A recent study by Dr. Chapman, published in Circulation, showed that implementation of high sensitivity cardiac troponin (hs-cTn) and the fourth universal definition of myocardial infarction (MI) increased the identification of patients at risk for cardiovascular and non-cardiovascular events, but failed to improve the outcomes. This study warrants the importance of seeking new strategies to improve outcomes in patients with type 2 MI and myocardial injury.
The fourth universal definition of MI recommends using hs-cTn and the 99th centile upper reference limit as the diagnostic threshold for MI. It also suggests the term “myocardial injury” as a sole increase in the hs-cTn value in the absence of other criteria for diagnosing myocardial infarction. The clinical implication of this modification, though, is yet to be fully discovered and recognized.
In a stepped-wedge cluster-randomized, controlled trial, a total of 48,282 consecutive patients with a history suggesting acute coronary syndrome were recruited. Participants were reclassified according to the Fourth Universal Definition of Myocardial Infarction. Type 1 or 4b MI or cardiovascular death at 1-year was considered as the primary outcome of the study. The secondary outcomes included all-cause death, cardiovascular death, cardiac death, non-cardiovascular death, duration of stay, myocardial infarction (type 1 or type 4b), unplanned coronary revascularization, hospitalization for heart failure, ischemic stroke, major hemorrhage, and unplanned hospitalization.
Using hs-cTn, the diagnosis of type 1 MI increased by 11% (510/4471), type 2 MI by 22% (205/916), acute myocardial injury by 36% (443/1233), and chronic myocardial injury by 43% (389/898). The primary outcome had the highest rate in those with type 1 MI when compared with those without myocardial injury (cause-specific HR 5.64 [95% CI, 5.12 – 6.22]). However, this outcome occurred with a qualitatively similar frequency among patients with type 2 MI (cause-specific HR 3.50 [95% CI, 2.94 – 4.15]), acute myocardial injury (cause-specific HR 4.38 [95% CI, 3.80 – 5.05]), and chronic myocardial injury (cause-specific HR 3.88 [95% CI, 3.31 – 4.55]). In contrast, non-cardiovascular deaths were highest in those with acute myocardial injury (cause-specific HR 2.65 [95% CI, 2.33 – 3.01]). No reduction was observed in the primary outcome of patients with type 1 MI (cause-specific HR 1.00 [95% CI, 0.82 – 1.21]) despite the increasing use of antiplatelet agents and coronary revascularization. Additionally, an increase in the recognition of type 2 MI and myocardial injury did not change their associated adverse outcomes.
This study showed similar cardiovascular outcomes in patients with type 2 MI and myocardial injury as well as a higher rate of non-cardiovascular death in these two groups. While the application of hs-cTn showed clear prognostic values, its clinical use has made no change to improve the outcomes. These data showed the importance of clinical attention to an increased hs-cTn value and its prognostic value as well as a need for considering new secondary preventive measurements to improve its associated clinical outcomes. Given the results of this study, a need to pursue additional non-invasive workup in patients without a clear cause of acute myocardial injury to identify unknown structural heart disease is felt.