Shift work worsens MI reperfusion injury

A recent study provides further proof that disruption of circadian rhythms by shift work leads to a higher risk of reperfusion injury in myocardial infarction (MI).

A group of researchers have identified a novel nuclear receptor subfamily 1 group D member 1/cardiotrophin-like cytokine factor 1 axis in the heart that appears to play a major role in mediating such process.

Patient data from the database of the EARLY-MYO-CMR (Early Assessment of Myocardial Tissue Characteristics by CMR in STEMI) registry, a prospective, multicentre registry of patients with ST-segment elevation myocardial infarction (STEMI) undergoing cardiac magnetic resonance (CMR) imaging after reperfusion therapy, were obtained.

CMR-defined postreperfusion infarct size was the primary endpoint, while the composite of major adverse cardiac events (MACE) during follow-up was secondary. The researchers also explored the potential mechanism using preclinical animal acute MI models.

The EARLY-MYO-CMR registry included 706 patients with STEMI, of whom 412 were included in the current analysis.

Shift work correlated with elevated CMR-defined infarct size (β, 5.94 percent, 95 percent confidence interval [CI], 2.94‒8.94; p<0.0001). Shift work also correlated with increased risks of MACE (adjusted hazard ratio [HR], 1.92, 95 percent CI, 1.12‒3.29; p=0.017) during a median follow-up of 5.0 years.

These findings were consistent with shift work simulation in mice and sheep, in which a significant augmented reperfusion injury in acute MI was observed.

In mechanism analyses, the researchers identified a nuclear receptor subfamily 1 group D member 1/cardiotrophin-like cytokine factor 1 axis in the heart that played a crucial role in mediating the detrimental effects of shift work on myocardial injury.

“Shift work is associated with increased risk of acute MI and worsened prognosis,” the researchers said.