The Ongoing Conundrum of the Type 2 Myocardial Infarction vs. a Myocardial Injury

The Task Force for the Universal Definition of Myocardial Infarction simultaneously published in 2007 and 2012 an international consensus document in the Journal of the American College of Cardiology, the European Heart Journal, and Circulation. The 2007 and 2012 documents were updated revisions of the original document published in 2000 by this task force.
A myocardial infarct as defined by the task force involves myocardial cell death due to prolonged ischemia. In the two most recent task force publications, various types of MI were defined. A type 1 MI was defined as an MI resulting from atherosclerotic coronary artery disease (CAD) with an occluded or partially occluded coronary artery secondary to an atherosclerotic plaque rupture or fissuring. Patients with type 1 MI were defined as individuals presenting with the typical clinical picture for MI.
However, recognizing that patients meeting the MI criteria without having coronary thrombi might require a different management strategy compared with those with coronary occlusion led the task force to create the category of a type 2 MI which is defined as occurring in individuals in whom myocardial necrosis was the result of a marked increase in myocardial oxygen demand or a marked decrease in myocardial blood flow leading to myocardial ischemic necrosis. Patients might have atherosclerotic coronary artery disease or they might have angiographically normal coronary arteries.
Unfortunately, patients may demonstrate abnormal blood troponin values in the absence of myocardial ischemia. Such patients are said to have suffered a non-ischemic myocardial injury. The use of the term non-ischemic myocardial injury mirrors the nomenclature of infarction and injury of other organs, for example, acute kidney injury.
In patients with serious comorbid illnesses the heart is presumably injured as an “innocent bystander”. Most of these individuals, however, have not had clinically important changes in their myocardial supply/demand status. Thus, the task force has defined these latter patients as not having suffered a type 2 MI. Rather they are said to have had a myocardial injury in the setting of a serious comorbid condition. Factors suggested in such situations as causative of myocardial necrosis included elevated circulating levels of inflammatory cytokines such as TNFα as well as catecholamines.
The complexity of the patients involved, and the potential for differing interpretations of the universal MI definition document by physicians have resulted in some uncertainty as to what constitutes a type 2 MI versus a non-ischemic myocardial injury. Clinical judgment is required to distinguish a type 2 MI from a non-ischemic myocardial injury. The latter is diagnosed when there has been no major hemodynamic or arterial oxygenation abnormality in the setting of a serious illness. The term “acute non-ischemic myocardial injury” avoids affixing the term myocardial infarction to these patients. Therapy for this entity is yet to be defined.