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      Cardiac remodelling and functional alterations in mild-to-moderate renal dysfunction: comparison with healthy subjects

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          Abstract

          Introduction

          Left ventricular (LV) hypertrophy (LVH) and reduced LV function correlate with poor prognosis in patients with chronic kidney disease (CKD). Our aim is to investigate whether mild-to-moderate CKD is associated with cardiac abnormalities.

          Methods

          Echocardiography, including tissue Doppler imaging, was performed in 103 patients with CKD at stages 2–3 and 4–5, and in 53 healthy controls. The systolic ( s′) and diastolic myocardial velocity ( e′), and the transmitral diastolic flow velocity ( E) were measured, and E/ e′ was calculated.

          Results

          Patients with chronic kidney disease had higher mean E/ e′ than controls (mean E/ e′: controls 5·00 ± 1·23 versus CKD 4–5 6·36 ± 1·71, P<0·001 and versus CKD 2–3 5·69 ± 1·47, P = 0·05), indicating altered diastolic function in the patients. The CKD groups showed lower longitudinal systolic function than controls, as assessed by atrio-ventricular plane displacement and s′ (mean s′: controls 11·5 ± 1·9 cm s −1 versus CKD 4–5 10·4 ± 2·1 cm s −1, P = 0·03 and versus CKD 2–3 10·4 ± 2·1 cm s −1, P = 0·02). The prevalence of LVH was higher in patients with CKD than in controls (controls 13% versus CKD 4–5 37%, P = 0·006 and versus CKD 2–3 30%, P = 0·03).

          Conclusion

          Alterations in systolic and diastolic myocardial function can be seen in mild-to-moderate CKD compared with controls, indicating that cardiac involvement starts early in CKD, which may be a precursor of premature cardiac morbidity.

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          Most cited references34

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          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)
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            Clinical epidemiology of cardiovascular disease in chronic renal disease.

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              Relation between renal dysfunction and cardiovascular outcomes after myocardial infarction.

              The presence of coexisting conditions has a substantial effect on the outcome of acute myocardial infarction. Renal failure is associated with one of the highest risks, but the influence of milder degrees of renal impairment is less well defined. As part of the Valsartan in Acute Myocardial Infarction Trial (VALIANT), we identified 14,527 patients with acute myocardial infarction complicated by clinical or radiologic signs of heart failure, left ventricular dysfunction, or both, and a documented serum creatinine measurement. Patients were randomly assigned to receive captopril, valsartan, or both. The glomerular filtration rate (GFR) was estimated by means of the four-component Modification of Diet in Renal Disease equation, and the patients were grouped according to their estimated GFR. We used a 70-candidate variable model to adjust and compare overall mortality and composite cardiovascular events among four GFR groups. The distribution of estimated GFR was wide and normally shaped, with a mean (+/-SD) value of 70+/-21 ml per minute per 1.73 m2 of body-surface area. The prevalence of coexisting risk factors, prior cardiovascular disease, and a Killip class of more than I was greatest among patients with a reduced estimated GFR (less than 45.0 ml per minute per 1.73 m2), and the use of aspirin, beta-blockers, statins, or coronary-revascularization procedures was lowest in this group. The risk of death or the composite end point of death from cardiovascular causes, reinfarction, congestive heart failure, stroke, or resuscitation after cardiac arrest increased with declining estimated GFRs. Although the rate of renal events increased with declining estimated GFRs, the adverse outcomes were predominantly cardiovascular. Below 81.0 ml per minute per 1.73 m2, each reduction of the estimated GFR by 10 units was associated with a hazard ratio for death and nonfatal cardiovascular outcomes of 1.10 (95 percent confidence interval, 1.08 to 1.12), which was independent of the treatment assignment. Even mild renal disease, as assessed by the estimated GFR, should be considered a major risk factor for cardiovascular complications after a myocardial infarction. Copyright 2004 Massachusetts Medical Society
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                Author and article information

                Journal
                Clin Physiol Funct Imaging
                Clin Physiol Funct Imaging
                cpf
                Clinical Physiology and Functional Imaging
                Blackwell Publishing Ltd (Oxford, UK )
                1475-0961
                1475-097X
                May 2015
                21 April 2014
                : 35
                : 3
                : 223-230
                Affiliations
                [1 ]Department of Clinical Physiology, Karolinska University Hospital Stockholm, Sweden
                [2 ]Department of Molecular Medicine and Surgery, Karolinska Institutet Stockholm, Sweden
                [3 ]Department of Nephrology, Karolinska University Hospital, Karolinska Institutet Stockholm, Sweden
                [4 ]Division of Nephrology, Department of Medicine, Västmanlands Hospital Västerås, Sweden
                [5 ]Division of Nephrology, Department of Clinical Sciences, Karolinska Institutet, Danderyd Hospital Stockholm, Sweden
                Author notes
                Anna M. Asp, Department of Clinical Physiology N2:01, Karolinska University Hospital, SE-171 76 Stockholm, Sweden, E-mail: anna.mathilda.asp@ 123456gmail.com
                Article
                10.1111/cpf.12154
                4405083
                24750894
                3d4690f6-45f0-4934-a309-39d11db4ef19
                © 2014 The Authors. Clinical Physiology and Functional Imaging published by John Wiley & Sons Ltd on behalf of Scandinavian Society of Clinical Physiology and Nuclear Medicine.

                This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                : 16 December 2013
                : 24 March 2014
                Categories
                Original Articles

                Anatomy & Physiology
                chronic kidney disease,left ventricular diastolic function,left ventricular mass,left ventricular systolic function,tissue doppler imaging

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