Type 2 MI

Here is a free full text review from the American Journal of Medicine.

Type 2 MI has received raised awareness but is the subject of a great deal of confusion.

The difference between type 1 MI (ACS due to an unstable coronary plaque) and type 2 MI (myocardial O2 supply/demand imbalance) is often possible on the basis of clinical findings and circumstances.

Another frequent distinction to be made involves the difference between MI (usually type 2) and non ischemic critical illness related troponin elevation. Chest pain, ischemic ECG changes and echocardiographic wall motion abnormalities are absent in the latter condition. (Another cause of troponin elevation that sometimes causes confusion is stress cardiomyopathy. However, it is more likely to mimic STEMI than the conditions described here).

For type 2 MI there is little evidence to drive treatment and no guidelines. Treatment is guided largely by pathophysiologic considerations, focusing on favorably impacting the myocardial oxygen supply and demand balance. From the review:

If a type 2 MI is suspected, the next clinical conundrum develops. Should the patient undergo coronary angiography; should aspirin, a P2Y12 inhibitor, and antithrombotic therapy be administered; should the patient be treated with beta-blockers, calcium channel blockers, angiotensin-converting enzyme inhibitors, an angiotensin receptor blocker, a statin, ranolazine, or nitrates? At this time, there is a dearth of scientific information that can help physicians make clinical decisions in this setting. Cardiac catheterBottom Line Available evidence, from underpowered pooled data, neither supports nor refutes an association of systemic antibiotic therapy with improved venous leg ulcer healing. Among topical antimicrobials, cadexomer iodine may be associated with better healing compared with usual care.ization almost certainly is associated with significant risk in such critically ill patients, as is antithrombotic therapy. Often, beta-blockers, nitrates, and low-dose aspirin are given, but without a strong sense on the part of the clinician involved that this therapy is beneficial in this setting. Clinical research involving patients with type 2 MI or myocardial injury is needed desperately to assist in differentiating these 2 entities and determining what, if any, specific therapy is indicated.

In conclusion, the authors feel that careful weighing of the clinical situation is important in guiding further diagnostic testing and possible therapy in patients with type 2 MI or a nonischemic myocardial injury with necrosis. Thus, a patient with one of these syndromes and a poor prognostic outlook might not undergo any further testing following recovery from an acute illness where blood troponin values were elevated, while a patient with a reasonably good prognosis would be offered additional diagnostic evaluation to assess the likelihood of important underlying coronary artery disease and to guide therapy.