Anticholesteremic Agents ; adverse effects ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; adverse effects

Anticholesteremic Agents ; adverse effects ; Dose-Response Relationship, Drug ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; adverse effects ; Liver ; drug effects

BACKGROUNDResearches in arterial elasticity have increased over the past few years. We investigated the effects of simvastatin on vascular stiffness in fat fed rabbits by ultrasonography.

METHODSThirty rabbits were assigned randomly to 3 groups: normal control group (A), the cholesterol group (B), simvastatin group (C: high fat diet for 4 weeks and high fat diet + simvastatin for further 4 weeks). Stiffness coefficient, pressure strain elastic modulus and velocity of pulse waves in abdominal aorta and femoral artery were measured by ultrasonographic echo tracking at the end of the 4th and the 8th weeks.

RESULTSAt the end of the 4th week, stiffness coefficient, pressure strain elastic modulus and pulse wave velocity of femoral artery were significantly increased in group B compared with those in group A. Similarly, at the end of the 8th week, the same parameters of abdominal aorta were significantly increased in group B compared with those in group A. In contrast, stiffness coefficient, pressure strain elastic modulus and pulse wave velocity of femoral artery were significantly decreased in group C compared with those in group B, however, there was no significant difference in parameters of abdominal aorta between groups B and C.

CONCLUSIONShort term administration of simvastatin can improve the elasticity of femoral artery but not abdominal aorta.

Animals ; Anticholesteremic Agents ; therapeutic use ; Aorta, Abdominal ; drug effects ; Blood Flow Velocity ; drug effects ; Dietary Fats ; adverse effects ; Femoral Artery ; drug effects ; Rabbits ; Random Allocation ; Simvastatin ; therapeutic use

OBJECTIVETo evaluate the effects of policosanol on serum lipid and heme oxygenase-1 (HO-1) in patients with hyperlipidemia.

METHODSThis randomized, open study included 72 patients with hyperlipidemia. The patients were randomly assigned to treatment group (policosanol, 20 mg/d, n = 36) or placebo group (placebo, two tablets/d, n = 36). The levels of serum lipids, hypersensitive C-reactive protein (hs-CRP), HO-1 were assessed before and after 16 weeks treatment. Drug-induced adverse effects and events were recorded during the observation period. The serum HO-1 was measured by ELISA.

RESULTS(1) After 16 weeks, all parameters remained unchanged in the placebo group; the level of TC decreased from (7.01 ± 1.03) mmol/L to (5.66 ± 0.83) mmol/L (-19.4%, P < 0.01), the level of LDL-C decreased from (4.78 ± 0.72) mmol/L to (3.70 ± 0.69) mmol/L (-22.5%, P < 0.01) in the treatment group. TG and HDL-C levels remained unchanged (P > 0.05) while the level of HO-1 significantly decreased from (1.82 ± 1.08) µg/L to (1.45 ± 0.81) µg/L (P < 0.01) and the level of hs-CRP decreased from (3.40 ± 3.64) mg/L to (1.86 ± 2.02) mg/L (P < 0.01) in the treatment group. (2) Safety index was similar between placebo and treatment groups (P > 0.05) and there was no adverse events including allergic reaction, muscle pain in all subjects during the observation period.

CONCLUSIONThe short-term data obtained from this small hyperlipidemia patient cohort suggest that policosanol is a safe lipid-lowering and anti-inflammatory agent for hyperlipidemia patients.

Anti-Inflammatory Agents ; adverse effects ; therapeutic use ; Anticholesteremic Agents ; adverse effects ; therapeutic use ; Fatty Alcohols ; adverse effects ; therapeutic use ; Female ; Heme Oxygenase-1 ; metabolism ; Humans ; Hyperlipidemias ; blood ; drug therapy ; Lipids ; blood ; Male ; Middle Aged

Humans ; Cardiovascular Diseases/chemically induced* ; East Asian People ; Risk Factors ; Heart Disease Risk Factors ; Lipids ; Anticholesteremic Agents/adverse effects* ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Treatment Outcome

