Carotid Beta-stiffness Research Articles

Vascular health years after a hypertensive disorder of pregnancy: The EPOCH study

Preeclampsia is associated with a two-fold increase in a woman's lifetime risk of developing atherosclerotic cardiovascular disease (ASCVD), but the reasons for this association are uncertain. The objective of this study was to examine the associations between vascular health and a hypertensive disorder of pregnancy among women ≥ 2 years postpartum. Pre-menopausal women with a history of either a hypertensive disorder of pregnancy (cases: preeclampsia or gestational hypertension) or a normotensive pregnancy (controls) were enrolled. Participants were assessed for standard ASCVD risk factors and underwent vascular testing, including measurements of blood pressure, endothelial function, and carotid artery ultrasound. The primary outcomes were blood pressure, ASCVD risk, reactive hyperemia index measured by EndoPAT and carotid intima-medial thickness. The secondary outcomes were augmentation index normalized to 75 beats per minute and pulse wave amplitude measured by EndoPAT, and carotid elastic modulus and carotid beta-stiffness measured by carotid ultrasound. Participants had a mean age of 40.7 years and were 5.7 years since their last pregnancy. In bivariate analyses, cases (N = 68) were more likely than controls (N = 71) to have hypertension (18% vs 4%, P = .034), higher calculated ASCVD risk (0.6 vs 0.4, P = .02), higher blood pressures (systolic: 118.5 vs 111.6 mm Hg, P = .0004; diastolic: 75.2 vs 69.8 mm Hg, P = .0004), and higher augmentation index values (7.7 vs 2.3, P = .03). They did not, however, differ significantly in carotid intima-media thickness (0.5 vs 0.5, P = .29) or reactive hyperemia index (2.1 vs 2.1, P = .93), nor in pulse wave amplitude (416 vs 326, P = .11), carotid elastic modulus (445 vs 426, P = .36), or carotid beta stiffness (2.8 vs 2.8, P = .86). Women with a prior hypertensive disorder of pregnancy had higher ASCVD risk and blood pressures several years postpartum, but did not have more endothelial dysfunction or subclinical atherosclerosis.

Social isolation and subclinical vascular pathways to cerebrovascular disease

ABSTRACT Social isolation and lack of social support are risk factors for cardiovascular and cerebrovascular disease (CVD). This study explored the relationship between measures of social support and subclinical measures of CVD risk. 58 healthy adults ages 18 to 85 years participated in this study. The Berkman-Syme Social Network Inventory (SNI) was used to assess social isolation, with higher scores signifying less isolation. Social support was defined using the 12-Item Interpersonal Support Evaluation List (ISEL-12) with a higher score signifying higher social support. Subclinical CVD measures included carotid-femoral pulse wave velocity (cfPWV), carotid beta-stiffness index, and middle cerebral artery (MCA) pulsatility index. Path analysis models for both the SNI and ISEL appraisal domain predicting cfPWV and cerebrovascular pulsatility fit the data well. Path analyses showed significant direct paths from the SNI (β = −.363, t = −2.91) and ISEL appraisal domain (β = −.264, t = −2.05) to cfPWV. From cfPWV, both models revealed significant direct paths to carotid stiffness (β = .488, t = 4.18) to carotid pulse pressure (β = .311, t = 2.45) to MCA pulsatility (β = .527, t = 4.64). Social isolation and appraisal of social support are related to unfavorably higher aortic stiffness, with subsequent detrimental effects on cerebrovascular hemodynamic pulsatility.

Age-related carotid extra-media thickening is associated with increased blood pressure and arterial stiffness.

