertise and poor track record of the center in this modality.
  • Pharmaco invasive  therapy is not a default in all STEMI .Do good quality , monitored  lysis , (Not necessarily new generation thrombolytic .(I prefer one hour sustained thrombolytic regimen , not the hit or miss bolus) .As a learned cardiologist we need to assess individual patients according to the type and risk of MI.Its not wise to blindly follow the guidelines ,because these guidelines , though based on evidence never answers a query in a single patient perspective !

The key “branch points”  in decision making  after lysis

  • Invasive strategy  should begin within one hour if the patient has failed  thrombolysis and has developed any mechanical issues.( Mind you, LVF requires good medical stabilization .Rushing  such patients to cath lab without application of mind can be disastrous )
  • If the Initial  lysis is excellent and the patient is asymptomatic  one need not proceed with invasive limb at all.(A significant chunk of apparently failed lysis by ECG are asymptomatic and comfortable , these are patients require delicate assessment regarding further intervention. )
  • If the MI is large and the clinical  stability is “not confirmed” one may  proceed urgently within 24 h.
  • In any case there is no role for invasive approach after 24 hours* Unless fresh ischemia  suspected to come from IRA or  non IRA.
  • Having  said that, there are many centers that do a diagnostic  angiogram alone just prior to discharge  (48-72h) for risk stratification and then take a genuine call for a possible PCI or  CABG. In my opinion it appears a sensible strategy , though a non invasive stress  test pre/post discharge can even avoid that  coronary angiogram !

One issue with Rescue PIA

Though by current definition  PIA is to be done  3-24 hours , don’t wait for the 4th hour if you have recognized a failed thrombolysis earlier than three hours.( Ofcourse , as the gap between P and I gets too narrowed it may  carry some adverse  effects witnessed in routine facilitated PCI -Refer FINESSE study ) Similarly,there need not be a blanket ban on PCI beyond 24 hours if residual ischemia is active.

Final message

PIA is a dynamic  coronary  re -perfusion strategy . Nothing is fixed in science. . The optimal gap between Pharmaco and invasive strategy  can be anywhere between  1 hour to “Infinitely deferred” depending upon individual risk perception and wisdom of the treating cardiologist.

 

 

 

I

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The ECG changes in ACS are “as dynamic as”  the occluding thrombus.The initial events include  sudden total occlusion, early lysis , trickle of flow, partial re-occlusion , reflow, no-flow etc. The extent of transmural vs sub-endocardial injury, the competing force of re-perfusing and necrotic  wave front, would define  ECG findings making  the ST segment labile in early hours of ACS.This is also the basis of  some cases of  STEMI evolving into NSTEMI and vice versa.

A 65 year old man  presented to with this ECG,

 

img-20160423-wa0012_1.jpg

Does this ECG allow you to go ahead for thrombolysis ? It actually looks like NSEACS with ST elevation in AVr suggesting left main lesion

The initial  diagnosis of  NSTEMI was made , and hence  thrombolysis was not considered. Even as the fellows  were mulling over the diagnosis , we subsequently came to know  there is one more  ECG available taken few hours ago  in  another hospital .

It had something on it ,

img-20160423-wa0009_1_1.jpg

This ECG taken few hours ago , shows ST elevation in 1 and AVL and few VPDS in chest leads unmasks the anterior ST elevation .

The moment we saw this ECG it was decided to go ahead with thrombolysis .The final ECG after thrombolysis with (Streptokinase) showed further stabilization .The question of thrombolysis  in NSTEMI though not indicated in general , in selected  situations we need to Introspect !

img-20160423-wa0011_1.jpg

How to mange  a patient who presents as NSTEMI but had STEMI  few hours ago ?

Four  ways to ponder !

  • This patient should not be lysed  as we have to treat the current event not the past.  ,(Its NSTEMI and no need for lysis) Just heparin,dual antiplatelets .That will do.
  • One can go ahead with lysis as there is evidence for STEMI in prior ECG.
  • There is ST elevation  in AVr even in the second ECG and so you have to thrombolyse !
  • “Come on guys , . . . are you still in the primitive era, of managing ACS in CCU , just forget  the ECG take him to cath lab , suck out all thrombus and deploy a stent and come out”.

