Posts Tagged ‘europcr’

  • It is a complex PCI procedure meant for  high risk  bifurcation /Trifurcation lesions
  • Two stents are simultaneously  deployed.
  • It aims to prevent sudden acute occlusion of one of the major  branches .
  • It is not an easy procedure , and be used only in rare circumstances .
  • Distal left main and ostio proximal LAD/LCX  is a  classical  example.
  • Navigation can be difficult , only well experienced operators should attempt it.

*Is there a ready made two lumen stent available ?

The image is meant for concept purpose only !


It is one of the techniques available to stent unprotected left main

An excellent review  in  ACC intervention journal for unprotected left main .

Click on the Image to reach the article


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Failed thrombolysis is an important clinical  issue  in STEMI   as  successful thrombolysis  occurs  only in  about 50-60%  of pateints . The typical criteria to define failed thrombolysis is  the  regression  of less than 50% of sum total( or maximum)  ST elevation in infarct leads.

So what do you do for these patients with failed thrombolysis ?

It depends upon the patient’s symptom, hemodynamic stability, LV dysfunction .

They  should  get one of the following .

  1. Conservative medical management  with /without CAG
  2. Repeat thrombolysis
  3. Rescue PCI
  4. CABG

Medical management is  thought to be  too inferior a  management,  many of the interventional cardiologists  do  not want to talk about . But  , there is  an important  group of patients (Not often addressed in cardiology literature)  who  technically fulfill the criteria  of failed thrombolysis  , but   still  very  comfortable , asymtomatic  and in  class 1. These patients ,  have  a strong option for continuing the conservative management .

Repeat thrombolysis does not have a consistent effect but can  be  tried in some  stable patients. CABG  can be a genuine option in few

Rescue PCI

This terminology  has become  the  glamorous one since the  catchy word  rescue is tagged in the title  itself. For most of the cardiac physicians ,  this has become the default treatment modality.This is an unfortunate perception . What  one should realise   here is  , we are  tying to rescue  the myocardium and  the patient ,   not the patient’s coronary artery !

Opening up a coronary obstruction is not synonymous with rescue .

For rescue PCI ,  to be effective it should be done within the same time window as that for thrombolysis (ie within 6 or at the most  12 hours) .This timing  is  of vital importance  for the simple reason , there will be nothing to rescue after 12 hours as most of the muscle  would be  dead. Reperfusing a dead myocardium has been shown to be hazardous in some ,  as it converts a simple  infarct into a hemorrhagic  infarct.This softens the core of the infarct and  carry a risk of rupture. Further,   doing a complex emergency  PCI  ,  in  a thrombotic milieu with   presumed  long term  benefit ,  is  a  perfect recipe for a potential  disaster.

While the above statement may be seen as pessimistic view , the optimistic cardiologist would vouch for the“Curious  open artery hypothesis” .This theory simply states , whatever be the status  of the distal myocardium ( dead or alive !)   opening an obstruction in the concerened coronary artery  will benefit the patient !

It is  huge surprise , this concept   continues to  be alive even after  repeatedly shot dead by number of very good clinical trials (TOAT, CTO limb of COURAGE etc ).

The REACT study (2004) concluded undisputed benefit of rescue PCI for failed thrombolysis  , only if the rescue was done  within  5-10 hours after the onset of symptoms.The mean time for  pain-to-rescue PCI was 414 minutes (6.5hours)

Final  message

It is fashionable to talk about time window for thrombolyis but not for PCI  .The time window for rescue PCI is an redundant issue  for many  cardiologists ! . But ,  the fact of the matter is ,  it is not . . .

The concept of time window in rescue PCI  , is as important as ,   that of  thrombolysis. Please , think twice or thrice !  if some body suggest you to do a rescue PCI in a stable patient  ,  12hours after the index event .

Important note : This rule   does not (  or need  not  ) apply for patients in cardiogenic shock  or patient ‘s with ongoing iscemia and angina.

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Coronary artery  perforation is a dreaded complication of PCI. Perforations are the Interventional cardiologists ultimate worry   as they need to  manipulate their  hardware for  long periods in many complex lesions.  Especially  it is a  real threat in chronic total occlusions.

