Influence Of Statins Research Articles

The Influence of Statin Medications on Prostate-specific Antigen Levels

Recent data suggest that statin use may be associated with a reduced risk of advanced prostate cancer. However, the influence of statins on prostate-specific antigen (PSA) levels and what effect this could potentially have on prostate cancer diagnosis are unknown. We conducted a longitudinal study of 1214 men who were prescribed a statin between 1990 and 2006 at the Durham Veterans Affairs Medical Center who were free of prostate cancer, had not undergone prostate surgery or taken medications known to alter androgen levels and who had at least one PSA value within 2 years before and at least one PSA value within 1 year after starting a statin. The change in PSA from before to after statin treatment was analyzed as a continuous variable using the Wilcoxon signed rank test. The association between change in PSA and change in cholesterol parameters (low-density lipoprotein [LDL], high-density lipoprotein [HDL], and total cholesterol) was analyzed using multivariate linear regression. All statistical tests were two-sided. Mean (SD) age when starting statins was 60.3 (8.3) years; median prestatin PSA concentration was 0.9 (1.9) ng/mL; and mean prestatin LDL cholesterol concentration was 144 (34) mg/dL. After starting a statin, the median LDL decline was 27.5%, and the median PSA decline was 4.1% (P < .001, for both comparisons). Changes in PSA concentration were strongly associated with statin dose and changes in LDL levels. For every 10% decrease in LDL after starting a statin, PSA levels declined by 1.64 (95 % confidence interval [CI] = 0.64% to 2.65%, p = .001). Among men most likely to be under consideration for prostate biopsy (prestatin PSA levels > or =2.5 ng/mL, n = 188), those with >41% declines in LDL (highest quartile) after starting a statin experienced a 17.4% (95% CI = 10.0% to 24.9%) decline in serum PSA. PSA levels declined by a statistically significant extent after initiation of statin treatment. The reduction was most pronounced among men with the largest LDL declines and those with PSA levels that would make them candidates for prostate biopsy. By lowering PSA levels, statins may complicate cancer detection, although further studies are needed to quantify the clinical significance of this effect.

Thienopyridine Resistance Among Patients Undergoing Intracoronary Stent Implantation and Treated With Dual Antiplatelet Therapy: Assessment of Some Modifying Factors

In this open, prospective study we assessed the prevalence of antiplatelet resistance among patients subjected to intracoronary stent implantation. In patients treated with aspirin + thienopyridine (N = 32), platelet reactivity index (PRI) significantly decreased after 2 and 7 days of dual antiplatelet treatment in comparison with the same patients on aspirin monotherapy (P<0.001, both). After 7 days of aspirin + thienopyridine treatment, insufficient antiplatelet response was observed in 28% (9/32) of the patients. High interindividual variability in response to aspirin + thienopyridine treatment emphasizes the significance of thienopyridine resistance, while the influence of statins on such a treatment should be reassessed.

Immediate effect of fluvastatin on lipid levels in acute coronary syndrome

It is widely assumed that acute benefit of statin therapy is mediated especially by non-lipid effects. The immediate influence of statins on lipid levels in patients with acute coronary syndrome (ACS) is, however, not clear. A total of 64 consecutive patients with ACS were randomized at admission to fluvastatin 80 mg (Group 1, N = 32) or standard therapy without statin (Group 2, N = 32). The levels of total cholesterol (TC), low-density-lipoprotein cholesterol (LDL-C), high-density-lipoprotein cholesterol (HDL-C), and triglycerides (TG) were examined at admission and after 24 h. Baseline characteristics were comparable in both groups. In Group 1, fluvastatin significantly decreased the levels of TC by 14.5%, LDL-C by 17.2%, and HDL-C by 10.0% (P < 0.001); TG were not influenced. In Group 2 only marginal reductions in TC (by 4.1%, P = 0.03) and HDL-C (by 7.5%, P < 0.01) were detected; the levels of LDL-C and TG were not changed. As compared with Group 2, in Group 1 the final levels of TC (P = 0.02) and LDL-C (P = 0.01) were significantly lower. Fluvastatin therapy, when started at admission in patients with ACS, significantly reduces TC and LDL-C already after 24 h. We suggest that the lipid-lowering effect of statins in the therapy of ACS is probably as prompt as non-lipid effects.

Influence of Statins on Perioperative Outcomes

Survey of Anesthesiology: April 2007 - Volume 51 - Issue 2 - p 97-98 doi: 10.1097/sa.0b013e318033652a

A medical therapy for aortic valve sclerosis and aortic valve stenosis? Rationale of the ASSIST study (Asymptomatic aortic Sclerosis/Stenosis: Influence of STatins): a large, observational, prospective, multicenter study of the Italian Society of Cardiovascular Echography

Progression of sclerosis and stenosis is substantially unpredictable in the individual patient: in some cases it is very slow, in others it is accelerated. In addition, different patterns of progression (linear and non-linear) are possible. It has been suggested that the aortic valve lesion can be considered a form within the spectrum of the same atherosclerotic disease. In this context it seemed reasonable to hypothesize that targeted medical therapy could retard the progression of the disease. In particular HMG-CoA reductase inhibitors (statins) and angiotensin-converting enzyme inhibitors have been tested. The first experimental and clinical studies are now available, even though they are not conclusive to date. Large, prospective, randomized trials are ideally needed, but they are quite difficult, if not even impossible, to realize in practice. The ASSIST study (Asymptomatic aortic Sclerosis/Stenosis: Influence of STatins) of the Italian Society of Cardiovascular Echography aims to create a large, prospective, observational investigation, involving many centers of echocardiography and thousands of patients, in order to provide from the real clinical world at least some of the answers to this unsolved question.

