Dr.S.Venkatesan MD

Rescue angioplasty as a concept in PCI is advocated for the past  two decades. Rescue angioplasty  continues to enjoy the  controversy over the years. A procedure which fails to shrug off the controversy for so long   inspite of multiple studies ,  would indicate there is something seriously wrong in the  procedure  or in the conceptualization.

The fundamental question   that  is often  and not answered properly is :

What is being rescued in R angioplasty ?

Is it the

• Patient’s life ?
• Myocardium  ?
• Rescues ischemic myocytes
• Infarct related  artery ?

*Or it simply rescues physician  from the legal issue arising out of  labeling his patient as  failed thrombolysis

The term rescue generally implies  tackling an  impending crisis .The threat is either  to the patient’s life or to the myocardium or both.

In STEMI when the initial reperfusion strategy fails (Usually thrombolysis)  R -angioplasty is considered. Here the aim is  to  rapidly  rescue  and salvage  myocardium . The problem  here is   , contrary to our expectation   the population of failed thrombolysis is not a homogenous one .In one end of the spectrum ,  is a patient with  persistent ST elevation ,   totally comfortable and pain free and  hemodynamically stable.The other end is , deteriorating blood pressure , tachycardia , progressive angina and impending cardiogenic shock. Considering the above situations it is very simple to guess who will  require the rescue  and  who will benefit more. In fact,  R -angioplasty  in   patients with  asymptomatic  failed thrombolysis  without ongoing  ischemia defies logic and conveys no meaning !  .This is especially true if the patient has crossed 12 hours of time since the first symptom.

In deteriorating patients R- PCI has a role where one can potentially  arrest the progression of cardiogenic shock  or even reverse it.

A third  group  among failed thrombolysis have  predominate  angina  with  hemodynamic stabilty. This group will benefit from R angioplasty  irrespective of time window , as the pain is often due to a critical non IRA lesion .Technically again we can’t call this PCI as rescue as nothing is done to salvage the myocardium . (Of course one wish to call it so ,  as the  patient is rescued from angina !)

A tricky issue is to know where does the pain come from in a post MI patient ?

It should be realised a post MI patient can have variety of source of chest pain. There has been instances where a persistent  pericardial pain has resulted in emergency  R-PCI !

The critical question that  has not  been  answered by cardiologists is

How long a STEMI pain last and when does post infarct angina begin in a  susceptible patient .

In other words how do differentiate present(Index event)  infarct angina from post infarct angina ?

Studies on pain signal transmission (medullated type c)  would suggest a dull aching retrosternal pain may occur in a substantial number of  patients  following STEMI .These pain signals come from  necrosed cells and not from  ischemic cells. This pain ceases after complete  ischemic destruction of nerve endings . The threshold , duration and central perception of this pain is highly variable.

One can imagine the importance of the above issue ,  as   there is a potential  to  misdiagnose recurrent post MI angina   for the relatively benign infarct related pain. Though experience have suggested a 12 hour cut off to define post MI angina ,  it is too empirical .

Final message

• Rescue angioplasty remain as  disputed entity in vast majority of  post MI population .
• It is most useful when  it is done in  impending cardiogenic shock .Note the word. Impending  . . . not established cardiogenic shock. (After prompt recognition of failed thrombolyis ,  within  overall time window < 6h*  ideally ,  but may be done  to up to 12h) There is no role for routine rescue in all failed thrombolysis patients , for the simple reason there may not be any clinical or  live myocardial  targets for rescue.

Need for seperate time window for rescue angioplasty

* Even this 6 hours is emprical . We need  seperate evidence based time window exclusive for rescue angiopalsty .I would personally believe this could  be as short as 1-2 hours .

Read Full Post »

Exercise stress test is the most commonly used non invasive  diagnostic test for CAD.

It is also useful in the functional capacity evaluation.Even though medical management of CAD is a proven and accepted  method of therapy in CAD . There  is always a   perception  even   among the  cardiologists  medical management  is an inferior form of treatment.  This is primarily due to peer group  pressure rather than based on solid scientific concepts.

What is the effect of medical  management on  the common CAD parameters ?

Relief of angina  . It is a simple , and easy parameter to assess.

