Stress related wall motion defect is a well-known entity . It is referred to as Takotsubo cardiomyopathy .
These stress are often
- 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
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 ! )
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 ?