Influence of statins on postoperative wound complications after inguinal or ventral herniorrhaphy

The lipid-lowering agents, statins, are the most commonly prescribed class of drugs in the western world. Because of their widespread use, many patients undergo surgical procedures while on statins. Statins, in addition to cholesterol-lowering effects, also have anticoagulant, immunosuppressive, and antiproliferative properties that may affect the risk of local wound complications. This study investigated the relationship between statins and postoperative wound complications in a large cohort of patients undergoing inguinal or ventral hernia repair. Data mining was performed in the Veterans Integrated Service Network (VISN)16 Data Warehouse. This database contains clinical and demographic information about all veterans cared for at the ten VA Medical Centers that comprise the South Central VA Healthcare Network in the mid-south region of the US. Aggregate data (age, body mass index, smoking history, gender, race, history of diabetes, statin use, and postoperative wound complications) were obtained for all patients who underwent inguinal or ventral hernia repair during the period October 1, 1996-November 30, 2004. During the period of the query, 10,782 patients (10,676 male, 106 female), 1,242 (11.5%) of whom received statins, underwent herniorrhaphy. Statin use did not affect the risk of wound infection or delayed wound healing. Statin use was, however, associated with an increased rate of local postoperative bleeding complications (P=0.01). When the type of hernia, age, smoking, diabetes, and body mass index were included in a multivariate analysis, statins remained borderline significant as an independent predictor of wound hematoma/postoperative bleeding (P=0.04), odds ratio 1.6 (95% CI 1.03-2.44). Patients who undergo inguinal herniorrhaphy while on statins have an increased risk of postoperative wound hematoma/hemorrhage. Focus on additional factors that may affect the propensity to postoperative bleeding and on meticulous intraoperative hemostasis are particularly important in such patients.

The influence of statins on the free intracellular calcium concentration in human umbilical vein endothelial cells.

BackgroundStatins are cholesterol-lowering drugs that are widely used to reduce the risk of cardiac infarction. Their beneficial clinical effects, however, are not restricted to their influence on cholesterol production. As several studies have shown that they have a potency of relaxing blood vessels.MethodsWe measured the effects of statins on the intracellular free calcium concentration ([Ca2+]i) in human umbilical vein endothelial cells (HUVEC) after acute application and 24-h-preincubation of statins.ResultsIncubation of the cells for 24 h with cerivastatin or fluvastatin significantly increased the resting [Ca2+]i. For cerivastatin this effect manifested at a concentration of 1 μM. Increase of resting [Ca2+]i in the presence of cerivastatin also occurred when the nitric oxide synthase was inhibited. Transient Ca2+ release induced by histamine was not affected.ConclusionsThe increase of resting [Ca2+]i after incubation with cerivastatin or fluvastatin may provide an explanation for the direct effects of statins on the endothelial-dependent vasodilatation and restoration of endothelial activity in vivo.

M.566 Influence of statins on LDL in vivo peroxidation

M.566 Influence of statins on LDL in vivo peroxidation

M.566 Influence of statins on LDL in vivo peroxidation

M.566 Influence of statins on LDL in vivo peroxidation

Effect of HMG-CoA reductase inhibitors on proliferation and protein synthesis by rat hepatic stellate cells

Background/Aims: 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors called statins, have besides their cholesterol-lowering function, therapeutic value in conditions such as neo-angiogenesis and atherosclerosis. We investigated the effect of two statins on the proliferation rate and protein steady state levels of hepatic stellate cells (HSC). Methods: Cellular DNA synthesis under the influence of statins and/or platelet derived growth factor (PDGF) and mevalonate was evaluated by measuring BrdU incorporation. Synthesis of collagens type I, III, IV and fibronectin was quantified by ELISA. Additionally, we examined the influence of simvastatin on isoprenylation of Ras and RhoA proteins. Results: Lovastatin and simvastatin induced a dose-dependent inhibition of the proliferation rate of HSC. Subsequent addition of PDGF and/or mevalonate, after long-term exposure of simvastatin to HSC, did not reverse simvastatins' antiproliferative effect. Lovastatin and simvastatin reduced the protein steady state level of collagens type I (−40%), III (−45%) and IV (−27%). Membrane bound Ras steady state levels decreased under the influence of simvastatin. Membrane bound RhoA remained unaltered, whereas, cytosolic RhoA protein level was strongly reduced. Conclusions: Our data showed that lovastatin and simvastatin inhibited HSC proliferation and collagen steady state levels by mechanisms independent of their lipid reducing activities.

Possible influence of statins on the paraoxonase activity

Possible influence of statins on the paraoxonase activity

Inflammatory response in stable angina pectoris: The possible influence of statins

Inflammatory response in stable angina pectoris: The possible influence of statins