Abstract 12918: Vitamin D Supplementation Did Not Have an Effect on Serum Total or Subclasses of High-Density Lipoprotein-Cholesterol; A Pilot Study

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Patricia G Weyland ◽  
Steven M Paul ◽  
Jill Howie-Esquivel
Keyword(s):  
Vitamin D ◽  
Repeated Measures ◽  
Reductase Inhibitor ◽  
Pearson Correlation ◽  
Causal Mechanism ◽  
Hmg Coa Reductase ◽  
Repeated Measures Anova ◽  
Significant Difference ◽  
Hmg Coa Reductase Inhibitor ◽  
Coa Reductase

Introduction: Both prevalent and incident CVD are negatively associated with 25-hydroxyvitamin D (25[OH] D) levels but the existence of a causal mechanism has yet to be determined. Vitamin D (D) supplementation may increase total HDL-c or one of the HDL subclasses; HDL2 and HDL3 and decrease CVD. The effect of D supplementation with HMG-CoA reductase inhibitor use on HDL-c, HDL2, and HDL3 also remains unclear. Hypotheses: We assessed the following two hypotheses; 1) HDL-c, HDL2, or HDL3 levels will increase with D supplementation for 12 weeks versus placebo and 2) HDL-c, HDL2, or HDL3 levels will increase with D supplementation for 12 weeks with HMG-CoA reductase inhibitor use versus without HMG-CoA reductase inhibitor use. Methods: Serum sample data, including 25(OH) D, HDL-c, HDL2, and HDL3 levels, from a randomized double-blinded placebo-controlled trial conducted between 2008 and 2012 were secondarily analyzed. Statistical analyses included Pearson correlation and Repeated-Measures ANOVA. Results: Hypothesis #1; of the 59 participants (mean age=56.0 years), 39 had a deficient (< 20 ng/mL) baseline 25(OH) D level. Hypothesis #2; of the 40 participants (mean age=56.5 years) 23 had a deficient (< 20 ng/mL) baseline 25(OH) D level. Pearson correlation showed 12-week 25(OH) D levels were moderately positively correlated with 12-week HDL-c (0.337, p ≤ 0.05) and 12-week HDL3 (0.356 p ≤ 0.05) levels but not at baseline. Hypotheses #1 and #2; baseline and 12-week levels for HDL-c, HDL2, and HDL3 were moderately to strongly positively correlated with female gender and moderately to strongly negatively correlated with BMI. Some participants did not achieve sufficient 25(OH) D levels. Repeated-Measures ANOVA with one between-subjects factor; group, and one within-subjects factor; time, showed no statistically significant difference in the mean change in HDL-c, HDL2 or HDL3 for D supplementation versus placebo or for D supplementation with versus without HMG-CoA reductase inhibitor use. Conclusions: Future studies may provide more informative results if they include; more participants, deficient 25(OH) D level as an inclusion criteria, and continued D supplementation until sufficiency is attained versus discontinuation after a pre-specified time period.

Effects of pravastatin, a new HMG-CoA reductase inhibitor, on vitamin D synthesis in man

Metabolism ◽  
1991 ◽  
Vol 40 (5) ◽  
pp. 524-528 ◽  
Author(s):  
Adrian S. Dobs ◽  
Michael A. Levine ◽  
Simeon Margolis
Keyword(s):  
Vitamin D ◽  
Reductase Inhibitor ◽  
Hmg Coa Reductase ◽  
Hmg Coa Reductase Inhibitor ◽  
Coa Reductase

Effects of an HMG-CoA reductase inhibitor, simvastatin, on human myeloma cells

2004 ◽  
Author(s):  
Takemi Otsuki ◽  
Haruko Sakaguchi ◽  
Tamayo Hatayama ◽  
Tomohiro Fujii ◽  
Takayuki Tsujioka ◽  
...  
Keyword(s):  
Reductase Inhibitor ◽  
Hmg Coa Reductase ◽  
Myeloma Cells ◽  
Hmg Coa Reductase Inhibitor ◽  
Coa Reductase ◽  
Human Myeloma Cells

Treatment of hypercholesterolemia with the HMG CoA reductase inhibitor, simvastatin

