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Archive for the ‘STEMI’ 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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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.

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100% occlusion of a coronary artery result in STEMI.This includes both thrombus and mechanical component .We are very much blinded till we touch , feel and see the lesion with a wire or IVUS to quantify the mechanical component’s  contribution in the genesis of  STEMI.It is generally believed (True as well ) thrombus is the chief culprit .It can even be 100 % thrombotic STEMI with  just a residual endothelial  erosion and hence
zero mechanical component .However , the point of contention that non flow limiting lesion is more likely to cause a thrombotic STEMI than a flow liming
lesion  seems to be biased and misunderstood scientific fact .

What happens once 100 % occlusion take place ?

Sudden occlusion , is expected to evoke a strong fire fighting response within the coronary artery.The immediate reaction is the activation of  tissue plasminogen system. In this aftermath  few succumb . ( Re-perfusion arrhythmia  generated as VF ) .The TPA system activates and tries to lyse the clot.The volume , morphology, attachment, content of thrombus ,  and the elasticity of fibrin mesh , location of  platelet core would determine the life and dissolvablity of thrombus. Even a trickle flow can keep the distal vessel patent .(Please note a timely TIMI 2 flow can be a greater achievement than a delayed TIMI 3  flow !)

thrombus propgation
What happens to the natural history of thrombus in STEMI ?
Thrombus formed over the culprit lesion can follow any of the following course

  •  Can remain static
  •  Get lysed by natural or pharmacological means
  •  Progress distally (By fragmentation or by moving en-mass )
  •  Grow proximal and and involve more serious proximal side branch obstruction
  • Organise and become a CTO

Factors determining thrombus migration

The interaction between the hemodynamic  forces that push a thrombus distally and hemo-rheological factors that promote fresh proximal thrombus formation are poorly understood. The altered intra-coronary milieu with a fissured plaque covered by  platelet vs RBC / fibrin core,  totally of obstruction,  reperfusing forces , re-exposure of raw areas and  the distal vessel integrity all matters.

While, logic would tell us,  thrombus more often migrates  distally  assisted by the direction of blood flow, an  opposite concept also seeks attention , ie since the blood flow is sluggish  in the proximal (to obstruction site )more thrombus forms in segments proximal to obstruction.

(In fact, its presumed  in any acute massive proximal LAD STEMI , it takes hardly few minutes for the thrombus to  queue up proximaly and  clog the bifurcation and spill over to LCX or even reach left main and result in instant mechanical death.)

What is the significance of length and longitudinal resistance of the thrombotic segment in STEMI ?

If thrombus is the culprit let us get rid of it , this concept looks nice on paper , but still  we don’t  know why thrombus aspiration in STEMI is not consistently useful. We also know little about  the length of the thrombotic  segment .When a guide wire is passed over a STEMI ATO it may cross smoothly like  “cutting a slice of  butter” in some , while in few we struggle and  end up with severe no-reflow inspite of great efforts .Why ?

What is the Impact of distal collateral flow in flushing fresh thrombus ?

The efficacy of collateral flow in salvaging myocardium is underestimated. Distal vessel flow if perfused partially by acute collaterals the thrombus load is not only less it’s soft and fail to get organised early that would help cross the lesion easily.

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A STEMI patient arrives late after 48 hours with chest pain .There is  persistent ST elevation.

What is the likely mechanism of this chest pain ?

  • Index infarct pain continuing . . .
  • Post infarct Angina-IRA territory
  • Re-infarction following intermittent re-perfusion  and re-occlusion
  • Remote  ischemia from a branch of IRA
  • Ischemia from a possible  non IRA lesion in a multivessel CAD

If this patient  comes to a non PCI eligible centre. Will you lyse him  ?

If post infarct angina is  unstable angina  . Isn’t  thrombolysis  contraindicated in UA  ?

How to differentiate Post Infarct Angina from Re-Infarction ?

