Arterial Stiffness and Cardiovascular Therapy

Abstract

The world population is aging and the number of old people is continuously increasing. Arterial structure and function change with age, progressively leading to arterial stiffening. Arterial stiffness is best characterized by measurement of pulse wave velocity (PWV), which is its surrogate marker. It has been shown that PWV could improve cardiovascular event prediction in models that included standard risk factors. Consequently, it might therefore enable better identification of populations at high-risk of cardiovascular morbidity and mortality. The present review is focused on a survey of different pharmacological therapeutic options for decreasing arterial stiffness. The influence of several groups of drugs is described: antihypertensive drugs (angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, calcium channel blockers, beta-blockers, diuretics, and nitrates), statins, peroral antidiabetics, advanced glycation end-products (AGE) cross-link breakers, anti-inflammatory drugs, endothelin-A receptor antagonists, and vasopeptidase inhibitors. All of these have shown some effect in decreasing arterial stiffness. Nevertheless, further studies are needed which should address the influence of arterial stiffness diminishment on major adverse cardiovascular and cerebrovascular events (MACCE).

Do arterial stiffness and wave reflections improve more with angiotensin receptor blockers than with other antihypertensive drug classes?

“…Previous meta-analyses have shown that antihypertensive agents of different classes may influence arterial stiffness and wave reflections to different extents, as summarized in Table 1 (2)(3)(4)(5). The results of the meta-analysis of Chen and co-authors add to previous evidence by specifically focusing on ARBs' effect and on AIx.…”

“…In addition, ARBs contrast the profibrotic action of the renin-angiotensin system, reducing the collagen content of the arteries and attenuating extracellular matrix remodeling, and they may reverse smooth muscle hypertrophy, increasing arterial distensibility (6). Such mechanisms are plausible and they have been documented in a number of studies (4). Unfortunately, in their metaanalysis Chen and coworkers do not provide data on the pressor effect of the antihypertensive drugs at the brachial artery level, and even more so at the aortic (central) level.…”

Sex-specific differences in cardiac maladaptation to hypertension and arterial stiffening

“…However, current non-invasive measures of arterial stiffness are BP-dependent, making it hard to distinguish the beneficial BP-lowering effects from those caused by de-stiffening of the arterial wall. In addition to BP-lowering drugs, statins, antidiabetic drugs, advanced glycation end-products, cross-link breakers, and anti-inflammatory drugs have been proposed to lower arterial stiffness, but are still under development or validation [80]. On the other hand, favourable effects of physical activity [81][82][83][84][85] and weight reduction [86] on arterial stiffness have been described in both healthy individuals and in patients with cardiovascular risk factors.…”

Aortic Stiffness and Disease

“…Promising results have been obtained with anti-inflammatory drugs such as tumor necrosis factor-α inhibitors, matrix metalloproteinase inhibitors, elastase inhibitors, and collagen crosslink breakers in preclinical studies. 12,13 However, experience in humans is limited, and results from human trials have been mixed. 12 Reducing blood pressure is proven to reduce arterial stiffening, and some antihypertensive drugs acting on the renin-angiotensin-aldosterone axis may have specific blood pressure-independent antistiffening effects.…”