Carotid-radial Pulse Wave Velocity Research Articles

Takayasu's arteritis: a cause of prolonged arterial stiffness

Cardiovascular disease is a major cause of mortality and morbidity in patients with Takayasu's arteritis (TA). Increased arterial stiffness is an independent risk factor and predictor of cardiovascular mortality in a variety of diseases. Pulse wave velocity (PWV) and the augmentation index (AI) are used as clinical measurements of arterial stiffness. Data are presented from 10 patients with TA and 11 normal controls obtained between 2000 and 2004. Arterial compliance was assessed non-invasively by measurement of PWV, using the Complior system, and calculation of the aortic AI. TA patients (mean age 40.8+/-13.2 yr) were compared with a control group of healthy women from a parallel study (mean age 32.3+/-5.5 yr). The mean carotid-femoral PWV (PWV-CF) was higher in TA patients (P = 0.03). In addition, both aortic AI derived from the radial artery (P = 0.002) and carotid AI (P = 0.03) were higher in TA patients compared with controls. PWV-CF did not correlate with CRP (r = - 0.23, P = 0.23) or ESR (r = - 0.19, P = 0.27). Similar results were obtained for the correlation of carotid-radial PWV with CRP (r = 0.15, P = 0.32) and ESR (r = 0.33, P = 0.14). Our data show that TA is associated with elevated arterial stiffness in the central aorta, which may persist when the disease is quiescent. These data suggest that PWV represents a means by which cardiovascular risk can be detected and monitored in TA, and highlights the importance of effective management of cardiovascular risk factors in these patients.

Clinical Implication of Carotid-Radial Pulse Wave Velocity for Patients with Coronary Artery Disease

Background and Objectives：Arterial stiffness assessed non-invasively with the aortic pulse wave velocity (PWV) has been associated with atherosclerosis in the coronary arteries and also cardiovascular mortality. The aim of this study was to determine whether arterial stiffness may predict the severity of coronary artery disease (CAD). Subjects and Methods：We enrolled 106 consecutive, symptomatic patients (males: 71 (67%), mean age: 57.0±10.5 years) who underwent coronary angiography. The extent of the CAD was defined by single or multiple vessel disease according to the number of coronary vessels with a ≥50% narrowing, the lesion type according to the AHA/ ACC guidelines, and a modified stenosis scoring system. Arterial stiffness was characterized by measurement of the carotid-radial PWV. In addition, such cardiovascular risk factors as the body mass index, hypertension, smoking, LDL-and HDL-cholesterol, ejection fraction (EF), left ventricle mass index (LVMI), pulse pressure, plasma homocysteine and C-reactive protein (CRP) were evaluated. Results：The carotid-radial PWV in multiple vessel CAD was faster than in single vessel CAD and the normal arteries (10.33±1.46 vs. 8.76±1.65 m/sec, respectively, p< 0.001). On the univariate analysis, the extent of the CAD, as expressed as a modified stenosis score, was associated with the total cholesterol, LDL-cholesterol, the EF and the PWV. However, on the multivariate analysis, the extent of CAD was associated with the carotid-radial PWV (p<0.001). Conclusion：Arterial stiffness identified by carotidradial PWV may predict the severity of the CAD after adjusting for other cardiovascular risk factors. (Korean Circulation J 2006;36:565-572)

Tu-P9:360 Coronary risk assessment by carotid-radial pulse wave velocity

Tu-P9:360 Coronary risk assessment by carotid-radial pulse wave velocity

Spironolactone reduces brachial pulse wave velocity and PIIINP levels in hypertensive diabetic patients

To assess whether spironolactone has beneficial effects on blood pressure (BP), N-terminal propeptide of type III procollagen (PIIINP) and pulse wave velocity (PWV) in hypertensive, type II diabetics. Ten patients with type II diabetes and hypertension were enrolled in a randomized, double-blind crossover study comparing 4 months' treatment with spironolactone and placebo with a 4-week washout phase. BP, PIIINP and carotid-radial PWV were measured at the end of each treatment phase. Compared with placebo, spironolactone reduced systolic BP by 15.6 +/- 46.1 mmHg (P = 0.005, 95% CI 2.7-28.5 mmHg), PIIINP by 0.6 +/- 0.3 microg l(-1) (P = 0.04, 95% CI 0.02-1.1 microg l(-1)) and PWV by 0.6 +/- 0.2 m s(-1) (P = 0.008, 95% CI 0.18-1.02 m s(-1)). Spironolactone is effective at reducing systolic BP and brachial artery stiffness as indicated by PWV. It also reduces PIIINP in type II diabetic patients with hypertension.

