MI type 1 is an event related to atherosclerotic plaque disruption (eg, rupture, ulceration, erosion) with super- imposed thrombus formation in a coronary artery, resulting in acute reduction in myocardial blood supply and/or distal embolization with subsequent myonecrosis. MI type 2 is myocardial injury caused by conditions other than coronary artery disease that results in an imbalance between myocardial oxygen supply and/or demand (eg, coronary artery embolism or spasm, tachyarrhythmias, anemia, respiratory failure, pro- found hypotension). The measure set developed by our writing committee applies only to MI type 1 and does not uniformly apply to the other 4 types of MI. In fact, some of those measures are even contraindicated with certain MI type, such as aspirin or receptor inhibitor therapies, which are contraindicated in patients with a MI type 2 resulting from severe hemorrhage and anemia. Given the widespread use of very sensitive assays for markers of myocardial necrosis (eg, the highly sensitive and specific cardiac troponin [cTn] biomarkers) and advanced imaging modalities, very small amounts of myonecrosis unre- lated to ischemia can be detected (eg, heart failure, renal fail- ure, myocarditis, pulmonary embolism). Our measures also do not apply to these myocardial injury events, which should be differentiated from true AMI events. For the sake of immediate treatment strategies (eg, reperfu- sion therapy),AMI is differentiated into STEMI and NSTEMI, depending on the existence of ST-segment elevation in 2 contiguous leads on the presenting ECG. Acute STEMI equiv- alent can, however, manifest as: hyperacute T-wave changes, true posterior MI, multilead ST depression with coexistent ST elevation in lead aVR, characteristic diagnostic criteria in the setting of left bundle branch block. The proportion of STEMI versus NSTEMI events varies in different registries and depends on the age of patients, their geographic location, and the type of surveillance used. 