Posts Tagged ‘primary pci’
Posted in bio ethics, cardiology-ethics, cath lab tips and tricks, medical quotes, Two line sermons in cardiology, tagged abandoning cath lab procedure, cath lab complications, cath lab tips and tricks, ethics in cath lab, extraordianry interventional cardiologist, interventional cardiologist, invasive cardiologist, pci ptca, primary pci, who is interventional cardiologist on March 4, 2014 | Leave a Comment »
Posted in Cardiology -Interventional -PCI, cath lab tips and tricks, tagged cath lab tips and tricks, ira vs nonira angioplasty, multivessel angioplasty in stemi, primary pci on May 19, 2013 | Leave a Comment »
Multivessel PCI during acute STEMI is forbidden except in cardiogenic shock . (or in some very unstable patients without cardiogenic shock)
- During acute MI hemodynamics are precariously balanced.We do not know yet how emergency multivessel plasty alters this .
- Our initial aim should be confined to myocardial salvage in the IRA . Total myocardial revascularization is niether the priority nor its desirable.
- The more time you spend within the inflamed coronary artery , more its hazardous.
- Multiple stenting is prone for thrombus and migration into side branch .
- Stent opposition is sub optimal in many thrombus infested lesions.
Still . . . in real world it is extremely difficult to curtail the urge to stent all eligible lesion during primary PCI !
How to avoid it ?
If the patient is poor or the insurance limit is low , the issue of multi vessel stenting does not arise at all !
Always ignore complex non IRA lesions during primary PCI. Be happy if a non IRA has a bifurcation lesion !
Still , some lovely looking lesions in non IRA would be tempting and inviting . Indulge at your own risk !
* Please remember if the proximal LAD has a non IRA lesion , it may be sensible to attempt simultaneous revascularisation even if the patient is stable !
Other unrealistic advice
- Keep the professional fee and other benefits fixed whether we do a single or multiple vessel stenting (Realise . . . surgeons do not charge more for a 4 vessel by-pass graft than a single ! )
- Keep the current AHA/ACC/ESC guidelines pasted right next to the fluroscopy monitor .
- Ask your subordinates to repeatedly caution you about the possible excesses and ask them to wave a red flag !
- You may empower the senior staff nurse with a veto power to shut off the cath lab once IRA plasty is completed and the patient is stable.
- In extreme situations , keep a cath marshal ready to manually evacuate the primary operator from cath lab !
For STEMI management there are 6 management protocols available
- Primary PCI
- Rescue PCI
- Facilitated PCI
- Pharmaco -Invasive approach
*CABG is rarely used except in severe mechanical complication.
There is some issues in differentiating facilitated PCI and Pharmaco Invasive Approach.
What do we facilitate ? How we do it ?
PCI in acute STEMI is done in a thrombotic milleu. So we get sub optimal results .Hence to facilitate it we try using
either 2B-3A antagonists, Newer Heparins, or even thrombolytic agents before submitting them for PCI
Where is this facilitation done ?
Facilitated PCI is done in small hospitals where there is no cath lab or cath lab is available only during office hours.
Facilitation can be done in either in same hospital or on the way to big hospital
Is there a time window to start this ?
The main aim was to was to facilitate the PCI .Hence time window was not considered vital in few studies (Wrongly though !) ideally it should be started as early as the first contact . Since facilitation can be started earlier the time window is 0-24 hours .
What happened to the concept of f-PCI ?
It died a premature death and last rites were completed when the FINNESE trial was out .
But it left behind a daughter concept ie in selected patients if the facilitation is done early , especially in those patients who are going to get the subsequent PCI late ,or in high risk individuals , the initial pharmacological facilitation* was indeed useful.)
*If facilitation was with fibrinolytic agents (Not 2a/2b ) .It is very important the benefits of facilitation is mainly attributed to the time gain in achieving partial opening of IRA making it more complete salvage of the subsequent PCI .
This aspect later on named as PIA .
Pharmaco- invasive approach(PIA)
We know p PCI is a race against time .We also know fibrinolytic therapy fares well in this race but pPCI beats in effectiveness .
