Circadian variation in ST-segment elevation myocardial infarction: a nationwide analysis of onset, treatment delays,

Artur Dziewierz1,2, Krzysztof Malinowski3,4, Natalia Dardzińska5

  • 1Second Department of Cardiology, Institute of Cardiology, Jagiellonian University Medical College, Kraków, Poland.

Insights

ST-segment elevation myocardial infarction (STEMI) onset follows a daily pattern, peaking in the morning. Nocturnal STEMI onset leads to significant treatment delays, with distinct circadian patterns observed for left anterior descending versus right coronary artery involvement.

Area of Science:

  • Cardiology
  • Circadian Biology
  • Public Health

Background:

  • ST-segment elevation myocardial infarction (STEMI) onset exhibits circadian variation.
  • Limited data exist on how STEMI onset time impacts treatment delays and coronary pathology in large contemporary registries.

Purpose of the Study:

  • To investigate the circadian patterns of STEMI onset.
  • To assess the influence of onset time on treatment delays, culprit vessel involvement, and mortality.

Main Methods:

  • Retrospective analysis of 153,543 STEMI patients from the Polish National PCI Registry (2014-2022).
  • Examination of hourly symptom onset distribution and its association with patient characteristics, treatment delays, and infarct-related artery location.

Main Results:

  • STEMI onset peaked at 8:00 AM, with earlier onset in males. Nocturnal onset (3:00 AM) was linked to doubled pain-to-first-medical-contact times compared to daytime onset (1:00 PM).
  • Opposing circadian rhythms were found for infarct-related artery location: Left Anterior Descending (LAD) artery involvement peaked nocturnally, while Right Coronary Artery (RCA) involvement peaked during the day.
  • Periprocedural mortality did not significantly differ based on STEMI onset time despite treatment delays.

Conclusions:

  • STEMI onset demonstrates a strong circadian pattern influencing system delays.
  • The time of day impacts STEMI triggering and its pathophysiological manifestation, as evidenced by opposing circadian rhythms in LAD versus RCA involvement.
Abstract

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