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      The reproducibility of cardiac magnetic resonance imaging measures of aortic stiffness and their relationship to cardiac structure in prevalent haemodialysis patients

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          ABSTRACT

          Background

          Aortic stiffness is one of the earliest signs of cardiovascular disease (CVD) in patients with chronic kidney disease and an independent predictor of mortality. It is thought to drive left ventricular (LV) remodelling, an established biomarker for mortality. The relationship between direct and indirect measures of aortic stiffness and LV remodelling is not defined in dialysis patients, nor are the reproducibility of methods used to assess aortic stiffness using cardiac magnetic resonance (CMR) imaging.

          Methods

          Using 3T CMR, we report the results of (i) the interstudy, interobserver and intra-observer reproducibility of ascending aortic distensibility (AAD), descending aortic distensibility (DAD) and aortic pulse wave velocity (aPWV) in 10 haemodialysis (HD) patients and (ii) the relationship between AAD, DAD and aPWV and LV mass index (LVMi) and LV remodelling in 70 HD patients.

          Results

          Inter- and intra-observer variability of AAD, DAD and aPWV were excellent [intraclass correlation (ICC) > 0.9 for all]. Interstudy reproducibility of AAD was excellent {ICC 0.94 [95% confidence interval (CI) 0.78–0.99]}, but poor for DAD and aPWV [ICC 0.51 (−0.13–0.85) and 0.51 (−0.31–0.89)]. AAD, DAD and aPWV associated with LVMi on univariate analysis (β = −0.244, P = 0.04; β =−0.315, P < 0.001 and β = 0.242, P = 0.04, respectively). Only systolic blood pressure, serum phosphate and a history of CVD remained independent determinants of LVMi on multivariable linear regression.

          Conclusions

          AAD is the most reproducible CMR-derived measure of aortic stiffness in HD patients. CMR-derived measures of aortic stiffness were not independent determinants of LVMi in HD patients. Whether one should target blood pressure over aortic stiffness to mitigate cardiovascular risk still needs determination.

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          Most cited references41

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          Chronic kidney disease: effects on the cardiovascular system.

          Accelerated cardiovascular disease is a frequent complication of renal disease. Chronic kidney disease promotes hypertension and dyslipidemia, which in turn can contribute to the progression of renal failure. Furthermore, diabetic nephropathy is the leading cause of renal failure in developed countries. Together, hypertension, dyslipidemia, and diabetes are major risk factors for the development of endothelial dysfunction and progression of atherosclerosis. Inflammatory mediators are often elevated and the renin-angiotensin system is frequently activated in chronic kidney disease, which likely contributes through enhanced production of reactive oxygen species to the accelerated atherosclerosis observed in chronic kidney disease. Promoters of calcification are increased and inhibitors of calcification are reduced, which favors metastatic vascular calcification, an important participant in vascular injury associated with end-stage renal disease. Accelerated atherosclerosis will then lead to increased prevalence of coronary artery disease, heart failure, stroke, and peripheral arterial disease. Consequently, subjects with chronic renal failure are exposed to increased morbidity and mortality as a result of cardiovascular events. Prevention and treatment of cardiovascular disease are major considerations in the management of individuals with chronic kidney disease.
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            Mechanical factors in arterial aging: a clinical perspective.

            The human arterial system in youth is beautifully designed for its role of receiving spurts of blood from the left ventricle and distributing this as steady flow through peripheral capillaries. Central to such design is "tuning" of the heart to arterial tree; this minimizes aortic pressure fluctuations and confines flow pulsations to the larger arteries. With aging, repetitive pulsations (some 30 million/year) cause fatigue and fracture of elastin lamellae of central arteries, causing them to stiffen (and dilate), so that reflections return earlier to the heart; in consequence, aortic systolic pressure rises, diastolic pressure falls, and pulsations of flow extend further into smaller vessels of vasodilated organs (notably the brain and kidney). Stiffening leads to increased left ventricular (LV) load with hypertrophy, decreased capacity for myocardial perfusion, and increased stresses on small arterial vessels, particularly of brain and kidney. Clinical manifestations are a result of diastolic LV dysfunction with dyspnea, predisposition to angina, and heart failure, and small vessel degeneration in brain and kidney with intellectual deterioration and renal failure. While aortic stiffening is the principal cause of cardiovascular disease with age in persons who escape atherosclerotic complications, it is not a specific target for therapy. The principal target is the smooth muscle in distributing arteries, whose relaxation has little effect on peripheral resistance but causes substantial reduction in the magnitude of wave reflection. Such relaxation is achieved through regular exercise and with the vasodilating drugs that are used in modern treatment of hypertension and cardiac failure.
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              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.
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                Author and article information

                Journal
                Clin Kidney J
                Clin Kidney J
                ckj
                Clinical Kidney Journal
                Oxford University Press
                2048-8505
                2048-8513
                December 2018
                21 June 2018
                21 June 2018
                : 11
                : 6
                : 864-873
                Affiliations
                [1 ]John Walls Renal Unit, University Hospitals Leicester NHS Trust, Leicester, UK
                [2 ]Department of Infection Immunity and Inflammation, School of Medicine and Biological Sciences, University of Leicester, Leicester, UK
                [3 ]National Centre for Sport and Exercise Medicine, School of Sport, Exercise and Health Sciences, Loughborough University, Leicestershire, UK
                [4 ]Department of Cardiovascular Sciences, University of Leicester, Leicester, UK
                [5 ]NIHR Leicester Cardiovascular Biomedical Research Centre, Glenfield Hospital, Leicester, UK
                Author notes
                Correspondence and offprint requests to: Matthew P.M. Graham-Brown; E-mail: mgb23@ 123456le.ac.uk
                Author information
                http://orcid.org/0000-0002-7717-8099
                Article
                sfy042
                10.1093/ckj/sfy042
                6275449
                30524722
                57954348-b87a-4d83-b6f6-44371b867a8a
                © The Author(s) 2018. Published by Oxford University Press on behalf of ERA-EDTA.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

                History
                : 12 April 2018
                : 27 April 2018
                Page count
                Pages: 10
                Funding
                Funded by: Clinician Scientist Award
                Award ID: CS2013-13-014
                Funded by: NIHR 10.13039/100006662
                Funded by: NHS
                Funded by: NIHR 10.13039/100006662
                Funded by: Department of Health 10.13039/501100000276
                Categories
                Hemodialysis

                Nephrology
                aortic stiffness,chronic kidney disease,end-stage renal disease,haemodialysis,left ventricular remodelling

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