Acute Effects of Caffeine on Arterial Stiffness in Young Healthy Subjects

Background and Objectives：Coffee is one of the most popular beverages in the world. Caffeine is one of the substances contained in coffee and it is well known to increase blood pressure and the peripheral vascular resistance, in part because it stimulates the sympathetic nervous system. Arterial stiffness is an important factor for the performance of the cardiovascular system and it is an independent prognosticator of cardiovascular disease. We investigated the acute effect of caffeine on arterial stiffness in young healthy subjects. Subjects and Methods：We enrolled 20 young healthy subjects, who were randomly divided two groups. The caffeine group (10 subjects, 4 males, mean age: 23.3±1.1 years) received 520 mL caffeinated coffee and the control group (10 subjects, 4 males, mean age: 23.1±1.3 years) received 520 mL water. The arterial stiffness was evaluated by the carotid-radial pulse wave velocity and the augmentation index as corrected by heart rate (75 bpm), and all the hemodynamic measurements were obtained at baseline, 30, 60, 120 and 180 minutes after ingestion of the coffee or water. Results：Arterial stiffness measured by carotid-radial pulse wave velocity increased progressively from 9.4±1.2 m/sec at baseline to 11.5± 1.6 m/sec (p<0.05) at 30 minutes after the coffee intake. In addition, peripheral systolic pressure increased progressively from 107.1±10.2 mmHg at baseline to 114.4±12.9 mmHg (p<0.05) at 60 minutes after the coffee intake. Such changes were not seen in control group. Conclusion：Caffeine affects increased the pulse wave velocity and systolic blood pressure. This means that coffee might have an adverse effect on arterial stiffness. (Korean Circulation J 2005;35:841-846)

Enhanced external counterpulsation does not alter arterial stiffness in patients with angina

Enhanced external counterpulsation (EECP) is a noninvasive treatment for angina that acutely augments diastolic pressure and reduces cardiac afterload. However, the mechanism of the sustained clinical benefit seen with this therapy is not known. The study aimed to determine whether EECP leads to an improvement in arterial stiffness. In all, 22 men and 1 woman with angina (age 63.6 +/- 6.7 years, mean +/- SD) were studied prior to and after 35 h of EECP therapy over 7 weeks. We measured carotid-radial (C-R) pulse wave velocity (PWV), and aortic augmentation index (AI) was derived from radial and carotid artery waveforms using applanation tonometry. Seventeen patients underwent treadmill exercise testing before and after the 7 weeks of EECP. After EECP therapy, despite a significant improvement in treadmill exercise time and a reduction in systolic and diastolic blood pressures, there was no significant change in any arterial stiffness parameters: Mean C-R PWV was 8.4 +/- 0.8 m/s at baseline and 8.0 +/- 1.2 m/s after 7 weeks of EECP, mean change: -0.4, 95% confidence interval (CI): -1.0, + 0.2, p = 0.17. Mean radial-derived AI was 25.7 +/- 10.4% before and 24.6 +/- 10.8% after, mean change: +1.1%, 95% CI: -2.3, +4.5, p = 0.53. Median AI-carotid was 31.5% before and 28.7% after; median change: -0.5, interquartile range: -9.5, +3.5, p = 0.32. Nineteen patients returned for 6-month recordings; neither blood pressure nor arterial stiffness readings were significantly different from baseline. Enhanced external counterpulsation therapy does not significantly alter arterial stiffness. Other than an initial reduction in blood pressure, the sustained clinical benefit seen with this therapy is unlikely to be effected through alterations in arterial wall mechanical properties.

