Mechanisms of ST Elevation Myocardial Infarction in Patients Hospitalized for Noncardiac Conditions

ST elevation myocardial infarction (STEMI) occurring in patients hospitalized for a noncardiac condition is associated with a high mortality rate and thus we sought to determine the mechanisms underlying STEMI in this patient population. This is a single center retrospective study of 70 patients who had STEMI while hospitalized on a noncardiac service and underwent coronary angiography. Thrombotic in-hospital STEMI was defined by angiographic or intravascular imaging evidence of intracoronary thrombus, plaque rupture, or stent thrombosis. Thirty-six (51%) inpatient STEMIs developed in the operating room or various postoperative stages and 6 (9%) after endoscopy or a percutaneous procedure. Thrombotic etiologies were found in 39 (56%) patients. Nonthrombotic etiologies included vasospasm, supply-demand mismatch, and takotsubo cardiomyopathy. Patients in the thrombotic group were more likely to have antiplatelet medications discontinued on admission, had higher peak troponin levels and were more likely to undergo percutaneous coronary intervention than patients in the nonthrombotic group. Exposure to vasopressors, time from ECG to angiography, post-STEMI ejection fraction, length of stay, and in-hospital mortality were similar in both groups. There was no difference in the use of percutaneous coronary intervention in patients but longer ECG to coronary angiography times and fivefold higher in-hospital mortality in thrombotic inpatient STEMI compared with 643 patients who presented with an out-of-hospital STEMI during the same time period. In conclusion, thrombotic and nonthrombotic mechanisms cause STEMI in hospitalized patients and are associated with a high mortality.