Ageing results in higher blood pressure and arterial stiffening leading to increased cardiovascular disease (CVD) risk. The extra-media thickness (EMT) is a composite measure of the arterial adventitia, perivascular adipose tissue (PVAT) and the jugular vein, but the association among EMT and ageing, blood pressure and arterial stiffness is largely unknown. We hypothesized that EMT is associated with ageing, blood pressure and arterial stiffness. Fifty (18M/32F, age range 20-79years.) individuals underwent measures of EMT (media-adventitia border to jugular lumen interface) via ultrasonography, blood pressure (brachial; carotid), arterial stiffness (carotid beta-stiffness, distensibility and Young's modulus) and body composition (dual X-ray absorptiometry). Independent two-tailed t-tests compared characteristics between young and middle-aged/older adults (MA/O). Bivariate correlations assessed the relation between EMT, ageing, blood pressure and arterial stiffness endpoints. Partial correlations were used to adjust for age, sex, body mass index (BMI) and body fat percentage. Compared to young, MA/O adults had higher EMT, blood pressure, arterial stiffness, BMI and BF% (all, p≤0.05). Carotid EMT was positively correlated with age (r=0.46), brachial SBP (r=0.32), carotid SBP (r=0.42), PP (r=0.42), beta-stiffness (r=0.37) and Young's elastic modulus (r=0.43) (all, p≤0.05), and negatively correlated with carotid distensibility (r=-0.34, p≤0.05). All endpoints correlated with EMT remained after adjusting for BMI, BF% and sex (p≤0.05). These data suggest EMT is a clinically relevant target that may be associated with age-related CVD risk in humans, yet further investigation is required to elucidate the role of EMT in age-related increases in blood pressure and arterial stiffness.

Carotid Beta Stiffness Association with Thyroid Function

Background: Thyroid hormone modulation of cardiovascular function has been associated with cardiovascular disease. Recent evidence suggests that free thyroxine (FT4) levels are associated with an increase in systemic arterial stiffness, but little is known about the effects of FT4 at the local level of the common carotid artery. β-stiffness index is a local elastic parameter usually determined by carotid ultrasound imaging. Methods: We conducted a cross-sectional analysis in the ProgeNIA cohort, including 4846 subjects across a broad age range. For the purpose of this study, we excluded subjects with increased thyrotropin (TSH) levels and those treated with levothyroxine or thyrostatic. We assessed β stiffness, strain, wall–lumen ratio, carotid cross-sectional area (CSA), and stress and flow in the right common carotid artery. We tested whether FT4, heart rate, and their interactions were associated with carotid parameters. Results: FT4 was positively and independently associated with β stiffness index (β = 0.026, p = 0.041), and had a negative association with strain (β = −0.025, p = 0.009). After adding heart rate and the interaction between FT4 and heart rate to the model, FT4 was still associated with the β stiffness index (β = 0.186, p = 0.06), heart rate was positively associated with the stiffness index (β = 0.389, p < 0.001) as well as their interaction (β = 0.271, p = 0.007). Conclusion: This study suggests that higher FT4 levels increase arterial stiffness at the common carotid level, consistent with a detrimental effect on elastic arteries. The effect of FT4 is likely to be primarily attributable to its effect on heart rate.

Sex Differences In Arterial Stiffness Following Acute Resistance Exercise

During resistance exercise there is an increase in blood pressure, with systolic pressure rising up to 400 mmHg. This transient elevation in pressure has been shown to result in acutely stiffer vessels in young males, however, this has not been well studied in young females. It is possible that the sex hormones of young females may be protective against this pressure load, resulting in differential responses following resistance exercise. PURPOSE: The purpose of this study was to determine if there are sex differences in arterial stiffness following an acute resistance exercise bout in young, healthy males and females who are not currently resistance training. METHODS: Carotid beta stiffness (β), arterial compliance (AC), and elastic modulus (Ep) measurements were taken in 23 young participants (10 males, 13 females; 26 ± 1 years) before, immediately after, and 30 minutes following full body resistance exercise. Exercise consisted of 2 sets of 10-12 repetitions performed on 8 resistance machines completed at 40% 1RM for the upper body and 60% 1RM for the lower body. Females were tested during the early follicular phase of their menstrual cycle to control for sex hormones. Exercise values (pre, post, post30) were compared between sexes using a repeated measures ANOVA, with significance set at p < 0.05. When the interaction was significant, the responses were evaluated with paired samples t-tests within each sex and independent t-tests between sexes. RESULTS: There were no sex differences in stiffness values prior to exercise, but males displayed significantly higher β and Ep and lower AC post and post30 compared to females. Males demonstrated significant increases in β (4.2 ± 0.4 to 6.6 ± 0.5 to 5.8 ± 0.5 AU) and Ep (48 ± 5 to 73 ± 6 to 65 ± 6 kPa) and decreases in AC (1.5 ± 0.2 to 0.9 ± 0.1 to 1.1 ± 0.1 mm2/kPa) both immediately and 30 min post resistance exercise compared to baseline values, while females had no change in AC (1.4 ± 0.1 to 1.2 ± 0.1 to 1.5 ± 0.1 mm2/kPa) or Ep (46 ± 4 to 52 ± 5 to 44 ± 5 kPa) with exercise and an immediate increase in β that returned to baseline at 30 min post (4.2 ± 0.3 to 5.1 ± 0.5 to 4.3 ± 0.4 AU). CONCLUSION: Acute resistance exercise in females does not result in the elevation of stiffness as seen in males. It appears females may be protected from this increased pressure load, which may be due to the vasodilatory effects of estrogen.

