16
views
0
recommends
+1 Recommend
1 collections
    0
    shares

      Clinical Interventions in Aging (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on prevention and treatment of diseases in people over 65 years of age. Sign up for email alerts here.

      36,334 Monthly downloads/views I 3.829 Impact Factor I 7.4 CiteScore I 1.83 Source Normalized Impact per Paper (SNIP) I 1.044 Scimago Journal & Country Rank (SJR)

      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Association of arteriosclerosis and/or atherosclerosis with hypertensive target organ damage in the community-dwelling elderly Chinese: the Northern Shanghai Study

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Objective

          Vascular abnormality includes two forms, arteriosclerosis (ARS) and atherosclerosis (ATS), which coexist in patients with cardiovascular (CV) diseases. However, whether their combination may lead to a worsening status in those patients remains unclear. We therefore aimed to investigate the association of ARS and/or ATS with hypertensive target organ damage (TOD).

          Methods

          From June 2014 to August 2015, a total of 1,599 community-dwelling elderly subjects (aged >65 years) from northern Shanghai were recruited. Vascular measurements, such as carotid–femoral pulse wave velocity (cf-PWV), ankle–brachial index (ABI) and carotid plaque, were conducted on each participant, and ARS was defined as cf-PWV >12 m/s, while ATS was defined as participants who have carotid plaque or ABI <0.9. Within the framework of comprehensive CV examinations, CV risk factors were assessed, and asymptomatic TOD was evaluated by measuring participants’ left ventricular mass index (LVMI), peak transmitral pulsed Doppler velocity/early diastolic tissue Doppler velocity (E/Ea), urinary albumin–creatinine rate (UACR) and estimated glomerular filtration rate (eGFR).

          Results

          Although LVMI, E/Ea and eGFR were significantly different among subjects with or without ARS and/or ATS ( P<0.02), in full adjustment model, only E/Ea showed the independent and significant difference ( P=0.023). Moreover, E/Ea was significantly different between participants with ARS or ATS and those without ARS or ATS ( P=0.045), while there was no significant difference between participants with ARS and ATS and those without ARS or ATS ( P=0.28). Similar results were obtained in the multivariate logistic regression of left ventricular diastolic dysfunction (LVDD). With similar adjustment, LVDD was significantly associated with ATS ( P=0.01) but not with ARS ( P=0.99).

          Conclusion

          In the community-dwelling elderly Chinese, among hypertensive TOD, LVDD was significantly associated with ATS but not with ARS. The proportion of patients with LVDD was not significantly different despite the presence of both ATS and ARS, when compared to patients with ATS alone.

          Most cited references33

          • Record: found
          • Abstract: found
          • Article: not found

          Echocardiographic assessment of left ventricular hypertrophy: comparison to necropsy findings.

          To determine the accuracy of echocardiographic left ventricular (LV) dimension and mass measurements for detection and quantification of LV hypertrophy, results of blindly read antemortem echocardiograms were compared with LV mass measurements made at necropsy in 55 patients. LV mass was calculated using M-mode LV measurements by Penn and American Society of Echocardiography (ASE) conventions and cube function and volume correction formulas in 52 patients. Penn-cube LV mass correlated closely with necropsy LV mass (r = 0.92, p less than 0.001) and overestimated it by only 6%; sensitivity in 18 patients with LV hypertrophy (necropsy LV mass more than 215 g) was 100% (18 of 18 patients) and specificity was 86% (29 of 34 patients). ASE-cube LV mass correlated similarly to necropsy LV mass (r = 0.90, p less than 0.001), but systematically overestimated it (by a mean of 25%); the overestimation could be corrected by the equation: LV mass = 0.80 (ASE-cube LV mass) + 0.6 g. Use of ASE measurements in the volume correction formula systematically underestimated necropsy LV mass (by a mean of 30%). In a subset of 9 patients, 3 of whom had technically inadequate M-mode echocardiograms, 2-dimensional echocardiographic (echo) LV mass by 2 methods was also significantly related to necropsy LV mass (r = 0.68, p less than 0.05 and r = 0.82, p less than 0.01). Among other indexes of LV anatomy, only measurement of myocardial cross-sectional area was acceptably accurate for quantitation of LV mass (r = 0.80, p less than 0.001) or diagnosis of LV hypertrophy (sensitivity = 72%, specificity = 94%).(ABSTRACT TRUNCATED AT 250 WORDS)
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Association between arterial stiffness and atherosclerosis: the Rotterdam Study.

