title: Smart damping modulation of carotid wall energetics in human hypertension: effects of angiotensin-converting enzyme inhibition.
abstract: Damping is the conversion of mechanical energy of a structure into thermal energy, and it is related to the material viscous behavior. To evaluate the role of damping in the common carotid artery (CCA) wall in human hypertension and the possible improvement of angiotensin-converting enzyme (ACE) inhibition, we used noninvasive CCA pressure (tonometry) and diameter (B-mode echography) waveforms in normotensive subjects (NT group; n=12) and in hypertensive patients (HT group; n=22) single-blind randomized into HT-placebo (n=10) or HT-treated (ramipril, 5 to 10 mg/d during 3 months; n=12). Vascular smooth muscle (VSM) null tonus condition was achieved from in vitro pressure and diameter waveforms (Konigsberg microtransducer and sonomicrometry) measured in explanted human CCA (n=14). Arterial wall dynamics was described by viscous (eta), inertial (M), and compliance (C) parameters, mean circumferential wall stress, viscous energy dissipation (WD), peak strain energy (WSt), damping ratio (xi=WD/WSt), and modeling isobaric indexes CIso and WSt(Iso). The lack of VSM tonus isobarically increased wall stress and reduced eta, CIso, and damping (P<0.01). Wall stress, eta, and WD were greater in HT than in NT (P<0.015) and arrived near normal in HT-treated (P<0.032 respect to HT), with no changes in HT-placebo. Whereas CIso increased in HT-treated (P<0.01) approaching the NT level, xi did not vary among groups. During hypertension, because of the WSt increase, the arterial wall reacts increasing WD to maintain xi. ACE inhibition modulates VSM activation and vessel wall remodeling, significantly improving wall energetics and wall stress. This protective vascular action reduces extra load to the heart and maintains enhanced arterial wall damping.
authors.affiliation: Facultad de Ingeniería y Ciencias Exactas y Naturales, Universidad Favaloro, Buenos Aires, Argentina. armen@favaloro.edu.ar
authors.forename: Ricardo L
authors.initials: RL
authors.lastname: Armentano
authors.forename: Juan G
authors.initials: JG
authors.lastname: Barra
authors.forename: Daniel Bia
authors.initials: DB
authors.lastname: Santana
authors.forename: Franco M
authors.initials: FM
authors.lastname: Pessana
authors.forename: Sebastian
authors.initials: S
authors.lastname: Graf
authors.forename: Damian
authors.initials: D
authors.lastname: Craiem
authors.forename: Laura M
authors.initials: LM
authors.lastname: Brandani
authors.forename: Hugo P
authors.initials: HP
authors.lastname: Baglivo
authors.forename: Ramiro A
authors.initials: RA
authors.lastname: Sanchez
mesh_terms: D000328:Adult; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D017536:Carotid Artery, Common / Q000000981:diagnostic imaging / Q000503:physiopathology*; D003187:Compliance; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D006973:Hypertension / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D008875:Middle Aged; D008955:Models, Cardiovascular; D017257:Ramipril / Q000627:therapeutic use; D016037:Single-Blind Method; D013314:Stress, Mechanical; D022722:Thermogenesis / Q000187:drug effects*; D014463:Ultrasonography; D014666:Vasomotor System / Q000503:physiopathology; D014783:Viscosity
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D017257:Ramipril