Age‐Related Increase in Extra‐Media Thickness is Associated with Arterial Stiffening and Carotid Blood Pressure

Older age is a primary risk factor associated with future cardiovascular disease (CVD) related events. Age‐related changes in perivascular adipose tissue (PVAT) and vascular remodeling both contribute to arterial stiffening and increased blood pressure which are established CVD risk factors. The non‐invasively measured extra‐media thickness (EMT) is a novel and composite measure, which includes PVAT, arterial adventitia, and the jugular vein that may provide translational insight for these factors contributing to age‐related arterial stiffening and higher blood pressure. However, it is unknown if aging increases EMT and is associated with arterial stiffness and blood pressure. We hypothesized that age‐related increases in EMT will be associated with higher arterial stiffness and blood pressure. Forty participants (young: 8M/12F, 23.2 ± 1.1 yrs and middle‐aged/older: 7M/13F, 60.7 ± 9.4 yrs) underwent measures of blood pressure (brachial; carotid), arterial stiffness (carotid b‐stiffness), EMT via ultrasonography and body composition with dual x‐ray absorptiometry. All measurements were taken in the supine position. Group mean differences between young and middle‐aged/older participants were analyzed with unpaired t‐tests and Pearson correlations were used to assess relations between EMT and arterial stiffness and blood pressure endpoints. Compared to younger participants, middle‐aged/older participants had higher EMT (0.80 ± 0.03 vs. 0.69 ± 0.02 mm), carotid beta stiffness (3.24 ± 0.08 vs. 2.60 ± 0.04), carotid SBP (116.5 ± 4.9 vs. 99.1 ± 2.3 mmHg), and carotid PP (44.6 ± 4.2 vs. 34.8 ± 1.5 mmHg) (all, p&lt;0.05). Brachial SBP was not different between groups (p&gt;0.05). Carotid beta stiffness (r= 0.410), carotid SBP (r= 0.501), and carotid PP (r= 0.5037) were all positively correlated with EMT for the entire cohort (all, p&lt;0.05). Our findings indicate that there is an age‐related increase in EMT that is associated with both carotid arterial stiffness and pressure. These data suggest that increases in arterial stiffness and blood pressure with advancing age may be attributable, in part, to increases in EMT, which may be due to changes in PVAT and arterial adventitial remodeling. Therefore, EMT, a potential surrogate for PVAT and arterial remodeling, may provide novel insight into age‐related arterial stiffening, higher blood pressure and increased CVD risk with aging.

Acute Effect of Aerobic Exercise on Carotid Strain in Individuals with Multiple Sclerosis

INTRODUCTIONIndividuals with multiple sclerosis (MS) have increased arterial stiffness, a known risk factor for cardiovascular disease. Acute aerobic exercise is a stressor affecting markers of arterial stiffness, such as carotid strain (CS) and beta stiffness index, which provides insight into aspects of arterial function. Individuals with MS may have different responses to exercise compared to healthy individuals due to arterial dysfunction, which can be evaluated via markers of arterial stiffness.PURPOSETo evaluate the acute effect of aerobic exercise on CS in individuals with MS.METHODSSixteen individuals with MS (42 ± 8 yrs; 27.5 ± 6.9 kg/m2) underwent treadmill walking at 60% of their peak aerobic capacity for 20 min. Images of the carotid artery were obtained in the radial view with ultrasonography at baseline, immediate and 30 min post‐exercise. Speckle tracking software was used to calculate the following variables of arterial function: CS, CS time to peak (TPK), CS rate, CS rate TPK, radial velocity (RV), RV TPK, radial displacement (RD) and RD TPK. Carotid systolic blood pressure (cSBP) was measured via applanation tonometry and longitudinal carotid beta stiffness index via ultrasonography.RESULTSSee Table. CS rate, RV and carotid systolic blood pressure (cSBP) increased immediate post‐exercise (p&lt;0.05). CS TPK and RD TPK decreased immediately post‐exercise and RD TPK remained decreased at 30 min post‐exercise (p&lt;0.05). HR and beta stiffness index increased immediately post‐exercise (p&lt;0.05) and returned to baseline at 30 min (p&gt;0.05).CONCLUSIONThe baseline levels of CS in individuals with MS are lower than values reported for middle‐aged adults in the literature, indicative of baseline arterial dysfunction. Beta stiffness index increased immediately after exercise. While CS rate increased after exercise in individuals with MS similar to beta stiffness index, the difference disappeared after statistically controlling for HR. Our results suggest that individuals with MS do not improve arterial stiffness with acute aerobic exercise, providing more evidence for arterial impairment.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Effect of upper body position on arterial stiffness: influence of hydrostatic pressure and autonomic function.

