Question special
Moderator

In patients with critical illness and NSTEMI, it can be difficult to distinguish demand-ischemia from an underlying plaque rupture, especially in patients with CKD or without CAD risk factors or prior coronary angiography. Troponin is usually trended but the rise may be gradual/plateaus. A TTE is useful for looking for signs of infarct, but it may be delayed in order to optimize fluid-status as a possible source of demand-ischemia. The delay may lead to a missed event.

In patients with acute illness (sepsis, volume overload, pneumonia), what pushes you to consider a Type 1 over a Type 2 NSTEMI? Are there biomarkers under development that are more specific for plaque rupture to differentiate a Type 1 from a Type 2 NSTEMI?