Effect of beta-adrenergic stimulation on pulse wave velocity in black and white subjects

Reduced beta-adrenergic sensitivity has been reported in black subjects. We hypothesized that beta-adrenergic stimulation by isoproterenol would affect pulse wave velocity (PWV), a marker of arterial stiffness, differently in black and white subjects. Healthy normotensive black subjects (n = 21) matched for age, gender, height and body mass index with healthy normotensive white subjects (n = 20), participated in a randomized, double-blind, placebo-controlled cross-over study. The PWV was determined using an automated device at baseline and after 30 min of an equal volume infusion of isoproterenol (8 mug/kg per min) or placebo (dextrose 5%), separated by a washout period of 25 min. At baseline, heart rate (HR), systolic and diastolic blood pressure (SBP, DBP) and PWV were comparable in black and in white subjects. Placebo had no significant effect on haemodynamic variables. Isoproterenol increased HR, SBP and pulse pressure and decreased DBP with a comparable magnitude in both groups. Compared with placebo, isoproterenol decreased carotid-femoral PWV in white (from 5.9 +/- 1.2 to 5.7 +/- 1.1 m/s, means +/- SD, P = 0.05), but not in black subjects (from 6.2 +/- 1.3 to 6.6 +/- 1.7 m/s, P = 0.1). The difference in response between black and white subjects was significant (P = 0.04). Isoproterenol decreased carotid-radial PWV only significantly in white subjects. These results are compatible with the hypothesis of an altered beta-adrenergic sensitivity, which is expressed by a blunted effect of isoproterenol on arterial stiffness in black subjects.

Arterial Stiffness and Wave Reflections in Patients With Sickle Cell Disease

We tested the hypothesis that lower blood pressure and increased vasodilatation reported in sickle cell disease (SCD) patients with hemoglobin SS genotype (SS) are translated by lower arterial stiffness determined by pulse wave velocity (PWV) and wave reflections assessed by augmentation index (AI). We enrolled 20 SS (8 females; 12 male) patients closely matched for age, gender, height, and body mass index to 20 subjects with hemoglobin AA genotype (AA). Carotid-femoral PWV (PWV(CF)) and carotid-radial PWV (PWV(CR)) were recorded with the Complior device. Aortic AI was derived from pressure wave analysis (SphygmocoR). PWV(CF) and PWV(CR) were lower in SS than in AA (4.5+/-0.7 m/s versus 6.9+/-0.9 m/s, P<0.0001 and 6.6+/-1.2 m/s versus 9.5+/-1.4 m/s, P<0.0001, respectively). AI was lower in SS than in AA (2+/-14% versus 11+/-8%, P=0.02). Multivariate analysis revealed that both PWV(CF) and PWV(CR) were negatively associated with hemoglobin SS type and positively related to mean arterial pressure (MAP), whereas AI was positively associated with MAP and total cholesterol (all P<0.0001). Multivariate analysis restricted to SS indicated a positive association between PWV(CF) and PWV(CR) with age but a negative association with MAP (R2=0.57 and 0.51, respectively, both P<0.001), whereas MAP and heart rate were independently associated with AI (R2=0.65, P<0.001). This study provides the first evidence that SCD is associated with both lower arterial stiffness and wave reflections. SS patients have a paradoxical negative association between PWV and MAP, suggesting that low MAP does not protect them against arterial stiffness impairment.

Non-invasive measures of pulse wave velocity correlate with coronary arterial plaque load in humans.