A very tricky issue indeed.

Unless fresh ST elevation with fresh enzyme peak is documented these entities  cannot be differentiated.

(Even  fresh ST elevation can be related to infarct expansion ,stretch or early acute remodeling.Fresh enzyme  release or new peak  may not represent new infarct always .It can be due to intermittent re-perfusion of IRA .It may  simply represent a  enzyme  flush from the index infarct zone)

What is the practical , realistic , (Unscientific !)  solution  ?

Why break our head ? Never bother to differentiate PIA   from Reinfarction  etc . Let  it  be any thing . Do a emergency CAG .Stent  whichever  lesion looks good  for the same . Of course , make sure he has enough insurance coverage .

 

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This  query often  evokes  confusion  among fellows and General physicians .

              The answer is simple .Yes ,  you can.(With few conditions)

  • Thrombolysis  or PCI  is  done  with reference to  the  presence  or absence of ST elevation and chest pain.
  • If there is ongoing chest pain  and  significant new onset ST elevation  thrombolysis or PCI is indicated whether there is associated q  waves or not.

Clinical situations 

 Ischemic  q waves: Q wave can occur  with transmural ischemia which result in electrical stunning and loss of R waves . (Many of them  regenerate this R within few days after STEMI ,  indicating the q  waves can be  ischemic  in origin)

Reinfarction : Patients with  old  MI can develop fresh ST elevation  in q leads due to tachycardia and dyskinetic infarct segment .This group  of patients  should be carefully evaluated before labeling them as  re-infarction

* q RBBB in early hours of  anterior STEMI is fairly common which  may revert later. qRBBB is not a contraindication for re-perfusion .

Final  message

Presence of q waves does not  imply one should not  entertain  thrombolysis or PCI .The decision  to reperfuse  , rather  goes with  presence of  chest pain , ST elevation and  of course  within the  acceptable   time window!

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.The  forgotten “Gem of a study” from lancet 2002 .

The fight between Primary angioplasty and thrombolysis was actually over in 2002 itself. But the cardiology community failed to ,( rather reluctant ) to accept the truth. The issue is being dragged without any useful purpose (for the patient !)  still trying to keep up the non existing superiority of pPCI.

A bolus thrombolytic agent (TPA/RPA) or even streptokinase  can do almost the same if not better than a highly complex procedure called  Primary PCI with lots of logistics issues and most important an unacceptable early procedure related  hazard.

Timely lysis can kick pPCI out of the ring . . . in three aspects with 100% certainty !

1.If symptom to TIMI 2/3 flow in IRA is the true parameter of success .pPCI can never ever come closer to pre hospital lysis.

2.The poor lytics do not differentiate in the efficacy . It simply acts whoever administer it. While results of pPCI are never reproducible and lots of expertise involved.

3.Thrombolytic agents never need to bother  about the complexity of lesions , (or  where is the IRA dilemma ? Is it a CTO or ATO confusion etc ) for the simple reason it doesn’t need to think before acting. It does its job fast.

What did CAPTIM prove ?

  • It proved pPCI has no mortality advantage over pre hospital lysis.
  • Perhaps the most Important conclusion from CAPTIM is pre hospital lysis significantly reduced  number of new onset cardiogenic shock . This alone nullifies the self inflicted pseudoscientific delay wasting the golden hour in the process ! (By the way who fixed the arbitrary acceptable delay conferred to pPCI of I hour .The whole evidence base for this delay to be scrutinised in view of CAPTIM !)

Final message

It is an irony,  a simple intravenous push of a drug (Thrombolytic agent)  very early after an STEMI can save many patients and reduce complication rate .But because it is simple ,it is considered  inferior .

Probably the only role for pPCI is high risk complicated STEMI at presentation or after an attempt of lysis has not stabilised the patient.(Where its referred to as Pharamco Invasive strategy )

2018 update

This post was originally posted in 2008. Now as I see this in 2018 . It is shocking  to know we haven’t  learnt any lesson from this study for 16 years since its published.