1989 ◽  
Vol 3 (2) ◽  
pp. 219-227 ◽  
Author(s):  
GMB Berger ◽  
AD Marais ◽  
HC Seftel ◽  
SG Baker ◽  
D Mendelsohn ◽  
...  
Keyword(s):  
Reductase Inhibitor ◽  
Hmg Coa Reductase ◽  
Hmg Coa Reductase Inhibitor ◽  
Coa Reductase

Serum lipoprotein Lp(a) concentrations are not influenced by an HMG CoA reductase inhibitor

1988 ◽  
Vol 66 (10) ◽  
pp. 462-463 ◽  
Author(s):  
J. Thiery ◽  
V. W. Armstrong ◽  
J. Schleef ◽  
C. Creutzfeldt ◽  
W. Creutzfeldt ◽  
...  
Keyword(s):  
Reductase Inhibitor ◽  
Serum Lipoprotein ◽  
Hmg Coa Reductase ◽  
Hmg Coa Reductase Inhibitor ◽  
Coa Reductase

Abstract 180: Synergistic Salutary Effects of HMG-CoA Reductase Inhibitor and Angiotensin II Receptor Blocker on Load-induced Heart Failure

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Yasuhiro Maejima ◽  
Mitsuaki Isobe
Keyword(s):  
Heart Failure ◽  
Angiotensin Ii ◽  
Reductase Inhibitor ◽  
Neonatal Rat ◽  
Receptor Blocker ◽  
Angiotensin Ii Receptor Blocker ◽  
Angiotensin Ii Receptor ◽  
Hmg Coa Reductase ◽  
Hmg Coa Reductase Inhibitor ◽  
Coa Reductase

We have shown previously that combined HMG-CoA reductase inhibitor (statin) and angiotensin II receptor blocker (ARB) therapy significantly improves both symptoms and left ventricular (LV) function over time in patients with heart failure (HF) by a clinical study [ HF-COSTAR Trial]. We elucidated the mechanisms of combination therapy with the ARB (losartan, LOS) and long-acting and statin (simvastatin, SIM) for the treatment of load-induced heart failure. Salt-loaded Dahl salt-sensitive (DS) rats were treated with vehicle, LOS (5mg/kg/day), SIM (2mg/kg/day) and LOS + SIM for 16 weeks. LOS and SIM in combination improved LV dysfunction (ΔLV fractional shortening; LOS = 60%, SIM = 42%, LOS + SIM = 24%, p <0.05), limited LV hypertrophy (ΔLV septal thickness; LOS = −21%, SIM = −18%, LOS + SIM = −13%, p <0.05) and reduced cardiac fibrosis (ΔLV collagen density; LOS = −26%, SIM = −16%, LOS + SIM = −28%, p <0.05) more than LOS or SIM alone. Both Rho and matrix metalloprotease-9 (MMP-9) activity in LV tissue were increased in untreated DS rats, and LOS and SIM in combination decreased these changes more than did LOS and SIM monotherapies. We confirmed that the plasma level of Exp-3174 (E3174), a LOS metabolite and a potent inverse agonist of angiotensin II receptor type 1, was higher in rats treated with LOS and SIM in combination than in those treated with LOS alone (E3174/LOS ratio; LOS = 2.6 ± 0.3 vs. LOS + SIM = 3.2 ± 0.2, p <0.05). Next, to mimic the response of volume-overload heart failure in vitro , cultured neonatal rat cardiomyocytes (CMs) were cyclically stretched. Stretch-induced increased CM hypertrophy was suppressed by pretreatment with both SIM and E3174 more than by pretreatment with LOS, E3174, SIM, or LOS and SIM in combination. Mechanical stretch also induced activation of extracellular signal regulated kinase (ERK) and the stretch-induced ERK activation of CMs was also significantly suppressed by SIM + E3174. In conclusion, LOS and SIM had beneficial myocardial effects in rats with salt-sensitive hypertension, partly through promoting the accumulation of plasma E3174. SIM enhanced the myocardial protective effects of LOS through suppression of Rho and MMP-9 activity. Thus, a combination of ARB with statin has a promising potential as a therapeutic strategy for HF.

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