Effect of atorvastatin to RANKL/OPG system in patients with acute coronary syndrome

Background: The prominent effect of statin therapy is the inhibition of hydroxymethyl glutaryl-Coenzyme A (HMG-CoA) reductase. This enzyme decreases the mevalonate level and prevents the synthesis of isoprenoids. This inhibition alters osteoclast activity. Osteoprotegerin (OPG) acts as a decoy receptor of the receptor activator of nuclear factor kB (NF-kB) ligand (RANKL), which is a key regulator of osteoclastogenesis. Objective: The aim of this study is to evaluate the effect of atorvastatin on the RANKL/OPG system in patients with acute coronary syndrome. Material and Methods: We studied 22 patients (17 men and 5 women, age 61 ± 8 years) referred to Hospital Rio Hortega with a diagnosis of acute coronary syndrome. The following parameters were determined: osteocalcin, paratohormone, 25-vitamin D, RANKL, and osteoprotegerin. Deoxypiridinoline was determined in urine samples. The same parameters were determined after 12 months. The patients were treated with atorvastatin. Results: Atorvastatin resulted in plasmatic level decreases of osteocalcin (3.8 ± 2 pmol/L vs 2 ± 1 pmol/L; P=0.022), RANKL (0.17 ± 0.13 vs 0.01 ± 0.02; P=0.02), and RANKL/OPG (0.02 ± 0.02; P=0.04). Conclusions: Atorvastatin decreases RANKL and osteocalcin levels in patients with acute myocardial infarction. Atorvastatin may increase the bone mineral density by inhibing the resorption through RANKL/OPG system.