Safety of benzodiazepines in patients with acute heart failure: A propensity score-matching study.

AIM: Benzodiazepines (BZDs) are one of the most used drugs to control symptoms in patients with acute heart failure (HF). However, the evidence on its safety is inconclusive. The objective was to describe the characteristics of patients admitted for HF and treated with BZDs and to assess the relationship of this treatment and mortality. PATIENTS AND METHODS: We performed a cross-sectional, multicentre (74 Spanish hospitals), cohort study. Patients admitted for HF were divided depending on whether they were treated with BZDs or not. Propensity score analysis matched patients in both groups in a 1:1 manner according to different factors. The primary outcome was mortality at day 7. Secondary outcomes were mortality at days 30 and 180, as well as readmissions and emergency room visits at 180 days. RESULTS: We included 1855 patients: 639 (34.4%) had prescribed BZDs treatment versus 1216 (65.6%) who had not been treated. Patients receiving BZDs had advanced heart disease, severe symptoms, need more HF intensive treatment and higher mortality. After propensity matching 381 balanced paired cases were included in each group. Treatment with BZDs was not associated with greater risk of mortality at day 7 of index hospitalization (7.6% vs 5.2%, adjusted OR 1.49, 95% CI 0.83-2.68, p = 0.186). There were also no differences between groups in terms of mortality at day 30 and 180, readmissions or visits to the emergency room. CONCLUSIONS: Our data support that benzodiazepines could be safely used for improving symptoms. in patients admitted for acute HF in terms of short-medium term mortality.

Hypothermia-induced Brugada-like electrocardiogram pattern.

A patient in whom moderate hypothermia developed after prolonged cardiopulmonary resuscitation is described. Hypothermia was manifested by transient electrocardiogram changes, including long QT, precordial J waves, and downsloping ST-segment elevation ending in a negative T wave in leads V(1) and V(2) resembling the Brugada syndrome. The physiopathologic mechanisms of these electrocardiographic findings are discussed.