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Any cardiac troponin value above the upper range limit is considered myocardial injury. If the elevation is static it is considered chronic myocardial injury. If there's a rise or fall it is considered acute. For this to be considered myocardial infarction there must be some additional clinical indicator which might be based on symptoms, ECG changes or imaging. There needs to be at least one.
The above criteria for troponin elevation apply to MI types one through three. For types four and five, different troponin cut offs apply. For these types of infarction troponin elevations must be greater than 5 or greater than 10 times the upper range limit, respectively. Troponin elevations that do not meet these cutoffs denote injury rather than infarction. (Note that a peri-PCI MI is termed type 4a. There is also a 4b and 4c MI and these terms refer to the more distant downstream complications of stent thrombosis and stent restenosis, respetively).
And now for an overview of types one through five. These categories are essentially unchanged from the prior edition of the universal definition. Type one MI is an acute coronary syndrome with plaque instability and thrombus, either occlusive or nonocclusive as indicated by the surrogates STEMI and NSTEMI respectively. Type 2 MI is not an acute coronary syndrome. It may occur in the presence or the absence of coronary disease. If coronary disease is present there is no plaque instability. The infarction is caused by an unfavorable balance and oxygen supply and demand. A couple of additional points are of note regarding type 2 MI. First of all in general patients with type 2 MI have a worse prognosis than those with type 1. This is due to the presence of comorbidity and is not surprising. Among patients with type 2 MI, those with coronary disease have a worse prognosis then those without. Of interest, studies have shown that ST elevation in type 2 MI occurs in between 3% and 24% of cases. In part this may be because coronary embolism and spontaneous coronary artery dissection (SCAD) are classified as type 2 MI. Finally it is not always possible to differentiate between type 2 MI and non-ischemic myocardial injury. In fact the two conditions may overlap. Type III MI is sudden cardiac death in which acute myocardial infarction was suspected but there was no opportunity to draw troponin levels. Type 4a is peri-PCI MI. Types 4 b and c represent the downstream manifestations already discussed. Type 5 MI is peri-CABG MI. The differences in troponin criteria for types four and five as opposed to types one through three have already been discussed.
A few special points should be made concerning perioperative ischemic events surrounding non-cardiac surgery. The ACC/AHA guidelines on perioperative evaluation and management for patients undergoing noncardiac surgery, updated in 2014, give troponin testing in the perioperative period a class I recommendation only for patients who exhibit signs or symptoms of myocardial ischemia. Troponin testing as a means of surveillance for patients deemed to be at high risk but without said signs or symptoms carries only a IIb recommendation. However a recent report and accompanying editorial published in the March 20, 2018 issue of Circulation suggest a role for pre and post operative troponin surveillance in selected high risk patients. There is still no consensus regarding this.
Acute exacerbation of heart failure is a special case. The article recommends troponin testing in all such patients. If troponin is elevated and it is dynamic, there should be a high index of suspicion for MI. A static elevation may represent chronic myocardial injury as part of the heart failure syndrome.
Takotsubo cardiomyopathy, nowadays more appropriately referred to as stress cardiomyopathy, is considered separately. It is distinguished from MI of any kind. The mechanism of myocardial injury is the subject of controversy but it's probably at least in part catecholamine mediated injury in which case it would be nonischemic myocardial injury. Another special situation is myocardial infarction with nonobstructive coronary arteries. This is known as MINOCA and may arise as a result of either type 1 or 2 MI.
What about patients with CKD? Many of these patients who have elevated troponins have chronic myocardial injury as a result of the CKD. Diagnosis of MI may be difficult in this setting. It is based on changes in troponin along with the other clinical criteria previously discussed.
Critical illness is commonly associated with troponin elevation. Either type 1 or type 2 MI may occur. Quite often patients with critical illness experience troponin elevation due to non-ischemic myocardial injury as an organ manifestation of the underlying critical illness. These cases may be difficult to distinguish from MI, especially type 2. In such patients, whether to evaluate for coronary disease, usually after recovery from critical illness, as a matter for clinical judgment.
The document contains some discussion of the ECG changes of myocardial infarction. The section makes several important points. First, when the initial tracing is nondiagnostic in a patient having active chest pain, serial tracings 15 to 30 minutes apart for the first couple of hours are recommended. ST segment elevation in lead aVR is mentioned as an important prognostic indicator and an indication of left main or multi vessel coronary artery disease. De Winter and Wellens T waves are described in that section, without calling them by name.
Bundle branch block gets a very superficial discussion. Scarbossa like changes are hinted at without using that eponym. New bundle branch block, either right or left, is mentioned. Mention is made of electrical remodeling (otherwise known as cardiac memory) in patients with pacemakers, in reference to non-paced complexes.
Section 31 has a nice discussion of normal versus pathologic Q waves and/ or QS complexes. Section 33 discusses ST segment and T wave negativity commonly seen in rapid atrial fibrillation and SVT. It states that the cause is poorly understood but that the phenomenon does not necessarily represent myocardial ischemia. It is mentioned that some degree of anomalous ventricular activation and or electrical remodeling may somehow explain these findings. In some cases it may represent a type 2 MI but this should not automatically be classified as such without additional clinical indicators.