Still , an important fact is ,  many of the coronary perforations are not life threatening ?

How is this possible ?  (Type 1 Ellis has zero mortality Read below)

As the guide wire injures and perforates the cor0nary vessel,  it results in  small puffs of dye extravasating  into peri coronary space .

The coronary artery , which is located   within the  atrioventricular groove  (LAD), or AV groove (LCX, RCA) have  two distinct anatomical relationship with reference to epicardium and pericardial space.

50 % 0f circumference of the coronary artery is  hugged  by the myocardium  another 50% or so is related directly to the pericardial aspect.

Guide wires hitting on the myocardial aspects face a stiff resistance than the pericardial aspect. So , generally the risk of perforating pericardial aspect is more than myocardial aspect

Even if , the coronary artery is punctured on myocardial aspect , no great danger occur as there is no potential space for the blood to drain and further,  the  elastic nature of myocardial muscle plane effectively seals the leak. At the most , mild myocardial staining is noted .


While ,  perforations  into  the pericardial space  , often threaten with a tamponade. The fact that pericardial space has negative pressure and  the mean  coronary arterial pressure around 40mmhg ,  it is  , all the more likely blood is sucked into the pericardial  space. Of course , very minute  perforations  even into the pericardial space ,  could  be self limited and  benign.


What is unrecognised coronary perforation?

Many times , the guidewire goes in a false track in the tissue plane.This is  nothing,  but perforation without hemodynamic implication. Most often , these are the instances of guide wire entering the epicardium.They mimic , false lumen entry , dissections, etc. There are occasion , where false lumen of the  coronary artery were  stented.

What are the  factors which increase risk of perforation ?


 How do you classify coronary perforations ?


*Ellis SG, Ajluni S, Arnold AZ,  Increased coronary perforation in the new device era. Incidence, classification, management, and outcomeCirculation. 1994;90:2725–2730


How do you manage coronary perforation?

Simple guide wire induced perforations are less trouble some unless we have crossed it with balloon without realising the fact the wire has entered the pericardial space. So, caution is required and always watch for guide wire tip movement which is often funny looking wihtin false lumens or very freely moving within pericardial space. Anticipate the complication especially so when you do CTOs and venous graft PCI.  Keep one cath lab  tamponade crash  bin  in ready mode before embarking upon a complex PCI

  • Neutralise the heparin action with protamine is the first step
  • Most are self limited, no intervention is required  but requires close observation for next 24 hours.
  • Temporary balloon occlusion may be suffice in many cases
  • Tamponade requires immediate tapping. Small collection without fall in BP can be observed.
  • keep doing the echocardiogram liberally to assess the leak and watch for any new collection.
  • PTFE covered stents if prolonged leak.
  • Emergency surgery may required in few.

2018 update 

This is  nearly 10 years old article. Now, we have gained much experience and hardware utilisation have rapidly expanded. While expertise has minimised this complication , more PCIs in complex lesion subset tend to keep the incidence static , if not higher.(Its around .5% )

Tips to use balloon occlusion during perforation

Perforations which are active and flowing should be immediately occluded with a balloon either at the site of leak or just proximal to it. Doing a proximal occlusion is easier in emergency , as often times its technically difficult to reach the site of leak especially in CTOs where the leaky site is not defined clearly or forward looking (Local balloon inflation across the leaky site is not feasible )


How long to occlude , Intermittent /complete, proximal ? or at the site of perforation ? These queries are answered in Ref 4


1.Largest report (1762 cases) of perforation from British Cardiovascular Intervention  Society Database Circ Cardiovasc Interv. 2016;9:e003449.

2.Al-Lamee R, Ielasi A, Latib A,. Incidence, predictors, management, immediate and long-term outcomes following grade III coronary perforation. JACC Cardiovasc Interv. 2011;4:87–95.

