The reduction or loss of arterial elasticity or distensibility
leads to arterial stiffness (AS), which has a substantial predictive
value for all-cause and cardiovascular disease (CVD)
mortality, as well as for non-fatal CVD events [1]. A plethora
of evidence consistently showed the prognostic value of
aortic stiffness for fatal and nonfatal CVD events in various
populations at different levels of CVD risk, including the
general population, elderly subjects and patients with hypertension,
type 2 diabetes mellitus (T2DM) and end-stage renal
disease (ESRD) [2]. It has been reported that 1-SD increase
in pulse wave velocity (PWV) is associated with a 47% increase
in the risk for total mortality [95% confidence interval
(CI), 1.31-1.64] and a similar 47% increase in the risk for
CVD mortality (95% CI, 1.29-1.66) [2].
Age is the major CVD risk factor and this is attributable
in part to stiffening of large elastic arteries, a natural process
[3]. During aging, the elastic lamella grows to be fragmented
and the mechanical load is transferred to collagen fibers,
which are several hundred times stiffer than elastic fibers.
This loss of the elastic properties (AS) mainly happens with
large arteries and causes arteriosclerosis different than atherosclerosis,
which refers to the arterial intima [4]. Arteriosclerosis
usually does not affect the smaller muscular arteries
[5]. Besides age, a number of changes in arterial wall, related
to CVD risk factors, also increase AS and contribute to
early arterial aging [3]. Matrix remodelling of the media and
adventitia may result from endothelial dysfunction, reduction
of elastin, increase of collagen metalloproteinases, vascular
smooth muscle cells and adhesion molecules, and deposition
of advanced glycation end-products and calcium due to lowgrade
inflammation, dyslipidaemia, T2DM, hypertension
(HTN) and chronic kidney disease (CKD) [3]. Arterial stiffness
increases PWV; this causes an early return of the reflection
wave in the aorta during left ventricular systole [6]. This
early return increases central aortic pressure and systolic blood pressure, while it reduces diastolic blood pressure 2/6
and thus coronary perfusion [6]. Central aortic pressure is
only an indirect, surrogate measure of AS. However, it provides
additional information concerning wave reflections
[6,7]. Central pulse-wave analysis should be optimally used
in combination with the measurement of aortic PWV value
to determine the contribution of AS to wave reflections [6,7].
Given the complex pathogenesis of AS, it is obvious that the
treatment of AS should also be multifactorial. Both lifestyle
and pharmacological approaches should be implemented in
these patients. Central pulse-wave analysis should be optimally
used in combination with the measurement of aortic
PWV value to determine the contribution of AS to wave reflections
[6,7]. Given the complex pathogenesis of AS, it is
obvious that the treatment of AS should also be multifactorial.
Both lifestyle and pharmacological approaches should
be implemented in these patients. Increased leisure time
physical activity, weight reduction, avoidance of diatery salt
and alcohol abuse as well as increased consumption of diatery
heavy chain omega fatty acids as recommended [7].
Drug treatment for arterial hypertension [diuretics,
angiotensin-converting enzyme inhibitors (ACE-I), angiotensin-
receptor blockers (ARBs), and calcium-channel
blockers (CCB)] [8-10]; lipid-lowering agents, mainly statins
[11,12], hypoglecaemic drugs (thiazolidinediones) [13]; and
potentially other novel agents, including AGE breakers [14].
There are been data suggesting that the reduction in AS during
treatment for arterial hypertension is not only attributed
to the reduction in BP per se but to additional BP loweringindependent
effects of antihypertensive drugs [15]. Indeed,
the renin – aldosterone - angiotensin –system (RAAS)
blockers, ACE inhibitors and ARBs, have been shown to
have a BP- independent beneficial effect on AS [16] and to
possess antifibrotic effects [17].
In antithesis, β-blockers do not reduce AS in the same
degree, because non-vasodilating -blockers are less effective
in reducing central pulse pressure than
other antihypertensive drugs [7]. In fact, older -blockers
may increase vasoconstriction and assist the early return of
the reflected pulse wave in late systole (and not in diastole), thus increasing central blood pressure and inducing a
mismatch between the heart and the arterial system [7].
The substudy of the Anglo-Scandinavian Cardiac Outcomes
Trial (ASCOT) [18], Conduit Artery Function
Evaluation (CAFE) trial [19], showed that amlodipine combined
with perindopril reduce central aortic pressure more
than atenolol 3/6 combined with thiazide despite a similar
impact on brachial BP. Moreover, central aortic pulse pressure
may be a determinant of clinical outcomes, and differences
in central aortic pressures may be a potential mechanism
to explain the different clinical outcomes between the
latter treatment arms in ASCOT [19]. In conclusion, even
AS increases with age, this process might be accelerated by
the simultaneous presence of other CVD risk factors, resulting
in early vascular aging. AS is associated with increased
risk for CVD and all-cause mortality, and it is possible that a
decrease in AS might improve outcomes. Various approaches,
particularly those targeting HTN, T2DM, dyslipidaemia,
metabolic syndrome and CKD, preferably combined
in a multifactorial approach, contribute to reduction in AS.
In addition, the potential role of newer therapies, including
AGE breakers and those aiming to break collagen crosslinks,
should be tested.
Impact of meal fatty acid composition on postprandial lipaemia, vascular function and blood pressure in postmenopausal women