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OBJECTIVE: Out-of-hospital cardiac arrest (OHCA) occurrence has been shown to exhibit a circadian rhythm, following the circadian rhythm of acute myocardial infarction (AMI) occurrence. Diabetes mellitus (DM) is associated with changes in circadian rhythm. We aimed to compare the temporal variation of OHCA occurrence over the day and week between OHCA patients with DM and those without. METHODS: In two population-based OHCA registries (Amsterdam Resuscitation Studies [ARREST] 2010-2016, n = 4163, and Danish Cardiac Arrest Registry [DANCAR], 2010-2014, n = 12,734), adults (≥18y) with presumed cardiac cause of OHCA and available medical history were included. Single and double cosinor analysis was performed to model circadian variation of OHCA occurrence. Stratified analysis of circadian variation was performed in patients with AMI as immediate cause of OHCA. RESULTS: DM patients (22.8% in ARREST, 24.2% in DANCAR) were older and more frequently had cardiovascular risk factors or previous cardiovascular disease. Both cohorts showed 24 h-rhythmicity, with significant amplitudes in single and double cosinor functions (P-range < 0.001). In both registries, a morning peak (10:00-11:00) and an evening peak (20:00-21:00) was observed in both DM and non-DM patients. No septadian variation was observed in either DM or non-DM patients (P-range 0.13-84). CONCLUSIONS: In these two population-based OHCA registries, we observed a similar circadian rhythm of OHCA occurrence in DM and non-DM patients.
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INTRODUCTION: In cardiac arrest, ventricular fibrillation (VF) waveform characteristics such as amplitude spectrum area (AMSA) are studied to identify an underlying myocardial infarction (MI). Observational studies report lower AMSA-values in patients with than without underlying MI. Moreover, experimental studies with 12-lead ECG-recordings show lowest VF-characteristics when the MI-localisation matches the ECG-recording direction. However, out-of-hospital cardiac arrest (OHCA)-studies with defibrillator-derived VF-recordings are lacking. METHODS: Multi-centre (Amsterdam/Nijmegen, the Netherlands) cohort-study on the association between AMSA, ST-elevation MI (STEMI) and its localisation. AMSA was calculated from defibrillator pad-ECG recordings (proxy for lead II, inferior vantage point); STEMI-localisation was determined using ECG/angiography/autopsy findings. RESULTS: We studied AMSA-values in 754 OHCA-patients. There were statistically significant differences between no STEMI, anterior STEMI and inferior STEMI (Nijmegen: no STEMI 13.0mVHz [7.9-18.6], anterior STEMI 7.5mVHz [5.6-13.8], inferior STEMI 7.5mVHz [5.4-11.8], p = 0.006. Amsterdam: 11.7mVHz [5.0-21.9], 9.6mVHz [4.6-17.2], and 6.9mVHz [3.2-16.0], respectively, p = 0.001). Univariate analyses showed significantly lower AMSA-values in inferior STEMI vs. no STEMI; there was no significant difference between anterior and no STEMI. After correction for confounders, adjusted absolute AMSA-values were numerically lowest for inferior STEMI in both cohorts, and the relative differences in AMSA between inferior and no STEMI was 1.4-1.7 times larger than between anterior and no STEMI. CONCLUSION: This multi-centre VF-waveform OHCA-study showed significantly lower AMSA in case of underlying STEMI, with a more pronounced difference for inferior than for anterior STEMI. Confirmative studies on the impact of STEMI-localisation on the VF-waveform are warranted, and might contribute to earlier diagnosis of STEMI during VF.