title: Low pulse pressure with high pulsatile external left ventricular power: influence of aortic waves.
abstract: Elevated pulse pressure (pp) is considered to be a risk factor for adverse cardiovascular events since it is directly related to an elevated myocardial workload. Information about both pressure and flow wave must be provided to assess hemodynamic complexity and true level of external left ventricular power (ELVP). pp value as a single feature of aortic waves cannot identify true level of ELVP. However, it is generally presumed that ELVP (and consequently LV workload) is positively correlated with pp. This study examined this positive correlation. The aim of this study was to test the hypothesis that aortic wave dynamics can create destructive hemodynamic conditions that increase the ELVP even though pp appears to be normal. To test this hypothesis, a computational model of the aorta with physiological properties was used. A Finite Element Method with fluid-structure interaction was employed to solve the equations of the solid and fluid. The aortic wall was assumed to be elastic and isotropic. The blood was assumed to be an incompressible Newtonian fluid. Simulations were performed for various heart rates (HR) and different aortic compliances while keeping the shape of the inlet flow and peripheral resistance constant. As expected, in most of the cases studied here, higher pp was associated with higher LV power demand. However, for a given cardiac output, mean pressure, and location of total reflection site, we have found cases where the above-mentioned trend does not hold. Our results suggest that using pp as a single index can result in an underestimation of the LV power demand under certain conditions related to the altered wave dynamics. Hence, in hypertensive patients, a full analysis of aortic wave dynamics is essential for the prevention and management of left ventricular hypertrophy (LVH) and congestive heart failure.
authors.affiliation: Option of Bioengineering, Division of Engineering & Applied Sciences, California Institute of Technology, Pasadena, CA, USA.
authors.forename: Niema M
authors.initials: NM
authors.lastname: Pahlevan
authors.forename: Morteza
authors.initials: M
authors.lastname: Gharib
mesh_terms: D001011:Aorta / Q000502:physiology* / Q000503:physiopathology; D001794:Blood Pressure / Q000502:physiology*; D002302:Cardiac Output / Q000502:physiology; D003187:Compliance / Q000502:physiology; D006333:Heart Failure / Q000503:physiopathology; D006339:Heart Rate / Q000502:physiology; D006352:Heart Ventricles / Q000503:physiopathology*; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology; D008955:Models, Cardiovascular; D011673:Pulsatile Flow / Q000502:physiology*; D011674:Pulse; D014655:Vascular Resistance / Q000502:physiology