LAUSR

Myocardial infarction (MI) type 2 (T2MI) has been a focus of attention since it was first described in 2007. T2MI is due to a critical imbalance between myocardial oxygen supply and demand resulting from various pathological mechanisms other than an acute atherosclerotic plaque disruption in the coronary arteries. Patients may or may not have atherosclerotic coronary artery disease. Often, myocardial oxygen supply/demand imbalance is related to tachycardia, hypotension/ shock, coronary artery spasm, myocardial microvascular dysfunction, coronary embolism, coronary artery dissection, or other conditions reducing coronary artery flow, but also altered myocardial oxygen carrying capacity secondary to anaemia or hypoxaemia associated with severe respiratory failure. Distinguishing patients with T2MI from those with type 1 MI (T1MI) is often straightforward but challenging at other times. Patients with T1MI usually present with spontaneous symptoms and signs suggesting acute myocardial ischaemia, with a rise and/or fall of cardiac troponin (cTn) values being diagnostic of acute MI that is considered to be related to an atherosclerotic plaque disruption. Patients with T2MI may also have symptoms and findings signalling acute myocardial ischaemia, which is considered to be the result of an important myocardial oxygen supply/demand imbalance, and which is accompanied by a rise and/or fall of cardiac troponin (cTn) values indicating acute MI. However, it appears from an all-comers’ study that cTn levels in T2MI patients tend to be lower compared to individuals with T1MI. This pattern is reflected in the present high sensitivity (hs)-cTnI study, to which patients with ST elevations MI (STEMI) were excluded, where the hs-cTnI values were lower at 0, 1, and 3 h after admission in T2MI patients, although a differentiation between T1MI and T2MI could not be done from a single elevated hs-cTnI value. In fact, this finding is unsurprising considering the varied cTn kinetics in non-STEMI (NSTEMI) patients. On the other hand, in an attempt to distinguish T2MI from T1MI patients utilizing hs-cTnI, the authors developed a logistic regression model that identified optimal hs-cTnI concentrations that were very strong predictors for T2MI at baseline and after 1 or 3 h. Furthermore, when inserting these predictors in addition to clinical parameters into a multivariable model, they developed a binary score showing that female sex, lack of typical chest pain, and a low baseline hs-cTnI <_40.8 ng/L were important forecasters for differentiation between T1MI and T2MI. However, it is important to emphasize that these calculations were made on an NSTEMI cohort rather than on an all-comers’ population. However, the issue of which population to include in a given study is important. Studies have shown variable frequencies of T2MI ranging from 2 30% of the total numbers of MIs. The present reported incidence of 34.5% of all MIs may not only reflect the exclusion of STEMI patients but also the inclusion of patients with pulmonary embolism (PE) or Takotsubo syndrome (TS) in the T2MI category. The Universal Definition of MI Task Force did not intend that conditions with non-ischaemic myocardial injury in the setting of PE or TS be designated as T2MI in the absence of clear evidence of acute myocardial ischaemia. Nevertheless, Neumann et al. have argued that these patients have had high cTnI dynamics together with symptoms and angiographic findings compatible with concomitant T2MI. As such, the inclusion of such patients may inadvertently increase the frequency of T2MI patients. Perhaps because of the manner in which the cohort of Neumann et al. was selected, the frequency of coronary artery disease (CAD) was lower in T2MI patients, who more often consisted of women, were older, did not present with typical radiating chest pain and were more likely to have atrial fibrillation, heart failure, hypertension, and worse renal function when compared to T1MI patients. Moreover, the high 1 year mortality rate of T2MI patients equals that of T1MI patients, in contrast to many other studies that have shown a poorer outcome for T2MI patients when compared to T1MI patients.