Arterial stiffness is an emerging major risk factor for cardiovascular morbidity and mortality. The aim of the present study was to assess if coronary artery plaque load correlates with non-invasive measures of arterial stiffness. Prospective investigational study. Tertiary university hospital centre. Patients undergoing elective diagnostic coronary angiography. Coronary artery plaque burden was assessed using a 30 MHz intravascular ultrasound catheter during an automated pullback. Proximal coronary artery plaque volume was determined using a validated edge-detection algorithm following three-dimensional computerized reconstruction. Central arterial stiffness was assessed in each patient using applanation tonometry to radial, carotid and femoral pulses, with derivation of aortic pressure augmentation and pulse wave velocity using pulse wave analysis. In 35 patients (61 +/- 2 years), proximal coronary arterial plaque volume was 5.9 +/- 0.6 mm3/mm of vessel. Plaque volume correlated positively with carotid-radial pulse wave velocity (r = 0.47, P = 0.008) and appeared to correlate with carotid-femoral pulse wave velocity (r = 0.34, P = 0.07). Aortic augmentation (r = 0.24, P = 0.16), augmentation index (r = 0.3, P = 0.08), and pulse pressure (r = 0.22, P = 0.2) did not correlate significantly with proximal coronary artery plaque volume. Non-invasive measures of carotid-radial pulse wave velocity correlate with the extent of coronary artery plaque volume and may be a useful non-invasive surrogate marker for the extent of coronary atherosclerosis. Our findings are consistent with the suggestion that central aortic stiffness may promote the development of coronary atherosclerosis and ischaemic heart disease.

Higher carotid-radial pulse wave velocity in healthy offspring of patients with Type 2 diabetes.

To determine whether carotid-radial pulse wave velocity (crPWV), a simple non-invasive measurement of muscular artery structure and function, is increased in offspring of patients with Type 2 diabetes compared with well-matched controls with no family history of diabetes. Serum levels of intercellular adhesion molecule-1 (sICAM-1) were also examined. Offspring (n = 19, M = 8) were recruited via contact with patients attending clinics. Controls (n = 19, M = 8) were recruited by advertisement. crPWV was measured using COMPLIOR. Blood pressure and heart rate were determined and fasting blood taken for measurement of metabolic and endothelial parameters. Offspring and controls were well matched [mean (sd)] for age [33.1 (9.6) vs. 32.8 (9.5) years], body mass index [24.8 (4.9) vs. 24.3 (3.4) kg/m2], waist circumference [78.3 (2.3) vs. 76.3 (2.5) cm], and systolic blood pressure [120 (9.3) vs. 119 (14.2) mmHg]. crPWV was 10% higher in the offspring [9.94 (1.3) m/s] compared with controls [9.01 (1.2) m/s, P = 0.02] despite similar pulse pressure [52 (10.5) vs. 53.5 (9.3) mmHg] and resting heart rate [71 (8.7) vs. 69 (14.0) beats/min]. They also showed a trend toward higher sICAM-1 [217 (55) vs. 188 (40) ng/ml, P = 0.07] concentrations which were also strongly correlated to crPWV in offspring (r = 0.63, P = 0.004). Vascular dysfunction in the form of increased muscular artery stiffness is present from an early stage in subjects at higher risk of developing diabetes. This may be secondary to impaired activation of endothelial signalling pathways in the context of inherited insulin resistance.

The relationship between androgens and arterial stiffness in older men.

To assess the relationship between endogenous androgen levels and arterial stiffness in older men. A retrospective, cross-sectional study. A London hospital-based, clinical research unit for the elderly. Fifty-five men (mean age+/-standard deviation=71.1+/-8.0). Sex hormone-binding globulin (SHBG), testosterone, and dehydroepiandrosterone sulfate (DHEAS) were measured in all subjects who had a stored serum sample drawn the same day as arterial stiffness measures were performed. Free testosterone index (FTI) was calculated ((total testosterone/SHBG) x 100 (%)). The measures of arterial stiffness used were pulse wave velocity (PWV) using the Complior system and systemic arterial compliance (SAC) using the area method. Relationship between arterial stiffness and serum androgens. : FTI showed a strong positive relationship with SAC (r=0.507, P<.001) and, correspondingly, an inverse relationship with carotid-femoral (C-F) and carotid-radial (C-R) PWV (r=-0.427 and -0.402, respectively, P<or=.002). With multiple regression, including age, blood pressure, cholesterol, body mass index, and waist/hip ratio, FTI remained a significant determinant of SAC and C-R PWV but not C-F PWV. In the subgroup of men without cardiovascular disease or vasoactive medication use (n=37), all three relationships remained significant. DHEAS was inversely related to C-F PWV only (r=-0.304, P=.041). The known association between lower androgenicity and increased cardiovascular risk in men might be explained by altered vascular stiffness.

