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

Coronary Heart Disease (CHD) is a multifactorial pathology whose progression is associated with the development of chronic heart failure (CHF) following myocardial infarction (MI). Recent studies have shown that vitamin D deficiency is an independent risk factor for CHD and its severity. Due to the lack of a unified understanding of the pathogenetic role of vitamin D deficiency, it is relevant to study the relationship between vitamin D deficiency and post-MI myocardial remodeling in rats. The aim of the study is to investigate echocardiographic and morphological parameters of post-infarction myocardial remodeling in rats with vitamin D deficiency, modeled in male Wistar rats (n = 41) by feeding a vitamin D-free diet (Delta Feeds) for two months, followed by MI induction. The animals were divided into three groups: Group 1—a comparison group, Group 2—rats that did not receive post-infarction cholecalciferol therapy, and Group 3—rats that received cholecalciferol post-MI. Echocardiography was performed using a MyLabTouchSL 3116 high-resolution ultrasound system (Esaote, Italy) on days 30 and 60 post-MI. Serum 25(OH)D levels were measured by ELISA in 5 animals from each group. Histological examination 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 therapy in Group 3 was accompanied by a reduced heart rate compared to Group 2 (p = 0.0004) on day 30 post-MI. Compared to Group 3, Group 2 exhibited a larger left ventricular end-diastolic dimension (LVEDD) (p = 0.002), left ventricular end-systolic dimension (LVESD) (p = 0.002), as well as lower left ventricular 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 of the left ventricular wall area), left ventricular wall thickness in the scar and interventricular septum region, as well as left ventricular hypertrophy and dilation indices, were higher in Group 2 than in Group 3 (p < 0.05). Thus, in an experimental rat model of MI, animals deficient in vitamin D and untreated with cholecalciferol post-MI exhibited a significant myocardial hypertrophy, reduced left ventricular function, and a larger post-infarction scar area compared to those treated with cholecalciferol.