            Studies of the association between arterial stiffness and atherosclerosis are contradictory. We studied stiffness of the aorta and the common carotid artery in relation to several indicators of atherosclerosis. This study was conducted within the Rotterdam Study in >3000 elderly subjects aged 60 to 101 years. Aortic stiffness was assessed by measuring carotid-femoral pulse wave velocity, and common carotid artery stiffness was assessed by measuring common carotid distensibility. Atherosclerosis was assessed by common carotid intima-media thickness, plaques in the carotid artery and in the aorta, and the presence of peripheral arterial disease. Data were analyzed by ANCOVA with adjustment for age, sex, mean arterial pressure, and heart rate. Both aortic and common carotid artery stiffness were found to have a strong positive association with common carotid intima-media thickness, severity of plaques in the carotid artery, and severity of plaques in the aorta (P: for trend <0.01 for all associations). Subjects with peripheral arterial disease had significantly increased aortic stiffness (P:=0.001) and borderline significantly increased common carotid artery stiffness (P:=0.08) compared with subjects without peripheral arterial disease. Results were similar after additional adjustment for cardiovascular risk factors and after exclusion of subjects with prevalent cardiovascular disease. This population-based study shows that arterial stiffness is strongly associated with atherosclerosis at various sites in the vascular tree.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Age-related intimal stiffening enhances endothelial permeability and leukocyte transmigration.

              Age is the most significant risk factor for atherosclerosis; however, the link between age and atherosclerosis is poorly understood. During both aging and atherosclerosis progression, the blood vessel wall stiffens owing to alterations in the extracellular matrix. Using in vitro and ex vivo models of vessel wall stiffness and aging, we show that stiffening of extracellular matrix within the intima promotes endothelial cell permeability--a hallmark of atherogenesis. When cultured on hydrogels fabricated to match the elasticity of young and aging intima, endothelial monolayers exhibit increased permeability and disrupted cell-cell junctions on stiffer matrices. In parallel experiments, we showed a corresponding increase in cell-cell junction width with age in ex vivo aortas from young (10 weeks) and old (21 to 25 months) healthy mice. To investigate the mechanism by which matrix stiffening alters monolayer integrity, we found that cell contractility increases with increased matrix stiffness, mechanically destabilizing cell-cell junctions. This increase in endothelial permeability results in increased leukocyte extravasation, which is a critical step in atherosclerotic plaque formation. Mild inhibition of Rho-dependent cell contractility using Y-27632, an inhibitor of Rho-associated kinase, or small interfering RNA restored monolayer integrity in vitro and in vivo. Our results suggest that extracellular matrix stiffening alone, which occurs during aging, can lead to endothelial monolayer disruption and atherosclerosis pathogenesis. Because previous therapeutics designed to decrease vascular stiffness have been met with limited success, our findings could be the basis for the design of therapeutics that target the Rho-dependent cellular contractile response to matrix stiffening, rather than stiffness itself, to more effectively prevent atherosclerosis progression.
                Bookmark

                Author and article information

                Journal
                Clin Interv Aging
                Clin Interv Aging
                Clinical Interventions in Aging
                Clinical Interventions in Aging
                Dove Medical Press
                1176-9092
                1178-1998
                2017
                02 June 2017
                : 12
                : 929-936
                Affiliations
                Department of Cardiology, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai, People’s Republic of China
                Author notes
                Correspondence: Yi Zhang; Yawei Xu, Department of Cardiology, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, 301 Yanchang Middle Road, Shanghai 200072, People’s Republic of China, Tel +86 21 6630 6920, Fax +86 21 6630 7239, Email yizshcn@ 123456gmail.com ; xuyaweicn@ 123456aliyun.com
                Article
                cia-12-929
                10.2147/CIA.S133691
                5472426
                84dabb2e-01ad-4f8e-8aa4-b97dbaafb7ff
                © 2017 Fan et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                History
                Categories
                Original Research

                Health & Social care
                arteriosclerosis,atherosclerosis,target organ damage,pulse wave velocity,carotid plaque

                Comments

                Comment on this article