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PubMed2003

Early use of statins in acute coronary syndromes.

This review examines the use of statin medications early in the clinical course of acute coronary syndrome (ACS). Available data demonstrate that there are clear clinical benefits to this practice. Numerous previous studies have documented the primary and secondary benefits of statins in the prevention of coronary events. Recent trials show that when statins are used during hospital admissions for ACS, patients experience decreased recurrent myocardial infarction, lower death rates, and fewer repeat hospitalizations for ischemia or revascularization. Several studies suggest that the positive effects of statins on plaque stabilization, inflammation, thrombosis, and endothelial function may be independent of lipid levels. There is also an emerging view that beneficial lipid-lowering with statins in high-risk patients has no lower limit. This information suggests that all patients admitted for ACS should be treated with statins, regardless of cholesterol levels.

Acute Disease↗
PubMed2005

Pharmacogenetics of response to statins: where do we stand?

Cardiovascular disease is one of the leading causes of death, especially in developed countries. Blood cholesterol lowering by way of statin therapy is a common risk-lowering therapy. The risk reduction for coronary artery disease for patients using statins is 27%. These reductions, however, are average effects for all patients included in the trials. There is notable interindividual variation in response to statins, and the origins of this variation are poorly understood. Pharmacogenetics seeks to determine the role of genetic factors in variation of drug response. In patients with primary hypercholesterolemia, 23 studies have examined the effects of genetic polymorphisms at 20 different loci on the lipid response to statin treatment, and 18 studies examined genetic polymorphisms involved in the benefits of statin therapy in the prevention of cardiovascular disease. Even though many studies have been performed, few results have been replicated. It is our contention that larger sample sizes and consideration of multiple genes are needed in the field of pharmacogenetics of statin response.

Carrier Proteins↗
PubMed2002

Early use of statins in acute coronary syndromes.

This review examines the use of HMG-CoA reductase inhibitor (statin) medications early in the clinical course of acute coronary syndrome. Available data demonstrate that there are clear clinical benefits to this practice. Numerous previous studies have documented the primary and secondary benefits of statins in the prevention of coronary events. Recent trials show that when statins are used during hospital admissions for acute coronary syndrome (ACS), patients experience decreased recurrent myocardial infarction, lower death rates, and fewer repeat hospitalizations for ischemia or revascularization. Several studies suggest that the positive effects of statins on plaque stabilization, inflammation, thrombosis, and endothelial function may be independent of lipid levels. There is also an emerging view that beneficial lipid-lowering with statins in high-risk patients has no lower limit. This information suggests that all patients admitted for ACS should be treated with statins, regardless of cholesterol levels.

Acute Disease↗
PubMed1992

Expression of the non-proliferation-specific protein, statin, in grey matter neuroglia of the aging rat brain.

The monoclonal antibody, S-44, identifies statin, a 57 kDa nuclear protein which appears to be expressed exclusively in non-proliferating cells. We previously demonstrated that in the aging rat corpus callosum approximately one third of neuroglia are statin-negative, suggesting the existence of an unexpectedly large cycling glial compartment. In the present study, double-labeling of individual cultured astroglia with [3H]thymidine and the S-44 antibody provided direct evidence for the non-proliferative status of statin-positive cells. The S-44 antibody was used to immuno-localize statin and thereby determine growth fractions for neuroglia in various grey matter regions of 3-, 18-, and 33-month-old rats. The proportion of statin-negative (cycling) cells for the three ages combined ranged from about 24% in the molecular layer of the dentate gyrus to 38% in the molecular layer of the parietal cortex. In most regions surveyed total glial counts and proportions of statin-positive and -negative cells did not vary significantly as a function of advancing age. These results suggest that (i) as in corpus callosum, pools of cycling neuroglia in various grey matter regions are far in excess of those previously predicted by S-phase labeling with [3H]thymidine or BUdR, and (ii) ratios of proliferating-to-quiescent neuroglia are tightly regulated over much of the animal's adult life span. These conserved ratios may be used as markers of normal CNS senescence, and deviations thereof may indicate the presence and extent of intervening neuropathologic processes.

Aging↗
PubMed2005

Lipid-independent effects of statins on endothelial function and bioavailability of nitric oxide in hypercholesterolemic patients.

