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Introduction: Several studies have reported circadian periodicity of sudden cardiac arrest (SCA), most commonly a nadir in event frequency during overnight hours. It remains unclear to what extent this circadian pattern is influenced by variation in patients’ physical activities. One way to elucidate this is to compare patients with out-of-hospital (OHCA) versus in-hospital (IHCA) cardiac arrests, which has not been previously done. We hypothesize that the circadian pattern of SCA will be preserved in a mixed contemporary cohort of OHCA and IHCA survivors. Methods: A total of 1,433 consecutive survivors of SCA in the Pittsburgh area from 2002 to 2012 were included. Patient demographics including clinical histories and details of SCA were collected using records from emergency medical services and rapid response teams. Unwitnessed SCA and those with potential non-cardiac confounders were excluded. The distribution of SCA throughout the day and associated patient characteristics were tested for differences using chi-square test and student’s t-test. Results: Of the 1,224 patients analyzed, 706 had IHCA and 518 OHCA. We observed a nadir of SCA in the nighttime hours between 0000 - 0600 in both IHCA and OHCA groups (p<0.001). Patients who arrested in this nighttime window had more co-morbidities (p=0.01) and lower percent of angiographically confirmed acute myocardial infarction (p=0.025). A similar circadian pattern was noted for patients with higher or lower comorbidity burden (p<0.001), although more blunted in sicker patients, as well as for patients whose arrest was due to a shockable rhythm (p<0.001). Correspondingly, the IHCA group had higher co-morbidity burden (p<0.001) and a blunted nighttime nadir compared to the OHCA group (p<0.001). We did not observe a temporal variation by day of week but did see a seasonal pattern with a peak in SCA in the Pittsburgh cold months (p<0.001). Conclusion: The typical pattern of nighttime nadir in SCA is seen in both OHCA and IHCA but is more blunted in sicker patients and in the hospital. This suggests a common mechanism that transcends differences between the two settings but may be influenced by non-cardiac comorbidities or environmental factors such as activity level.

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