Pulmonary congestion evaluated by lung ultrasound predicts decompensation in heart failure outpatients

Background Pulmonary congestion is the main cause of hospital admission among heart failure (HF) patients. Lung ultrasound (LUS) assessment of B-lines has been recently proposed as a reliable and easy tool for evaluating pulmonary congestion. Objective To determine the prognostic value of LUS in predicting adverse events in HF outpatients. Methods Single-center prospective cohort of 97 moderate-to-severe systolic HF patients (53 ± 13 years; 61% males) consecutively enrolled between November 2011 and October 2012. LUS evaluation was performed during the regular outpatient visit to evaluate the presence of pulmonary congestion, determined by B-lines number. Patients were followed up for 4 months to assess admission due to acute pulmonary edema. Results During follow-up period (106 ± 12 days), 21 hospitalizations for acute pulmonary edema occurred. At Cox regression analysis, B-lines number ≥ 30 (HR 8.62; 95%CI: 1.8–40.1; p = 0.006) identified a group at high risk for acute pulmonary edema admission at 120 days, and was the strongest predictor of events compared to other established clinical, laboratory and instrumental findings. No acute pulmonary edema occurred in patients without significant pulmonary congestion at LUS (number of B-lines < 15). Conclusion In a HF outpatient setting, B-line assessment by LUS identifies patients more likely to be admitted for decompensated HF in the following 4 months. This simple evaluation could allow prompt therapy optimization in those patients who, although asymptomatic, carry a significant degree of extravascular lung water. Condensed abstract Pulmonary congestion is the main cause of hospital admissions among heart failure patients. Lung ultrasound can be used as a reliable and easy way to evaluate pulmonary congestion through assessment of B-lines. In a cohort of heart failure outpatients, a B-lines cutoff ≥ 30 (HR 8.62; 95%CI: 1.8–40.1) identified patients most likely to develop acute pulmonary edema at 120-days.