Dr.S.Venkatesan MD

Regional wall motion defect is the sine qua non of STEMI. Whenever there is sudden occlusion of a coronary artery , the segment  it supplies is expected to go in for mechanical dysfunction. This is the fundamental principle of ischemic cascade . But , in NSTEMI ,wall motion defects are not a consistent feature. In fact absence of WMA is much more common than it’s  presence.The concept of ischemic cascade tells us  that chest pain is the last  thing to occur in the series of events following ischemia.

But in reality it seems the myocardium rarely obeys  this rule

The incidence of WMA in unstable angina or NSTEMI could be  at best 25 % . How and why the majority  do not manifest it ?

1. The ischemia has to be extensive to produce WMA.
2. Presence  of even minimal  collateral circulation  could prevent WMA.
3. Sub epicardial or transmural  ischemia are more likely to result in WMA. Isolated subendocardial ischemia could not manifest the WMA as the epicardial band of non ischemic  contractile  myocardial tissue has a  piggyback effect on the ischemic segment and  hence WMA do not manifest.
4. Presence of LVH has an attenuating effect on the WMA.It is  a well realised fact ( Of course ,with very little published evidence !) LVH is a great protector of mechanical dysfunction during ACS.It can even  nullify the  mechanical effects of   STEMI sometimes  . Read my blog advantages of LVH .
5. Some  myocardial segments  which are less exposed to wall stress than others do not manifest WMA. For example, the myocardial segments supplied by the LCX territory are notorious for  being totally silent .
6. WMA equivalents. Some times,  the WMA defect is  very subtle for the eyes , but still good enough to result in  ischemic MR.
7. Electrocardiographically  T wave ischemias rarely produce WMA ,  while  resting ST segment depression > 2mm invariably result in WMA.
8. Some  would  suggest ( Especially the researchers !) WMA  is always there  concealed within as   we are unable to pick it up with  available imaging modalities.Trans thoracic echo has well known   limitations. If we do tissue doppler studies.(TDI) and myocardial strain rate it may show the WMA which is otherwise missed.

*Finally and most importantly  , it need to be emphazised even  few ischemic myocytes can trigger a clinical chest pain while it requires the collective efforts  few million ischemic myocytes  to apply the  “vice like   grip ” on the  myocardial contractility that result in WMA.

Just think about this

The concept of pharmocological stress testing like doutamine stress echo  , relies hugely on the phenomenon of ischemia induced wall motion defect , which is picked up by echocardiography.As we  recognise ,  even  in   real life , true  ACS the incidence of WMA  is very less  , how can ,  it be  logical to expect  pharmocological stressors to give us authentic  information regarding hidden  subclincal CAD.