Editorial: Arterial stiffness and cardiovascular disease. Prognostic value and applicability in clinical practice

Stiffness is the resistance offered by an elastic body to deformation. In the vascular system arterial stiffness (AS) increases with age, especially from the ages of 50-55, due to the gradual replacement of collagen fibres in the arterial wall, affecting the central and conducting arteries more frequently than the peripheral arteries. AS is a biomarker of vascular ageing, and develops not only according to biological age, but also to the presence and degree of control of several vascular risk factors.¹ The impact of hypertension, hyperglycaemia, smoking and other classical risk factors on vascular ageing is well known, but the mechanisms causing it remain unclear; complex factors appear to be involved that are still not sufficiently understood.²

Data from classical epidemiological studies have shown that systolic and diastolic blood pressure (BP) increase up to the age of 50 to 55, but they then diverge, and systolic BP increases, and diastolic BP stabilises or decreases, which results in an increase in differential pressure or pulse pressure (PP). This increase in PP is an indirect marker of AS and is associated with increased cardiovascular morbidity and mortality.³

Although there is no consensus on the evidence, AS could be a mechanism of disease, inducing heart, kidney, and brain damage.⁴ AS reduces coronary perfusion pressure, causing increased left ventricular overload that can result in heart dysfunction and failure even in the absence of heart disease. It also influences pulse pressure and flow, which leads to increased pulsatile energy penetration into the microcirculation of target organs, especial those with high flow requirements and low arteriolar resistance.^1,4

An original study⁵ is published in this issue of Clínica e Investigación en Arteriosclerosis on the role of increased central AS in macro-and microvascular damage in patients with heart disease. Forty-eight patients were assessed: 11 had no significant heart damage, 24 had significant damage to one or two coronary arteries, and 13 to 3 or more coronary arteries. Patients with acute coronary syndrome were excluded, brachial BP was measured (mean of 3 readings) 12 hours before the coronary angiography, and central BP was measured in the same arm as the brachial BP. Pulse wave was measured by applanation tonometry using a micromanometer connected to a Sphygmocor device (AtCor Medical, Sydney, Australia), and the same device was used to measure carotid-femoral pulse wave velocity, obtaining the pulse wave using applanation tonometry sequentially over the common carotid and femoral artery. Although the sample is small, the authors observed data of interest: in these patients who underwent coronary angiography for suspected stable coronary artery disease, carotid-femoral pulse wave velocity (as an expression of aortic AS) was independently associated with coronary artery disease and its extent. Regarding kidney involvement, when age was introduced in the multiple linear regression model, no association was observed with estimated glomerular filtration rate, and although a significant association with albuminuria was observed, this association disappeared when other parameters of brachial and central BP related to it were introduced.

The results of some studies suggest that target organ involvement may be caused by microcirculatory disturbances due to excess transmission of pressure pulsatility secondary to increased AS, beyond the effect of raised peripheral BP. Mitigating AS could therefore reduce the overall burden of target organ damage and in turn reduce cardiovascular events.^4,6 Inflammatory and endocrine mechanisms mediated by the renin-angiotensin-aldosterone system (RAAS) appear to be involved in this process, and the use of RAAS inhibitors could achieve a more significant reduction in central BP compared with β-blockers and diuretics even after the same reduction in brachial BP.^4,7,8 The use of statins has also been shown to reduce arterial stiffness and central aortic pressure by mechanisms that are not fully understood.⁹

Pulse wave velocity (PWV) is the speed at which the pulse wave travels along a given arterial segment and is considered the standard for non-invasive investigation of AS. The stiffer the artery, the higher the PWV.

Based on extensive experience of its use in large populations, the current benchmark method would be to measure carotid-femoral PWV by applanation tonometry, or by Doppler, given the advantage of the superficial location of both arteries.¹ The guidelines of the European Society of Cardiology (ESC) and the European Society of Hypertension (ESH)¹⁰ consider a PWV score of more than 10 m/s to be a conservative estimate of impaired aortic function. Several studies have shown that a PWV score > 10 m/s provides additional information to that given by the classical risk factors, including the SCORE or Framingham risk charts.¹¹

Although central arterial stiffness can currently be measured by non-invasive methods,¹² as in the original study that we mention, for it to be routinely used in clinical practice, some concerns are still to be addressed. First, the different devices need to be validated and normal values determined in the general population, according to age.^13–16 Second, the situations in which they can provide additional information that adds prognostic value to brachial BP measurements need to be established, especially those obtained by 24-hour ambulatory BP monitoring. The studies published in recent years on central BP in hypertensive patients are not conclusive, and in general central BP readings, including those taken over 24 hours, do not provide additional value to ambulatory BP in its association with target organ damage, whether analysed overall¹⁷ or differentiating between heart and kidney involvement.^18–20 Finally, central BP readings taken non-invasively over 24 hours vary according to the calibration, which is an unresolved methodological problem.^21,22 It has been suggested that calibration for the measurement of peripheral pulse waves would be better if based on mean BP and diastolic BP, rather than on systolic and diastolic BP.²¹ These same authors suggest that systolic BP should be used when assessing the relative risk of central aortic BP versus brachial BP.

We can conclude that non-invasive measurements of AS are likely to be of value in vascular risk stratification compared to the classical risk factors, especially in low or intermediate risk patients. However, we have no data on whether modifying them with treatment would result in an improved prognosis.²³