Association of cardio-ankle vascular index with blood pressure indices: mathematical and methodological perspectives

Abstract

First, we would like to congratulate Nagayama et al. for their recent study [1], which provides novel information concerning the association of cardio-ankle vascular index (CAVI), a surrogate of arterial stiffness, with four different blood pressure indices; systolic (SBP), diastolic (DBP), pulse pressure (PP), and mean arterial pressure (MAP). We would like to further discuss the findings of this study and stimulate additional thinking regarding their interpretation, under the light of new published evidence concerning: (i) different formulas for MAP estimation, (ii) the association of arterial stiffness with resting heart rate, and (iii) the recent 2017 ACC/AHA guidelines for prevention, detection, evaluation, and management of high blood pressure (BP) in adults. Nagayama et al. used the traditional formula for MAP estimation (MAP=DBP+ 0.333 × PP). It would be of interest to estimate MAP using alternative formulas and particularly the one proposed by Meaney et al. [2]; MAP= DBP+ 0.412 × PP, using a factor (f) 0.412 instead of f= 0.333. The alternative formula yielded more accurate MAP estimations than the traditional one (f= 1/3), when compared with invasive direct intra-arterial MAP measurement [2, 3]. Moreover, MAP calculated by an f= 0.412 exhibited a stronger association, compared with the traditional formula (f= 0.333), with left ventricular and carotid wall hypertrophy, as well as increased aortic stiffness assessed by carotid-to-femoral pulse wave velocity [4]. This finding might be also applicable on the reported association between CAVI and MAP [1] and it is worth further examination. Finally, although PP was found to be less useful for the assessment of arterial stiffness (assessed by CAVI) compared with other BP indices [1], the fractional PP (defined as the ratio of PP to MAP) might be considered as another BP-related biomarker with clinical relevance according to previous observations [5]. Mounting epidemiological, cross-sectional studies investigated the association of arterial stiffness and particularly pulse wave velocity (PWV) with resting heart rate [6]. It is evident that under specific circumstances resting heart rate influences arterial stiffness measurements either due to the viscoelastic nature of the arterial wall or due to other mediating factors such as BP or/and shear stress which are directly affected by heart rate changes. Although heart rate was not measured in this study, it should be recommended to be co-evaluated in studies involving arterial stiffness assessment, according to previous recommendations by the American Heart Association [7]. Finally, it was recently reported [8] that the reclassified subjects as stage 1 hypertensive (SBP between 130–139 mmHg or DBP between 80–89 mmHg) according to the recent 2017 ACC/AHA guidelines [9], have a significantly increased aortic stiffness and greater prevalence in asymptomatic aortic damage compared with subjects with “elevated BP” (SBP between 120–129 mmHg and DBP < 80 mmHg). This finding might be applicable on the results of this study [1], which reported that adjusted CAVI was lower in normotensive subjects compared with different subgroups of hypertensive subjects and that no significant differences in adjusted CAVI exists among the three examined groups of hypertensive individuals. Therefore, it would be of great importance to re-examine the differences in CAVI between reclassified normotensive and hypertensive subgroups, according to the new BP cut-off values proposed by the 2017 ACC/AHA guidelines [9].