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      Lower serum 25-hydroxyvitamin D level is associated with impaired myocardial performance and left ventricle hypertrophy in newly diagnosed hypertensive patients

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          Abstract

          Objective:

          Vitamin D deficiency is an independent risk factor for cardiovascular mortality. The relationship between vitamin D level and left ventricle (LV) myocardial performance index (MPI=Tei index), which incorporates both LV systolic function and diastolic function, was not investigated in previous studies. We hypothesized that vitamin D level may be associated with LV function and geometry. We aimed to investigate the association between serum 25-hydroxyvitamin D (25 [OH] D) levels and MPI and LV hypertrophy in hypertensive patients with newly diagnosed and preserved ejection fraction.

          Methods:

          We studied 151 sequential newly diagnosed hypertensive subjects who lived in the Çukurova region without known cardiovascular risk factors or overt heart disease (mean age: 62.8±10.4 years). Serum 25 (OH) D was measured using a direct competitive chemiluminescent immunoassay. The patients were divided into two groups according to serum 25 (OH) D level: vitamin D-non-deficient group (vitamin D> 20.00 ng/mL, n=53) and vitamin D-deficient group (vitamin D< 20.00 ng/mL, n=98). MPI was defined as the sum of isovolumic contraction and relaxation times divided by the ejection time. LV mass index (LVMI) was calculated by using the Devereux formula and body surface area.

          Results:

          MPI and LVMI values were lower and low-density lipoprotein (LDL) levels were higher in patients who were vitamin D-non-deficient than patients who were vitamin D-deficient (p<0.05 for all). Multivariate linear regression analysis showed that serum 25 (OH) D was indepen-dently associated with MPI (β=-0.426, p<0.001), LVMI (β=-0.345, p=<0.001), and LDL (β=0.140, p<0.026).

          Conclusion:

          Lower serum 25 (OH) D levels are significantly associated with impaired myocardial performance and LVMI.

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          Most cited references33

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          New index of combined systolic and diastolic myocardial performance: a simple and reproducible measure of cardiac function--a study in normals and dilated cardiomyopathy.

          Because systolic and diastolic dysfunction frequently coexist, it is hypothesized that a combined measure of left ventricular chamber performance may be more reflective of overall cardiac dysfunction than systolic or diastolic measures alone. METHODS Study patients consisted of 170 subjects: 70 normals, 47 patients with severe dilated cardiomyopathy in NYHA class III-IV awaiting cardiac transplantation and 53 patients with idiopathic dilated cardiomyopathy of intermediate severity [NYHA class II, ejection fractions (EF) 30-50%]. EF, stroke volume and cardiac indexes were measured using conventional echo-Doppler methods. Pre-ejection period/ejection time (PEP/ET), isovolumetric relaxation time (IRT), isovolumetric contraction time/ET (ICT/ET) were also measured. A new derived index of myocardial performance: (ICT+IRT)/ET, was obtained by subtracting ET from the interval between cessation and onset of the mitral inflow velocity to give the sum of ICT and IRT. RESULTS The index was easily measured, reproducible, and had a narrow range in normals. The mean value of the index was significantly different between normal, intermediate and pre-transplant subjects (0.39 +/- 0.05, 0.59 +/- 0.10 and 1.06 +/- 0.24, respectively, p < 0.001 for all comparisons). The degree of inter-group overlap was smaller for the index compared to PEP/ET, ICT/ET and other parameters. Within functional groups, the value of the index did not appear to be related to heart rate, mean arterial pressure and the degree of mitral regurgitation. CONCLUSION (ICT+IRT)/ET is a conceptually new, simple and reproducible Doppler index of combined systolic and diastolic myocardial performance in patients with primary myocardial systolic dysfunction.
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            1,25(OH)2 vitamin d inhibits foam cell formation and suppresses macrophage cholesterol uptake in patients with type 2 diabetes mellitus.

