Sympathetic Markers are Different Between Clinical Responders and Nonresponders After Left Ventricular Assist Device Implantation

Background: Clinical response to left ventricular assist devices (LVADs), as measured by health-related quality of life, varies among patients after implantation; however, it is unknown which pathophysiological mechanisms underlie differences in clinical response by health-related quality of life. Objective: The purpose of this study was to compare changes in sympathetic markers (beta-adrenergic receptor kinase-1 [beta ARK1], norepinephrine [NE], and 3,4-dihydroxyphenylglycol [DHPG]) between health-related quality of life clinical responders and nonresponders from pre- to post-LVAD implantation. Methods: We performed a secondary analysis on a subset of data from a cohort study of patients from pre- to 1, 3, and 6 months after LVAD implantation. Clinical response was defined as an increase of 5 points or higher on the Kansas City Cardiomyopathy Questionnaire Clinical Summary score from pre- to 6 months post LVAD implantation. We measured plasma beta ARK1 level with an enzyme-linked immunosorbent assay and plasma NE and DHPG levels with high-performance liquid chromatography with electrochemical detection. Latent growth curve modeling was used to compare the trajectories of markers between groups. Results: The mean (SD) age of the sample (n = 39) was 52.9 (13.2) years, and most were male (74.4%) and received LVADs as bridge to transplantation (69.2%). Preimplantation plasma beta ARK1 levels were significantly higher in clinical responders (n = 19) than in nonresponders (n = 20) (P =.001), but change was similar after LVAD (P =.235). Preimplantation plasma DHPG levels were significantly lower in clinical responders than in nonresponders (P =.002), but the change was similar after LVAD (P =.881). There were no significant differences in plasma NE levels. Conclusions: Preimplantation beta ARK1 and DHPG levels are differentiating factors between health-related quality of life clinical responders and nonresponders to LVAD, potentially signaling differing levels of sympathetic stimulation underlying clinical response.