* The last one , though appear practical (and most of us would love to indulge ) is an unprofessional way of practicing cardiology.Management of ACS requires sound principles of ECG and its correlation  with the Intra-coronary  and myocardial  pathology.

What happened to this patient ?

He did well, free of angina with minimal LV dysfunction. He was discharged .Will be reviewed two weeks later,for further evaluation.This is typical example of a patient with ACS managed without  even entering cath lab.

Final message

ECG changes are as dynamic as the Intra-coronary blood flow in ACS. Various factors  determine  the ST elevation or depression.While ,thrombolysis is reserved for STEMI,  NSTEMI has little or no benefits to accrue with thrombolysis .However this is applicable only for de-novo NSTEMI  and may not apply for a STEMI in transition into NSTEMI as in the above patient .

 

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Answer  : I guess all mechanisms  contribute.Though E appears unlikely,  its backed by evidence (Ref 5)

Balloon pericardiotomy is done as a drainage procedure in recurrent pericardial effusion. It is is actually a replication of surgical window  by interventional cardiologist.The window not only drains the effusion it also act as a continuous drain. Though the  benefits are real,( In that the pericardial fluid is shunted away from the pericardial space)  the exact mechanism of its benefit is not clear .

By concept , the catheter and  balloon should not cross pleural space , (As pneumothorax may ensue) but still pleural effusion is a common consequence of this procedure .How is this possible ? One probable explanation is,  the pleural space has some hidden communication with pericardial space .The other possibility is, the balloon creates patent tissue channels  in the para-cardiac spaces of mediastinum .The extra-cardiac lymphatics does the drainage job without true shunting  pericardial space into the pleural space..

There is a from Annals of thoracic surgery which specifically   looked  into the  mechanism of benefit of  surgical pericardial window and came to a surprise conclusion that it is not the continuous  drainage (As  we don’t create patent drain ) rather,  the window  somehow helps obliterate  the the peicardial space.(Sugimoto 1990,Annals of thoraic surgery )

Future  Innovation  : A technical add on could be delivering a covered stent across the pericardial space  into  peritoneal space like a VP shunt done by  Neurosurgeons.( If no body has done this I can claim the patent rights !)

The procedure

 

percutaneous balloon pericarditomy

Image used from Daniel A. Jones & Ajay K. Jain, Journal of thoracic Oncology , 2011

Risk of procedure

The procedure carries a definite risk especially  if done in an  emergency fashion. The aim of  procedure is two fold one to drain pericardial effusion second to prevent recurrence of effusion  .Since procedure carries risk its to be performed  only in malignant effusion that are documented to be recurrent.

Surgical vs Balloon window  and other alternatives

Surgical window  creation is well known procedure , ever since Palacios (Ref 1) in 1991 described this per cutaneous approach as an alternative to surgery has become less popular. The risk of anesthesia and co-morbidity makes balloon pericardiotomy attractive. But surgical window creation still may have a role. A video  assisted pericardiotomy by thoracoscopy is also possible .Another option is injecting scerlosing agents into pericardial space .This time tested simple modality probably requires  more attention.

Need for subsequent pleural tapping

It should be realised this procedure may just the shift the  fluid from pericardium to pleural space. Some of them become significant effusion that requires pleural space drainage.

Concern of risk of dissemination of malignancy

Its a real issue , there has been instances of accelerated death after the procedure. Hence this procedure is a trade of  between patient comfort and quality of life with a  potential risk of dissemination impacting  the longevity of life .

1.Palacios IF, Tuzcu EM, Ziskind AA, Younger J, Block PC. Percoutaneous balloon pericardial window for patients with malignant pericardial effusion and tamponade. Cathet Cardiovasc Diagn 1991: 22;244-249.

5.

 

 

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