            Cardiovascular disease is the leading cause of death among those with diabetes mellitus. Vitamin D deficiency is associated with an increased risk of cardiovascular disease in this population. To determine the mechanism by which vitamin D deficiency mediates accelerated cardiovascular disease in patients with diabetes mellitus, we investigated the effects of active vitamin D on macrophage cholesterol deposition. We obtained macrophages from 76 obese, diabetic, hypertensive patients with vitamin D deficiency (25-hydroxyvitamin D <80 nmol/L; group A) and 4 control groups: obese, diabetic, hypertensive patients with normal vitamin D (group B; n=15); obese, nondiabetic, hypertensive patients with vitamin D deficiency (group C; n=25); and nonobese, nondiabetic, nonhypertensive patients with vitamin D deficiency (group D; n=10) or sufficiency (group E; n=10). Macrophages from the same patients in all groups were cultured in vitamin D-deficient or 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] -supplemented media and exposed to modified low-density lipoprotein cholesterol. 1,25(OH)(2)D(3) suppressed foam cell formation by reducing acetylated or oxidized low-density lipoprotein cholesterol uptake in diabetic subjects only. Conversely, deletion of the vitamin D receptor in macrophages from diabetic patients accelerated foam cell formation induced by modified LDL. 1,25(OH)(2)D(3) downregulation of c-Jun N-terminal kinase activation reduced peroxisome proliferated-activated receptor-gamma expression, suppressed CD36 expression, and prevented oxidized low-density lipoprotein-derived cholesterol uptake. In addition, 1,25(OH)(2)D(3) suppression of macrophage endoplasmic reticulum stress improved insulin signaling, downregulated SR-A1 expression, and prevented oxidized and acetylated low-density lipoprotein-derived cholesterol uptake. These results identify reduced vitamin D receptor signaling as a potential mechanism underlying increased foam cell formation and accelerated cardiovascular disease in diabetic subjects.
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              Vitamin D status is associated with arterial stiffness and vascular dysfunction in healthy humans.

              The primary objective of this study was to elucidate mechanisms underlying the link between vitamin D status and cardiovascular disease by exploring the relationship between 25-hydroxyvitamin D (25-OH D), an established marker of vitamin D status, and vascular function in healthy adults. Mechanisms underlying vitamin D deficiency-mediated increased risk of cardiovascular disease remain unknown. Vitamin D influences endothelial and smooth muscle cell function, mediates inflammation, and modulates the renin-angiotensin-aldosterone axis. We investigated the relationship between vitamin D status and vascular function in humans, with the hypothesis that vitamin D insufficiency will be associated with increased arterial stiffness and abnormal vascular function. We measured serum 25-OH D in 554 subjects. Endothelial function was assessed as brachial artery flow-mediated dilation, and microvascular function was assessed as digital reactive hyperemia index. Carotid-femoral pulse wave velocity and radial tonometry-derived central augmentation index and subendocardial viability ratio were measured to assess arterial stiffness. Mean 25-OH D was 31.8 ± 14 ng/ml. After adjustment for age, sex, race, body mass index, total cholesterol, low-density lipoprotein, triglycerides, C-reactive protein, and medication use, 25-OH D remained independently associated with flow-mediated vasodilation (β = 0.1, p = 0.03), reactive hyperemia index (β = 0.23, p < 0.001), pulse wave velocity (β = -0.09, p = 0.04), augmentation index (β = -0.11, p = 0.03), and subendocardial viability ratio (β = 0.18, p = 0.001). In 42 subjects with vitamin D insufficiency, normalization of 25-OH D at 6 months was associated with increases in reactive hyperemia index (0.38 ± 0.14, p = 0.009) and subendocardial viability ratio (7.7 ± 3.1, p = 0.04), and a decrease in mean arterial pressure (4.6 ± 2.3 mm Hg, p = 0.02). Vitamin D insufficiency is associated with increased arterial stiffness and endothelial dysfunction in the conductance and resistance blood vessels in humans, irrespective of traditional risk burden. Our findings provide impetus for larger trials to assess the effects of vitamin D therapy in cardiovascular disease. Copyright © 2011 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Anatol J Cardiol
                Anatol J Cardiol
                Anatolian Journal of Cardiology
                Kare Publishing (Turkey )
                2149-2263
                2149-2271
                September 2015
                15 October 2014
                : 15
                : 9
                : 744-750
                Affiliations
                [1]Department of Cardiology, Adana Numune Training and Research Hospital; Adana- Turkey
                [1 ]Department of Cardiology, Yenimahalle State Hospital; Ankara- Turkey
                Author notes
                Address for Correspondence: Dr. Taner Şeker, Adana Numune Eğitim ve Araştırma Hastanesi, Kardiyoloji Kliniği, 01170 Adana- Türkiye Phone: +90 532 509 03 54 Fax: +90 322 338 33 69 E-mail: atanerseker@ 123456hotmail.com
                Article
                AJC-15-744
                10.5152/akd.2014.5637
                5368484
                25592096
                41120487-d350-4cd7-ac55-bbcc431ab1b9
                Copyright © 2015 Turkish Society of Cardiology

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License

                History
                : 20 August 2014
                Categories
                Original Investigation

                vitamin d,tei index,myocardial performance index,hypertension

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