3Xiangfei Wang and Junbo Ge Balloon Occlusion Types in the Treatment of Coronary Perforation during Percutaneous Coronary Intervention   Cardiology Research and Practice Volume 2014, Article ID 784018,

4.A very good review comes from Royal Hospital, Muscat, Sultanate of Oman


iFAQs in coronary perforations

1.Does the plane of the coronary artery (Sub epicardial within the fat layers)  determine the likely hood of tamponade ?

While myocardial tissue can resist flow we are not sure about sub-epicardial fat on the pericardial aspect.

2.How common is Intra-cavitory perforation ?

Perforations into chamber is invariably associated with septal branches (PCI to septal branch itself is less common )

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Coronary stents have revolutionised the management of CAD. Stents are metallic scaffolding devices that help keep the atherosclerotic plaque  plastered within the coronary arterial wall.Thus it gained the name angioplasty. Stents have aradial strength that  exerts a constant force on  the plaque . Since metals are unfriendly partners for coronary artery , we need to have minimum metal within the coronary artery.The stent struts weave around the lumen generally the stento/ artery area ratio should be as less as possible (15%).

But this has a trade off .The uncovered area of plaque tend to project into the lumen .This is many times not significant.But can be a problem if the plaque is very soft and bulk of the lipid core may reenter the lumen.this event is called plaque prolapse.


What is the time taken for plaque to prolapse ?

Generally it is late event.But it can happen immediately after the procedure also.

Which type of lesions are more likely to have plaque prolapse ?

Eccentric and complex lesions especially with overhanging edges are prone for prolapse

What is the sequale ?

It can be benign.If there is a erosion due to stent struts can precipitate an ACS.It progresses into instent restnosis in many.

What is the angiographic appearnce ?

Angiographically it often appears as luminal  irregularity withi stented segment .

Many times , it may appear as a filling defect also.

Is there any specific issues in plaque prolapse in drug eluting stents ?

Coornary artery is not drugged uniformly by the drug eluting stents.In fact contact  lines of metalic struts  , through it’s micropore oozes the drug with polymer.Pathological studies have revelaed non homogenous drug penetration and resultant irregularity on the plaque surface.This could amplify the plaque penetration preferentially in few areas.

How to manage plaque prolapse ?

It should be managed as any other instent restenosis.Plaque resection with atherectomy devices has not solved the problem to the desired levels.A second stent is the most common approach advocated by the cardiologists.(Whic is not ideal though !)

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                                                    Drugs are poisons , whenever it is administered without valid purpose. it can enter human body  in many ways (Oral, intravenous, percutaneous etc ) And now we have another route namely intracoronary !

                                                   In quest for prevention of restenosis, many of the anti cancer drugs are now delivered directly inside the coronary arteries .These drugs are secreted  like a sustained release  tablet from the drug coated stents.These drugs are expected to prevent restenosis within the stented segment.But, after years of  intense debate and research  , we realised that ,  drugs  eluted from the stent  could damage the distal coronary vascular bed and coronary microcirculation.( And thus came the epidemic of acute stent thrombosis ! )

                                                The tender and sensitive coronary microvasculature  is constantly exposed to  these  powerful anticancer and immmunosuppresive  drugs .It is a great surprise , no body thought of  this dangerous drug -coronary artery interaction ! It required the genius of Renu virmani and others to point out this.

But still , the cardiology community by and large , fails to consider  this an important issue.This is proven by the fact, usage of DES is  still increasing  and used mainly as an off label indication.

Read this land mark article from circulation




Questions that need to be answered

  • What is the long term effects of drugging a coronary artery ?
  • Is no reflow or slow flow  more common after DES , because of the adverse drug reaction in the distal vascular bed ?
  • If a patient  with  DES  undergoes a CABG later what  would be  the impact of the  drug on the graft ? Will the functional vasodilatation   affected ?

Final message

                                  A drug , to get a legal clearance it has to undergo  hundreds of rigorous tests . Finally it is cleared for that  specific indication for which it is tested  .Just because a drug is cleared for one purpose ( Paclitaxel for malignancy ) it does not mean it is safe to use for any other  purpose for which it is deemed to be useful . Exactly the  opposite is happening   in the  the field of interventional cardiology . No body wondered to think what would be the effect of these drugs on the normal coronary endothelial cells and vasculature.Is it not a crime ,  without analysing this particular issue  , dozens of drug eluting stents have been released in the market . And now,  sounds of crying  foul is heard world wide !