So what prevents us to combine the swiftness the fibrinolysis and the robustness of pPCI ? That is like getting the best of both world .( It is not that easy thing accomplish after all 1+1 in medicine is rarely 2 !)
In it’s core principle it is same as f-PCI . But facilitation is done only with fibrinolytic agent (Not 2B-3A) . Pharmaco Invasive strategy can be started in any small hospital/ In the ambulance /. It is routinely followed by PCI whether the initial thrombolysis is successful or not . PIA should not be done before 3 hours window if a timely pPCI is feasible. Hence PIA has a typical time window of 3-24 hours .
f-PCI is combining various anti-platelet and fibrinlytic strategy prior to PCI . It was found to be useless if it is used routinely in all cases of pPCI. (Rather 2B-3A was useful if only the facilitation was done within the cath lab to prevent procedure related issues) .Time window can be between 0-24h .
Pharmaco Invasive approach (PIA) is actually a type of f-PCI where fibrinolytic agents are used routinely which is followed by mandatory angiogram and PCI in all deserving cases.Many still believe the facilitation in PIA is primarily accured in shortening the time to reperfusion rather than altering the thrombus load and morphology ! Time window is usually between 3-24 hours.
Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Primary PCI, STEMI-Primary PCI, tagged Pre hospital fibrinolysis, primary pci, STREAM study on March 31, 2013 | Leave a Comment »
Primary PCI is presumed to be the ultimate , undisputed reperfusion strategy in STEMI . Still , time and again one study or other strips down this “Numero Uno” status of pPCI . If it is really supreme , such awkward situation shouldn’t arise too often . More importantly , the major reason for dubious real world record of pPCI goes beyond the time and logistic factors (which is considered the only issue for pPCI by most interventionist ! ) There is something more to it that is invisible ! (Is it the no reflow ?)
The major surprise was pre-hospital fibrinolysis showed less incidence of cardiogenic shock . ( pPCI
group had more of this ( 4.4 VS 5.9 % in STREAM )
Now . . . shall I make a provocative statement ?
while pPCI may be treatment of choice for cardiogenic shock . . . but it may also confer a risk of cardiogenic shock in otherwise low risk MI !
Caution and conclusion
STREAM population applies strictly to 1 to 3 hour time window . It does not apply to either before or after that ! Simply put,we do not have guts to compare fibrinolysis and pPCI in patients who arrive within one hour into a facility where 24 hour cath lab facility is available . We call it unethical to do a study like that ! I personally feel it is really unethical if we do not do a study in this time frame . The reasoning is simple and very personal .In a large Government hospital where we do not have primary PCI program our net mortality for STEMI never exceeded 7-8 % over a period of 10 years , Which is almost at par with global data on pPCI. (Our door to needle time is an unbelivebale 8-12 minutes ! that too only streptokinase !)
Adding Further controversy
pPCI is indeed a superior reperfusion strategy . No one can dispute that .But its superiority is not realised in every patient who gets it. The benefits are accrued if and only if it is used most judiciously . In Low risk , small regional , branch vessel STEMI , pPCI has never been shown superior . It is well recognised , upto 15 % of STEMI is likely to spontaneously abort or experience very good spontaneous recannalisation . By rushing these patients very early into cath lab pPCI meddles with the natural anti fibrinolytic mechanisms . It is this population who invite all the procedural hazards. .
Is this the reason STREAM had more cardiogenic shocks in pPCI limb ?
I think STREAM has strengthened the case in favor of fibrinolysis in this ever ending debate .
I would seriously believe pPCI is hanging it’s superiority over fibrinolysis with a wafer thin mortality advantage . pPCI may not be recommended in a routine fashion to all STEMI population even if they arrive within 6 hours and able to perform the plasty fast . Science is . . . after all . . . continuing confrontations with our assumptions !
STREAM is not an exclusive study comparing fibrinolysis and PCI . It is a study comparing Pharmaco Invasive approach vs pure invasive approach . 80 % of patients in the fibrinolytic limb ultimately received PCI and stenting . It simply doesnot make sense to conclude fibrinolysis is superior to PCI . Most of the beneficial effects on 30 day outcome may reflect the timely PCI in the lytic group.
