Arterial Stiffening

Abstract

A ortic and large artery stiffening, hallmarks of vascular aging, 1 are predictive of cardiovascular events, particularly in subjects with hypertension and components of the metabolic syndrome. 2,3 One hypothesis is that stiffening is a consequence of the combined insult of risk factors on the vascular wall. 3 However, cross-sectional studies show little association of arterial stiffness with conventional risk factors other than blood pressure. 4 The interrelationship of arterial stiffness with blood pressure makes it fascinating for the hypertensionologist. An elevation in mean arterial pressure stretches the arterial wall, leading to a functional increase in stiffness. Stiffening associated with a chronic elevation of blood pressure (ie, hypertension) may be because of distention of the arterial wall but could also be explained by structural changes of the arterial wall. The degree to which the latter explains hypertension-associated stiffening is still disputed. 5 Finally, the effect of increased stiffening is to increase pulse pressure and systolic blood pressure. Disentangling these interrelationships is challenging, and the causal link between blood pressure and arterial stiffness has not been elucidated. Longitudinal studies that provide insight into the role of blood pressure and novel risk factors on arterial stiffening are, thus, particularly useful.In this issue of Hypertension, McEniery et al 6 present an analysis of prospective risk factors for aortic stiffness in men from the Caerphilly Prospective Study. In a cohort of 825 men of mean age 74 years, aortic pulse wave velocity (PWV), regarded by many as the gold-standard measure of arterial stiffness, was measured during the most recent follow-up phase of the Caerphilly Prospective Study. The relationship of PWV to blood pressure and risk factors at the time of its measurement and over an average follow-up of 20 years was examined. PWV (adjusted for "current risk factors") was closely correlated with the pulse pressureϫheart rate product over the 20-year follow-up. There was also a highly significant correlation of PWV with baseline and subsequent measures of C-reactive protein. Aside from weak correlations with blood glucose, triglycerides, and waist diameter, PWV was not correlated with any other risk factor. A limitation of the study, which the authors were keen to point out, is that they did not have longitudinal measures of PWV. Thus the association of PWV with longitudinal measures of pulse pressure could be explained by pulse pressure acting as a surrogate for PWV. Similarly, the contribution of heart rate could be explained in part by the functional increase in PWV that accompanies an acute elevation in heart rate and that is probably attributable to visco-elastic properties of the arterial wall. Nonetheless, the finding of a relationship between PWV and repetitive cyclic stress is appealing, because such stress is thought to result in stress fracturing of elastin and consequent stiffening.

Adverse effect of diabetes and hyperglycaemia on arterial stiffness in Europeans, South Asians, and African Caribbeans in the SABRE study

“…Our findings therefore also provide a potential mechanism to explain why diabetes and hyperglycemia are particularly adverse for risk of CHD in South Asian people(2) since they are associated with greater arterial stiffness in South Asian people than in Europeans or African-Caribbean people. Diabetes and hyperglycemia have been reported to be associated with increased arterial stiffness,(32) although the strength of association has previously been reported as weak,(33) and we observed no significant relationship between diabetes or glycosylated haemoglobin in Europeans or African Caribbeans in this study. It is possible that more aggressive management of BP in people with diabetes contributes to this effect.…”

The effect of hypertension on aortic pulse wave velocity in type-1 diabetes mellitus patients: assessment with MRI

“…Age and blood pressure have consistently been shown to be independently associated with PWV [16]. The impact of hypertension on aortic stiffening may be twofold: 1. mechanistic stretching of the arterial wall may result in aortic stiffening; 2. structural changes of the arterial wall due to cyclic stress, resulting in stress fracturing of elastin and consequent stiffening [16, 23]. In contrast to the predominant effect of hypertension on aortic stiffening, only weak correlations have been shown with diabetes, accounting for a mean of 5% of the variation in PWV [16].…”

Evaluation of aortic 18F-NaF tracer uptake using PET/CT as a predictor of aortic calcification in postmenopausal women: A longitudinal study

“…1–6 The mechanism by which the presence of aortic calcification is predictive of cardiovascular outcome is unknown but is likely to involve negative effects of calcification on plaque rupture, arterial stiffening and predisposition to isolated systolic hypertension. 9–14 Despite the prognostic importance of vascular calcification there are currently no interventions available to reduce or prevent vascular calcification. Developing novel therapeutic interventions targeting vascular calcification may further be impeded by current imaging techniques, which are limited to detecting macro-calcification rather than biologically active areas of novel mineralisation, which may be more susceptible to therapy.…”

“…9 Medial calcification occurs in association with elastin fragmentation 10 and is associated with stiffening of large arteries independently of atherosclerosis. 11–13 Large artery stiffness predisposes to the development of isolated systolic hypertension and is an independent predictor of cardiovascular morbidity and mortality. 14 Despite the negative impact of vascular calcification and its association with cardiovascular outcomes there are currently no therapies that target aortic calcification.…”