Brain mimickers of myocardial infarction

I read with interest the paper by A. Sharma and colleagues [ ]. Electrocardiographic (ECG) changes mimicking an acute coronary syndrome are relatively common among patients with acute disorders of the central nervous system such as subarachnoid hemorrhage, stroke and status epilepticus. These changes are transient in most cases and are postulated to reflect a reversible, non-ischemic myocardial injury caused by the adrenergic storm and the activation of neurocardiogenic pathways triggered by the inciting CNS event. However, a probably not negligible subset of these patients fit the clinical, ECG and laboratory characteristics for the diagnosis of type 2 myocardial infarction (MI) [ ]. According to a case definition that has been widely promulgated, type 2 MI happens because of an imbalance between blood supply and myocardial oxygen demand under circumstances where conditions other than obstructive coronary artery disease substantially contribute to the mismatch that causes myocardial injury and necrosis [ ]. Furthermore, type 2 MI is linked with early and late mortality and an excess rate of adverse events, being an independent predictor of death with a 2-year mortality rate of approximately 50% [ ]. There are no key features favoring type 2 MI over the apparently transient myocardial injury of CNS acute disorders or an acute coronary syndrome. Clinical presentation, electrocardiographic findings, and biomarker profiles are similar and neither ECG or cut-off troponin levels can definitely differentiate between them. This implicates that the clinical meaningfulness of the appearance of ECG changes during acute CNS disorders is still an unresolved issue. In particular, it is unclear if patients with acute brain disorders in whom a type 2 MI can be diagnosed are at risk for a worse outcome than patients in whom the appearance of an ischemic ECG pattern is not associated with increased troponin levels.