A patient with extensive anterior STEMI presented 18 hours after onset of chest pain . He was other wise stable and free from angina but had persistent ST elevation (5mm in V 1 to V 5 ). He had a total occlusion of LAD with TIMI zero flow . He had a tight PDA lesion as well . A bed side echo revealed LV EF of 50% . The septum was hypo-kinetic but did not appear severely dysfunctional .
So , it was decided to open up the LAD. The moment LAD was opened he developed severe acute LVF / flash pulmonary edema . Even after a 30 minutes of heart (Fire ) fighting he could not be resuscitated .
What is the mechanism of death here ? Expert STEMI interventionist from core labs may answer this !
An acute ischemic MR with myocardial disruption was suggested . Why it was triggered after opening the IRA ?
Three mechanisms were discussed
- Re-perfusion injury
- Collateral damage
- Physiological de-stabilisation of Contra -Lateral lesion (Remote lesions )
Re-perfusion Injury ? How relevant it is in cath lab ?
Is re-perfusion injury electrical , mechanical or both ?
In this particular patient even though there was a total LAD occlusion , the segments supplied by the LAD was partially functional and it was contributing to LV pump function. The moment a trickle of flow was established , some thing happened and the whatever little mechanical function his LV had was also interrupted . The LV came to standstill and the patient died .
If re-perfusion Injury is simply an electrical event like VF , it can be resuscitated . If it is mechanical outcome is bad ! This is not a new concept . It is part of the once famous concept called myocardial stunning . There are lots of reasons for stunning to be a clinically relevant phenomenon .Unfortunately if any cardiologist talks about it in 2012 , he is at risk of labeled as old fashioned !
One more mechanism which we feel that might have contributed to death here is the “collateral damage” .(This is not cross fire !)
We know collaterals can be recruited within 12 hours in many STEMI patients . In some it can even salvage significant mass of myocardium . The acute collaterals to LAD may be interrupted during primary PCI . Once you poke the lesion the coronary vascular bed which had dilated (as a response to total occlusion ) may react with inappropriate vasoconstriction . This raises the local hydrostatic pressure (Myocardial edema) and further impede the incoming micro collateral flow . This a very critical time for the myocardium where antegrade and retrograde flow are kept in a fine balance .
Interference with remote lesion Hemodynamics .
Another possibility is the opening the LAD lesion some how impact on remote lesional flow as well (PDA in this patient )
Please remember ,
Even a transient hypo- tension can have devastating effect in the hemo -dynamics of non IRA territory especially if it harbors a critical lesion !
Coming to the title question , Is no – flow better than slow- flow in late presenters of STEMI ?
Common sense dictates whenever an artery is obstructed just get rid of it. When it comes to the heart it must be done in an urgent basis That is the essence of primary angioplasty . . . agreed . But in this patient I believe , the common sense was proved wrong !
Truths are always hidden. The science of myocardial re-perfusion is a perfect example . We need to learn a lot still !
This I call as Para cardiology : Heart facts without evidence !
One may argue this is an exceptional case in STEMI intervention. Don’t hype exceptions and undermine the importance of a great concept ! Exceptions and rules are directly related to our experience we have accrued. Exceptions are the great knowledge substrates and help crack medical mysteries !
Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology- coronary care, tagged export catheter, primary pci, thrombo suction, thrombus aspiration, tornus catheter on February 29, 2012 | Leave a Comment »
The key word for successful primary PCI is
- Suction & Aspiration of thrombus with micro catheters like export catheters
- One can do away with a stent during primary PCI but can never do away aspiration
- Distal protection as concept is rapidly dying out as we aim to remove all the thrombus .
Tips for effective thrombus aspiration
- Apply continuous negative pressure once catheter reaches the thrombus do not release it till you enter back into the guide.
- Make sure you are sucking only blood products not the endothelium
- Watch out for side branch spill over.
- 7F sheath 7F catheter ideal for aspirating with a micro catheter
- Please be informed some thrombus require more negative pressure especially in the late presenters of STEMI
* During dire emergency when you do not have a specialized suction catheter do not hesitate to push even a diagnostic catheter into the coronary .We have saved few lives !