Let us thank  , the so called negative forces in cardiology  for making this an  issue . In science ,  the watch dogs should bark  at  times of danger not wag the tail !

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Stents are mechanical  devices like  a  spring ,  used to  keep an artery open after a PTCA or PCI.


                                Bare metal stents(BMS) were found to have restenois rate of about 25%.  So it was perceived a stent should have it’s own protective coat , so that it won’t get restenosed.For this the researchers thought  anti cancer drugs are ideal as they block cell proliferation and thus neovascualrisation and restenosis.Alas, they were found dismally wrong ,  after all , neointiaml proliferation is only a part of the problem of restenosis  and simple blocking of cell growth is insufficient . The issue doesn’t stop with that, the anti cancer drugs incorporated within the stent simply can not differentiate normal from abnormal cells and

DES effectively blocks the normal endothelisation over the stents and make this highly vulnerable for acute stent thrombosis .

This complication is unique to DES and can result in SCD.Further ,during the last 6 years of DES , we recognised the restenosis rate has increased form the much hyped O % to almost 15% and it’s still growing . These  complications  has made a huge question mark over the future of drug eluting stents !


The concept of DES may not die , but which drug it should elute should be answered ! This  again is  going to be a long battle. So it is currently   adviced,  based  on common sense ( With due respects to  those RCTs  funded by industry )

Whenever you encounter a block within the coronary artery* Ask the following  questions in sequence  ,

  • Whether we can leave it alone  with medical therapy  ,  if the answer is no , proceed  to the next step !
  • Is there a possibility for plain balloon angioplasty in a given vessel (POBA, Yes !  the concept is not dead yet !)
  • If you decide a stent is required , Will  the  bare metal  do the job ?
  • In multivessel CAD  , Did the issue of increased metal load on the  long term outcome was considered ?
  • If lesions appear complex,  should we  not strongly consider CABG as an option ?

However  if we  have the habit of  ask ing the following  question  you are likely to deviate from scientific approach  

Is it possible to put a stent  across  the block ?

Yes , will be the answer most of the time ,and the patient will invariably get one or more stents  and carry a life long  stent related problems.

*The rule does not apply in Acute coronary syndromes

Also read this letter  posted by the author published in  British medical journal

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 Rescue thrombolysis in acute   myocardial   Infarction  

 *Venkatesan sangareddi ,Madras medical college,Chennai.India



   Back ground  Failed thrombolysisin acute myocardial infarction occurs in 30-40% of patients. The incidence of progressive pathological remodelling and cardiac failure is high in these patients. The approach to the patient with failed thrombolysis is generally considered to be catheter based and the outcome is not clear. Bleeding can be troublesome in patients, taken for interventional procedures in the immediate post thrombolytic state. The option of repeat thrombolysis has not been studied widely and is not popular among cardiologists.

Methods:We present our experience with six patients (Age 42-56, M-6, F-0) who were thrombolysed for failed first thrombolysis. All had anterior MI and had received either urokinse or streptokinase (between four to nine hours) after the onset of chest pain. All of them had persistent ST elevation, angina not responsive to maximal doses of IV NTG and beta blockers. The initial thrombolysis was deemed to have failed. Repeat thrombolysis with streptokinase (15 lakhs) was given between 16 and 24 th hour. The clinical outcome following the second thrombolysis was rewarding. It relieved the angina, ST segment elevation came down by 50% and coronary angiogram done at 2-4 weeks showed complete IRA patency in four out of six patients. The factors responsible for failed thrombolysis is complex and multifactorial. A logical explanation from the fundamentals of clinical pharmacology would suggest that a common cause of failure of any drug is due to a inadequate first dose.

Conclusion :We conclude that repeat (Rescue) thrombolysis can be an effective medical intervention for failed thrombolysis in AMI.

