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      Left Ventricular Hypertrophy and Chronic Renal Insufficiency in the Elderly

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      Cardiorenal Medicine

      S. Karger AG

      Renal insufficiency, Elderly, Left ventricular hypertrophy

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          Abstract

          Background: The global population is aging. Cardiovascular disease is the leading cause of death in both men and women older than 65 years. In particular, elderly patients have an increased prevalence of left ventricular hypertrophy (LVH) and chronic kidney disease (CKD), both of which predict increased cardiovascular morbidity and mortality. LVH and CKD frequently coexist in the elderly, and LVH is a powerful predictor of mortality in patients with end-stage renal disease. Key Messages: Several hemodynamic factors contribute to LVH and CKD in the elderly. Increased arterial stiffness in the elderly is associated with LVH and CKD. Studies using noninvasive measures of arterial stiffening have shown a correlation between these measures and LVH in patients with CKD. Hypertensive patients with an altered circadian blood pressure pattern such as nondippers have an increased incidence of LVH and CKD. Anemia is a risk factor for LVH in patients in all stages of CKD, and studies have shown correlations between age, anemia and LV mass. Nonhemodynamic factors include chronic inflammation, increased oxidative stress, and reduced autophagy, all of which are present in the elderly. Disordered mineral metabolism in the elderly with reduced levels of vitamin D and elevated levels of parathyroid hormone and phosphorus is associated with LVH and CKD. Conclusions: Multiple pathophysiologic mechanisms contribute to the development of LVH and CKD in the elderly. Future research should be directed at interfering with this development and reducing the burden of cardiovascular and renal diseases in this growing population. i 2014 S. Karger AG, Basel

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          Most cited references 46

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          Inflammatory markers and onset of cardiovascular events: results from the Health ABC study.

          Inflammation plays an important role in cardiovascular disease. The aim of this study is to investigate the predictive value of several inflammatory markers on the incidence of cardiovascular events in well-functioning older persons. The subjects were 2225 participants 70 to 79 years old, without baseline cardiovascular disease, who were enrolled in the Health, Aging, and Body Composition study. Incident coronary heart disease (CHD), stroke, and congestive heart failure (CHF) events were detected during an average follow-up of 3.6 years. Blood levels of interleukin-6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor-alpha (TNF-alpha) were assessed. After adjustment for potential confounders, IL-6 was significantly associated with all outcomes (CHD events, per IL-6 SD increase: RR, 1.27; 95% CI, 1.10 to 1.48; stroke events, per IL-6 SD increase: RR, 1.45; 95% CI, 1.12 to 1.86; CHF events, per IL-6 SD increase: RR, 1.72; 95% CI, 1.40 to 2.12). TNF-alpha showed significant associations with CHD (per TNF-alpha SD increase: RR, 1.22; 95% CI, 1.04 to 1.43) and CHF (per TNF-alpha SD increase: RR, 1.59; 95% CI, 1.30 to 1.95) events. CRP was significantly associated with CHF events (per CRP SD increase: RR, 1.48; 95% CI, 1.23 to 1.78). A composite summary indicator of inflammation showed a strong association with incident cardiovascular events, with an especially high risk if all 3 inflammatory markers were in the highest tertile. Findings suggest that inflammatory markers are independent predictors of cardiovascular events in older persons.
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            Cardiac hypertrophy in vitamin D receptor knockout mice: role of the systemic and cardiac renin-angiotensin systems.

            Our recent studies suggest that 1,25-dihydroxyvitamin D3 functions as an endocrine suppressor of renin biosynthesis. Genetic disruption of the vitamin D receptor (VDR) results in overstimulation of the renin-angiotensin system (RAS), leading to high blood pressure and cardiac hypertrophy. Consistent with the higher heart-to-body weight ratio, the size of left ventricular cardiomyocytes in VDR knockout (KO) mice was markedly increased compared with wild-type (WT) mice. As expected, levels of atrial natriuretic peptide (ANP) mRNA and circulating ANP were also increased in VDRKO mice. Treatment of VDRKO mice with captopril reduced cardiac hypertrophy and normalized ANP expression. To investigate the role of the cardiac RAS in the development of cardiac hypertrophy, the expression of renin, angiotensinogen, and AT-1a receptor in the heart was examined by real-time RT-PCR and immunostaining. In VDRKO mice, the cardiac renin mRNA level was significantly increased, and this increase was further amplified by captopril treatment. Consistently, intense immunostaining was detected in the left ventricle of captopril-treated WT and VDRKO mice by use of an anti-renin antibody. Levels of cardiac angiotensinogen and AT-1a receptor mRNAs were unchanged in the mutant mice. These data suggest that the cardiac hypertrophy seen in VDRKO mice is a consequence of activation of both the systemic and cardiac RAS and support the notion that 1,25-dihydroxyvitamin D(3) regulates cardiac functions, at least in part, through the RAS.
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              Mineral metabolism and arterial functions in end-stage renal disease: potential role of 25-hydroxyvitamin D deficiency.

              In ESRD, arterial function is abnormal, characterized by decreased capacitive function (arterial stiffening) and reduced conduit function, shown by diminished flow-mediated dilation (FMD). The pathophysiology of these abnormalities is not clear, and this cross-sectional study analyzed possible relationships among arterial alterations and cardiovascular risk factors, including mineral metabolism parameters, such as serum parathormone, and vitamin D "nutritional" and "hormonal" status by measuring serum 25-hydroxyvitamin D [25(OH)D(3)] and 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] levels. Aortic stiffness (pulse wave velocity), brachial artery (BA) distensibility (echotracking; n = 42), BA FMD (hand-warming; n = 37), and arterial calcification scores (echography and plain x-rays) were measured in 52 stable and uncomplicated patients who were on hemodialysis. 25(OH)D(3) and 1,25(OH)(2)D(3) serum levels were low and weakly correlated (r = 0.365, P < 0.05). After adjustment for BP and age, multivariate analyses indicated that 25(OH)D(3) and 1,25(OH)(2)D(3) were negatively correlated with aortic pulse wave velocity (P < 0.001) and positively correlated with BA distensibility (P < 0.01) and FMD (P < 0.001). Arterial calcification scores were not independently associated with 25(OH)D(3) and 1,25(OH)(2)D(3) serum concentrations. These results suggest that nutritional vitamin D deficiency and low 1,25(OH)(2)D(3) could be associated with arteriosclerosis and endothelial dysfunction in patients who have ESRD and are on hemodialysis.
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                Author and article information

                Journal
                CRM
                Cardiorenal Med
                10.1159/issn.1664-5502
                Cardiorenal Medicine
                S. Karger AG
                1664-3828
                1664-5502
                2014
                December 2014
                17 September 2014
                : 4
                : 3-4
                : 168-175
                Affiliations
                Coronary Care Unit, Hadassah-Hebrew University Medical Center, Jerusalem, Israel
                Author notes
                *David Leibowitz, MD, Coronary Care Unit, Hadassah-Hebrew University Medical Center, Mount-Scopus, Jerusalem 91240 (Israel), E-Mail oleibo@hadassah.org.il
                Article
                366455 PMC4299265 Cardiorenal Med 2014;4:168-175
                10.1159/000366455
                PMC4299265
                25737681
                © 2014 S. Karger AG, Basel

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                Page count
                Pages: 8
                Categories
                Review

                Cardiovascular Medicine, Nephrology

                Elderly, Renal insufficiency, Left ventricular hypertrophy

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