Arterial Stiffness: Pathophysiological and Genetic Aspects

Abstract

Cardiovascular diseases (CVD) are the main cause of mortality and it represents a significant percentage of hospitalizations. In the scenario of minimization of costs of the health system, methods that identify subclinical CVD would be important. Some guidelines include the measures of aortic stiffness and intima-media thickness of the carotid artery as methods to identify subclinical CVD in hypertensive patients. The pulse wave velocity (PWV) is the gold standard for the evaluation of arterial stiffness. In this review, we report the pathophysiology, the determinants of arterial stiffness, and justify its inclusion in the assessment of hypertensive patient due its direct association with cardiovascular risk, as show in the I Diretriz Brasileira de Prevenção Cardiovascular. In addition, we raised the main genetic studies of this phenotype, due to its complexity, can be modulated by dozens of genes. However, a better understanding of the relationship genetic-arterial stiffness and, even an intervention based on genotypes, should be achieved in future studies.

Blockade of angiotensin AT1 receptors prevents arterial remodelling and stiffening in iron‐overloaded rats

“…Notwithstanding, the major finding in the present study was the ability of AT 1 receptor blockade to prevent the increase in aortic stiffness in a rat model of iron‐overload, as indicated by lower PWV, β‐index, and EM/WS ratio compared to rats treated with vehicle. Increased aortic PWV, an indicator of arterial stiffness, is a strong and independent predictor of cardiovascular risk not only in patients with vascular diseases (Alvim et al, ; Alvim, Santos, Bortolotto, Mill, & Pereira, ; Baldo et al, ; Georgianos, Sarafidis, & Lasaridis, ; Mitchell, ) but also in patients with haemochromatosis (Cash et al, ). This increased risk could be due to a loss of the ability of a stiffer aorta to buffer pulsatile changes in BP.…”

“…This increased risk could be due to a loss of the ability of a stiffer aorta to buffer pulsatile changes in BP. In fact, for both man and experimental animals, the loss of aortic distensibility increases BP and pulsatile pressure and places vulnerable tissues at risk of microvascular damage, by reducing capillary proliferation and increasing thrombosis, atherosclerosis, and vasomotor dysfunction (Alvim et al, ; Mitchell, ; Safar, ). In our study, we did not identify significant changes in the BP or pulse pressure of the rats subjected to iron‐overload, which suggests that altered control of vascular tone remained normal despite the signs of vascular stiffness.…”

“…Especially in smaller arteries and arterioles, it is also determined by other mechanisms modulating smooth muscle tone, including endothelial function and NO availability. Thus, the endothelial dysfunction induced by iron‐overload could increase peripheral vascular resistance and, therefore, potentially change the elastic properties of the aortic wall (Alvim et al, ; Lacolley et al, 2017). However, as discussed above, because the vasoresponses to phenylephrine both in vivo and in vitro were not different between control and iron‐overload rats, a possible contribution of endothelial dysfunction or altered smooth muscle cell tone to the vessel wall stiffness is unlikely.…”

“…Increased aortic PWV, an indicator of arterial stiffness, is a strong and independent predictor of cardiovascular risk not only in patients with vascular diseases (Alvim et al, 2013;Alvim, Santos, Bortolotto, Mill, & Pereira, 2017;Baldo et al, 2018;Georgianos, Sarafidis, & Lasaridis, 2015;Mitchell, 2009) but also in patients with haemochromatosis (Cash et al, 2013). This increased risk could be due to a loss of the ability of a stiffer aorta to buffer pulsatile changes in BP.…”

Associations of Cardiorespiratory Fitness and Muscular Strength with Arterial Stiffness in Older Adults

“…Arterial stiffness is the reduction in the compliance and distensibility of the large central arteries, and it is associated with the presence of CVD risk factors, vascular dysfunction, and inflammatory and metabolic diseased states (Alvim et al, 2017;Kohn, Lampi, & Reinhart-King, 2015;Niiranen et al, 2016;Stehouwer, Henry, & Ferreira, 2008;van Sloten, 2017;Charalambos Vlachopoulos et al, 2010). More importantly, AS is an independent predictor of future hypertension, CVD events, CVD mortality, and allcause mortality, in adults and older adult populations (Avolio, 2013;Ben-Shlomo et al, 2014;Fagard et al, 2007;Mitchell et al, 2010;Niiranen et al, 2016;Sutton-Tyrrell et al, 2005;Van Bortel et al, 2012;Vlachopoulos et al, 2010;Zheng et al, 2015).…”