PURPOSE: We hypothesized that acute systemic inflammation (ASI)-induced endothelial dysfunction is a significant and under-appreciated risk factor for sudden cardiac death (SCD) in ICU patients with pre-existing atherosclerotic cardiovascular disease (ASCVD). The relationship between acute systemic inflammation and sudden cardiac arrest in patients with sepsis and adult respiratory distress syndrome (ARDS) has not been investigated.
METHODS: Retrospective analysis of eligible patients from two randomized trials investigating the use of prolonged glucocorticoid treatment in sepsis (N = 74) and early ARDS (N = 89). SCD was defined as an unexpected cessation of cardiac mechanical activity in the absence of shock or acute changes in CV hemodynamic and pulmonary mechanics. Dysregulated systemic inflammation was defined by a less than 50% reduction in CRP by day 7.
RESULTS: 44 patients (27%) had ASCVD. 13 of 46 deaths (28.2 %) were SCD. SCD accounted for 38% and 20% of death in sepsis and ARDS, respectively. Among patients that died after study day 1 (N = 40), dysregulated SI was observed in 18 (45%); as for those who had SCD dysregulation was seen in 9 of 13 (69%), and 4 of 6 with progression of MODS. Patients with sepsis who had known history of cardiovascular diseases (CAD, PVD, and stroke) were more likely to die from SCD than other causes (75% Vs 25%, 100% Vs 0%, 100% Vs 0% respectively). Similar findings could not be demonstrated in the ARDS group. Presence of CV risk factors did not increase the risk of SCD in either sepsis or ARDS patients.
CONCLUSION: Patients with ASCVD (with or without DM) admitted to a medical ICU are at increased risk for SCD. These findings provide proof of concept for a potential relationship between systemic inflammation and SCD in patients with ASCVD.
CLINICAL IMPLICATIONS: If these findings are confirmed by larger studies, secondary prevention with ASA, B-blockers, statins, etc. should also be investigated in patients with ASCVD admitted with non-cardiac systemic inflammation.
DISCLOSURE: Amr El Gamal, None.