Type 2 myocardial infarction

Type 2 myocardial infarction (T2MI) results from ischemia due to reduced oxygen supply, heightened demand, or both, without acute atherothrombosis. Numerous nonatherosclerotic factors, including coronary abnormalities like vasospasm, dissection, or embolism, as well as noncoronary issues like anemia, hypoxemia, and hypotension, can diminish myocardial oxygen supply. Similarly, factors such as severe hypertension, tachycardia, and fever can escalate oxygen demand. Moreover, T2MI can manifest in patients with or without obstructive coronary artery disease (CAD), although the threshold for ischemic necrosis induction is considerably higher in those without obstructive CAD. While type 1 myocardial infarction (T1MI), stemming from acute plaque disruption and subsequent thrombosis, benefits from a substantial evidence base guiding its evaluation and treatment, there is a scarcity of high-quality studies addressing T2MI.