In this era of medical  commerce and  simple ,cheap ,and effective treatment can never compete with  sophisticated , glamorous , less effective  treatment modalities !

Read the full version of CAPTIM and comments

Comparison of Angioplasty and Prehospital Thrombolysis in Acute Myocardial Infarction (CAPTIM) study group, are published in the September 14, 2002 issue of theLancet.

Primary angioplasty “no better” than prehospital fibrinolysis: CAPTIM

London, UK – In a finding that would appear to go against the swelling tide of support for primary angioplasty as the treatment of choice for acute MI, investigators comparing primary angioplasty with prehospital administration of alteplase with rescue angioplasty have concluded that the 2 strategies are comparable. The results, from the Comparison of Angioplasty and Prehospital Thrombolysis in Acute Myocardial Infarction(CAPTIM) study group, are published in the September 14, 2002 issue of theLancet.1

“Our findings indicate that primary angioplasty is no better than prehospital fibrinolysis followed by transfer for possible emergency coronary angioplasty in patients presenting within 6 hours of an acute myocardial infarction,” the researchers, led by Dr Eric Bonnefoy and Dr Paul Touboul(Hopital Louis Pradel, Hospices Civils de Lyon, Lyon, France), write.

However, they point out that cessation of funding during the trial resulted in a lower-than-expected enrollment, 840 of 1200 planned patients, reducing their statistical power. “The CI (confidence interval) for the primary end point shows that there could be a real difference in the treatment effects,” they write.

Still, the researchers feel their conclusion is valid. “This was and is for us a very pragmatic question for our care system in France,” Bonnefoy told heartwire. “Is our current management, with prehospital thrombolysis with transfer, in a time when primary angioplasty is promoted as the best-of-the-best treatment, still sufficient? Even if the power of the study is lower than expected, we think that we have our answer, and we can go on with that practice.”

The strategy also means less strain on their cath labs, Bonnefoy added, since only 1 in 4 patients underwent rescue angioplasty. A cost analysis comparing the 2 strategies is currently being carried out.

Earlier thrombolysisPrevious studies comparing primary angioplasty with in-hospital thrombolysis have shown a “definite, albeit modest” benefit of angioplasty over thrombolysis, with lower rates of recurrent infarction and higher patency rates, Bonnefoy et al write. However, it does impose additional treatment delays, and “delay to treatment is an essential consideration for any revascularization strategy.”
In France, where this multicenter trial was carried out, ambulance crews include a physician, and so thrombolysis with intravenous tPA is possible in the prehospital setting. In this trial, they randomized MI patients to either prehospital administration of accelerated alteplase or primary angioplasty and transferred all of the patients to a center where emergency angioplasty could be carried out if it were determined that thrombolysis had not been successful.
The primary end point was a composite of death, nonfatal reinfarction, and nonfatal disabling stroke at 30 days, with analysis by intention to treat.
Of the 840 patients, 419 were randomized to prehospital fibrinolysis and 421 to primary angioplasty. Rescue angioplasty was used “liberally,” they write, in 26% of patients assigned to fibrinolysis.

Time to treatment, as expected, was longer in the primary angioplasty group: the median delay between onset of symptoms and treatment was 130 minutes in the prehospital fibrinolysis group, and time to first balloon inflation was 190 minutes in the angioplasty group.

At 30 days, there was no significant difference in the primary end point between groups. Overall mortality was lower than expected, they note. Deaths were fewer in the prehospital thrombolysis group, but mortality was not significantly different between groups. There was a trend toward less reinfarction and less disabling stroke favoring the primary angioplasty strategy.

