Continuation or Discontinuation of Statin Therapy Did Not Influence Patient Outcomes after the Development of Acute Respiratory Distress Syndrome

Background. The anti-inflammatory effects of statin therapy may be beneficial in the treatment and prevention of acute respiratory distress syndrome (ARDS). Objectives. Determine if continuation or discontinuation of prior statin therapy is associated with ventilator-free days (VFDs) at day 28 in patients with ARDS. Methods. Patients with ARDS admitted to the intensive care units of a tertiary care medical center were evaluated in this retrospective cohort study. Included patients were allocated to three groups: patients in whom statin therapy was given before and continued after ARDS diagnosis (Group 1), patients with statin therapy only before ARDS diagnosis (Group 2), and patients never exposed to statins (Group 3). Results. Of 244 patients evaluated, 187 were included; 17 (9.1%) patients in Group 1, 20 (10.7%) in Group 2, and 150 in Group 3. There were no differences among groups in APACHE II or SOFA scores. VFDs were not significantly different among groups (median 0 versus 4.5 versus 13.5 days, ). After adjustment for baseline characteristics, including propensity for statin administration, statin therapy was not associated with increased VFDs on linear regression. Conclusions. Exposure to statins before or after ARDS diagnosis was not associated with improved VFDs in this cohort of patients with ARDS. 1. Introduction Acute respiratory distress syndrome (ARDS) is a common and devastating illness in the intensive care unit (ICU), with mortality rates exceeding 30–50% [1]. ARDS occurs secondarily in a number of disease processes, most commonly sepsis, pneumonia, aspiration, trauma, pancreatitis, blood transfusions, smoke or toxic gas inhalation, and certain types of drug toxicity [2]. The pathogenesis of ARDS is not completely clear. The disease process is characterized by diffuse damage to the alveoli resulting in disruption of the endothelium and epithelium. In the acute phase of ARDS, fluid accumulates in the alveolar spaces and is accompanied by severe inflammation, increased pulmonary vascular permeability, and gas exchange abnormalities. The subsequent fibrotic phase results in diffuse interstitial thickening, fibrosis, increased dead space, and loss of lung compliance [3]. Disappointingly, anti-inflammatory therapies for ARDS have been utilized with limited success in past studies [4–9]. Despite preliminary data suggesting reduced inflammation with ketoconazole and lisofylline, these effects were not demonstrated in clinical trials of patients with ARDS, and the studies were terminated early due to futility [4, 5]. Corticosteroids have been