Arteriosclerosis and arterial remodeling; different mechanisms in young adults

Subclinical vascular damage can present with various forms, each one reflecting different—but sometimes overlapping—underlying pathophysiological mechanisms. Two of the most important and clinically relevant types of vascular damage are arteriosclerosis (ie, increased arterial stiffness) and arterial remodeling or hypertrophy; the former can be expressed and quantified by means of aortic pulse wave velocity (PWV) and the latter through measurement of the intima‐media thickness (IMT) of the carotid artery.1 Both of the aforementioned biomarkers have established prognostic ability for future cardiovascular (CV) events and mortality and can be assessed through various techniques and methods.1

The gold standard noninvasive method for the evaluation of aortic stiffness is the measurement of carotid to femoral pulse wave velocity.2 It is well established that PWV is highly age dependent, increasing steadily with aging and is also closely related to blood pressure (BP) levels.3, 4, 5 On the other hand, IMT can be evaluated through B‐mode ultrasonography and is associated with traditional CV risk factors,6 representing an established CV risk modifier,7 possibly allowing for the reclassification of subjects to a higher CV risk level.

In the current issue of the journal, Cecelja et al present us the results of their study8 carried out in a rural, low‐income, young population of southern India, concerning the association of functional and structural indices, namely PWV and IMT, with traditional risk factors. In 1400 participants aged 20‐24 years old, they identified that—after adjustment for different confounders—only mean arterial BP (MAP) remained a significant determinant of PWV. Specifically, MAP was able to explain 37% of the variability of PWV in multivariate models, while other risk factors such as age, sex, smoking, blood cholesterol, and indices of impaired glycemia did not exert a significant effect. On the other hand, HDL cholesterol was the only parameter—negatively—associated with IMT in this population, with only 2% of its variability being attributed to HDL cholesterol.

This study provides further evidence that arteriosclerosis and arterial remodeling arise from different and distinct pathophysiological basis in a rural population of young and apparently healthy subjects, coming from a low‐income country but with high CV mortality. Most relevant studies have focused in older populations from western countries,4, 9 in which aortic stiffness and arterial remodeling or even plaque formation are overt, not allowing the evaluation of the pathophysiological mechanisms in early stages of these conditions. Moreover, the western lifestyle may also play a significant predisposing role in the development of these conditions. It is important to remember that especially in early subclinical arterial damage—as in our case—the distinction between loss of elasticity (elastin degradation and smooth muscle cell dysfunction) and arterial remodeling/hypertrophy is even clearer.10 In later stages, formation of plaques arises, which get calcified (ie, develop atherosclerosis) but in completely different way than the media calcification of arterial stiffening (arteriosclerosis).11 At these later stages, the two arterial pathologies may “come closer,” though in these stages the loss of elasticity in atherosclerosis is local (ie, only in the vicinity of plaque) but in arteriosclerosis segmental (ie, affects long segments of elastic arteries).

In recent years, a variety of noninvasive and operator‐independent devices have been developed, allowing the assessment of central hemodynamics with use of cuffs.12 In the study by Cecelja et al, the Vicorder apparatus was used for the assessment of PWV, which uses cuffs that are being placed at the neck and upper thigh of the subject. This device has been evaluated for the accuracy of the derived indices13, 14, 15 and—given its operator‐independent nature—can be considered more appropriate for use in large epidemiological studies. However, in the era of constant technological advances and introduction of novel devices for the assessment of central hemodynamics, rigorous efforts must be made for the proper validation of these devices with use of standardized protocols and always bear in mind that these indices should not necessarily be considered interchangeable.12

Last, in view of the cross‐sectional nature of this study, prospective evaluation of the participants—with use of the same techniques—for the assessment of structural and functional subclinical vascular damage could help identify the prognostic ability of the exposure parameters in the prevalence of vascular damage and further elucidate/dissociate the pathophysiological basis of arteriosclerosis and arterial remodeling/hypertrophy in young populations.

CONFLICT OF INTEREST

Authors have nothing to disclose.