BACKGROUND: Experimental evidence suggests a lipid-independent effect of statins on endothelial function and nitric oxide (NO) availability in humans. We investigated whether improvement in NO availability in hypercholesterolemia can be achieved rapidly with statins before lipid-lowering therapy is complete. METHODS: We studied 41 patients (52 +/- 11 years) with low-density lipoprotein (LDL) cholesterol > or = 130 mg/dL (179 +/- 45 mg/dL) randomly assigned to treatment either with atorvastatin (20 mg/day) or cerivastatin (0.4 mg/day). Endothelium-dependent vasodilation of the forearm vasculature was measured by plethysmography and intra-arterial infusion of acetylcholine (ACh) after 3 days (n = 18) and 14 days (n = 39) of treatment. NO availability and oxidative stress were assessed by coinfusion of l-NMMA and vitamin C. RESULTS: After 3 days of treatment, LDL-cholesterol decreased by 11.9% with a further decrease to 29.6% after 14 days ( P < .001). Endothelium-dependent vasodilation improved by +46.7% after 3 days of statin therapy compared with before therapy (ACh 48 microg/min: +15.7 +/- 10.6 vs +10.7 +/- 10.8 mL/min per 100 mL, P < .05). No further improvement in endothelium-dependent vasodilation (+42.7% compared with before therapy) could be demonstrated after 14 days of treatment (ACh 48 microg/min: +17.7 +/- 10.3 vs +12.4 +/- 9.3 mL/min per 100 mL before therapy, P < .001). Coinfusion of ACh plus vitamin C was able to improve endothelium-dependent vasodilation before but not after 3 or 14 days of statin therapy either. The improvement in endothelium-dependent vasodilation after therapy was no longer observed when the NO-synthase inhibitor l-NMMA was coinfused together with ACh. CONCLUSIONS: Short-term lipid-lowering therapy with statins is able to improve endothelial function and NO availability almost completely after 3 days in hypercholesterolemic patients probably by decreasing oxidative stress. This improvement seems to be more rapid than the accompanying decline in LDL-cholesterol and not related to these lipid changes. This finding can support the concept of lipid-independent effects of statins in humans.

Acetylcholine↗
PubMed2007

Therapy with angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, and statins: no effect on ablation outcome after ablation of atrial fibrillation.

BACKGROUND: The renin-angiotensin-aldosterone system and inflammation are supposed to play a key role in the pathogenesis of atrial fibrillation (AF). This retrospective clinical study was intended to assess the influence of drugs with antiinflammatory and/or renin-angiotensin-aldosterone system-modulating properties, namely angiotensin-converting enzyme inhibitors (ACE-Is), angiotensin II receptor blockers (ARBs), and statins, on AF-free survival after AF ablation. METHODS: The study included 234 patients (23-80 years; 71.8% men) with drug-resistant paroxysmal (n = 165) or persistent AF (n = 69) who either underwent a Lasso-guided segmental pulmonary vein isolation (n = 83) or a CARTO-guided left atrial circumferential ablation (n = 151). Treatment with statins (n = 113), ACE-Is, or ARBs (n = 124), or a combination of a statin and an ACE-I or ARB (n = 75) was started >3 months before ablation and was continued during follow-up. RESULTS: After a median follow-up of 12.7 months, 64% of patients with paroxysmal and 45% of patients with persistent AF were free of AF. Statin use (hazard ratio [HR], 1.06; P = .79), ACE-I or ARB use (HR, 1.12; P = .59), and their combined use (statin + ACE-I/ARB; HR, 1.17; P = .54) did not significantly influence ablation outcome as assessed by Cox regression analysis. In addition, after multivariate adjustment for potential confounders, the examined drugs did not significantly affect ablation outcome. Ablation induced an acute up-regulation of C-reactive protein levels (preablation vs 48 hours postablation, 5.9 +/- 8.1 vs 33.7 +/- 30 mg/L; P < .001) and other inflammatory markers. The examined drugs did not significantly alter baseline levels or ablation-induced up-regulation of inflammatory markers. CONCLUSIONS: The routine use of statins, ACE-Is, or ARBs did not result in an improved outcome of AF ablation.

Adult↗
PubMed2004

Statin and aspirin therapy are associated with decreased rates of choroidal neovascularization among patients with age-related macular degeneration.

PURPOSE: To investigate the relationship between statin and aspirin use and the risk of choroidal neovascularization (CNV) in patients with age-related macular degeneration (AMD). DESIGN: Retrospective consecutive case series. METHODS: All patients 60 years and older with AMD who were seen between January 1, 1990, and March 1, 2003, at the San Francisco Veterans Affairs Hospital Eye Clinic with fundus photographs were included. Patients with other diagnoses predisposing to CNV or incomplete medical records were excluded. The main outcome measure was angiographically evident CNV. Diagnosis was based on review of fundus photographs and fluorescein angiograms in masked fashion; medical records were reviewed for variables possibly predisposing to CNV or statin use. For patients with CNV, age of onset was recorded; those without CNV were treated as censored. Age-related macular degeneration disease status and time of onset of CNV was compared between patients treated or not treated with statins for at least 6 months. RESULTS: Of 326 patients with AMD, 104 had CNV, 204 had dry AMD, and 18 had geographic atrophy (GA). Of CNV subjects, 21 (20%) used statins, compared with 77 (38%) of dry AMD subjects without GA and 6 (33%) of controls with GA (hazard ratio = 0.51, 95% confidence interval (CI) = 0.31-0.86, P =.01). Aspirin use was also significantly associated with decreased rates of CNV; 62 CNV subjects (60%) used aspirin, compared with 154 (75%) dry AMD subjects without GA or 12 (67%) with GA (hazard ratio = 0.63, 95% CI = 0.40-0.98, P =.04). CONCLUSIONS: Therapy with statins or aspirin is associated with decreased rates of CNV among AMD patients. Additional study with a prospective and/or randomized trial of statin and aspirin use in AMD patients is warranted.

