Background-Doppler ultrasound is the clinical gold standard for noninvasive blood pressure (BP) measurement among continuous-flow left ventricular assist device patients. The relationship of Doppler BP to systolic BP (SBP) and mean arterial pressure (MAP) is uncertain and Doppler measurements require a clinic visit. We studied the relationship between Doppler BP and both arterial-line (A-line) SBP and MAP. Validity and reliability of the Terumo Elemano BP Monitor, a novel slow cuff-deflation device that could potentially be used by patients at home, were assessed. we tested the success rate, reliability, and validity of a novel slow cuff-deflation system, which enhances sensitivity for detection of BP in patients with reduced arterial PP. The Terumo Elemano BP Monitor was compared with BP measurements taken with either A-line (gold standard) or Doppler ultrasound (clinical standard). We also compared the performance of an automated BP monitor (GE CARESCAPE V100) with A-line and Doppler, as this automated device is routinely used at our Institution, in patients on CF-LVAD support. Methods and Results-Doppler Methods Patient PopulationA total of 60 patients were prospectively studied at 2 time points as follows: (1) 30 inpatients were assessed immediately following implantation of an axial flow CF-LVAD, the Heart Mate II (Thoratec Corporation, CA; inpatient visit v1), and the second encounter (inpatient v2) occurred a minimum of 3 days later after the patient was no longer in the intensive care unit and no longer had an A-line; and (2) a separate group of 30 outpatients on Heart Mate II LVAD support, who presented to clinic for routine follow-up, were assessed at 2 separate visits (outpatient v1 and outpatient v2, respectively). Patients enrolled in the inpatient group could not be enrolled in the outpatient group. The study protocol was approved by the local institutional review board and all subjects signed provided informed consent. Study ProtocolDuring their first encounter (inpatient v1), LVAD inpatients had BP measurements by a radial A-line obtained immediately prior to each of the 3 noninvasive modalities tested (see below). Before measurements were recorded, the A-line was flushed once and leveled to the pressure transducer (IntelliVue, Phillips, the Netherlands). BP measurements were done in triplicate for each method. A-line BP was recorded in a paired fashion, prior to each of the triplicate measurements by each noninvasive modality. All BP measurements were obtained in the same arm as the A-line.For all patients, 3 separate BPs were taken 4 with each of the following 3 different noninvasive BP measurement methods: Doppler ultrasound (Lumeon Doppler System, Houston, TX), GE CARESCAPE V100 (Fairfield, CT) automated BP monitor, and Terumo Elemano BP (Somerset, NJ) monitor.Doppler ultrasound BP measurements were obtained using a calibrated sphygmomanometer as previously described. 4 Briefly, the Doppler probe was placed over the brachial artery while the examiner verified that the brachial pulse could be...

Peripheral venous congestion causes release of inflammatory mediators, neurohormones, and activation of ECs. Overall, venous congestion mimicked, notable aspects of the phenotype typical of advanced and of acute HF and RF.

Endothelin‐1 (ET‐1) is a pivotal mediator of vasoconstriction and inflammation in congestive states such as heart failure (HF) and chronic kidney disease (CKD). Whether peripheral venous congestion (VC) increases plasma ET‐1 at pressures commonly seen in HF and CKD patients is unknown. We seek to characterize whether peripheral VC promotes time‐ and dose‐dependent increases in plasma ET‐1 and whether these changes are sustained after decongestion. We used a randomized, cross‐over design in 20 healthy subjects (age 30 ± 7 years). To experimentally model VC, venous pressure was increased to either 15 or 30 mmHg (randomized at first visit) above baseline by inflating a cuff around the subject's dominant arm; the nondominant arm served as a noncongested control. We measured plasma ET‐1 at baseline, after 20, 60 and 120 min of VC, and finally at 180 min (60 min after cuff release and decongestion). Plasma ET‐1 progressively and significantly increased over 120 min in the congested arm relative to the control arm and to baseline values. This effect was dose‐dependent: ET‐1 increased by 45% and 100% at VC doses of 15 and 30 mmHg, respectively (P < 0.05), and declined after 60 min of decongestion though remaining significantly elevated compared to baseline. In summary, peripheral VC causes time‐ and dose‐dependent increases in plasma ET‐1. Of note, the lower dose of 15 mmHg (more clinically relevant to HF and CKD patients) was sufficient to raise ET‐1. These findings support the potentially contributory, not merely consequential, role of VC in the pathophysiology of HF and CKD.

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.