Personal perspective                  

                             Repeat  thrombolysis for failed ( initial ) thrombolysis  is still   considered  a  fantasy treatment  by most of the cardiologists !  The utility and efficacy of this modality of  treatment (Rescue thrombolyis ) , will never be known to humanity , as planning  such a  study , in a large population  would  promptly be  called unethical by the modern day cardiologists.

                     While a cathlab based cardiologist  take on the lesion head on with multiple attempts  , it is an irony , poor  thrombolytic agents are given only one shot  and if failed in the first attempt,  it is doomed to be a  failure for ever.Currently,  the incidence of  failed thromolysis could be up to a whooping 50 %  .There has not been much scientific initiative  to enhance the efficacy of these drugs.

                            Common sense and logic would suggest it  is the  inadequate first dose ,  improper delivery , pharmacokinetics is   the major cause of failure of action of  a drug in clinical therapeutics.

If the first  dose is not working ,  always think about another  incremental dose if found safe to administer.

Can we increase the dose of thrombolytic agents  as we like ? Will it not increase the bleeding risk to dangerous levels ?

This is a clinical trial  question.

  • In patients with prosthetic valve thrombosis and acute pulmonary embolism we have safety data of administering of  1 lakh units for an hour for up to 48 hours.

Can  the same regimen be tried in STEMI if the initial thrombolysis has  failed  and emergency intervention is not possible  ?

Logic would say yes . Unfortunately we can’t go with logic alone in medicine .We need scientific data ( with or without logic ! ).But now ,  as we realise common sense is also a integral part of therapeutics  It is called as level 3 evidence / expert consensus by AHA/ACC .

Applying  mind , to all relevant issues ,  continuous streptokinase infusion 1 lakh/hour for 24-48 hours in patients with failed thrombolysis can indeed be an option,  especially when the patient is sinking and  no immediate catheter based intervention  possible .This study question is open to all researchers , and may be tested in a scientific setting if feasible.

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No reflow is the terminology used primarily in cath labs where, even  after a successful opening and stenting  of a coronary artery the coronary blood flow is not  restored to myocardium . The point to be emphazised here is blood do cross  successfully the site of  the obstruction but fails to enter the muscle segment  to which the coronary artery is supplying. So the paradoxical situation of artery  being open but the  myocardium is closed to receive  blood flow  happens . This is termed as no -reflow.  Actually it is a  misnomer , and  ideally it should be called “no flow” because  normal distal flow  does not  occur (After PCI)  in the first instance  to get interrupted  later on  and be labeled as  no re-flow.  .The only positive effect of PCI in these situation is blood flow would have improved by few centimeters ie till it reaches  but falls short of myocardium . In fact no reflow , can be termed as  glorified and concealed  terminology  for  PCI failure . It needs urgent action . No reflow is also called as myocardial epicardial dissociation.

Mechanism of no reflow.

Curious case of open coronary artery and closed myocardium !

Coronary  microvascular plugging  is mainly  due to thrombus and atheromatous debri , myocardial  edema , microvascular spasm may also contribute.

Where can it occur ?

  • First described in cath lab, especially following primary angioplasty.
  • It can very  well happen following thrombolysis in STEMI.
  • Can occur in venous grafts.

How do you recognise no reflow?

In cath lab it will be self evident from the check angiogram. Some times it is less obvious and may  require, myocardial  blush score, TIMI frame  count, contrast echocardiography, PET scan etc. In post MI a very simple method to recognise this entity could be the observation of persistent ST elevation in ECG .


Extremely difficult. Almost every coronary vasodilator has been tried.(Nitrates, nicorandil, calcium blockers, etc).Success is less than 30%.  High pressure flushing with saline inside the coronary artery is advocated by some.Others believe it’s dangerous to do it. So prevention is the key. Avoid doing PCI in complex, thrombotic lesions. Use thrombus suction device like export catheter(Medtronic). Distal protective devices are double edged devices , useful only in experienced hands.

Unanswered question

What is the size of the particle (thrombotic and atheromatous  debri)  the   coronary microcirculation safely handle and push it into the coronary venous circulation and the coronary sinus for disposal ?

