Posts Tagged ‘akinetic myocardium’

The answer to this question  is not  easy  , as   one  would tend to believe . In fact this question , takes it for granted     revascularisation  will  improve the LV dysfunction in patients  with severe LV dysfunction.

The truth is , we  are not sure   about the mechanisms . How   revasculariastion  will have an effect  on  chronically dying or dead myocardium  ? (Acutely dying myocardium is a different story, where revascualrisation has a profound effect , that is called salvaging the myocardium )

This  issue is  of great clinical significance  in end stage ischemic heart disease  .A typical  myocardial segment in ischemic cardiomyopathy  has millions of  the dead cells  interwoven with dying cells  with  occasional  clusters if live cells scattered all over .Once the process of myocardial apotosis sets in ,  myocardial cell death does not result  in segmental destruction  instead  an universal cell death.(Paracrine signals of  cell death that spills over to adjacent segments  )  The current standards of revascualrisation (PCI and CABG) aims to provide blood flow  in a segmental fashion. Even if the blood flow is restored in an obstructive vessel it is not clear , how it is going to enter the chronically atrophied myocytes.

Meanwhile , many studies are available   suggesting  coronary revascularisation does indeed improve LV dysfunction. These  evidence has never been  conclusive .Real world experience would also  confirm this  simple fact , that   angina relief is definite following revascularisation but not dyspnea  relief  in patients  with LV dysfunction .

So ,  when seeking the  guidelines  for revascularisation  ( PCI or CABG )  in patients  with CAD one need to ask  this  specific  question

Does the patient has

A.Angina alone

B.Angina and dyspnea

C.Only  dyspnea

If the answer is C ,  assess the patient again , rule out systemic causes of dyspnea (Anemia, renal function etc)  rethink  or postpone  revascularisation.If primary  or secondary LV muscle dysfunction has set in revascularisation has little value.

Also read

Viable myocardium

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Post myocardial infarction revascularistation either by PCI or CABG forms the bulk of the coronary interventions world wide.There has been considerable controversy in selecting the patients for the procedure.

Certain basic rules are to be applied.

  • Never do any thing on a totally asymptomatic and fully functional patient.(Functional , means good exercise capacity of atleast( 10Mets).Just medical treatment with good doses of statins, beta blockers will do.
  • If a patient has persistent angina  following MI  ,the issue is relatively simple as  they are  candidates  for CAG  and intervention .
  • The issue becomes little complex when the primary complaint is breathlessness and echo showing  LV dysfunction.

This dilemma is due to a  simple fact

coronary revascularisation has a  great impact in relieving angina but has  less impact in reversing

left ventricular  dysfunction

So,  how do you approach a patient with LV dysfunction and exertional  breathlessness and absolutely no chest pain ?

  1. Do a  CAG
  2. Assess the lesions if any (Some times,  to our surprise there may not be any critical lesions at all ! )
  3. If there is / there are critical lesions try to corroborate with infarct segments.(Use Echo for this correlation)
  4. Don’t bother much,  if a  vessel has a lesion  that is supplying a scarred myocardium.
  5. If there is gross LV dilatation, mitral regurgitation and LV clot refer these pateints  may benefit  from surgical management

One of the rules written by the cardiology community over the past few decades has been

We must document viable myocardium before doing a revascularisation procedures on them.

This rule was self imposed ,  to prevent inappropriate revascularisation in  post MI population.

So , a  gamut of investigations (Both invasive and non invasive came into vogue) to identify viable myocardium in post MI population. Stress echo, Thallium-sesta MIBI, PET  to name a few .

Even after liberal usage of these invesitgations , we realised ,  the confusion in the  optimal selection of candidates for revascularisation has not settled.

In fact,  the correlation between viabilty and subsequent interventional benefit is  inconsistent .Not withstanding this  issue  ,cardiologists inspite of the negative results of OAT and TOAT trials ,  started  opening or by passing any occluded vessel irrespective of viability status.

Unanswered  &  Unasked questions in myocardial revascularisation ?

1.Why viable myocardium is viable even in the adverse compromised vascular  environment ?

It  is viable for the simple reason it has some capacity to be alive . By it’s inherent survival capacity (Survival of the fittest ) or it somehow gets the nutrients by cell to cell perfusion.

2. It is viable allright  ,  why it is not contracting ?

Because ,  it is biochemically and metabolically alive (Can be documented by FDG PET scan mismatch ) but it can not synthesise adequate ATPs to make the muscle contractile.

3.”Viable myocardium is viable ” what more you want from it   ?

Simple viability is not suffice . How to make it mechanically active and contractile ?

4.Is viable  myocardium    synonymous with ischemic myocardium ?.

No,  it is not (Contrary to the popular perception ) .

5. Is it not  common to find dysfunctional segments with good TIMI 3 flow ?. So what is the purpose to document viability ?

It is not suffice to simply document viable myocardium but it is an absolute necessity to prove this viable segment is also  critically ischemic .

7.If angina is  a sign of viabilty why most of viable myocardium is painless ?

This again confirms the fact , much of the viable myocardium in the post MI phase is not ischemic but” still dysfunctional” waiting for healing time. This concept  was  introduced with great fanfare* as  stunned myocardium ,  20 years ago , which was subsequently rejected my mainstream cardiologists , as this concept tend to  restrict the  freedom of interventionists. * Even though ,the concept was genuine and proven scientifically !

6.Are we  certain , the  viable ,  non contractile myocardium  (Which we painstakingly document )  will get back the contractility once the  segment is    revascularised?

Absolutely not. (With lot of PET study doumentation )  This,  we can not guarantee even in ischemic, viable segments  ,  while in the  non ischemic, viable segment it is all the more unlikely.

7. What are the chances of these viable but  non contractile myocardium  regain the contractility  by natural course ?
Very significant chances .In fact every patient recover some LV  function spontaneously over time .

Final message.

  • Revascularisation is non controversial in patients with angina
  • In patients with  primary symptoms of dyspnea  ,  it is less effective and documentation of myocardial viabilty per se will not guarantee successful outcome following revascularisation.Out come depends on  multiple factors .

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