To evaluate changes in arterial stiffness with positional change and whether the stiffness changes are due to hydrostatic pressure alone or if physiological changes in vasoconstriction of the conduit arteries play a role in the modulation of arterial stiffness. Thirty participants' (male = 15, 24 ± 4 years) upper bodies were positioned at 0, 45, and 72° angles. Pulse wave velocity (PWV), cardio-ankle vascular index, carotid beta-stiffness index, carotid blood pressure (cBP), and carotid diameters were measured at each position. A gravitational height correction was determined using the vertical fluid column distance (mmHg) between the heart and carotid artery. Carotid beta-stiffness was calibrated using three methods: nonheight corrected cBP of each position, height corrected cBP of each position, and height corrected cBP of the supine position (theoretical model). Low frequency systolic blood pressure variability (LFSAP) was analyzed as a marker of sympathetic activity. PWV and cardio-ankle vascular index increased with position (P < 0.05). Carotid beta-stiffness did not increase if not corrected for hydrostatic pressure. Arterial stiffness indices based on Method 2 were not different from Method 3 (P = 0.65). LFSAP increased in more upright positions (P < 0.05) but diastolic diameter relative to diastolic pressure did not (P > 0.05). Arterial stiffness increases with a more upright body position. Carotid beta-stiffness needs to be calibrated accounting for hydrostatic effects of gravity if measured in a seated position. It is unclear why PWV increased as this increase was independent of blood pressure. No difference between Methods 2 and 3 presumably indicates that the beta-stiffness increases are only pressure dependent, despite the increase in vascular sympathetic modulation.

Abstract P270: First Trimester Elevation in Circulating Endothelin-1 and Arterial Stiffness are Predictive of Late Pregnancy Preeclampsia

Preeclampsia (PE) is characterized by late pregnancy hypertension and proteinuria. PE causes significant morbidity for the maternal-fetal unit. Circulating endothelin-1 (ET-1), a potent vasoconstrictor, is elevated at the time of diagnosis of human PE. In addition, women with PE demonstrate arterial stiffness as early as the end of the first trimester. However, it is unknown if arterial stiffness is associated with a first trimester elevation in ET-1 and post-delivery placental ET-1. We hypothesized that 1) first trimester plasma ET-1 is elevated and is associated with arterial stiffness in women who develop PE; 2) first trimester ET-1 is predictive of PE; and 3) placental ET-1 is increased in PE. To address these questions, we performed a nested case-control study in women at risk for PE. First trimester plasma ET-1 was measured via ELISA; aortic stiffness and carotid beta-stiffness (CβS) were measured by carotid-femoral pulse-wave velocity (CFPWV) and carotid tonometry/ultrasound, respectively. While the maternal age of controls (n=126; age 30 ± 0.45 years) and PE (n=15; age 31 ± 1.3 years) were similar, the PE group had a higher first trimester BMI (35 ± 3 vs. 29 ± 1 kg/m 2 , p = 0.01), systolic (125 ± 2 vs. 113 ± 1 mmHg, p&lt; 0.01) and diastolic blood pressure (68 ± 2 vs. 60 ± 1 mmHg, p&lt; 0.01) compared with controls. In addition, first trimester plasma ET-1 (2.7 ± 0.4 vs. 2.0 ± 0.2 pg/mL, p &lt; 0.01), CFPWV (7.2 ± 0.5 vs. 6.1 ± 0.2 m/s, p = 0.016), and CβS (8.4 ± 1.9 vs. 6.3 ± 0.3, p = 0.055) were higher in the PE group. Consistent with previous studies, third trimester plasma ET-1 was elevated in the PE group (2.9 ± 1.1 vs. 1.6 ± 0.1 pg/mL, p &lt; 0.01) which paralleled a 2.5 fold increase in placental decidual ET-1 mRNA (p &lt; 0.0001). ROC analyses showed that first trimester plasma ET-1 (AUC=0.71, p &lt; 0.001) and CFPWV (AUC=0.70, p=0.014) were predictive of PE. This study supports the novel concept that elevated ET-1 in preeclampsia begins early in the first trimester and is associated with premature arterial stiffness. Further, these novel data suggest that ET-1 may play an important role in the first trimester prediction and pathogenesis of preeclampsia.

