Type 2 myocardial infarction (T2MI), also known as supply/demand MI, is a commonly encountered clinical challenge, and, according to Yader Sandoval, MD, and colleagues, one that deserves more notice from the cardiology community. In an article recently published in JACC, Dr. Sandoval et al. reviewed the definition of T2MI, the controversies surrounding its acceptance in clinical practice, and future directions for research that may improve its diagnosis.

Published in 2007, the Second Universal Definition of MI expanded clinical classification of MIs, describing T2MI as an MI due to supply/demand mismatch, without plaque rupture (e.g., coronary artery spasm, anemia, hypertension), but with myocardial necrosis (evidenced by a rise and/or fall of cardiac biomarkers above the 99th percentile reference value of a normal population), in addition to at least one other criteria for MI. In a further refinement, 2013's Third Universal Definition of MI added coronary endothelial dysfunction as a variable to consider when encountering supply/ demand ischemia.

While major cardiology societies endorsed the definitions and subtypes of MI, clinical practice and research trials have been reluctant to adopt this definition. The multifactorial nature of supply/demand ischemia further complicates development of strict criteria for the diagnosis of T2MI. Patients may have any number of factors leading to increased demand or decreased supply, and certain scenarios make adjudicating a T1MI (spontaneous related to plaque rupture) versus T2MI even more challenging. These include heart failure, the postoperative setting, and critically ill patients—all of which can be associated with increases in cardiac troponin (cTn), making their etiologic assessment "remarkably difficult."

Confirmation of a T2MI diagnosis relies on currently available cTn assays; when novel high-sensitivity cTn (hs-cTn) assays become available in the United States, Sandoval et al. predict increased incidence of cTn elevations above the 99th percentile in clinical settings—consistent with T2MI. There are a limited number of studies offering epidemiologic data, perhaps owing to the disparity in diagnosis definitions, that make distinguishing between T1MI and T2MI a great challenge for research, clinical, and regulatory purposes.

Given the paucity of systematic data regarding diagnosis and management of T2MI, Sandoval et al. noted that several questions face the clinical cardiology community, including:

• Should clinicians embrace the five subtypes of MI (and therefore increase the recognition of T2MI), or advocate for the more familiar acute coronary syndrome (ACS) classification and utilize a "non-ACS" label that includes supply/demand MI?
• Given the challenges surrounding the clinical distinction between T1MI and T2MI, should there be a "default" diagnosis when diagnostic uncertainty prevails, with consequential clinical and research implications?
• Should strict and standardized criteria be used to define T2MI? Or should an individualized approach assessing all involved variables be favored?
• Should clinicians preferably order cTn on patients with a higher pretest probability for T1MI? Or should cTn be obtained in allcomers with suspected ischemic symptoms?
• Do T2MI patients have independently worse outcomes? Or is this a reflection of the underlying unadjusted comorbidities?

One major institutional change that needs to be made before T2MI is universally adopted: the ICD must recognize the condition to facilitate quality review evaluations, including resource utilization, and outcomes assessments. Dr. Sandoval and colleagues note that this is particularly true in the United States, "because clinicians are unable to diagnose a patient with T2MI without being penalized by ICD coders for deviating from the accepted, guideline-driven ACS therapies that are required by Centers for Medicaid and Medicare Services (e.g., aspirin on arrival and discharge, beta-blocker, statin prescribed on discharge, etc.) even though these therapies might not be appropriate for T2MI."

Sandoval Y, Smith SW, Thordsen SE, et al. J Am Coll Cardiol. 2014 March 13. [Epub ahead of print]