The cardio-ankle vascular index (CAVI) is a new index of arterial stiffness that can be measured with a VaSera VS-1000 device. An association between certain arterial stiffness indices and cardiac function has been found but has not yet been validated. The aim of this study was to establish whether any significant relationship exists between cardiac index (CI) and CAVI. Twenty healthy male volunteers with a mean age of 30 ± 5 years and a mean BMI of 23.1 ± 1.1 kg/m2 participated in the study. CO was estimated using a Doppler technique, and CAVI was measured with a VaSeraVS-1000 device. A motorised tilting table was used to achieve head-up tilt (HUT) angles of 0°, 30°and 60°, to modify the peripheral sympathetic outflow. We found that there was a significant inverse correlation between CI and the degree of head-up tilt, ( for 0°and 30°; for 0° and 60°, p < 0.001 for both; for 30° and 60°, ). CAVI showed a significant positive correlation relative with the degree of HUT, ( for 0° and 30°; for 0° and 60°; for 30° and 60°, for all). A significant negative correlation was found between CI and CAVI r = - 0.47, p < 0.05. Additionally, a significant p < 0.001 increase in PVR values was observed for increasing HUT values. In conclusion: An inverse relationship between CI and CAVI was shown; a decrease in cardiac output is associated with an increase in CAVI values at different degrees of HUT. This association provides further insight into the postural link between cardiac output and arterial compliance.
The cardiac index (CI) is a normalized metric of cardiac output (CO) and is based on a person’s body size (l/min/ m2); CI increases proportionally with an individual’s body surface area (BSA), which is commonly measured with the Mosteller formula [
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CO can be calculated from stroke volume (SV) and heart rate (HR) based on the following equation [
(where D is the aortic diameter and VTI is the velocitytime integral).
CI is considered the most important indicator of the cardiovascular system function. The normal range of CI at rest is 2.6 - 4.2 l/min/m [2-4], and an age-related variation in indexed cardiac output has been well established [5,6]. Unlike the left ventricular ejection fraction (LVEF), CI offers a more precise estimate of the pumping action of the heart: because it does not change with increased heart rate or concomitant decreases in stroke volume, when pacing a normal-size heart [
Reports linking CI values with overt or subtle changes in arterial compliance are scarce. Studies have related indices of cardiac function, including CI, to neuropsychological impairment [9,10], dementia and cognitive dysfunction among patients with severe cardiomyopathies [
Interestingly, both obese and non-obese individuals were shown to have similar cardiac indexes, despite an increased LV-EF in the obese individuals [
In a population-based study, arterial stiffness was shown to be strongly associated with atherosclerosis at various sites in the vascular tree [
Hayashi et al. [
(where p is blood density, and dP is pulse pressure)
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PWV is obtained by dividing the vascular length (L) by the time (T) required for a pulse wave to propagate from aortic valve to the ankle. L is obtained by measuring the length between the aortic valve and the ankle [
The aim of this work was to establish whether a significant relationship exists between CI and CAVI. Furthermore, we aimed to propose a new index, CI/CAVI, as a haemodynemic parameter.
We created varied levels of vasoconstriction by baroreceptor-sympathetic outflow activation using, graded degrees of HUT [30,31]. This technique caused changes in the arteriolar vascular system stiffness, and simulated a clinical condition of varying degrees of atherosclerosis in the arteries.
Twenty healthy non-smoking male subjects, with, a mean age of 30 ± 5 years were recruited for the study. All the subjects signed an informed consent upon their arrival at the study venue. All were in stable clinical condition, none was on medication, and they all had normal blood pressure, CVS, renal, and hepatic functions, as well as, blood sugar, serum cholesterol and uric acid levels. Prior to beginning the test, all the study subjects were reassured about its safety and non-invasive nature to minimize any anxiety.
The subjects were examined in the supine position on tilt a table, in a quiet, temperature-controlled room. The measurements were performed after at least 10-min of supine rest to achieve a steady state, in which the heart rate changed less than 3 beats/min from one minute to the next [
CAVI was measured by a VaSera VS-1000 (Fukuda Denshi, Tokyo, Japan) using soft-ware version 08-01, which assesses the state of the vessels with high accuracy. The reliability of the VaSera VS-1000 in estimating arterial stiffness has been previously validated [
Cardiac output was calculated using the Sonos 7500 echo-Doppler equipment (M2424A Ultrasound system, Andover Masssachuses 01810, Philips, made in USA) with a 2.5 MHz phased array cardiac probe, a PW Doppler and a built-in ECG. To obtain the left ventricular outflow tract (LVOT) VTI, the Doppler sample volume was placed at the middle of the LVOT, just below the aortic cusp [
culated using the following equation [
where D is the aortic diameter, and VTI is the velocity time integral. CO was calculated according the equation:. CI was obtained by dividing CO by the body surface area.