Functional capacity . Increased exercise capacity  is a good marker of successful medical therapy

The effect  on stress ischemia could be most objective way to assess the success of medical therapy.

But , unfortunately this does not come in the regular scheme of things  for many  cardiologists following medical  management. If we are able to document reversal of stress  test positivity it could be the ultimate marker of success in medical revascularisation. EST is an approved method of assessment of efficacy of optimal medical  management .Still ,  in day to day cardiology practice this is rarely done for the simple reason the patient often stumbles upon an  interventionist and lands up in a PCI or CABG !

Following  things can happen over EST following medical management

• Complete correction of inducible   ischemia
• Delayed appearance of ST depression with increased exercise capacity
• Duration of ST depression can be reduced
• Convert painful  ischemia into silent ischemia*
• No response **

* Conversion of painful episodes into silent episodes may not be a real success  in physiological terms.But in patient point of view it is .It should be  recalled  even in  CABG  pain relief  is a major clinical  outcome .

** Could be termed as failure of medical management , but there  is a  group of patients who have increased exercise  capacity but still EST is positive

Real world experience of large case studies (Individual communication : Large community based stress test in over 9000 patients ( Gnanavel et all Ganesh clinic Thiruvannamalai ,India ) strongly suggest optimal medical management would indeed reverse exercise induced ST depression.

Why can’t we call medical therapy as a revascularisation procedure ?

Human mind does not accept certain things. Simply swallowing few drugs can never make us believe ( Especially the current generation cardiologists !  )  it can be  equivalent to a PCI/CABG

While , restoration of  TIMI flow ,  %  stenosis , Net luminal gain,  are the popular   scientific parameters fro effective revascularisation , the following are  the  desired outcomes  clinical well being , relief from pain, reduction of plaque volume, plaque stabilisation, maintenance of  collaterals , microvascular patency ,  reduction of recurrent events .The irony in CAD management  is  in many points clinical endpoints can be achieved without mechanical  the above  mechanical end points !( As we learn from the OAT, COURAGE trials where we learn t arterial patency is nothing to do with major  clinical end points )

While PCI and CABG inherently convey they are revascularsation procedures , realistically looking medical  therapy also does improve the vascularisation espcially where it is needed (Micro)

In the overall interest of  CAD community , and with good scientific basis ,  it is vital  to  emphazise medical management of CAD  is  also a  form revascualrisation .It is better to call OMT(Optimal medical therapy )  as medical revascularisation .This will help us  to neutralise the unfair” semantic  advantage” the PCI and CABG enjoys as   revascularisation modalities !

Refer: 1.AVERT study :Atorvastatin equals PCI .2.Regular excercise equivalent to PCI (esc2009)

Final message

Medical management , do reverse  the positive EST in most of the patients provided the drugs are optimally used

Stability provided by  medical management   in coronary micro and macrocircualtion is  often  significant and it can either directly  or indirectly improve coronary perfusion .  attenuate ischemia ,  improve exercise capacity and relieve symptoms. To confirm this , every patient  with medical management should periodically undergo exercise stress testing.

* One may argue , without knowing coronary anatomy  it is dangerous to  assume things and every patient with positive EST should udergo CAG. Yes ,  It may be true, ischemia due to  critical lesions in proximal locations can never be corrected with drugs

Read Full Post »

Left main disease  is an important subset of CAD , and it has special interest for the interventionist. Traditionally cardiologist have   a fear to touch this lesion , as they thought a sudden occlusion within this vessel is life threatening   . Later on as  they gained experience  it was thought  we could intervene safely at least in protected left main . Subsequently  it was realised this fear was largely unfounded  , after all  the proximal LAD is equally  dangerous and we spend hours together inside an LAD ! .Now we have technology and expertise to do successful PCI any where in LM. And  unfortunately , the same expertise is not applied in selecting the ideal patients who will benefit the most . LMD has become a glorified indication for PCI.

The terminology of protected and unprotected LMD is in vogue for many years . Unfortunately it do not convey a uniform meaning . In next few minutes ,  I shall share  my views on the nuances of protected and unprotected LMD .

