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Properties of the Arterial Wall
Published in Wilmer W Nichols, Michael F O'Rourke, Elazer R Edelman, Charalambos Vlachopoulos, McDonald's Blood Flow in Arteries, 2022
Frohlich and colleagues studied the changes in cardiovascular mass, left ventricular pumping ability (Frank–Starling curves), and aortic distensibility after chronic ingestion of angiotensin-converting enzyme (ACE) inhibitors or calcium antagonists (Frohlich et al., 1992a) in normotensive and spontaneously hypertensive rats. As stated previously, aortic distensibility was obtained by ligating a segment of the intact vessel proximal and distal to the carotid artery and constructing pressure–volume curves. All agents tested were vasodilators (or smooth muscle relaxants); they improved aortic distensibility (i.e. a rightward shift of the pressure–volume curve; an example is shown in Figure 4.18), decreased left ventricular mass (in hyper-tensive rats) and improved left ventricular pumping ability. Reduction in elastance (or stiffness) with vasodilators in the elastic aorta of rats may be exaggerated because of the small caliber and large proportion of SMC. In larger human elastic arteries, vasoactive drugs have minimal direct (or active) effects on vessel wall properties (Nichols and Edwards, 2001; Weber et al., 2003), however, elastic artery wall properties will change with a change in distending pressure caused by the drug’s action on muscular arteries (see Figure 4.18). Hajdu et al. (1990) studied the effects of aging on mechanics and composition of cerebral arterioles in rats (see later discussion). Pressure and diameter were measured in pial arterioles through an open skull preparation (Baumbach et al., 1988).
Atherosclerosis and Mechanical Forces
Published in Michel R. Labrosse, Cardiovascular Mechanics, 2018
The pulsatile nature of blood flow exposes the vessel to cyclic mechanical stretch or strain. Stretch describes the change in dimension of the vessel, and strain expresses the ratio of this change in dimension to its original dimension. The force per unit area that produces the deformation is called stress (Nichols et al. 2011). During systole, blood vessels experience both longitudinal and circumferential stretches that are counteracted by the vessels’ elasticity. Under physiological conditions, a large elastic artery such as the aorta undergoes about 10% circumferential strain between diastole and systole (Bell 2014).
Overview of the cardiovascular system
Published in Neil Herring, David J. Paterson, Levick's Introduction to Cardiovascular Physiology, 2018
Neil Herring, David J. Paterson
Collagen is the other major extracellular protein of elastic arteries. Collagen fibrils are ~100 times less distensible than elastin. They form a partly slack network in the media and prevent overdistension if BP rises. The elastic artery wall is thus a composite material, similar in many respects to a car tyre; the rubber/elastin allows expansion up to a certain volume, beyond which increasing tension in inelastic fibres prevents overexpansion. As elastin fragments with age, the stiffer collagen increasingly dominates the properties of elastic vessels. This is a process called ‘arteriosclerosis’ (Chapter 18).
More than a matter of the heart: the concept of intravascular multimorbidity in cardiac rehabilitation
Published in Expert Review of Cardiovascular Therapy, 2020
Chueh-Lung Hwang, Ahmed Elokda, Cemal Ozemek, Ross Arena, Shane A. Phillips
The carotid artery is an elastic artery and distributes blood to the brain. Noninvasive ultrasound imaging can be used to determine the presence of carotid atherosclerosis by quantifying the carotid intima-media thickness (IMT), which measures the thickness of intima (endothelium) and media (smooth muscle) layers of the vessel. The increases in carotid IMT are associated with increased atherosclerotic risks and increased incidents of cardiovascular events such as stroke, heart attack, or heart failure (reviewed in [2]). A carotid IMT of 0.81mm or higher may indicate the presence of significant CAD (i.e., ≥50% coronary artery stenosis) [15]. In patients who underwent a coronary artery bypass graft surgery, every increase in carotid IMT by 0.03mm was associated with a ~2% increase in risk of non-fatal myocardial infarction or coronary death and with a ~3% increase in risk of any coronary events [16].
Autophagy as an emerging therapeutic target for age-related vascular pathologies
Published in Expert Opinion on Therapeutic Targets, 2020
Dorien G De Munck, Guido RY De Meyer, Wim Martinet
Finally, there is a link between lifestyle recommended adjustments in preventing vascular aging such as certain dietary adjustments and the process of autophagy. Caloric restriction (CR) can prevent all important features of arterial aging. In mice, it has been shown that life-long CR reduces age-related aortic stiffness and large elastic artery hypertrophy. Similarly, age-related impaired endothelial dysfunction and increases in blood pressure could be prevented by life-long CR [106]. A comparable effect on endothelium dysfunction is also observed after short-term CR [107]. Considering that nutrient availability is an important regulator of autophagy and starvation is one of the strongest stimuli for autophagy induction, it is possible that some of the advantageous effects of CR are, at least partially, related to autophagy induction in the vasculature. In support of this hypothesis, it has already been shown that the life prolonging effects of CR are mediated by the induction of autophagy [83,108].
Local carotid arterial stiffness is an independent determinant of left ventricular remodeling in never-treated hypertensive patients
Published in Blood Pressure, 2019
Olga Vriz, Julien Magne, Joanna Jarosh, Eduardo Bossone, Victor Aboyans, Paolo Palatini
In the present study, BP load determined by ABPM was directly responsible for LV adaptation, mean day-time for LVM and mean night-time for RWT, which is consistent with previous data from the literature [8–10]. Arterial stiffness was coupled with LV structure, and local carotid stiffness was independently related to LVM and left atrial volume. This stronger correlation with carotid stiffness is likely due to at least two factors: (i) the carotid artery is a short artery with a homogeneous elastic structure unlike the aorta that starts as an elastic artery and ends as a muscular one, and (ii) the ageing process accelerated by high BP is faster at the carotid level than in the aorta and may impose a direct pressure-independent effect on the left ventricle. On the other hand, LV remodeling (RWT) and LV filling pressure (E/Em) were related to night BP load. Our results are in line with previous reports [5,6,33,36,37] where local carotid stiffness is coupled with LV structure and left atrial volume over and above cfPWV and, in the present study, also on top of BP load either as mean day-time or night-time BP as more accurately measured by ABPM.