The above-cited measurements of VTI using Doppler echocardiography, and CAVI, using the VaSeraVS-1000 were performed after the subject achieved a steady state, with an HUT of 0˚ (the pre-test supine position), 30˚ or 60˚ (
The statistical analysis was performed using SPSS, version 12. All values were expressed as the means ± SD. The haemodynamic parameters (CI, CAVI and CI/CAVI) were compared at different degrees of HUT, using Student’s paired t-test, and Pearson’s correlation (r). A p value <0.05 was considered statistically significant.
The results were consistent for all twenty participants.
The baseline control value of CI (lying flat in the supine position) was 2.58 ± 0.25 (range, 2.55 - 3.20) l/min/m2. The CI values at 30˚ and 60˚ were 2.06 ± 0.42 (range, 1.30 - 2.90) and 1.85 ± 0.45 (range, 1.20 - 2.70) l/min/ m2, respectively. There were significant correlations between the CI values at 0˚ of HUT and those at 30˚ and 60˚ (0˚ and 30˚; 0˚ and 60˚:). A significant correlation existed between CI values at 30˚ and 60˚. The CI values at 30˚ and 60˚ of HUT were significantly lower than that at 0˚. The CI at 60˚ of HUT was significantly lower than that at 30˚. As demonstrated in
The baseline control value of CAVI was (range, 5.60 - 8.05). The CAVI values at 30˚ and 60˚ were 8.60 ± 0.73 (range, 7.10 - 9.90) and 9.20 ± 0.98 (range, 7.75 - 10.45), respectively. As shown in
The value of CI/CAVI at 0˚ of HUT was (range, 0.23 - 0.48). The values at 30˚ and 60˚ were 0.25 ± 0.06 (range, 0.14 - 0.37) and 0.19 ± 0.05 (range, 0.12 - 0.30), respectively. There were significant correlations between the CI/CAVI value at 0˚ of HUT and those at 30˚ and 60˚ (for 0˚ and 30˚, , for 0˚ and 60˚, ). In addition, a significant correlation existed between CI/CAVI values at 30˚ and 60˚ (, for 30˚ and 60˚,). As demonstrated in
There was a significant increase in the PVR (mean arterial blood pressure value divided by cardiac output value) values with increases in HUT. The baseline control value was 25.33 ± 5.01 mmHg·min−1/dl (range 14.4 - 33.6 mmHg·min−1/dl). The PVR values at 30˚ and
60˚ were mmHg·min−1/dl (range 18.0 - 37.63 mmHg·min−1/dl) and mmHg·min−1/dl (range 20.01 - 47.57 mmHg·min−1/dl), respectively.
The cardiovascular response to a postural change from the supine to the upright position has been extensively studied. This response reflects both mechanical changes due to the effects of gravity on the circulatory system and the changes caused by the resulting nervous reflex responses [
As mentioned previously, the estimation of CAVI is dependent on the pulse wave transmission between the aortic valve and peripheral blood vessels and can be used to express changes in the arterial diameter [27,28]. Such changes in arterial diameter which are evoked by the baroreceptor-sympathetic nerves, in response to incremental changes in the HUT, are precisely expressed by the estimated graded CAVI values at 30˚ and 60˚ of tilt, compared to the baseline supine value (Figures 7(a)-(c)). Thus, CAVI can be used as an index of arterial stiffness, to estimate the degree of vascular bed compliance, which can be altered in various metabolic and/or cardiovascular disorders, as atherosclerosis, which is known to result in
greatly increased vascular stiffness [
Notably, a considerable body of evidence has implicated both vascular compliance and total peripheral resistance in the determination of after-load, (and, therefore, CO and CI) [38,39]. In this study, we noninvasively demonstrated an inverse correlation between varied degrees of peripheral resistance, reflected by changes in arterial diameter (estimated by CAVI), and overall cardiac performance, expressed as the cardiac index. A consistent and significant inverse relationship was revealed, at different degrees of HUT (
This study was investigative, and we do not advocate CAVI assessments or the use of CI/CAVI correlations in patients with valvular heart diseases or severe obliterative vascular disorders, because CAVI depends on generation of pressure waveforms which are impossible to achieve with these maladies.
In this investigation, a novel technique (the measurement of CAVI) was employed to assess changes in arterial compliance caused by postural changes in normal individuals, and an inverse correlation between cardiac index (CI) and cardio-ankle vascular index (CAVI) was established Therefore, our approach may have clinical implications for the treatment of patients suffering from metabolic and/or atherosclerotic disorders.