With the introduction of more sensitive cardiac biomarkers, the European Society of Cardiology (ESC) and the American College of Cardiology (ACC) collaborated to redefine MI using a biochemical and clinical approach, and reported that myocardial injury detected by abnormal biomarkers in the setting of acute myocardial ischaemia should be labelled as MI. Continue reading
The TIMI risk score, based upon data from 15,000 patients with an ST segment elevation myocardial infarction eligible for fibrinolytic therapy, is a simple arithmetic sum of eight independent predictors of mortality.
Acute: Subtle low signal (hypointense) on T1, often difficult to see at this stage, and high signal (hyperintense) on spin density and/or T2-weighted and proton density-weighted images starting 8 h after onset; should follow vascular distribution. Mass effect maximal at 24 h, sometimes starting 2 h after onset, even in the absence of parenchymal signal changes. No parenchymal enhancement with paramagnetic contrast agent. Territorial intravascular paramagnetic contrast enhancement of “slow-flow” arteries in hyperacute infarcts; at 48 h, parenchymal and meningeal enhancement can be expected.
Infarction: focal hypodense area, in cortical, subcortical, or deep gray or white matter, following vascular territory, or watershed distribution. Early subtle findings include obscuration of gray/white matter contrast and effacement of sulci, or “insular ribbon.”
Criteria for acute, evolving or recent MI
Either one of the following criteria satisfies the diagnosis for an acute, evolving or recent MI:
1) Typical rise and gradual fall (troponin) or more rapid rise and fall (CK-MB) of biochemical markers of myocardial necrosis with at least one of the following: