Isabella Tan

Arterial stiffness index beta and cardio-ankle vascular index inherently depend on blood pressure but can be readily corrected

Objectives: Arterial stiffness index &bgr; and cardio-ankle vascular index (CAVI) are widely accepted to quantify the intrinsic exponent (&bgr;0) of the blood pressure (BP)-diameter relationship. CAVI and &bgr; assume an exponential relationship between pressure (P) and diameter (d). We aim to demonstrate that, under this assumption, &bgr; and CAVI as currently implemented are inherently BP-dependent and to provide corrected, BP-independent forms of CAVI and &bgr;. Methods and results: In P = Prefe&bgr;0[(d/dref)-1], usually reference pressure (Pref) and reference diameter (dref) are substituted with DBP and diastolic diameter to accommodate measurements. Consequently, the resulting exponent is not equal to the pressure-independent &bgr;0. CAVI does not only suffer from this ‘reference pressure’ effect, but also from the linear approximation of (dP/dd). For example, assuming &bgr;0 = 7, an increase of SBP/DBP from 110/70 to 170/120 mmHg increased &bgr; by 8.1% and CAVI by 14.3%. We derived corrected forms of &bgr; and of CAVI (CAVI0) that indeed did not change with BP and represent the pressure-independent &bgr;0. To substantiate the BP effect on CAVI in a typical follow-up study, we realistically simulated patients (n = 161) before and following BP-lowering ‘treatment’ (assuming no follow-up change in intrinsic &bgr;0 and therefore in actual P–d relationship). Lowering BP from 160 ± 14/111 ± 11 to 120 ± 15/79 ± 11 mmHg (p < 0.001) resulted in a significant CAVI decrease (from 8.1 ± 2.0 to 7.7 ± 2.1, p = 0.008); CAVI0 did not change (9.8 ± 2.4 and 9.9 ± 2.6, p = 0.499). Conclusion: &bgr; and CAVI as currently implemented are inherently BP-dependent, potentially leading to erroneous conclusions in arterial stiffness trials. BP-independent forms are presented to readily overcome this problem.

Heart Rate Dependency of Large Artery Stiffness

Carotid-femoral pulse wave velocity (cfPWV) quantifies large artery stiffness, it is used in hemodynamic research and is considered a useful cardiovascular clinical marker. cfPWV is blood pressure (BP) dependent. Intrinsic heart rate (HR) dependency of cfPWV is unknown because increasing HR is commonly accompanied by increasing BP. This study aims to quantify cfPWV dependency on acute, sympathovagal-independent changes in HR, independent of BP. Individuals (n=52, age 40–93 years, 11 female) with in situ cardiac pacemakers or cardioverter defibrillators were paced at 60, 70, 80, 90, and 100 bpm. BP and cfPWV were measured at each HR. Both cfPWV (mean [95% CI], 0.31 [0.26–0.37] m/s per 10 bpm; P<0.001) and central aortic diastolic pressure (3.78 [3.40–4.17] mm Hg/10 bpm; P<0.001) increased with HR. The HR effect on cfPWV was isolated by correcting the BP effects by 3 different methods: (1) statistically, by a linear mixed model; (2) mathematically, using an exponential relationship between BP and cross-sectional lumen area; and (3) using measured BP dependency of cfPWV derived from changes in BP induced by orthostatic changes (seated and supine) in a subset of subjects (n=17). The BP-independent effects of HR on cfPWV were quantified as 0.20 [0.11–0.28] m/s per 10 bpm (P<0.001, method 1), 0.16 [0.11–0.22] m/s per 10 bpm (P<0.001, method 2), and 0.16 [0.11–0.21] m/s per 10 bpm (P<0.001, method 3). With a mean HR dependency in the range of 0.16 to 0.20 m/s per 10 bpm, cfPWV may be considered to have minimal physiologically relevant changes for small changes in HR, but larger differences in HR must be considered as contributing to significant differences in cfPWV.

Arterial viscoelasticity: role in the dependency of pulse wave velocity on heart rate in conduit arteries

Experimental investigations have established that the stiffness of large arteries has a dependency on acute heart rate (HR) changes. However, the possible underlying mechanisms inherent in this HR dependency have not been well established. This study aimed to explore a plausible viscoelastic mechanism by which HR exerts an influence on arterial stiffness. A multisegment transmission line model of the human arterial tree incorporating fractional viscoelastic components in each segment was used to investigate the effect of varying fractional order parameter (α) of viscoelasticity on the dependence of aortic arch to femoral artery pulse wave velocity (afPWV) on HR. HR was varied from 60 to 100 beats/min at a fixed mean flow of 100 ml/s. PWV was calculated by intersecting tangent method (afPWVTan) and by phase velocity from the transfer function (afPWVTF) in the time and frequency domain, respectively. PWV was significantly and positively associated with HR for α ≥ 0.6; for α = 0.6, 0.8, and 1, HR-dependent changes in afPWVTan were 0.01 ± 0.02, 0.07 ± 0.04, and 0.22 ± 0.09 m/s per 5 beats/min; HR-dependent changes in afPWVTF were 0.02 ± 0.01, 0.12 ± 0.00, and 0.34 ± 0.01 m/s per 5 beats/min, respectively. This crosses the range of previous physiological studies where the dependence of PWV on HR was found to be between 0.08 and 0.10 m/s per 5 beats/min. Therefore, viscoelasticity of the arterial wall could contribute to mechanisms through which large artery stiffness changes with changing HR. Physiological studies are required to confirm this mechanism.NEW & NOTEWORTHY This study used a transmission line model to elucidate the role of arterial viscoelasticity in the dependency of pulse wave velocity on heart rate. The model uses fractional viscoelasticity concepts, which provided novel insights into arterial hemodynamics. This study also provides a means of assessing the clinical manifestation of the association of pulse wave velocity and heart rate.

Effects of cardiac timing and peripheral resistance on measurement of pulse wave velocity for assessment of arterial stiffness

To investigate the effects of heart rate (HR), left ventricular ejection time (LVET) and wave reflection on arterial stiffness as assessed by pulse wave velocity (PWV), a pulse wave propagation simulation system (PWPSim) based on the transmission line model of the arterial tree was developed and was applied to investigate pulse wave propagation. HR, LVET, arterial elastic modulus and peripheral resistance were increased from 60 to 100 beats per minute (bpm), 0.1 to 0.45 seconds, 0.5 to 1.5 times and 0.5 to 1.5 times of the normal value, respectively. Carotid-femoral PWV (cfPWV) and brachial-ankle PWV (baPWV) were calculated by intersecting tangent method (cfPWVtan and baPWVtan), maximum slope (cfPWVmax and baPWVmax), and using the Moens-Korteweg equation (

Effects of pacing modality on noninvasive assessment of heart rate dependency of indices of large artery function

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Cerebral Haemodynamics: Effects of Systemic Arterial Pulsatile Function and Hypertension

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Systolic time intervals assessed from analysis of the carotid pressure waveform

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