Relationship between carotid arterial properties and cerebral white matter hyperintensities.

Since arterial stiffness is a functional measure of arterial compliance and may be an important marker of cerebrovascular disease, we examined the association of carotid artery stiffness with white matter hyperintensity volume (WMHV) in a cross-sectional study of 1,166 stroke-free participants. Carotid beta stiffness index (STIFF) was assessed by M-mode ultrasound of the common carotid artery and calculated as the ratio of natural log of the difference between systolic and diastolic blood pressure over STRAIN, a ratio of the difference between carotid systolic and diastolic diameter (DD) divided by DD. WMHV was measured by fluid-attenuated inversion recovery MRI. The associations of STIFF, DD, and STRAIN with WMHV were examined using linear regression after adjusting for sociodemographic, lifestyle, and vascular risk factors. In a fully adjusted model, larger carotid DD was significantly associated with greater log-WMHV (β = 0.09, p = 0.001). STIFF and STRAIN were not significantly associated with WMHV. In adjusted analyses stratified by race-ethnicity, STRAIN (β = -1.78, p = 0.002) and DD (β = 0.11, p = 0.001) were both associated with greater log-WMHV among Hispanic participants, but not among black or white participants. Large carotid artery diameters are associated with greater burden of white matter hyperintensity (WMH) in this multiethnic population. The association between increased diameters, decreased STRAIN, and greater WMH burden is more pronounced among Hispanics. These associations suggest a potential important pathophysiologic role of extracranial large artery remodeling in the burden of WMH.

Abstract 17026: Serum Adropin Level is Associated With Exercise Training-induced Improvement of Arterial Stiffness in Obese Adults

Introduction: Obesity-induced deterioration of arterial stiffness is reduced by habitual exercise, and increased production of nitric oxide (NO) participates in this effect. Adropin is a regulator of endothelial NO synthase and NO release, and circulating adropin level decreases in obese patients. However, the association between exercise-training effects of arterial stiffness and circulating adropin level in obese subjects remains unclear. Hypothesis: This study aimed to determine the serum adropin level related to exercise-training effects of arterial stiffness in obese subjects. Methods: Eighteen Japanese obese subjects (age: 65.7 ± 1.6 years, % body fat: 34.8 ± 1.6 %) and nine Japanese non-obese subjects (age: 69.1 ± 1.0 years, % body fat: 19.9 ± 2.4 %) participated in this study. Obese subjects completed 8-week of aerobic exercise training (60-70% peak oxygen uptake [VO2peak] for 45 min, 3 days/week). Before and after the intervention, we evaluated plasma nitrite/nitrate (NOx) and serum adropin concentrations, carotid beta-stiffness as an indicator of arterial stiffness, and VO2peak as an index of cardiorespiratory fitness. VO2peak was measured using an incremental cycle exercise test on a cycle ergometer. Results: Serum adropin level in the obese subjects was lower than that in the non-obese subjects. After the 8-week intervention, VO2peak was significantly increased and carotid beta-stiffness was significantly decreased (P &lt; 0.05). Moreover, plasma NOx level and serum adropin level was significantly increased after the 8-week intervention (P &lt; 0.05). Additionally, the exercise training-induced reduction in beta-stiffness was negatively correlated with the training-induced changes in serum adropin (r = -0.481, P &lt; 0.05) and plasma NOx levels (r = -0.668, P &lt; 0.01). Furthermore, a significant correlation was observed between the training-induced changes in serum adropin and plasma NOx levels (r = 0.677, P &lt; 0.01). Conclusions: These results suggest that the plasma adropin level is increased by aerobic exercise training intervention and is associated with exercise training-induced alternation of arterial stiffness in obese subjects. Thus, the increase in adropin may participate in the exercise-induced reduction of arterial stiffness.

