Changes in blood pressure and arterial stiffness monitored using the cardio–ankle vascular index during hemodialysis

Abstract

During hemodialysis (HD), blood pressure (BP) changes are frequently observed. However, the mechanism of BP changes during HD has not been fully clarified. The cardio–ankle vascular index (CAVI) reflects the arterial stiffness of the arterial tree from the origin of the aorta to the ankle independent from BP during measurement. Additionally, CAVI reflects functional stiffness in addition to structural stiffness. We aimed to clarify the role of CAVI in regulating the BP system during HD. We included 10 patients undergoing 4-hour HD (total 57 HD sessions). Changes in the CAVI and various hemodynamic parameters were evaluated during each session. During HD, BP decreased and CAVI significantly increased (CAVI, median [interquartile range]; 9.1 [8.4–9.8] [0 min] to 9.6 [9.2–10.2] [240 min], p < 0.05). Changes in CAVI from 0 min to 240 min were significantly correlated with water removal rate (WRR) (r = −0.42, p = 0.002). Changes in CAVI at each measurement point were negatively correlated with ΔBP (Δsystolic BPeach MP, r = −0.23, p < 0.0001; Δdiastolic BPeach MP, r = −0.12, p = 0.029). Whereas one patient exhibited a simultaneous decrease in BP and CAVI during the initial 60 min of HD. Arterial stiffness monitored with CAVI generally increased during HD. CAVI elevation is associated with decreased WWR and BP. An increase in CAVI during HD may reflect the contraction of smooth muscle cells and play an important role in BP maintenance. Hence, measuring CAVI during HD may distinguish the cause of BP changes.

The Responses of Arterial Stiffness Parameter Beta-Derived Index of the Aorta and Illiac-Femoral Artery to Acute Hypovolemia in Rabbits

“…CAVI reflects vascular smooth muscle contraction [14‒19] and relaxation as well as structural stiffness of the arterial wall such as atherosclerosis [10‒13]. CAVI is not only a surrogate marker of arterial stiffness but also that of peripheral resistance or compliance.…”

“…The cardio-ankle vascular index (CAVI) was developed as a BP-independent index of arterial stiffness based on the stiffness parameter β theory [8] and Bramwell and Hill's equation [9]. It has been clinically pointed out that the CAVI reflected not only structural stiffness due to aging, atherosclerosis, and diabetes [10][11][12][13] but also functional stiffness due to contraction and dilatation of arterial smooth muscle cells [14] such as dialysis [15,16], septic shock [17], and administration of vasodilating drug [18]. Nagasawa et al [19] reported in rabbits that the CAVI increased whereas heart-to-ankle PWV decreased in response to a decrease in BP induced by the depletion of 25-30% of total blood volume.…”

Arterial stiffness of the aorta and iliofemoral artery and their responses to nitroglycerin administration in myocardial infarction-prone Watanabe heritable hyperlipidemic rabbits

“…The conspicuous feature of CAVI is independency of blood pressure (BP) at measuring time. It becomes clear that CAVI reflects not only the organic stiffness of the arterial wall induced by aging or atherosclerosis but also functional change in stiffness induced by medial smooth muscle contraction [ 4 , 7 ].…”

Effect of balloon pulmonary angioplasty on cardio-ankle vascular index and biventricular remodeling in patients with chronic thromboembolic pulmonary hypertension

“…The CAVI reflects arterial stiffness from the aortic root to the ankle. In addition, it reflects functional stiffness due to smooth muscle cell contraction or relaxation and plays an important role in hemodynamics by reflecting LV afterload (14)(15)(16)(17)(18). Therefore, the CAVI is suitable for evaluating arterial stiffness in patients with CTEPH.…”

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A and Shimizu K (2023) Effect of balloon pulmonary angioplasty on cardio-ankle vascular index and biventricular remodeling in patients with chronic thromboembolic pulmonary hypertension.

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