Posts Tagged ‘remote ischemia’

Stress related wall motion defect  is a well-known entity . It is referred to as Takotsubo cardiomyopathy .

These stress are often

  • Emotional
  • Neurological
  • General systemic stress

The culprit seems to be pooling of adrenaline and nor adrenaline in myocardium .These remote  neurogenic stress can cause significant wall motion defect due to adrenergic  downpour

The image depicts the wide variation in the density of beta receptors in heart.The stress of MI can result in varying degrees of wall motion defect .It is important to realise the wall motion defect in STEMI has two components .One is related to ischemia and other is due to excess catecholamines. This explains many of the unexplained remote wall motion defects during STEMI .This  may be referred to as Intrinsic Takosubo effect !

Then   . . . the following    questions arise

When systemic stress can have a profound  effect on myocardium , what   about local stress ?

Acute STEMI  is  a huge stress for the heart   . . .   isn’t  . If  so , can it   alter  the wall motion defect in adjacent  or remote myocardial segments  independent of ischemia ?

With the distribution  of adrenergic receptors  showing  huge variation ,  we do not know how an acutely ischemic heart  spills the adrenaline all over .  Is there a pattern to it  ?  or it happens at random ?  Further , the  response to  accumulated  catecholamines  is  not  going to be  uniform. This will explain why certain patients  go into ischemic  LVF  , very early in the course of STEMI  even before the myocardium is necrosed. It will  also explain  the  benefits that accrue in selected patients  who receive early IV beta  blockade  ( Which is  of course currently not popular after COMET study ! )

Final message

We  have seen at least  two patients  with severe  transient ballooning  wall  motion defect in LAD region  (LV apex)  with isolated RCA lesion and inferior Infarct .

The question raised is this 

Can  the  stress of  Inferior  STEMI   . . . result in  apical Takatsubo  like  effect ?




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ST segment depression is a fairly common observation in anterior precardial leads. It   is  due to

  1.  Pure electrical phenomenon (Referred to as reciprocal changes)*
  2.  Additional  ischemia in LAD territory
  3.  It could imply  the IRA  is  a critically occluded  LCX and STEMI is actually an   infero -posterior STEMI
  4.  Simply  indicate a  multi vessel disease.
  5. Many times  reciprocal changes may simply indicate extensive nature of the  index  inferior MI.

How to differentiate reciprocal ischemia from true  remote ischemia ?*

  • Logically true ischemia patients  should suffer from double dose of angina (Infarct pain plus ischemic). Most of these patients will present in a   scenario of  post infarct persistent  angina . Patients with   pure electrical reciprocal  changes are relatively  quiet and  severe distress is uncommon.
  • In true ischemia  , both patterns are  not temporally related  in time. If its a  pure electrical phenomenon they should be linked in time .
  • Disproportionate ST segment depression  (ST elevation  in inferior lead  is  2 mm  while ST depression in v1,v2, v3 is >  3 mm )
  • Persistence of ST depression even after thrombolysis  or PCI to IRA.
  • Worsening with thrombolysis would suggest ST depression in V1V2 and v3  is indeed an  episode of  true NSTEMI  of LAD , where thrombolysis is contraindicated. (Also  read  – A  related article  dual acute coronary syndrome in this site )
  • Echocardiogram will give us a clue .One can  detect ischemic the wall motion defect in the segment in dispute .(Reciprocals do not show WMA )
  • Coronary angiogram   would provide   definite  answer to the speculations in most  . Still , it may   require a FFR  to confirm ischemia in the contra lateral artery.

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