Physical activity, adiponectin, and cardiovascular structure and function

Physical activity (PA) may modify cardiovascular structure and function as well as insulin sensitivity and level of plasma adipokines in relation to its extent, duration, and intensity. To evaluate the associations of average daily PA and bouts of moderate-to-vigorous-intensity PA with cardiovascular and metabolic measures, 45 healthy volunteers (mean age = 42 ± 9 years) not involved in regular intensive exercise training and competitive sport activity underwent the following examinations: (1) accelerometer monitoring of ambulatory movements (average monitoring time = 6.1 ± 1.3 days); (2) complete carotid and cardiac ultrasound; (3) measurement of carotid-femoral pulse-wave velocity; (4) anthropometric measurements; (5) euglycemic hyperinsulinemic clamp; and (6) assessment of plasma levels of leptin, adiponectin, and high-sensitivity C-reactive protein (hsCRP). Average PA measured by accelerometer correlated with carotid beta-stiffness index (inversely) and with longitudinal systolic myocardial velocity (directly), independently of age, anthropometric, hemodynamic, and metabolic parameters. Subjects with periods of moderate-to-vigorous-intensity PA lasting at least 10 min (n = 28) had higher left ventricular (LV) mass index and lower plasma adiponectin, leptin, and hsCRP (P < 0.05 for all) compared with those who spent the monitoring time only in sedentary and light-intensity PA (n = 17). Minutes per day spent in moderate-to-vigorous PA correlated with LV mass index (directly) and with plasma adiponectin (inversely). Plasma adiponectin was an independent determinant of LV mass, together with body surface area, stroke volume, and systolic blood pressure (cumulative r (2) = 0.80). We conclude that in healthy subjects, average daily PA is independently related to longitudinal systolic myocardial function and to local carotid stiffness. Bouts of moderate-to-vigorous PA seem to induce LV mass increase, which may be partially related to a decrease in plasma adiponectin level.

Genome-Wide Association Study of Habitual Exercise-Induced Improvement of Arterial Stiffness in Japanese Adults

An increase in arterial stiffness is causal factor of cardiovascular diseases. Habitual exercise improves arterial stiffness and has a protective effect against these diseases. However, not all individuals may benefit equally from exercise. These genetic variations in association with the regular exercise-induced improvement of arterial stiffness remain unclear. PURPOSE: To identify genetic variants, which influence individuals respond to regular exercise-induced improvement of arterial stiffness, using genome-wide association studies (GWAS) in Japanese adults. METHODS: 285 Japanese adults aged from 25 to 70, who were recruited from Nutrition and EXercise Intervention Study (NEXIS) totally enrolled 838 persons, participated in this study. Mean daily amount of physical activity for 14 days at >3 METs was measured by using triaxial accelerometry at both baseline and 1 year later. Also, arterial stiffness was assessed by carotid beta-stiffness with ultrasonography and tonometry. Active subjects (n=45), which has kept more than 5.1 METs*h/day (the highest quintile at baseline) at both baseline and 1 year measurements, were divided into two groups; high values of beta-stiffness (High-Stif) and low values of beta-stiffness (Low-Stif) based on the median value of beta-stiffness in each sex and decade. A GWAS between two groups was performed by Human660W-Quad BeadChip (illumina). RESULTS: There were no significant differences in age, sex, BMI, blood pressure and fasting blood glucose, triglyceride, and HDL-C concentrations between High-Stif and Low-Stif groups, whereas there was a significant difference in beta-stiffness (13.2±1.2 vs 7.0±0.4 AU, P<0.0001). The >550,000 genetic polymorphisms were analyzed by using JMP Genetics (SAS Institute), then 10 and 27 SNPs were significantly associated with the individual variation of regular exercise-induced improvement of arterial stiffness (genotype and allele frequency respectively, P<0.0001). These polymorphisms were located on gene locus involved in the cadherin superfamily, cGMP, and endothelial progenitor cell, and lipoprotein related protein, etc. CONCLUSIONS: These genetic variations may be associated with the regular exercise-induced improvement of arterial stiffness. Supported by grant in KAKENHI 22650166

Associations Between Cardio-Ankle Vascular Index and Microvascular Complications in Type 2 Diabetes Mellitus Patients