This paper presents a case of reversible dysphasia occurring in a patient prescribed atorvastatin in combination with indapamide. A milder dysphasia recurred with the prescription of rosuvastatin and was documented on clinical examination. This resolved following cessation of rosuvastatin. The case highlights both a need for a wider understanding of potential drug interactions through the CYP 450 system and for an increased awareness, questioning and reporting of drug side-effects.
Anticholesteremic Agents/adverse effects/*therapeutic use ; Antihypertensive Agents/therapeutic use ; Anxiety/diagnosis ; Aphasia/diagnosis/*etiology ; Cytochrome P-450 Enzyme System/metabolism ; Depression/diagnosis ; Drug Interactions ; Female ; Fluorobenzenes/adverse effects/*therapeutic use ; Heptanoic Acids/adverse effects/*therapeutic use ; Humans ; Hypercholesterolemia/drug therapy ; Indapamide/therapeutic use ; Middle Aged ; Pyrimidines/adverse effects/*therapeutic use ; Pyrroles/adverse effects/*therapeutic use ; Sulfonamides/adverse effects/*therapeutic use

OBJECTIVETo compare the efficacy and safety of atorvastatin, rosuvastatin and xuezhikang capsule in elderly.

METHODSA total of 314 60-to-94-year-old (average (73.6 ± 7.9) years old) patients who were given different doses and types of statins were divided into three groups: the atorvastatin group (108 patients), the rosuvastatin group (104 patients) and the xuezhikang capsule group (102 patients). The serum TG, TC, LDL-C, HDL-C,ALT and CK were examined before and after the treatment which lasted for at least 4 weeks. All patients were divided into moderate risk group (13, 12 and 21 patients respectively in 3 groups); high risk group (40, 44 and 48 patients respectively in 3 groups) and very high risk group (55, 48 and 33 patients respectively in 3 groups ) according to guidelines on prevention and treatment of dyslipidemia in chinese adults (2007 version). The rate of reaching target goal and the dose when reaching target levels in different risk stratification groups were calculated and compared.

RESULTSSerum TC, LDL-C and non-HDL-C were significantly reduced after the 4-week-treatment in all the three groups (P < 0.01). Serum LDL-C level before and after treatment were (3.14 ± 0.78)mmol/L vs. (2.14 ± 0.65)mmol/L in atorvastatin group (the arevage dose was (16.4 ± 4.8)mg/d), (2.92 ± 0.77)mmol/L vs. (1.96 ± 0.55)mmol/L in rosuvastatin group (the arevage dose was (8.7 ± 3.0) mg/d), and (2.70 ± 0.62)mmol/L vs. (2.16 ± 0.61) mmol/L in xuezhikang capsule group (the arevage dose was (0.9 ± 0.3) g/d ). Among all the three groups of patients, the cases of reaching target levels of LDL-C were 13, 11 and 20 in patients at moderate risk, were 38(95.0%), 38(86.4%) and 40 (83.3%) in patients at high risk, and were 22(40.0%), 30(62.5%) and 17(51.5%) in patients at very high risk. There were no statistical differences in the rate of reaching target levels of LDL-C, non-HDL-C and TC in the three groups and at different risks (P > 0.05). One patient in the atorvastatin group showed ALT level elevation >3 times of the upper limit of normal value, there was no patient with CK level elevation >5 times of the upper limit of normal value.

CONCLUSIONAtorvastatin, rosuvastatin and xuezhikang capsule at low dose and/or standard dose are effective and safety in elderly patients.

Aged ; Aged, 80 and over ; Anticholesteremic Agents ; Atorvastatin Calcium ; Cholesterol, LDL ; Dose-Response Relationship, Drug ; Dyslipidemias ; drug therapy ; Female ; Fluorobenzenes ; adverse effects ; therapeutic use ; Heptanoic Acids ; adverse effects ; therapeutic use ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; adverse effects ; therapeutic use ; Male ; Middle Aged ; Pyrimidines ; adverse effects ; therapeutic use ; Pyrroles ; adverse effects ; therapeutic use ; Rosuvastatin Calcium ; Sulfonamides ; adverse effects ; therapeutic use

OBJECTIVESThis study was designed to evaluate the efficacy and safety of rosuvastatin on treating Chinese patients with hypercholesterolemia.

METHODSThis randomized double-blind multi-center study enrolled the patients with LDL-C > or = 160 mg/dL but < 250 mg/dL and TG < 400 mg/dL after six-week dietary run-in. Patients were randomized to receive either rosuvastatin 10 mg/d (R) or atorvastatin (A) 10 mg/d in 2:1 ratio for 12 weeks. Patients with LDL-C levels not reaching goal defined by ATP III guideline in R group were titrated to 20 mg for additional 8 weeks.