If we can lyse the thrombus into micro particles by some mechanism and make it traverse the coronary circulation this complication of microvascular  plugging can be treated and prevented .

What is the final message ?

  • No reflow is relatively common condition during emergency PCI done for ACS patients
  • More common in complex thrombotic lesions.
  • Can also  occur in STEMI
  • Treatment is often vexing . In fact the treatment of this condition is so difficult , it can be termed  almost synonymously with “Failed PCI” if flow is not restored.
  • Successful treatment of no- reflow  means not momentry restoration of  myocardial flow  by mechanical and pharmacological modalities ,but to maintain sustained myocardial   perfusion. This we realise, as patients who have had a no reflow during  a PCI, do not perform as well in the follow up  .
  • So prevention is the key.

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There are numerous complex grading for bifurcation lesions available.

The one proposed by Medina is simple and most useful.

In this grading three segments

  • Proximal main vessel
  • Distal main vessel
  • Branch vessel

Are given a code 0, and 1 if  lesion is present or absent .

This grading gives simple and fast method to label a bifurcatiuon lesion and to asssess the response to PCI. The only issue here is the individual  lesions are not graded , for example branch vessel ostium just involved about 20 % is not addressed . Further TIMI flow in these vessels may also be incorporated

How medina grading can be used to assess effectiveness of

angioplasty  ?

A patient with 1.1.1  after the treatment should revert back to 0.0.0.  if converted into 0.0.(.5) may indicate a residual side branch lesion  .5 shall indicate 50% residual lesion, .3 , 30% etc


What is the best management strategy for bifurcation lesions?

The topic has been discussed extensively for over a decade in various forums.

Though the lesions and intervention techniques  appear complex the basic concept is simple.

Following is the 8 point algorithm

1. Assess the bifurcation lesion accurately.

2. Apply the general rule and ask the first question whether PCI is neccessary at all ? if decided for PCI

3. Stent the main vessel.Protect the side branch.  

4. Dilate the side branch with a balloon.(KIss or through the struts) 

5. Very rarely,  if the side vessel is more significant and large  stent it and balloon the main vessel.

6. Use drug eluting stents with caution .

7. Resist the temptation of using two stents unless the situation demands and is absolutely required.

8. Never attempt to do bifurcation angioplasty during ACS as apart of primary angioplasty.( Unless you’re extremely competent, even then aim of primary PCI is to salvage myocarium quickly , not to provide TIMI 3 flow in non IRA vessel.)

Dr.S.Venkatesan.Madras medical college.Chennai.

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                                                          Left main coronary  lesions are  fairly common  during routine coronary angiogram.These may be a critical or a innocuous lesion.The  word “left main” triggers a sort of alarm reaction to many cath lab staff as well as the cardiologists and surgeon.Many times, these left main lesions are detected in patients   with chronic stable angina who have stable symptoms. Left main disese has not been graded  clearly in literature . Often it is perceived , any lesion in LM is serious.

There is an unwritten rule,  rather a medical compulsion  to take a patient  with left main disease  for emergency CABG ( Now some centres ,emergency PCI) .Some institutions make it  a rule these patients  are posted  in the  next available slot in the theatre.

 The basic question we raise here is   “Should we consider all  left main  disease  as  an  emergency”?

Not really , especially when it occurs in a stable angina .One can wait , buy some time to fully evaluate and prepare  the patient  and may be the patient can be posted  as an elective case. It is a well recognised fact that, CABG carries adverse outcome when done as an emergency procedure. This is primarily due to inadequate pre op work up and resultant complications. It is also well known ,  surgical  back up team may not be available in full strength in odd hours .

This post is  to convey the message , that left main is  a serious disease but that doesn’t  mean it should elicit  a panic reaction and be taken as an ultra emergency . There has been many morbid and fatal outcomes in many hospitals due to this apparent  pseudo emergency !


Note* 1.Left main  disease during acute coronary syndrome is to be seen in different perspective.2.Some of the proximal LAD lesions are so tight and  could be more significant than left main lesions.

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