Type 2 diabetes mellitus (T2DM) is a risk factor for increased arterial stiffness. We evaluated associations between the cardio-ankle vascular index (CAVI) and carotid plaque, intima media thickness (IMT), and diabetic microvascular complications in Korean T2DM patients. We conducted a retrospective, cross-sectional study of 320 Korean T2DM patients without a history of macrovascular disease or macroalbuminuria. We measured 24-hour urinary albumin excretion (UAE) levels and performed funduscopic and neuropathy examinations to assess the extent of diabetic microvascular complications. Arterial stiffness was assessed using CAVI. We also measured the ankle-brachial index (ABI), common carotid artery IMT, and carotid beta stiffness index. Among the 320 patients enrolled in this study, 64 (20%) had increased CAVI (≥ 9). We found that CAVI was correlated with systolic blood pressure, pulse pressure, IMT, carotid beta stiffness index, log-transformed UAE, and total cholesterol. In multiple logistic regression analysis, mean IMT and the presence of carotid plaque were independently associated with increased CAVI (≥ 9) (OR=5.77, P < 0.01; OR=5.36, P < 0.001, respectively). Furthermore, an increased CAVI was associated with peripheral neuropathy (OR=2.03, P = 0.03) and microalbuminuria (OR=2.47, P < 0.01) after adjusting for possible confounding variables. The results of this study suggest that increased CAVI is associated with the presence of arterial plaque, increased IMT, and microvascular complications, such as nephropathy and neuropathy, in T2DM patients.

Arterial function of carotid and brachial arteries in postmenopausal vegetarians

Background:Vegetarianism is associated with a lower risk of cardiovascular disease. However, studies of arterial function in vegetarians are limited.Methods:This study investigated arterial function in vegetarianism by comparing 49 healthy postmenopausal vegetarians with 41 age-matched omnivores. The arterial function of the common carotid artery was assessed by carotid duplex, while the pulse dynamics method was used to measure brachial artery distensibility (BAD), compliance (BAC), and resistance (BAR). Fasting blood levels of glucose, lipids, lipoprotein (a), high-sensitivity C-reactive protein, homocysteine, and vitamin B12 were also measured.Results:Vegetarians had significantly lower serum cholesterol, high-density and low-density lipoprotein, and glucose compared with omnivores. They also had lower vitamin B12 but higher homocysteine levels. Serum levels of lipoprotein (a) and high-sensitivity C-reactive protein were no different between the two groups. There were no significant differences in carotid beta stiffness index, BAC, and BAD between the two groups even after adjustment for associated covariates. However, BAR was significantly lower in vegetarians than in omnivores. Multiple linear regression analysis revealed that age and pulse pressure were two important determinants of carotid beta stiffness index and BAD. Vegetarianism is not associated with better arterial elasticity.Conclusion:Apparently healthy postmenopausal vegetarians are not significantly better in terms of carotid beta stiffness index, BAC, and BAD, but have significantly decreased BAR than omnivores. Prevention of vitamin B12 deficiency might be beneficial for cardiovascular health in vegetarians.

Physical Activity Duration, Intensity, and Arterial Stiffening in Postmenopausal Women

Aerobic exercise training is associated with lower central arterial stiffness, but little information exists on the effects of physical activity intensity or duration on central arterial stiffness. Using a cross-sectional and interventional approach, we tested the hypothesis that both moderate and vigorous physical activity reduce central arterial stiffness in postmenopausal women. Carotid arterial stiffness (via ultrasound and applanation tonometry) and duration of physical activity at low, moderate, and vigorous intensities (via electronic accelerometer) were measured in 103 apparently healthy sedentary or recreationally active women 47 to 82 years of age. Moderate intensity physical activity was defined as 4.0 to 6.0 metabolic equivalents (MET) in subjects aged <65 years and as 3.0 to 5.0 MET in subjects >or=65 years. A subgroup of 17 sedentary subjects was randomly assigned to moderate (n = 8) or vigorous (n = 9) intensity cycling exercise training (900 kcal/week, three to five sessions per week, for 12 weeks). Carotid arterial stiffness was measured before and after training. Carotid beta-stiffness index was significantly correlated with the duration of moderate and vigorous intensity physical activity (r = -0.25 and r = -0.22) even after adjustment for age, height, and mean BP. Carotid beta-stiffness index significantly decreased after moderate and vigorous intensity cycling training. There were no significant group differences in the magnitude of beta-stiffness index change even after adjustment for expected confounders (eg, baseline beta-stiffness index, height, body mass index, heart rate, and post-training body mass, body mass index, and mean BP). These results suggest that both moderate and vigorous physical activities have favorable effects on central arterial stiffness in postmenopausal women.