RESULTSAltogether, 304 patients were included in the study, 201 patients in R group and 103 in A group. The ITT population is 290 and PP is 263. The LDL-C level decreased after 12 weeks in R group than that in A group, (45.6% vs 39.0%, P < 0.001). The rate reaching the target level defined by ATP III in R group tended to be higher than that in A group (78.0% vs 72.7%), especially in patients with high risk (56.5% vs 35%), however the difference did not reach statistical significance. The magnitudes of TG reduction (-22.8%), HDL-C (+6.6%) and ApoA-1 increase (+12.5%) in R group had no significant difference compared to those in A group (-16.6%, +4.3% and +9.8%, respectively). 29 patients were titrated to receive 20 mg of rosuvastatin. 10 of 22 patients reached the LDL-C target. There were no drug related SAE found during the study.

CONCLUSIONSThe efficacy of rosuvastatin in reducing LDL-C is more effective than atorvastatin in the same dose, however, the safety data is similar between them in the period of 3-month follow-up.

Adolescent ; Adult ; Aged ; Anticholesteremic Agents ; therapeutic use ; Asian Continental Ancestry Group ; Atorvastatin Calcium ; Double-Blind Method ; Female ; Fluorobenzenes ; adverse effects ; therapeutic use ; Heptanoic Acids ; therapeutic use ; Humans ; Hypercholesterolemia ; drug therapy ; Hypolipidemic Agents ; therapeutic use ; Male ; Middle Aged ; Pyrimidines ; adverse effects ; therapeutic use ; Pyrroles ; therapeutic use ; Rosuvastatin Calcium ; Sulfonamides ; adverse effects ; therapeutic use ; Young Adult

Aged ; Androgen Antagonists/adverse effects* ; Anticholesteremic Agents/therapeutic use* ; Cholesterol, HDL/blood* ; Cholesterol, LDL/blood* ; Humans ; Hypercholesterolemia/chemically induced* ; Lipids/blood* ; Male ; Middle Aged ; Prostatic Neoplasms/therapy* ; Retrospective Studies ; Testosterone/blood*

Matrix metalloproteinase-9 (MMP-9) may play an important role in emphysematous change in chronic obstructive pulmonary disease (COPD), one of the leading causes of mortality and morbidity worldwide. We previously reported that simvastatin, an inhibitor of HMG-CoA reductase, attenuates emphysematous change and MMP-9 induction in the lungs of rats exposed to cigarette smoke. However, it remained uncertain how cigarette smoke induced MMP-9 and how simvastatin inhibited cigarette smoke-induced MMP-9 expression in alveolar macrophages (AMs), a major source of MMP-9 in the lungs of COPD patients. Presently, we examined the related signaling for MMP-9 induction and the inhibitory mechanism of simvastatin on MMP-9 induction in AMs exposed to cigarette smoke extract (CSE). In isolated rat AMs, CSE induced MMP-9 expression and phosphorylation of ERK and Akt. A chemical inhibitor of MEK1/2 or PI3K reduced phosphorylation of ERK or Akt, respectively, and also inhibited CSE-mediated MMP-9 induction. Simvastatin reduced CSE-mediated MMP-9 induction, and simvastatin-mediated inhibition was reversed by farnesyl pyrophosphate (FPP) or geranylgeranyl pyrophosphate (GGPP). Similar to simvastatin, inhibition of FPP transferase or GGPP transferase suppressed CSE-mediated MMP-9 induction. Simvastatin attenuated CSE-mediated activation of RAS and phosphorylation of ERK, Akt, p65, IkappaB, and nuclear AP-1 or NF-kappaB activity. Taken together, these results suggest that simvastatin may inhibit CSE-mediated MMP-9 induction, primarily by blocking prenylation of RAS in the signaling pathways, in which Raf-MEK-ERK, PI3K/Akt, AP-1, and IkappaB-NF-kappaB are involved.
1-Phosphatidylinositol 3-Kinase/metabolism ; Alkyl and Aryl Transferases/metabolism ; Animals ; Anticholesteremic Agents/pharmacology ; Cells, Cultured ; Enzyme Inhibitors/metabolism/pharmacology ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Gene Expression Regulation, Enzymologic/*drug effects ; I-kappa B Kinase/antagonists & inhibitors/metabolism ; Macrophages, Alveolar/cytology/*drug effects/*enzymology ; Matrix Metalloproteinase 9/genetics/*metabolism ; Mitogen-Activated Protein Kinase Kinases/metabolism ; Polyisoprenyl Phosphates/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Rats ; Sesquiterpenes/metabolism ; Signal Transduction/physiology ; Simvastatin/*pharmacology ; Smoke/*adverse effects ; *Tobacco/adverse effects/chemistry