CAPTIM: Primary end point

Outcome    

 

Prehospital fibrinolysis    

 

Primary angioplasty    

 

Risk difference (95% CI)    

 

p    

 

Composite end point 8.2% 6.2% 1.96
(-1.53-5.46)
0.29
Mortality 3.8% 4.8% -0.93
(-3.67-1.81)
0.61
Reinfarction 3.7% 1.7% 1.99
(-0.27-4.24)
0.13
Disabling stroke 1.0% 0 1.00
(0.02-1.97
0.12

To download table as a slide, click on slide logo below

Among secondary end points, the researchers noted a nonsignificant trend toward a higher frequency of cardiogenic shockthe most common cause of death in this studyin the primary angioplasty group, noting that cardiogenic shock between randomization and hospital admission occurred only in that group.

The CAPTIM results were first presented at the European Society of Cardiology Congress in September 2001 and reported by heartwire.

 

Strong wordsIn an accompanying commentary, Dr Gregg W Stone (Lenox Hill Heart and Vascular Institute, New York, NY) calls the CAPTIM results “the latest salvo in the ‘primary PTCA vs thrombolytic therapy wars’,” a “well-designed and carried out” trial.2
“Unfortunately,” because of funding issues and slow enrollment, the trial ended before the planned recruitment of 1200 patients that would have been required to show a 40% reduction in the primary end point with primary PTCA, he writes. “Nonetheless, the results demonstrate a trend toward a 24% relative reduction in the occurrence of adverse events favoring the interventional strategy, driven by strong reductions in reinfarction and stroke (which would be expected, after all, to be largely independent of reperfusion time),” Stone notes.
He attributes the lack of mortality benefit from primary angioplasty to the lower-than-expected mortality risk in this population, since the survival benefit of primary angioplasty is seen primarily in the highest-risk patients, the elderly and those with anterior MIs or shock. The lack of mortality benefit, though, “does not diminish the clinical relevance of fewer strokes, reinfarctions, a reduction in urgent revascularization procedures, and the shorter hospital stay” seen with the interventional strategy in this and other studies, he writes.
Perhaps the most novel finding is the reduction in early-onset cardiogenic shock with prehospital thrombolysis, a result that “adds fuel to the fire calling for facilitated primary PTCA trials.” However, several trials of the combined approach to date have shown it to be either inferior to or no better than primary PTCA, he notes. Even in CAPTIM, prehospital thrombolysis was supported by rescue angioplasty in 26% of patients, and Stone speculates these patients may have been “better off” if they had simply been transferred for routine immediate primary PTCA.

“Thus, until the large trials of facilitated PTCA are completed (none of which have even begun enrolling), the best therapy for most patients with evolving AMI should no longer be debated; administer antiplatelet therapy (aspirin, a thienopyridine, and possibly abciximab), withhold thrombolytic therapy, and transfer the patient for primary PTCA, regardless of whether the nearest catheterization suite is 3 floors or 3 hours away,” Stone concludes.

“To do less should no longer be considered standard care. Strong words, yes, but it is time for a wake-up call.”

 

CAPTIM researchers respondAsked to respond, Bonnefoy pointed out that “Dr Stone is surely a primary angioplastician and very convinced, but it’s quite ideological. CAPTIM is quite pragmatic. His arguments are acceptable, but they are not convincing; that is his opinion rather than scientific data.”
Bonnefoy asserts that no study has clearly demonstrated the superiority in terms of mortality of primary angioplasty over prehospital thrombolysis. “And in CAPTIM, we have the surprise and intriguing observation to have lower mortality in the prehospital thrombolysis groupit may be hazard, but it is present.”
Moreover, while high-risk patients may benefit from primary angioplasty, high-risk patients do not represent the majority of the MI population. In patients such as those in the CAPTIM study, he said, “our conclusions are quite valid.”
 

 

 

Sources
  1. Primary angioplasty versus prehospital fibrinolysis in acute myocardial infarction: a randomized study2002; 360:825-829
  2. Primary angioplasty versus “earlier” thrombolysis–time for a wake-up call2002; 360:814-815

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