For a study, researchers sought to determine the effect of shift work on reperfusion damage, which is a significant driver of clinical outcomes in AMI. Patients’ data for the study were obtained from the EARLY-MYO-CMR (Early Assessment of Myocardial Tissue Characteristics by CMR in STEMI) registry, which was a prospective, multicenter registry of patients with ST-segment elevation myocardial infarction (STEMI) who underwent cardiac magnetic resonance (CMR) imaging after reperfusion therapy. The main outcome was the size of the CMR-defined post-reperfusion infarct. The composite of major adverse cardiac events (MACE) during follow-up was a secondary clinical objective. Potential causes were investigated using preclinical animal AMI models.
About 412 STEMI patients were eventually included in the EARLY-MYO-CMR registry out of 706 patients recruited. Shift employment was linked to larger CMR-defined infarcts (β=5.94%; 95% CI: 2.94-8.94; P<0.0001). Shift employment was linked with an elevated risk of MACE over a 5.0-year follow-up (adjusted HR: 1.92; 95% CI: 1.12-3.29; P=0.017). Mechanism investigations revealed a unique nuclear receptor subfamily 1 group D member 1/cardiotrophin-like cytokine factor 1 axis in the heart, which was critical in mediating the negative effects of shift work on myocardial damage. A recent study discovered that shift employment causes myocardial infarction reperfusion damage. It discovered a new nuclear receptor subfamily 1 group D member 1/cardiotrophin-like cytokine factor 1 axis in the heart that may be important in mediating this process.