Posts Tagged ‘primary angioplasty’


 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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Is it a crime to do a plain balloon angioplasty in 2008 ?

Plain balloon angioplasty,   the greatest  innovation in   cardiology  when it was introduced in 1977 in a Zurich cath lab , has now become an  ugly  word for most of the cardiologist !

Why this turn around ?  Has technology ,  really overtaken a great procedure and made it obsolete now ?

The answer is a definite ” No”

The restenosis which was the villian in the plain old angioplasty has never been overcome even today. Stents initally used as a bail out procedure during  abrupt closure , later it was used conditionally, followed by provisional stenting and now in 2008  we are made to believe  it is mandatory.

When we realised , bare metal stents are equally  bad (If not slightly better ) in arresting the restenosis drug eluting stents came into vogue with a big bang in 2002. It was projected as the ultimate breakthrough in interventional cardiology and  in 5 years the truth was exposed and it not only failed to prevent the restenois but also had a dreaded complication of acute stent thrombosis.

Now we know , metals  inside a coronary artery  carry  a life long  risk of sudden occulusion , and we talk about biodegradable stents (With poly lactic acid ).

 Common sense ( Unscientific truths)  would suggest

Plain balloon angioplasty still has a major role in our global  cardiovascualr population.

Since restenosis is the  only issue here, ( about 30% )  we can choose patients in whom even if restenosis is likely to happen  no major harm is done . A vast majority of chronic stable angina patients  fall in this category.

Aggressive lipid lowering with plain  balloon angioplasty has never been tested properly . In future also it is unlikely,  such trials will be done as it would be considered unethical . But that would be a premature conclusion.

The other major issue is the cost of stenting , the procedure of PCI/PTCA  has become unaffordable for most of the population in developing countries .The primary reason being the PCI without stenting is considered  ” A untouchable” . If only we remove this stigma from the cardiology community   a signiificant population will be benefited.

A patient with chronic stable angina treated with POBA ,if develop further angina after few years , he  is likely to get a recurrence of  relatively safe  stable angina.  While in a post PCI patient  any angina after the procedure becomes a unstable angina ( Braunwald classification)  and requires emergency care . Angina in a  stented patient is can not be taken lightly as  the the course of angina is unpredictable .

POBA in primary PCI ?

Many may think it is a foolish idea . It has been found many times,  when we rush the pateint to   cath lab after a STEMI  we are in for a surprise !. About 30% of times it is a very complex lesion profile  like diffuse disese,  tight bifurcation lesions , loaded with thrombus or a left main disese.

We fail to realise a basic  fact  , the  initial aim of primary PCI is to salvage the myocardium ,and the next comes the prevention of restenosis . It may even , be argued salvaging  myocardium is the only aim ! Myocardial salvage sould be done urgently . And even  removing the thrombus and opening a IRA can be suffice in a patient who is crashing on table.  Of course stenting can be done whenever possible. But for IRAs which has complex anatomy attempting a perfect stent PCI   (Some may require more than few stents)  as an emergency procedure invariably affects the outcome. One should spend  shortest possible time  inside the  illfated coronary artery. Prolonged manipulations within the coronary artery in an unstable patient  aiming at  longterm patency of an IRA  is to be avoided .The pending procedures can always planned in a next stage. 

Final message

So it is not a crime to think about plain balloon  angioplasty  in some of  our  patients  with acute or chronic coronary syndromes .  Hope Gruentzig  is listening from the heaven and hopefully agree with me !

Dr.S.Venkatesan, madras medical college, chennai, India .

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