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 ?
- The ischemia has to be extensive to produce WMA.
- Presence of even minimal collateral circulation could prevent WMA.
- 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.
- 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 .
- 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 .
- WMA equivalents. Some times, the WMA defect is very subtle for the eyes , but still good enough to result in ischemic MR.
- Electrocardiographically T wave ischemias rarely produce WMA , while resting ST segment depression > 2mm invariably result in WMA.
- 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.
nice chapter, i really like it
This is a good chapter, but it would be even better after an edit for grammatical errors and sentence construction.
Again, great work!
I love it!. Very nice! Perfect! Subject is interesting to me. Can I ask some references from you basing in this chapter, because I have to report this week on chest pain as a sole basis of revascularization, and not relying on WMA in transthoracic echocardiography and stress echo in the decision of sending patients to Cath lab and then revascularization. I wouuld be very grateful if you can send me a list of your references on this chapter or possible related journals or randomized clinical trials. Thank you again.