Blood flow in arteries is dominated by unsteady flow phenomena. The cardiovascular system is an internal flow loop with multiple branches in which a complex liquid circulates. A nondimensional frequency parameter, the Womersley number, governs the relationship between the unsteady and viscous forces. Normal arterial flow is laminar with secondary flows generated at curves and branches. The arteries are living organs that can adapt to and change with the varying hemodynamic conditions. In certain circumstances, unusual hemodynamic conditions create an abnormal biological response. Velocity profile skewing can create pockets in which the direction of the wall shear stress oscillates. Atherosclerotic disease tends to be localized in these sites and results in a narrowing of the artery lumen—a stenosis. The stenosis can cause turbulence and reduce flow by means of viscous head losses and flow choking. Very high shear stresses near the throat of the stenosis can activate platelets and thereby induce thrombosis, which can totally block blood flow to the heart or brain. Detection and quantification of stenosis serve as the basis for surgical intervention. In the future, the study of arterial blood flow will lead to the prediction of individual hemodynamic flows in any patient, the development of diagnostic tools to quantify disease, and the design of devices that mimic or alter blood flow. This field is rich with challenging problems in fluid mechanics involving three-dimensional, pulsatile flows at the edge of turbulence.

Blood flow in arteries

Normal vascular aging: Differential effects on wave reflection and aortic pulse wave velocity - The Anglo-Cardiff Collaborative Trial (ACCT)

SUMMARYThe relationship between the shape of the ascending aortic pressure wave form and aortic input impedance was studied in 18 patients who underwent elective cardiac catheterization but in whom no heart disease was found. Ascending aortic flow velocity and pressure were simultaneously recorded from a multisensor catheter with an electromagnetic velocity probe and a pressure sensor mounted at the same location. Another pressure sensor at the catheter tip provided left ventricular pressure or a second aortic pressure to determine pulse-wave velocity. Fick cardiac outputs were used to scale the velocity signal to instantaneous volumetric flow. Input impedance was calculated from 10 harmonics of aortic pressure and flow. For each patient, impedance moduli and phases from a minimum of 15 beats during a steady state were averaged. Peripheral resistance was 1137 ± 39 dyn-sec-cm-5 (± SEM) and characteristic impedance was 47 ±4 dyn-sec-cm-5; pulsewave velocity was 6.68 ± 0.32 m-sec-1. In all patients, a well-defined systolic inflection point divided the aortic pressure wave form into an early and late systolic phase. The patients were classified into three groups: group A (n = 7) patients whose late systolic pressure exceeded early systolic pressure; group B (n = 7) patients whose early and late systolic pressures were nearly equal; group C (n = 4) - patients whose early systolic pressure exceeded late systolic pressure. Group A and B patients all demonstrated oscillations of the impedance moduli about the characteristic impedance. Group C patients demonstrated flatter impedance spectra. Thus, a larger secondary rise in pressure was associated with a more oscillatory impedance spectrum. These results suggest that the differences in pressure wave forms are due to differences in reflections in the arterial tree and not secondary to differences in cardiac function. Using pulse-wave velocity, the \"effective\" reflection site distance was determined from both pressure (48 cm) and impedance (44 cm) data, implying that the region of the terminal abdominal aorta acts as the major reflection site in normal adult man.

Aortic input impedance in normal man: relationship to pressure wave forms.

https://hal.inria.fr/inria-00071499/document

Added-mass effect in the design of partitioned algorithms for fluid-structure problems

Damage of large arteries is a major factor in the high cardiovascular morbidity and mortality of patients with end-stage renal disease (ESRD). Increased aortic pulse wave velocity (PWV) and brachial pulse pressure (PP) are the principal arterial markers of cardiovascular mortality described in these patients. Whether central (carotid) PP and brachial-carotid PP amplification may predict all-cause (including cardiovascular) mortality has never been investigated. A cohort of 180 patients with ESRD who were undergoing hemodialysis was studied between January 1990 and March 2000. The mean duration of follow-up was 52±36 months (mean±SD). Mean age at entry was 51.5±16.3 years. Seventy deaths occurred, including both cardiovascular and noncardiovascular fatal events. At entry, patients underwent carotid PP measurements (pulse wave analysis), echocardiography, and aortic PWV (Doppler ultrasonography), together with standard clinical and biochemical analyses. On the basis of Cox analyses, after adjustment of age, time on dialysis before inclusion, and previous cardiovascular events, 3 factors emerged as predictors of all-cause mortality: carotid PP, brachial/carotid PP, and aortic PWV. Adjusted hazard ratios for 1-SD increments were 1.4 (1.1 to 1.8) for carotid PP, 0.5 (0.3 to 0.8) for brachial/carotid PP, and 1.3 (1.0 to 1.7) for PWV. Brachial blood pressure, including PP, had no predictive value for mortality after adjustment. These results provide the first direct evidence that in patients with ESRD, the carotid PP level and, mostly, the disappearance of PP amplification are strong independent predictors of all-cause (including cardiovascular) mortality.

Donald A. McDonald

Papers

Blood flow in arteries