Non invasive estimation of central pulse pressure: comparison of 2 methods

Several techniques have been proposed for the non-invasive measurement of central pulse pressure (PP). The aim of the present study was to compare 2 different methods: measurement of central PP by applanation tonometry of the carotid artery and estimation from the Pulse Wave Velocities (PWV) using the ’water-hammer’ formula. Applanation tonometry is considered as a reference method for the measurement of PP in the right common carotid artery (CCA) which has been shown to be identical to the PP in the ascending aorta at the branching off from the CCA. In 111 haemodialysis patients (H) and 40 patients free of cardiovascular treatment and event/injury (N), carotid PP was measured by applanation tonometry (Sphygmocor®) at the right CCA by alternatively calibrated tonometer-derived pressure waves [1]. BP was measured with a mercury sphygmomanometer at the right arm following the WHO guidelines and PParm calculated. Complior® was used for the measurements of carotid-femoral PWV (PWVCF) and carotid-radial PWV (PWVCR). Central PP was then calculated as PParm x √(PWVCF/PWVCR) The H patients had significant higher SBP, DBP and PParm than the N patients. Age and genders were not different between the 2 groups. Central PP obtained by the water-hammer formula (PPPWV) tended to be overestimated (p<10−5): The overestimation was higher in the N group (p=0.031). (PPPWV) is a segmental (carotid femoral) PP, when the central PP measured by tonometry is a local one, this might explain the observed difference between the 2 methods. (See Table) m ± sd m ± sd

MATTERS ARISING: Facco replies:

<h3>Introduction</h3> We studied if motivational interviewing (MI) added to standard educational care (SEC) improves vascular health in adolescents with poorly controlled type 1 diabetes. <h3>Research design and methods</h3> 47 adolescents with type 1 diabetes of at least 2 years duration and hemoglobin A1c &gt;75 mmol/mol (&gt;9.0%) on two visits were randomized to MI+SEC or SEC. We also compared vascular health parameters of patients with type 1 diabetes at trial baseline with a group of healthy historical controls matched for age and body size. <h3>Results</h3> 39 adolescents (20 MI+SEC) completed the vascular health study. At 12 months, parameter changes were not statistically significantly different between MI+SEC and SEC (carotid-femoral pulse wave velocity (cfPWV): mean difference 0.052 m/s (95% CI −0.395 to 0.500, p=0.81); carotid-radial PWV (crPWV): 0.118 m/s (95% to 0.478 to 0.713, p=0.69), carotid intima-media thickness (IMT): 0.002 mm (95% CI −0.37 to 0.40, p=0.93), systolic blood pressure (BP) z-score: 0.495 (95% CI −0.099 to 1.09, p=0.10). At baseline, duration of type 1 diabetes was associated with radial IMT (r=0.430, p=0.007) and cfPWV (r=0.373, p=0.018), and carotid, femoral and brachial IMT were correlated with continuous glucose monitoring (CGM) SD (r=0.440, p=0.017; r=0.377, p=0.048; r=0.387, p=0.038). There was an inverse association between CGM time-in-range (3.9–10.0 mmol/L) and crPWV (r=−0.476, p=0.022) changes. Systolic BP change was associated with body mass index change (r=0.374, p=0.019) and IMT change (r=0.461, p=0.016 for carotid IMT; r=0.498, p=0.010 for femoral IMT). PWVs were higher and common carotid compliance lower among patients with type 1 diabetes at baseline compared with healthy controls, but no other differences were found. <h3>Conclusion</h3> There was no effect of MI added to SEC on vascular health parameters. Although disease duration and glycemic control were associated with vascular health at baseline, there were only limited associations between glycemic control and vascular health parameter changes. Vascular health parameter changes were interrelated suggesting clustering of cardiovascular risk. <h3>Trial registration number</h3> NCT02637154.