Vitamin D deficiency is a risk factor for osteoporosis and other chronic diseases, including type 1 diabetes, hypertension, metabolic syndrome, and ischemic heart disease. Cholesterol and vitamin D share the 7-dehydrocolesterol metabolic pathway. This study evaluated the possible effect of atorvastatin on vitamin D levels in patients with acute ischemic heart disease. Eighty-three patients (52 men and 31 women) with an acute coronary syndrome (75 with acute myocardial infarction and 8 with unstable angina) were included. After diagnosis, patients received atorvastatin as secondary prevention. Serum vitamin D was measured by high-performance liquid chromatography at baseline and at 12 months. Atorvastatin treatment produced a statistically significant decrease in cholesterol and triglyceride levels and an increase in vitamin D levels ( Vitamin D deficiency is a risk factor for osteoporosis and other chronic diseases, including type 1 diabetes, hypertension, metabolic syndrome, and ischemic heart disease. 1 Vitamin D is synthesized in the skin by ultraviolet radiation that acts on 7-dehydrocolesterol, which is hydroxylated into carbon-25 by 25-hydroxyvitamin D-1␣ hydroxylase or CYP27B1, an enzyme located in the mitochondria of the hepatocyte. The resulting metabolite, 25-hydroxyvitamin D, is the best way to measure individual vitamin D levels. 2 Cholesterol and vitamin D share the 7-dehydrocolesterol metabolic pathway. 3 Statins have beneficial effects on morbidity and mortality of patients with acute ischemic heart disease; these may be mediated by vitamin D. These patients have a greater prevalence of vitamin D deficiency and are often treated with statins as secondary prevention. 1 This led us to study the possible effect of atorvastatin on vitamin D levels in this group of patients. Increased levels of vitamin D could explain some of the beneficial effects of atorvastatin at the cardiovascular and bone metabolism levels that are unrelated to cholesterol levels. Methods and ResultsPatients hospitalized for an acute coronary syndrome, defined as high-risk unstable angina, non-ST-elevated myocardial infarction, or ST-elevated myocardial infarction, were eligible for inclusion. Eighty-three patients (52 men and 31 women) with an acute coronary syndrome (75 with acute myocardial infarction and 8 with unstable angina) were included. Patients were recruited at hospital admission. Exclusion criteria were alcoholism, neoplasia, hyperor hypocalcemia, and treatment with phosphocalcium metabolism-modifying drugs. After diagnosis, patients received atorvastatin as secondary prevention. Low (10 to 20 mg) and high (40 to 80 mg) doses were used according to baseline levels of cholesterol and triglycerides and index of vascular risk. Only patients completing follow-up were evaluated. A control group of 73 hypertensive patients (38 men and 35 women) not receiving treatment with statins was included.Blood samples were obtained after 8 or 9 hours of fasting. Total calcium, phosphorus, total cholesterol, and triglycerides were mea...

Adequate vitamin D levels are necessary for good vascular health. 1,25-dihydroxycholecalciferol activates CYP3A4, an enzyme of the cytochrome P450 system, which metabolizes atorvastatin to its main metabolites. The objective of this study was to evaluate the response of cholesterol and triglycerides to atorvastatin according to vitamin D levels. Sixty-three patients with acute myocardial infarction treated with low and high doses of atorvastatin were included. Levels of total cholesterol, triglycerides, HDL cholesterol, and LDL cholesterol were measured at baseline and at 12 months of follow-up. Baseline levels of 25-hydroxyvitamin D (25-OHD) were classified as deficient (<30 nmol/L), insufficient (30–50 nmol/L), and normal (>50 nmol/L). In patients with 25-OHD <30 nmol/L, there were no significant changes in levels of total cholesterol (173 ± 47 mg/dL versus 164 ± 51 mg/dL), triglycerides (151 ± 49 mg/dL versus 177 ± 94 mg/dL), and LDL cholesterol (111 ± 48 mg/dL versus 92 45 ± mg/dL); whereas patients with insufficient (30–50 nmol/L) and normal vitamin D (>50 nmol/L) had a good response to atorvastatin. We suggest that vitamin D concentrations >30 nmol/L may be required for atorvastatin to reduce lipid levels in patients with acute myocardial infarction.

The atherosclerosis that appears in coronary, cerebrovascular and peripheral arterial disease is responsible for most cardiovascular diseases. It is characterized by chronic arterial inflammation caused and exacerbated by disorders of the lipidic metabolism and other clearly identified risk factors [1]. Calcification, which is initiated by an active process in which inflammatory cytokines and other mediators that regulate the phospho-calcium metabolism intervene, is characteristic of atherosclerosis [2]. These mechanisms can intervene in an opposite phenomenon that takes place at the level of the bone characterized by a reduction in bone mineral content and alterations in the microarchitecture that define osteoporosis. The association between the two diseases, which share mechanisms but have a different expression, is noteworthy.The Wnt-LPR5 signalling pathway plays an important role in skeletal homeostasis, especially in regulating osteoblastic activity. It is formed by a series of elements, WnT ligands, and a receptor complex, which is constituted by the Frizzled protein and . Recently, a missense mutation in LPR6 that codifies a coreceptor has been described in an Iranian family. Cysteine is replaced by arginine, damaging in vitro Wnt signalling. These patients have a greater risk of coronary disease, low bone mineral density (BMD) and osteoporotic fracture, suggesting that the two diseases may be pleiotropic consequences of the alteration of the Wnt signalling pathway [4].Wnt signalling pathway activation is regulated by various inhibitors, including DKK1, which interacts with a transmembrane protein, kremen, to prevent the activation of the LPR5 coreceptor, leading to internalization of the DKK/LPR complex with a loss of the Wnt signal [5]. Studies in experimental animals have shown a possible role of DKK1 in the regulation of bone homeostasis, although there are few studies in humans and in patients with acute coronary syndrome.The objective of this study was to evaluate DKK1 levels in patients with acute myocardial infarction, the response to atorvastatin and the relationship with bone mass.Patients with acute myocardial infarction were included. Exclusion criteria were chronic alcohol abuse, neoplasia, chronic renal failure, hyper-and hypocalcaemia, hyperparathyroidism and the use of drugs modifying BMD. Patients were allocated to low (10-20 mg) and high doses (40-80 mg) of atorvastatin according to baseline levels of cholesterol and triglycerides and the index of vascular risk. Measurements were made at baseline and at 12 months of follow up. The control group was patients of the same age and sex without coronary disease.Blood samples were obtained after 8 fasting hours. DKK1 was determined by immunoassay (Biomedica, Wien, Austria) with a 9% interassay coefficient of variation. Densitometric studies were conducted in the lumbar spine (L2-L4) and femoral neck and trochanter using an X-ray densitometer (DXA, Lunar Corporation, Madison, Wisconsin, USA).The results are expressed as mean± standard deviation....

No abstract