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      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)

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      Vascular aging and subclinical atherosclerosis: why such a “never ending” and challenging story in cardiology?

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          Abstract

          The true onset of atherosclerosis remains one of the biggest challenges for cardiologists. Is atheroma plaque development considered the earliest step of vascular aging? If so, when it starts? Before or after birth? If it starts before birth or early during childhood, it seems that Thomas Sydenham was right: “A man is as old as his arteries.” Except disorganization of elastic fibers, less is known about the morphology of vascular aging and also about the molecular events influencing the age of arteries, arterial stiffness, and their role in the appearance of future complications. Cellular and molecular events responsible for the switch from physiologic to pathologic aging of human arteries are less known. Epigenetic, genetic, and environmental influences at the onset of early vascular aging (EVA) should specifically influence the process. This paper briefly reviews the controversial data regarding vascular aging with an emphasis on the less known facts about the morphology of EVA.

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          Fatty streak formation occurs in human fetal aortas and is greatly enhanced by maternal hypercholesterolemia. Intimal accumulation of low density lipoprotein and its oxidation precede monocyte recruitment into early atherosclerotic lesions.

          A Postiglione, S. Napoli, W Palinski … (1997)
          To determine whether oxidized LDL enhances atherogenesis by promoting monocyte recruitment into the vascular intima, we investigated whether LDL accumulation and oxidation precede intimal accumulation of monocytes in human fetal aortas (from spontaneous abortions and premature newborns who died within 12 h; fetal age 6.2+/-1.3 mo). For this purpose, a systematic assessment of fatty streak formation was carried out in fetal aortas from normocholesterolemic mothers (n = 22), hypercholesterolemic mothers (n = 33), and mothers who were hypercholesterolemic only during pregnancy (n = 27). Fetal plasma cholesterol levels showed a strong inverse correlation with fetal age (R = -0.88, P < 0.0001). In fetuses younger than 6 mo, fetal plasma cholesterol levels correlated with maternal ones (R = 0.86, P = 0.001), whereas in older fetuses no such correlation existed. Fetal aortas from hypercholesterolemic mothers and mothers with temporary hypercholesterolemia contained significantly more and larger lesions (758,651+/-87,449 and 451,255+/-37,448 micron2 per section, respectively; mean+/-SD) than aortas from normocholesterolemic mothers (61,862+/-9,555 micron2; P < 0.00005). Serial sections of the arch, thoracic, and abdominal aortas were immunostained for recognized markers of atherosclerosis: macrophages, apo B, and two different oxidation-specific epitopes (malondialdehyde- and 4-hydroxynonenal-lysine). Of the atherogenic sites that showed positive immunostaining for at least one of these markers, 58.6% were established lesions containing both macrophage/foam cells and oxidized LDL (OxLDL). 17.3% of all sites contained only native LDL, and 13.3% contained only OxLDL without monocyte/ macrophages. In contrast, only 4.3% of sites contained isolated monocytes in the absence of native or oxidized LDL. In addition, 6.3% of sites contained LDL and macrophages but few oxidation-specific epitopes. These results demonstrate that LDL oxidation and formation of fatty streaks occurs already during fetal development, and that both phenomena are greatly enhanced by maternal hypercholesterolemia. The fact that in very early lesions LDL and OxLDL are frequently found in the absence of monocyte/macrophages, whereas the opposite is rare, suggests that intimal LDL accumulation and oxidation contributes to monocyte recruitment in vivo.
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            Vascular Fibrosis in Aging and Hypertension: Molecular Mechanisms and Clinical Implications

