High Pulsatile Load Decreases Arterial Stiffness: An ex vivo Study

Measuring arterial stiffness has recently gained a lot of interest because it is a strong predictor for cardiovascular events and all-cause mortality. However, assessing blood vessel stiffness is not easy and the in vivo measurements currently used provide only limited information. Ex vivo experiments allow for a more thorough investigation of (altered) arterial biomechanical properties. Such experiments can be performed either statically or dynamically, where the latter better corresponds to physiological conditions. In a dynamic setup, arterial segments oscillate between two predefined forces, mimicking the diastolic and systolic pressures from an in vivo setting. Consequently, these oscillations result in a pulsatile load (i.e., the pulse pressure). The importance of pulse pressure on the ex vivo measurement of arterial stiffness is not completely understood. Here, we demonstrate that pulsatile load modulates the overall stiffness of the aortic tissue in an ex vivo setup. More specifically, increasing pulsatile load softens the aortic tissue. Moreover, vascular smooth muscle cell (VSMC) function was affected by pulse pressure. VSMC contraction and basal tonus showed a dependence on the amplitude of the applied pulse pressure. In addition, two distinct regions of the aorta, namely the thoracic descending aorta (TDA) and the abdominal infrarenal aorta (AIA), responded differently to changes in pulse pressure. Our data indicate that pulse pressure alters ex vivo measurements of arterial stiffness and should be considered as an important variable in future experiments. More research should be conducted in order to determine which biomechanical properties are affected due to changes in pulse pressure. The elucidation of the underlying pulse pressure-sensitive properties would improve our understanding of blood vessel biomechanics and could potentially yield new therapeutic insights.

Pulsatile Load and Wasted Pressure Effort are Reduced Following an Acute Bout of Aerobic Exercise

Following aerobic exercise, sustained vasodilation and concomitant reductions in total peripheral resistance (TPR) result in a reduction in blood pressure that is maintained for two or more hours. However, the time course for postexercise changes in reflected wave amplitude and other indices of pulsatile load on the left ventricle have not been thoroughly described. Therefore, we tested the hypothesis that reflected wave amplitude is reduced beyond an hour after cycling at 60% V̇O2peak for 60 min. Aortic pressure waveforms were derived in 14 healthy adults (7 men, 7 women; 26 ± 3 yr) from radial pulse waves acquired via high-fidelity applanation tonometry at baseline and every 20 min for 120 min postexercise. Concurrently, left ventricle outflow velocities were acquired via Doppler echocardiography and pressure-flow analyses were performed. Aortic characteristic impedance (Zc), forward (Pf) and backward (Pb) pulse wave amplitude, reflected wave travel time (RWTT), and wasted pressure effort were derived. Reductions in aortic blood pressure, Zc, Pf, and Pb were all sustained postexercise while increases in RWTT emerged from 60-100 min post exercise (all P<0.05). WPE was reduced by ~40% from 40-100 min post exercise (all P<0.02). Stepwise multiple regression analysis revealed that the peak ∆WPE was associated with ∆RWTT (β=-0.57, P=0.003) and ∆Pb (β=0.52, P=0.006), but not ∆cardiac output, ∆TPR, ∆Zc, or ∆Pf. These results suggest that changes in pulsatile hemodynamics are sustained for ≥100 min following moderate intensity aerobic exercise. Moreover, decreased and delayed reflected pressure waves are associated with decreased left ventricular wasted effort after exercise.

Dynamic and isometric handgrip exercise increases wave reflection in healthy young adults

This study demonstrated that wave reflection magnitude is increased while reflected wave transit time is decreased during handgrip exercise in healthy young adults. The larger backward pressure waves and earlier return of these pressure waves were not different between dynamic and isometric handgrip exercise. These acute changes in wave reflection during handgrip exercise transiently augment pulsatile load.

Aortic stiffness, pressure and flow pulsatility, and target organ damage

Measures of aortic stiffness and pressure and flow pulsatility have emerged as correlates of and potential contributors to cardiovascular disease, dementia, and kidney disease. Higher aortic stiffness and greater pressure and flow pulsatility are associated with excessive pulsatile load on the heart, which increases mass and reduces global longitudinal strain of the left ventricle. Excessive stiffness and pulsatility are also associated with microvascular lesions in high-flow organs, such as the brain and kidney, suggesting that small vessels in these organs are damaged by pulsatility. This brief review will summarize evidence relating aortic stiffness to cardiovascular, brain, and kidney disease.