The Role of Monitoring Arterial Stiffness with Cardio-Ankle Vascular Index in the Control of Lifestyle-Related Diseases

Abstract

Arteriosclerosis is a major contributor to cardiovascular diseases. One of the difficulties in controlling those diseases is the lack of a suitable indicator of arteriosclerosis or arterial injury in routine clinical practice. Arterial stiffness was supposed to be one of the monitoring indexes of arteriosclerosis. Cardio-ankle vascular index (CAVI) is reflecting the stiffness of the arterial tree from the origin of the aorta to the ankle, and one of the features of CAVI is independency from blood pressure at a measuring time. When doxazosin, an α1-adrenergic blocker, was administered, CAVI decreased, indicating that arterial stiffness is composed of both organic stiffness and functional stiffness, which reflects the contraction of arterial smooth muscle. CAVI shows a high value with aging and in many arteriosclerotic diseases, and is also high in persons possessing main coronary risk factors such as diabetes mellitus, metabolic syndrome, hypertension and smoking. Furthermore, when the most of those risk factors were controlled by proper methods, CAVI improved. Furthermore, the co-relationship between CAVI and heart function was demonstrated during treatment of heart failure. This paper reviews the principle and rationale of CAVI, and discusses the meaning of monitoring CAVI in following up so-called lifestyle-related diseases and cardiac dysfunction in routine clinical practice.

Keywords: Arterial stiffness; Arteriosclerosis; Cardiac dysfunction; Cardio-ankle vascular index; Coronary risk factor; Diabetes mellitus; Hypertension; Pulse wave velocity.

Fig. 1

The equation of CAVI and its measuring method. PWV from the heart to the ankle is obtained by measuring the length from the origin of the aorta to the ankle, and by calculating T = t_b + t_ba. Blood pressure is measured at the brachial artery. Ps = Systolic blood pressure; Pd = diastolic blood pressure; ΔP = pulse pressure, Ps – Pd; ρ = blood density; L = length from the origin of the aorta to the ankle; T = time taken for the pulse wave to propagate from the aortic valve to the ankle; t_ba = time between the rise of brachial pulse wave and the rise of ankle pulse wave; t_b = time between aortic valve closing sound and the notch of brachial pulse wave; t′_b = time between aortic valve opening sound and the rise of brachial pulse wave. Reproduced from Shirai et al. [12].

Fig. 2

Effects of the β₁-blocker metoprolol and α₁-blocker doxazosin on CAVI and baPWV [16]. a When the selective β₁-adrenergic blocker metoprolol (80 mg) was administered, both systolic and diastolic blood pressures decreased and baPWV also decreased, but CAVI did not change. This study indicates that CAVI is independent of blood pressure at the time of measurement. b Furthermore, with the administration of the selective α₁-adrenergic receptor blocker doxazosin (4 mg), systolic and diastolic blood pressures as well as CAVI and baPWV decreased, indicating that CAVI decreased with a relaxation of smooth muscles induced by the α₁-adrenergic receptor blocker. * p < 0.05, ** p < 0.01 vs. baseline, Bonferroni test. Reproduced from Shirai et al. [16].

Fig. 3

Effects of age on CAVI. CAVI was measured in Japanese workers and their families. CAVI increased with age, and the values of CAVI were higher in men than women at any age. CAVI = 0.5 by 10 years; men > women by 0.2 (= difference of 5 years). Modified from Namekata et al. [17].

Fig. 4

The relationship between the number of affected coronary arteries and CAVI. * p < 0.05; ** p < 0.001. Reproduced from Nakamura et al. [18].

Fig. 5

Comparison of CAVI in estimated glomerular filtration rate (eGFR) quartiles. CAVI was negatively correlated with eGFR. CAVI might be a possible indicator of chronic kidney disease. * p < 0.05; ** p < 0.001. Reproduced from Nakamura et al. [19].

Fig. 6

Comparison between the effects of amlodipine and efonidipine on CAVI. Blood pressure (BP) decreased with both agents at almost the same rates, but the rate of decrease was different. Efonidipine decreased CAVI to a much greater extent than amlodipine. Reproduced from Sasaki et al. [57].

Fig. 7

Changes in CAVI following the huge East Japan earthquake in hypertensive patients who lived 250 km away from the epicenter. Data are presented as mean ± SD. * p < 0.05; *** p < 0.0001.

Fig. 8

CAVI in arteriosclerotic diseases and coronary risk factors. CAVI showed high value in typical arteriosclerotic diseases and also in persons with cardiovascular risk factors. Also, CAVI decreased with improvement of those risk factors. EPA = Eicosapentaenoic acid.

Fig. 9

The correlation of CAVI and baPWV with E/A and deceleration time of the E wave (EDCT) in patients with chest pain syndrome who underwent coronary angiography. Reproduced from Takaki et al. [79].

Fig. 10

The meaning of CAVI. CAVI reflects the proper arterial stiffness, which is a surrogate marker of arteriosclerosis, but is also involved in the interrelationship with left ventricular function as a windkessel. ΔD = Change in diameter; D = diameter of the vessel.