Crazy questions in primary PCI ( or Is it futuristic )
Can we connect the suction apparatus into LAD micro catheter ?
Do we have camera guided suction catheter ?
Can you flush the thrombus if you are not succeeding in aspiration ?
Is ultrasonic desiccation of thrombus possible ?
Some of the tips were gathered from the recently concluded India Live 2012 conference in New Delhi .
A middle-aged man was rushed to cath lab with extensive antero- lateral STEMI . Primary angioplasty was planned.The coronary angiogram showed a critical LAD and a total LCX lesion just beyond the bifurcation . Both lesions looked irregular and hazy . RCA had insignificant lesions . Patient was stable hemo-dynamicaly .
The moment we saw the angiogram, we knew , we had a real problem on hand ! . First of all , It looked a complex lesion for a pPCI .(A brief thought about an emergency CABG creeped in, but was dropped with enthusiastic residents voted unequivocally in favor of PCI . Of course , to be frank we didn’t have a CABG team ready either ! )
So the plan was : To open the IRA . . . & forget the non IRA ( for the time being ) which is the current management mantra as on 2012 !
Trouble from unusual quarters ! By the way . . . which is the IRA ?
Even as the consultant was initiating the rituals with wires and balloons to tackle the LCX , some one behind the consultant mumbled “why can’t the LAD be the IRA ” After all , it also has a critical lesion and mind you we are dealing a case of anterior MI !) . That mumble was loud enough to create buzz of confusion in cath lab .
Now everyone quipped , ” IRA is what ?
Is that the critical mid LAD lesion ?
(or ) Is it the total LCX (or ) Both ?
Logic would suggest in the setting of STEMI any total occlusion should be considered as IRA . Of course , one can not be dogmatic about it. When a patient is having anterolateal MI both LAD and LCX can contribute to the MI .
What about proposing a new concept of “Double IRA” ?
When multiple plaques are activated suddenly in unstable angina , it is possible for multiple IRAs to occur in STEMI as well . But this issue is rarely discussed in literature .
The 100 % lesion in LCX could still be the primary culprit and a thrombus migration into LAD might have resulted in infarct extension into anterior wall .
Further , confounding may occur if a patient with chronic total occlusion develop a SEMI . It makes it really difficult to identify the IRA.
When the supposedly gold standard coronary angiogram fails to identify the IRA , what shall we do ?
Go to the basics . The good old ECG might help .
(Please beware in a patient with pre- existing multi-vesel CAD , none of the ECG algorithms work to localise IRA !(Especially the famous Wellen’s miserably fails ! )
Still unclear ? Look for the wall motion defects in echo . An echo cardiogram (Need to be meticulous ) will help match the dysfunctional segment with IRA.
Wall motion defects are notoriously error prone in ACS for two reasons.
- We do not have easy and accurate methods to differentiate ischemic wall motion defect from infarct related wall motion defects.
- Tethering artifacts , differential behavior epicardial vs endocardial ischema on contractility will confound the issue .
So what is left ?
One need to go back to the CAG again . Have a critical look at the lesion once more. Look for thrombus or eccentric /unstable lesions . If present it is going to be the IRA in 90 % of times. Let it be a wild guess in the remaining 10 % .
There is also a practical solution . Poke the lesions with your favorite guidewire ! . The one that gives way easily is likely to be the IRA !
Finally, if the confusion still prevails ,
Stent both the lesions. That’s what , was done to this patient . Many would have thought , this should have been the default approach instead of scratching our heads to identify the IRA , wasting crucial minutes !
Final message :
Current guidelines do not recommend pPCI for non -IRA at the same sitting of IRA pPCI . However the issue of IRA “too close to call “ is rarely addressed.I do not know how commonly this issue is encountered in angiographic core labs that deal huge loads of pPCI world wide .
Our early experience suggest the problem is real , unique and definitely not rare .
What is your take ? We argue guidelines committee to specifically address the issue of uncertain IRA as a branch point in the pPCI decision making tree !