            Adam Harvey, Augusto C. Montezano, Rhéure Alves Moreira Lopes … (2016)
            Aging is the primary risk factor underlying hypertension and incident cardiovascular disease. With aging, the vasculature undergoes structural and functional changes characterized by endothelial dysfunction, wall thickening, reduced distensibility, and arterial stiffening. Vascular stiffness results from fibrosis and extracellular matrix (ECM) remodelling, processes that are associated with aging and are amplified by hypertension. Some recently characterized molecular mechanisms underlying these processes include increased expression and activation of matrix metalloproteinases, activation of transforming growth factor-β1/SMAD signalling, upregulation of galectin-3, and activation of proinflammatory and profibrotic signalling pathways. These events can be induced by vasoactive agents, such as angiotensin II, endothelin-1, and aldosterone, which are increased in the vasculature during aging and hypertension. Complex interplay between the “aging process” and prohypertensive factors results in accelerated vascular remodelling and fibrosis and increased arterial stiffness, which is typically observed in hypertension. Because the vascular phenotype in a young hypertensive individual resembles that of an elderly otherwise healthy individual, the notion of “early” or “premature” vascular aging is now often used to describe hypertension-associated vascular disease. We review the vascular phenotype in aging and hypertension, focusing on arterial stiffness and vascular remodelling. We also highlight the clinical implications of these processes and discuss some novel molecular mechanisms of fibrosis and ECM reorganization.
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              Stiffness of capacitive and conduit arteries: prognostic significance for end-stage renal disease patients.

              Bruno Pannier, Sylvain Marchais, P Guérin … (2005)
              The aorta is the principal capacitive element of the arterial tree and its increased stiffness, determined by measurement of aortic pulse wave velocity (PWV), is a strong independent predictor of cardiovascular mortality in the general population and end-stage renal disease (ESRD) patients. Whether stiffness of ESRD patients' peripheral arteries has the same prognostic value has never been investigated. A cohort of 305 ESRD patients was followed for 70+/-49 months (mean+/-SD). Ninety-six deaths of cardiovascular origin occurred. At entry into the study, together with standard clinical and biochemical analyses, patients' aortic, brachial artery, and femorotibial PWV were determined. Based on Kaplan-Meier survival curve analyses and Cox proportional hazards analyses, adjusted for age, pulse pressure, and clinical data, aortic PWV was a significant and independent predictor of outcome. Neither brachial artery nor femotibial artery stiffness was able to predict cardiovascular outcome. Receiver operating characteristic curve analysis of aortic PWV indicated the cutoff value of 10.75 m/s, with 84% sensitivity, 73% specificity, 87% negative predictive value, and 72% positive predictive value. These results provide evidence that, in ESRD, increased stiffness of capacitive arteries, like the aorta, is an independent strong predictor of cardiovascular mortality, whereas stiffness of peripheral conduit arteries had no prognostic value.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Clin Interv Aging
                Journal ID (iso-abbrev): Clin Interv Aging
                Journal ID (publisher-id): Clinical Interventions in Aging
                Title: Clinical Interventions in Aging
                Publisher: Dove Medical Press
                ISSN (Print): 1176-9092
                ISSN (Electronic): 1178-1998
                Publication date Collection: 2017
                Publication date (Electronic): 23 August 2017
                Volume: 12
                Pages: 1339-1345
                Affiliations
                [1 ]Department of Preventive Medicine, Angiogenesis Research Center, “Victor Babes” University of Medicine and Pharmacy
                [2 ]Clinical Emergency County Hospital “Pius Brînzeu,”
                [3 ]Department of Microscopic Morphology/Histology, Angiogenesis Research Center, “Victor Babes” University of Medicine and Pharmacy, Timisoara
                [4 ]Department of Cardiology, “Grigore T Popa” University of Medicine and Pharmacy, Iasi
                [5 ]Department of Pathology, Louis Turcanu Children Hospital, Timisoara, Romania
                Author notes
                Correspondence: Anca Maria Cimpean, Department of Microscopic Morphology/Histology, Angiogenesis Research Center, “Victor Babes” University of Medicine and Pharmacy, Piata Eftimie Murgu 2, 300041 Timisoara, Romania, Tel +40 720 060 955, Email ancacimpean1972@ 123456yahoo.com
                Article
                Publisher ID: cia-12-1339
                DOI: 10.2147/CIA.S141265
                PMC ID: 5574695
                PubMed ID: 28883714
                SO-VID: 4e9b7c5a-b022-45f9-99a0-03959b571a7f
                Copyright © © 2017 Iurciuc et al. This work is published and licensed by Dove Medical Press Limited
                License:

                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.

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                Subject: Expert Opinion

                ScienceOpen disciplines: Health & Social care
                Keywords: arterial stiffness,blood pressure variability,arterial aging,telomeres
                Data availability:
                ScienceOpen disciplines: Health & Social care
                Keywords: arterial stiffness, blood pressure variability, arterial aging, telomeres

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