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Abstract <p>Coronary Heart Disease (CHD) is a multifactorial pathologywhose progression is associated with the development of chronicheart failure (CHF) following myocardial infarction (MI). Recentstudies have shown that vitamin D deficiency is an independent riskfactor for CHD and its severity. Due to the lack of a unified understandingof the pathogenetic role of vitamin D deficiency, it is relevantto study the relationship between vitamin D deficiency and post-MImyocardial remodeling in rats. The aim of the study is to investigateechocardiographic and morphological parameters of post-infarctionmyocardial remodeling in rats with vitamin D deficiency, modeledin male Wistar rats (<i>n</i> = 41)by feeding a vitamin D-free diet (Delta Feeds) for two months, followedby MI induction. The animals were divided into three groups: Group1—a comparison group, Group 2—rats that did not receive post-infarction cholecalciferoltherapy, and Group 3—rats that received cholecalciferol post-MI.Echocardiography was performed using a MyLabTouchSL 3116 high-resolutionultrasound system (Esaote, Italy) on days 30 and 60 post-MI. Serum25(OH)D levels were measured by ELISA in 5 animals from each group. Histologicalexamination assessed scar size and the severity of myocardial remodeling.The 25(OH)D level in Group 3 was higher than in Groups 1 and 2 [59.70(50.50–64.80), 9.00 (8.12–9.54), and 8.20 (7.60–8.31) nmol/L, respectively; <i>p</i> = 0.04]. Cholecalciferol therapyin Group 3 was accompanied by a reduced heart rate compared to Group2 (<i>p</i> = 0.0004) on day 30 post-MI.Compared to Group 3, Group 2 exhibited a larger left ventricularend-diastolic dimension (LVEDD) (<i>p</i> =0.002), left ventricular end-systolic dimension (LVESD) (<i>p</i> = 0.002), as well as lower leftventricular fractional shortening (FS) (<i>p</i> = 0.002)and ejection fraction (EF) (<i>p</i> =0.002) on days 30 and 60 post-MI. The scar area (as a percentage ofthe left ventricular wall area), left ventricular wall thicknessin the scar and interventricular septum region, as well as leftventricular hypertrophy and dilation indices, were higher in Group2 than in Group 3 (<i>p</i> &lt; 0.05).Thus, in an experimental rat model of MI, animals deficient in vitaminD and untreated with cholecalciferol post-MI exhibited a significantmyocardial hypertrophy, reduced left ventricular function, and alarger post-infarction scar area compared to those treated withcholecalciferol.</p>

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Vitamin D Deficiency Impairs Post-Infarction Left Ventricular Remodeling in Rats

  • 期刊论文

  • 发表日期：

    2025年5月1日

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  • Zh. I. Ionova,
  • A. A. Karpov,
  • O. A. Berkovich,
  • S. G. Cefu,
  • L. A. Shilenko,
  • M. G. Butskikh,
  • A.-Kh. A. Chervaev,
  • D. S. Chepurnaya,
  • D. Yu. Ivkin,
  • T. D. Vlasov

摘要

Abstract

Coronary Heart Disease (CHD) is a multifactorial pathologywhose progression is associated with the development of chronicheart failure (CHF) following myocardial infarction (MI). Recentstudies have shown that vitamin D deficiency is an independent riskfactor for CHD and its severity. Due to the lack of a unified understandingof the pathogenetic role of vitamin D deficiency, it is relevantto study the relationship between vitamin D deficiency and post-MImyocardial remodeling in rats. The aim of the study is to investigateechocardiographic and morphological parameters of post-infarctionmyocardial remodeling in rats with vitamin D deficiency, modeledin male Wistar rats (n = 41)by feeding a vitamin D-free diet (Delta Feeds) for two months, followedby MI induction. The animals were divided into three groups: Group1—a comparison group, Group 2—rats that did not receive post-infarction cholecalciferoltherapy, and Group 3—rats that received cholecalciferol post-MI.Echocardiography was performed using a MyLabTouchSL 3116 high-resolutionultrasound system (Esaote, Italy) on days 30 and 60 post-MI. Serum25(OH)D levels were measured by ELISA in 5 animals from each group. Histologicalexamination assessed scar size and the severity of myocardial remodeling.The 25(OH)D level in Group 3 was higher than in Groups 1 and 2 [59.70(50.50–64.80), 9.00 (8.12–9.54), and 8.20 (7.60–8.31) nmol/L, respectively; p = 0.04]. Cholecalciferol therapyin Group 3 was accompanied by a reduced heart rate compared to Group2 (p = 0.0004) on day 30 post-MI.Compared to Group 3, Group 2 exhibited a larger left ventricularend-diastolic dimension (LVEDD) (p =0.002), left ventricular end-systolic dimension (LVESD) (p = 0.002), as well as lower leftventricular fractional shortening (FS) (p = 0.002)and ejection fraction (EF) (p =0.002) on days 30 and 60 post-MI. The scar area (as a percentage ofthe left ventricular wall area), left ventricular wall thicknessin the scar and interventricular septum region, as well as leftventricular hypertrophy and dilation indices, were higher in Group2 than in Group 3 (p < 0.05).Thus, in an experimental rat model of MI, animals deficient in vitaminD and untreated with cholecalciferol post-MI exhibited a significantmyocardial hypertrophy, reduced left ventricular function, and alarger post-infarction scar area compared to those treated withcholecalciferol.