Arterial elastance and heart-arterial coupling in aortic regurgitation are determined by aortic leak severity.
BACKGROUND
In aortic valve regurgitation (AR), aortic leak severity modulates left ventricle (LV) arterial system interaction. The aim of this study was to assess (1) how arterial elastance (E(a)), calculated as the ratio of LV end-systolic pressure and stroke volume, relates to arterial properties and leak severity and (2) the validity of E(a)/E(max) (with E(max) the slope of the end-systolic pressure-volume relation) as a heart-arterial coupling parameter in AR.


RESULTS
Our work is based on human data obtained from a study on vascular adaptation in chronic AR. These data allowed us to assess the parameters of a computer model of heart-arterial interaction. In particular, total peripheral resistance (R) and aortic leak severity--expressed as leak resistance (R(L,ao))--were quantified for different patient subgroups (group I/IIa/IIb: E(max) = 2.15/0.62/0.47 mm Hg/mL; E(a) = 1.24/0.66/0.90 mm Hg/mL; R = 1.9/0.6/0.85 mm Hg.s/mL, R(L,ao) = 0.35/0.05/0.20 mm Hg.s/mL). A parameter study demonstrated that R(L,ao) was the main determinant of E(a). With all other parameters constant, valve repair would increase E(a) to 2.81, 1.08, and 1.54 mm Hg/mL in groups I, IIa, and IIb, respectively. For a given E(a)/E(max), LV pump efficiency (estimated as the ratio of stroke work and LV systolic pressure-volume area) was lower than the theoretical predicted value, except for the simulations with intact aortic valve.


CONCLUSIONS
In AR, E(a) is determined by aortic leak severity rather than by arterial system properties. Using E(a)/E(max) as a coupling parameter in general or as a mechanico-energetic regulatory parameter in particular is questionable.
D001022:Aortic Valve Insufficiency / Q000503:physiopathology*; D002908:Chronic Disease; D004548:Elasticity; D006801:Humans; D008875:Middle Aged; D008955:Models, Cardiovascular; D013318:Stroke Volume / Q000502:physiology; D013599:Systole; D018924:Vascular Capacitance / Q000502:physiology; D014655:Vascular Resistance / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology*; D017725:Ventricular Pressure / Q000502:physiology