Calcifediol supplementation did not reduce left ventricular remodeling incidence (30.8% vs 28.6%, p=1.000) or improve cardiac MRI parameters after anterior STEMI.
Does calcifediol prevent left ventricular remodelling in patients with anterior STEMI?
Calcifediol supplementation for 12 months does not improve left ventricular remodeling or biomarker profiles in patients with anterior STEMI.
Tasa de eventos absoluta: 0% vs 0%
Abstract Introduction The information regarding the potential benefit of Vitamin D supplements (VDSs) on left ventricular (LV) remodelling is controversial. We investigated whether VDSs improve LV remodelling in pts. with anterior ST-segment elevation acute myocardial infarction (STEMI). Methods VITDAMI (VITamin D in Acute Myocardial Infarction) is a multicentre, randomized, double-blind, placebo-controlled trial in pts. with anterior STEMI. A total of 93 pts. were randomly allocated (2:1) to receive calcifediol (0.266 mg/15 days) or placebo for 12 months. The primary endpoint was LV remodelling (defined as 10% increase in LV end-diastolic volume EDV) assessed by magnetic resonance imaging (MRI) at baseline and at 1 year (the investigators interpreting the MRI were unaware of the treatment received by the pts.). Secondary objectives included: change in EDV, end-systolic volume (ESV) and LV ejection fraction (EF), and change in N-Terminal pro-brain natriuretic peptide (NT-proBNP), galectin-3, and fibroblast growth factor-23 (FGF23) plasma levels. Results Sixty-five pts. received calcifediol and 28 placebo. There were no differences in baseline characteristics between the two groups. At baseline, the calcifediol group had similar EDVs (155±42.8 vs 171±48.4 ml; p=0.114), ESV (82.4±34.5 vs 96.1±39.5 ml; p=0.096), EF (48.0±9.8 vs 45.0±9.5%; p=0.182), and calcidiol (26.4±12.5 vs 27.0±10.7 ng/mL; p=0.834), NT-proBNP (1180 632, 2335 vs 1210 872, 2555 pg/ml; p=0.481), galectin-3 (9408±3187 vs 10773±4049 ng/mL; p=0.087), and FGF23 (79.0 54.2, 101 vs 80.5 63.2, 99.0 RU/mL; p=0.831) plasma levels as compared to the placebo group. Calcidiol levels increased in the intervention vs the control group (24.4±22.1 vs 0.72±10.9 ng/mL; p0.001). There were no differences in the incidence of LV remodelling (primary endpoint, 30.8% vs 28.6%; p=1.000), increase in EDV (3.63±29.6 vs 5.63±32.8 ml; p=0.773), ESV (-6.05±26.6 vs -5.33±29.8 ml; p=0.908), EF (6.1±7.93% vs 6.12±8.64%;p=0.992) or in changes in NT-proBNP, Galectin-3 and FGF23 levels in the calcifediol versus the placebo group at the end of follow-up. The interobserver correlation (r=0.907 to 0.999) and agreement (intraclass correlation coefficient= 0.922 to 0.999) for MRI analyses were excellent (p0.001 for all), and similar results were obtained for intraobserver correlation (r=0.867 to 0.988) and agreement (intraclass correlation coefficient= 0.928 to 0.991) (p0.001 for all). All the analyses were repeated in the subgroup of pts. with FGF23 levels above the median (79.0 RU/mL; N=44) and in the subgroup with low calcidiol levels (30 ng/mL; N=58) and no benefits were found in the described MRI parameters nor in the changes of NT-proBNP, galectin-3, and FGF23 plasma levels. Conclusion Administration of calcifediol to pts. with anterior STEMI does not improve LV remodelling as compared with placebo and it is not related to significant changes in NT-proBNP, galectin-3 or FGF23 plasma levels.Effect of calfediol on left ventricular
Fernandez et al. (Sat,) reported a other. Calcifediol supplementation did not reduce left ventricular remodeling incidence (30.8% vs 28.6%, p=1.000) or improve cardiac MRI parameters after anterior STEMI.