Key result
Active-phase MI onset worsens infarct size and mortality via exaggerated neutrophil inflammation.
Why the study?
Does the time-of-day of myocardial infarction onset affect cardiac healing and neutrophil recruitment in a mouse model?
Does the time-of-day of myocardial infarction onset affect cardiac healing and neutrophil recruitment in a mouse model?
p-value: p=0.0006
The time-of-day of myocardial infarction onset determines infarct size and cardiac function through circadian oscillations in CXCR2-dependent neutrophil recruitment, suggesting timing is critical for anti-inflammatory treatments.
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MI timing by circadian phase may influence outcomes; hypothesis-generating for time-targeted or CXCR2 therapies in humans.
Schloss et al. (2016) studied Myocardial infarction. Myocardial infarction onset during active phase (ZT13) vs. Myocardial infarction onset during resting phase (ZT5) was evaluated on Infarct size, cardiac function, and survival (p=0.0006). Myocardial infarction onset during the active phase (ZT13) resulted in exaggerated neutrophilic inflammation, larger infarct size, worsened cardiac function, and higher mortality compared to the resting phase (ZT5).
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