Abstract 13993: Soluble CD146 is a Marker of Peripheral Congestion in Global Heart Failure Patients

Abstract

Introduction: CD146 is a component of the endothelial junction. We previously showed that its soluble form (sCD146) is as powerful as plasma natriuretic peptides to detect cardiac origin of acute dyspnea. The source of plasma sCD146 in heart failure (HF) is however unknown. Hypothesis: We make the hypothesis that peripheral venous congestion (VC), a typical sign of global ventricular failure, might be the source of increased sCD146. Methods: A total of 44 outpatients with heart failure, NYHA functional class II or III, and LVEF <40%, no evidence of VC on physical exam and on stable medical therapy were studied. Patients gave informed consent. To experimentally model VC, venous arm pressure was increased to 30 mmHg above baseline by inflating a pressure cuff around the dominant arm. Blood was sampled from test and control arm (lacking an inflated cuff) before and after 90 minutes of venous congestion. Plasma concentrations of sCD146 were determined by ELISA. Values are expressed as mean ± SEM and groups were compared with paired-samples t-test. Results: The age of the study cohort was 54±2 years, 32% were female, 32% had an ischemic etiology and the LVEF was 22±1%. The induction of VC was associated with an increase in circulating levels of sCD146 in the congested arm when compared to baseline (506±33 vs 463±33 ng/ml, p=0.001) and to control arm (476±32 ng/ml, p=0.035). In contrast, no significant increase occurred in the control arm when compared to baseline values (Figure). Conclusions: Plasma sCD146 acutely increases in response to experimental peripheral VC. sCD146 could be particularly useful to titrate diuretic treatment in HF patients with global heart failure, possibly preventing end-organ dysfunction and damage from severe and/or long-standing peripheral VC.

Effect of an Emergency Department Care Bundle on 30-Day Hospital Discharge and Survival Among Elderly Patients With Acute Heart Failure

“…Based on previous cohort analysis, the mean (SD) number of days alive and out of the hospital at 30 days was estimated at 14 (9). 10,12,18 To be clinically relevant and consistent with previous literature, it was estimated that the intervention should improve this end point by 20% (ie, ≥3 days). 8,9 For 80% power and an α of 5%, 283 patients needed to be included.…”

“…10,11 The failure of recent acute heart failure studies to report clinical benefits with specific treatments may be attributable to both the delay from presentation to treatment, because recent studies suggest that an early therapy is associated with better prognosis, and the lack of management of precipitating factors, because acute heart failure prognosis has been reported to be associated with the underlying precipitant of worsening heart failure. 12,13 Whether early ED management of congestion and precipitating factors improves outcomes is unknown.…”