Читать книгу Practical Cardiovascular Medicine - Elias B. Hanna - Страница 22

In patients with a recent infarction (a few days earlier), the diagnosis of reinfarction relies on:

 CK or CK-MB re-elevation, as they normalize faster than troponin, or

 Change in the downward trend of troponin (re-increase > 20% above the nadir)¹

Type 3 MI is defined as sudden death with preceding clinical and ECG features suggestive of MI, such as VF.

In the post-PCI context, MI is diagnosed by a troponin elevation > 5× normal, along with ischemic ST changes or Q waves, new wall motion abnormality, or angiographic evidence of procedural complications.¹ In patients with elevated baseline cardiac markers that are stable or falling, post-PCI MI is diagnosed by > 20% reincrease of the downward trending troponin to a value >5x normal, along with the other features (most studies use a 50% rather than a 20% cutoff in the post-PCI context). Note that spontaneous NSTEMI carries a much stronger prognostic value than post-PCI NSTEMI, despite the often mild biomarker elevation in the former (threefold higher mortality).^33,34 In fact, in spontaneous NSTEMI, the adverse outcome is related not just to the minor myocardial injury but to the ruptured plaques that carry a high future risk of large infarctions. This is not the case in the controlled post-PCI MI. Along with data suggesting that only marked CK-MB elevation carries a prognostic value after PCI, an expert document has proposed the use of CK-MB ≥ 10× normal or troponin ≥70x normal to define post-PCI MI, rather than the mild troponin rise.³⁴

In the post-CABG context, MI is diagnosed by a troponin elevation > 10× normal, associated with new Q waves or new wall motion abnormality.¹