Physiologic effects of stress dose corticosteroids in in-hospital cardiac arrest (CORTICA): A randomized clinical trial.

Aim: Postresuscitation hemodynamics are associated with hospital mortality/functional outcome. We sought to determine whether low-dose steroids started during and continued after cardiopulmonary resuscitation (CPR) affect postresuscitation hemodynamics and other physiological variables in vasopressor-requiring, in-hospital cardiac arrest. Methods: We conducted a two-center, randomized, double-blind trial of patients with adrenaline (epinephrine)-requiring cardiac arrest. Patients were randomized to receive either methylprednisolone 40 mg (steroids group) or normal saline-placebo (control group) during the first CPR cycle post-enrollment. Postresuscitation shock was treated with hydrocortisone 240 mg daily for 7 days maximum and gradual taper (steroids group), or saline-placebo (control group). Primary outcomes were arterial pressure and central-venous oxygen saturation (ScvO2) within 72 hours post-ROSC. Results: Eighty nine of 98 controls and 80 of 86 steroids group patients with ROSC were treated as randomized. Primary outcome data were collected from 100 patients with ROSC (control, n = 54; steroids, n = 46). In intention-to-treat mixed-model analyses, there was no significant effect of group on arterial pressure, marginal mean (95% confidence interval) for mean arterial pressure, steroids vs. control: 74 (68-80) vs. 72 (66-79) mmHg] and ScvO2 [71 (68-75)% vs. 69 (65-73)%], cardiac index [2.8 (2.5-3.1) vs. 2.9 (2.5-3.2) L/min/m2], and serum cytokine concentrations [e.g. interleukin-6, 89.1 (42.8-133.9) vs. 75.7 (52.1-152.3) pg/mL] determined within 72 hours post-ROSC (P = 0.12-0.86). There was no between-group difference in body temperature, echocardiographic variables, prefrontal blood flow index/cerebral autoregulation, organ failure-free days, and hazard for poor in-hospital/functional outcome, and adverse events (P = 0.08->0.99). Conclusions: Our results do not support the use of low-dose corticosteroids in in-hospital cardiac arrest.Trial Registration:ClinicalTrials.gov number: NCT02790788 ( https://www.clinicaltrials.gov ).

Metabolic syndrome, independent of its components, affects adversely cardiovascular morbidity in essential hypertensives.

BACKGROUND: The metabolic syndrome (MS) is widespread among hypertensive patients. However, the net impact of MS on major atherosclerotic events beyond the cardiovascular risk imposed by its individual components remains controversial in this group. We sought to assess both the independent and incremental prognostic role of MS for unfavorable cardiovascular events in a cohort of essential hypertensives. METHODS: We followed up 2176 essential hypertensives free of cardiovascular disease for a median period of 40 months. All subjects had at least one annual visit. MS was defined according to the updated NCEP III criteria. Endpoint of interest was the incidence of stroke, coronary artery disease (CAD) and their composite. RESULTS: MS was present at baseline in 819 hypertensives (37.6%). MS group presented increased prevalence of resistant hypertension in comparison to MS free group (18.4% versus 10.6%, p < 0.001). The incidence of the composite end-point was 3.1% (69 events) across the follow-up period. Patients with MS were more likely to experience major adverse cardiovascular events (MACE) in comparison to reference category (3.7% versus 1.9%, log rank p = 0.024). While MS was an independent predictor for MACE, none of the individual components of the syndrome was associated independently with the endpoint. MS provided incremental discriminative value (Harrell's c, p < 0.05 for all) over individual risk factors for the incidence of MACE. CONCLUSIONS: MS predicts adverse cardiovascular events in hypertensives incrementally of its individual components. Early identification of MS in this population may enable more accurate prediction of future cardiovascular risk and could implement more efficient strategies in terms of primary prevention.