The term   protected was  not  coined by  cardiovascular physiologists   but by   interventional  cardiologists . Hence it connotes a  anatomical  meaning rather than physiological.  Protected LMD  meant there must be a at least one  graft to either LAD or circumflex . And this graft should be functional . The presence of this graft is supposed to increase the comfort levels of the interventionist as well as  the patient.

A left main coronary artery disease angiographically  can be  classified  as

Common types of Left main lesion

• Asymptomatic , non flow limiting , angiographically insignificant disease(< than50%)
• Ostial
• Ostio proximal
• Shaft : Mid, distal or diffuse Left main
• Bifurcation

Unprotected left main

• All the above lesions
• Non functional GABG grafts ( eg: LIMA occlusion makes LAD unprotected)

Protected left main

• Post CABG  with atleast one functional graft to LAD /LCX
• ? Left main   with total  LAD and very good LAD collaterals from RCA /LCX

Partially protected Leftmain

It could mean any of the following,     Left main Plus  .  . .

1. Incomplete occlusion of single  LIMA graft
2. Occlusion of  SVG-LCX and patent LAD-LIMA
3. Occlusion of LIMA-  LAD graft but patent SVG-LCX  graft
4. Patent LIMA-LAD  but a  critical  LM / LCX  bifurcation lesion with no grafts for LCX*

The above 3  situations may demand a  PCI .But logic would  suggest one would try to open up the partially occluded graft rather than open the left main . Of course the decision involves status of RCA .

*The only indication for a  PCI  in protected  LMD could be 4

Unusual ( Crazy !) questions  about  left main disease

Can left main be protected by collateral circulation ?

It is very common to find Left main   bifurcation  lesion   with LAD having  very good collaterals from RCA sometimes filling up to proximal  LAD .This can be considered   “protected left main equivalent”

As on today , cardiologists would rather   believe  a surgeon’s graft  rather than a naturally grown  collateral from RCA however extensive it may be !

But logics and real case experience would indicate in a patient  with LMD and an  extensively collateralised LAD can in fact be  considered a protected left main.

If a  left main is well protected by a functional LAD graft , why should we do a PCI for left main at all ?

This question was risen in one of our cath conferences , a patient   who had functioning  LIMA to  LAD graft.His   RCA had a functioning  venous graft  and his circumflex had a partially functioning  graft.The left main had a near total  obstruction and the proximal  LAD was  faintly visible .

Since the  patient  had class  2 angina Options were discussed .He  satisfied  the  current criteria of protected LMD .Just because he fulfils the criteria of protected left main , he  does not  become eligible for  left main    PCI .  After all he is having this LMD for many years. Protecting again the left main which is already protected is not a big deal in terms  of outcome .  Double protection is waste of resource at additional risk. It was decided to attempt a PCI to SVG graft to LCX. If it does n’t work leave him with medical management.

Does  every patient  after a CABG   has a high chances of developing LMD ?

What is accelerated atherosclerosis of Left main following LAD /LCX  grafts ? It is  true  left main  has high risk of  accelerated atherosclerosis and it   undergoes  gradual obstruction once the LAD and LCX is grafted.This is due to low flow across the native left main as distal grafts maintain the flow . This is all the more likely in good bulk of patients who had undergone  CABG  where   LMD  was the indication .

A typical scenario

A left main patient   who undergoes a CABG  a follow up for a suspected  angina  angio after 5 years show the  totally  or near totally occluded native left main . Sudden   Visualisation of worsened leftmain disease    makes this patient eligible for  a  PCI as he fulfills the criteria for  protected leftmain .

Final message

A well protected left main  with a good  functioning graft especially to LAD   most often do not require a fresh revascularisation  procedure  irrespective of the tightness of left main disease . Most of such patients will be candidates for medical therapy .Contrary   to the popular belief ,   left main  intervention   could  be    confined  to   ” unprotected LMD   rather than well protected LMD” as the  potential benefits are more .Further interventional resources need not be wasted in giving second alternate protective channel  for an already protected vessel !

Of  course it should be remembered  in any given patient  with  protected or unprotected  LMD  the indication for  revascualrisation  is based on  the severity of lesion , symptoms,  LV function ,  residual ischemia, viability  etc .

Suggestions  , comments  and  corrections  welcome

Read Full Post »