Reduced common carotid artery longitudinal wall motion and intramural shear strain in individuals with elevated cardiovascular disease risk using speckle tracking

2015 ◽  
Vol 37 (2) ◽  
pp. 106-116 ◽  
Author(s):  
Jimmy Tat ◽  
Jason S. Au ◽  
Peter J. Keir ◽  
Maureen J. MacDonald
Author(s):  
Zhili Hao ◽  
Leryn Reynolds ◽  
John M. Herre

Abstract In light of recently recognized independent clinical values of longitudinal wall motion ux(t) at the common carotid artery (CCA) and the struggle on appropriate arterial indices for interpreting ux(t), this paper hypothesizes a mechanistic model of ux(t) and explores clear implications of the antegrade amplitude ux0-ante and retrograde amplitude ux0-retro of ux(t) in systole to the cardiovascular (CV) system. By examining findings on ux(t) and other relevant findings through the lens of the engineering essence of ux(t), a mechanistic model of ux(t) is hypothesized: the left ventricle (LV) base rotation is the excitation source for initiating the longitudinal elastic wave propagating along the arterial tree; wall shear stress at an artery serves as a local external source for supplying energy to the longitudinal elastic wave; and longitudinal elasticity at the arterial wall dictates the wave propagation velocity. Integrating the mechanistic model with findings on ux(t) gives rise to interpretation of ux0-ante and ux0-retro for their clear implications: longitudinal elasticity Exx at the common carotid artery (CCA) is estimated from ux0-ante, and ux0-retro is an inverse indicator of the maximum base rotation of the LV and a positive indicator of longitudinal elasticity at the ascending aorta (AA). For the first time, this model reveals the mechanisms underlying those statistical-based findings on ux(t).


Author(s):  
Susan A. Everson‐Rose ◽  
Emma J. M. Barinas‐Mitchell ◽  
Samar R. El Khoudary ◽  
Hsin‐Hui Huang ◽  
Qi Wang ◽  
...  

Background The menopausal transition is characterized by increased cardiovascular risk, weight gain, and increased adiposity for many women. The adipose‐derived secretory proteins adiponectin and leptin are associated with insulin resistance, metabolic syndrome, and cardiovascular disease but their role in subclinical atherosclerotic disease is unclear. This cross‐sectional study evaluated the associations of adiponectin and leptin with carotid artery intima‐media thickness, adventitial diameter, presence of carotid plaques, and brachial‐ankle pulse wave velocity (baPWV) in women aged 54 to 65 years. Methods and Results Participants were 1399 women from SWAN (Study of Women's Health Across the Nation), a community‐based study of women transitioning through menopause. Carotid ultrasound and baPWV measures were obtained at SWAN follow‐up visits 12 or 13, when 97% of participants were post‐menopausal. Adipokines were assayed from serum specimens obtained concurrently at these visits. Linear and logistic regression models were used to evaluate adiponectin or leptin, both log‐transformed attributable to skewness, in relationship to carotid artery intima‐media thickness, adventitial diameter, baPWV, and presence of carotid plaque. Covariates included age, race, study site, smoking, alcohol use, obesity, cardiovascular disease risk factors, and menopausal status. Lower levels of adiponectin were related to greater carotid artery intima‐media thickness, wider adventitial diameter, and faster baPWV; associations were attenuated after adjusting for cardiovascular disease risk factors. Higher levels of leptin were associated with greater carotid artery intima‐media thickness and wider adventitial diameter in minimally and fully adjusted models, and contrary to expectation, with slower baPWV, particularly among women with diabetes mellitus or obesity. Conclusions Adiponectin and leptin are 2 important inflammatory pathways that may contribute to adverse subclinical cardiovascular disease risk profiles in women at midlife.


Author(s):  
Ryan J. Pewowaruk ◽  
Yacob Tedla ◽  
Claudia E. Korcarz ◽  
Matthew C. Tattersall ◽  
James H. Stein ◽  
...  

Elastic arteries stiffen via 2 main mechanisms: (1) load-dependent stiffening from higher blood pressure and (2) structural stiffening due to changes in the vessel wall. Differentiating these closely coupled mechanisms is important to understanding vascular aging. MESA (Multi-Ethnic Study of Atherosclerosis) participants with B-mode carotid ultrasound and brachial blood pressure at exam 1 and exam 5 (year 10) were included in this study (n=2604). Peterson and Young elastic moduli were calculated to represent total stiffness. Structural stiffness was calculated by adjusting Peterson and Young elastic moduli to a standard blood pressure of 120/80 mm Hg with participant-specific models. Load-dependent stiffness was the difference between total and structural stiffness. Changes in carotid artery stiffness mechanisms over 10 years were compared by age groups with ANCOVA models adjusted for baseline cardiovascular disease risk factors. The 75- to 84-year age group had the greatest change in total, structural, and load-dependent stiffening compared with younger groups ( P <0.05). Only age and cessation of antihypertensive medication were predictive of structural stiffening, whereas age, race/ethnicity, education, blood pressure, cholesterol, and antihypertensive medication were predictive of increased load-dependent stiffening. On average, structural stiffening accounted for the vast majority of total stiffening, but 37% of participants had more load-dependent than structural stiffening. Rates of structural and load-dependent carotid artery stiffening increased with age. Structural stiffening was consistently observed, and load-dependent stiffening was highly variable. Heterogeneity in arterial stiffening mechanisms with aging may influence cardiovascular disease development.


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