Does third generation left ventricular assist device alter heart failure-related microvascular dysfunction?. Issue 4 (1st August 2016)

• Record Type: Journal Article
• Authors: Esmaeilzadeh, Fatemeh; Dendievel, Renaud; Wauters, Aurélien; Vachiery, Jean-Luc; Van Nooten, Guido; Van De Borne, Philippe; Argacha, Jean-François
• Is Part Of: Acta cardiologica. Volume 71:Issue 4(2016)
• Page Start: 403
• Page End: 410
• Publication Date: 2016-08-01
• Subjects: Left ventricular assist device -- endothelial function -- heart failure.; Cardiology -- Periodicals; Cardiology; Cardiologie -- Périodiques; Cardiology; Cardiologie; Periodicals; Periodicals; 616.12005
• DOI: 10.1080/AC.71.4.3159692
• Languages: English
• ISSNs: 0001-5385

Abstract

Abstract : Background Left ventricular assist device (LVAD) is a promising new therapy in patients with advanced heart failure. Previous studies suggested that continuous blood flow impairs endothelial function. Whether the third-generation LVAD (HeartWareR, HeartWare Inc., Framingham, MA, USA) system affects endothelial regulation of microvascular flow, endothelial nitric oxide (NO) bioavailability and endothelial production of vWF is not known. Methods Fifteen LVAD-supported heart failure patients and 13 age/body mass index matched heart failure patients (HF) were included. The microvascular endothelial function of skin vessels was assessed with laser Doppler imager (LDI) using 3 different hyperaemic challenges: acetylcholine (Ach) iontophoresis, sodium nitroprusside (SNP) iontophoresis and local heating to 44°C. NO-mediated vasodilation was further evaluated by comparing heating hyperaemic response in skin area pretreated either by a saline solution (control) or a specific NO-synthase inhibitor (L-N-arginine-methyl-ester, L-NAME). vWF antigen was also measured in LVAD and HF patients. Results SNP-induced vasodilation did not differ between LVAD and HF patients, and we observed a trend towards an increased vasodilator response to Ach in LVAD patients ( P = 0.06). Compared to HF patients, skin thermal hyperaemia was increased in LVAD patients in both control and L-NAME pretreated skin (all P < 0.001). The hyperaemic reaction attributable to NO-mediated vasodilation correlated negatively with HF duration (r = –0.50, P < 0.01, n = 28), but did not differ between LVAD and HF patients. Both groups disclosed also similar vWF antigen serum levels. Conclusion This case-control study indicates that third-generation LVAD therapy does not alter skin microvascular endothelial function and vWF production of patients with HF