Age of Onset↗
PubMed2003

A propensity score-matched cohort study of the effect of statins, mainly fluvastatin, on the occurrence of acute myocardial infarction.

This investigation quantified the effect of statins on acute myocardial infarction (AMI) in an observational setting where fluvastatin represented most of the statin use. The study applied propensity scores to match statin initiators to statin noninitiators and followed them for the occurrence of AMI. Serum low-density lipoprotein levels were reduced by statin therapy, and there were fewer incidents of AMI in statin initiators than in noninitiators.

Cholesterol, LDL↗
PubMed2004

Comparisons of effects of statins (atorvastatin, fluvastatin, lovastatin, pravastatin, and simvastatin) on fasting and postprandial lipoproteins in patients with coronary heart disease versus control subjects.

The effects of atorvastatin at 20, 40, and 80 mg/day on plasma lipoprotein subspecies were examined in a randomized, placebo-controlled fashion over 36 weeks in 97 patients with coronary heart disease (CHD) with low-density lipoprotein (LDL) cholesterol levels of >130 mg/dl and compared directly with the effects of fluvastatin (n = 28), pravastatin (n = 22), lovastatin (n = 24), and simvastatin (n = 25). The effects of placebo and 40 mg/day of each statin were also examined in subjects with CHD with subjects in the fasting state and in the fed state 4 hours after a meal rich in saturated fat and cholesterol and compared with results in age- and gender-matched control subjects. At all doses tested in the fasting and fed states, atorvastatin was significantly (p <0.01) more effective in lowering LDL cholesterol and non-high-density lipoprotein (HDL) cholesterol than all other statins, and significantly (p <0.05) more effective than all statins, except for simvastatin, in lowering triglyceride and remnant lipoprotein (RLP) cholesterol. At 40 mg/day in the fasting state, atorvastatin was significantly (p <0.01) more effective than all statins, except for lovastatin and simvastatin, in lowering cholesterol levels in small LDL, and was significantly (p <0.05) more effective than all statins, except for simvastatin, in increasing cholesterol in large HDL and in lowering LDL particle numbers. Our data indicate that atorvastatin was the most effective statin tested in lowering cholesterol in LDL, non-HDL, and RLP in the fasting and fed states, and getting patients with CHD to established goals, with fluvastatin, pravastatin, lovastatin, and simvastatin having about 33%, 50%, 60%, and 85% of the efficacy of atorvastatin, respectively, at the same dose in the same patients.

Anticholesteremic Agents↗
PubMed2005

Statins and postoperative risk of atrial fibrillation following coronary artery bypass grafting.

Atrial fibrillation (AF) is a common complication after coronary artery bypass grafting. Atrial remodeling has been observed in AF and has been associated with the development of this arrhythmia. Because 3-hydroxy-3-methylglutaryl coenzyme A inhibitors (statins) have been demonstrated to modify remodeling, we hypothesized a protective role of statins against postoperative AF. We also hypothesized that extracellular matrix turnover and brain natriuretic peptide (BNP) might be related to such atrial remodeling. We studied 234 consecutive patients who underwent coronary artery bypass grafting (173 men; 65 +/- 9 years of age) in whom the occurrence of postoperative AF was monitored. In a subgroup of 66 patients, we measured plasma levels of matrix metalloproteinase-1 (MMP-1), its inhibitor, tissue inhibitor matrix metalloproteinase-1 (TIMP-1; as indexes of extracellular matrix remodeling), and N-terminus pro-BNP (related to left ventricular function) at baseline and at 24 hours after surgery. Of 234 patients, 66 (28.2%) developed postoperative AF. In multivariate analysis, previous AF was related to an increase in the development of AF (odds ratio 11.92, 95% confidence interval 2.37 to 59.98, p = 0.026), whereas statin use was related to a decrease in arrhythmia (odds ratio 0.52, 95% confidence interval 0.28 to 0.96, p = 0.038). A higher TIMP-1/MMP-1 ratio at 24 hours after surgery was present in those who did not develop postoperative AF (p = 0.043). Statin use was associated with increased TIMP-1 levels and TIMP-1/MMP-1 ratio (p = 0.027 and 0.036, respectively). No significant relations to N-terminus pro-BNP were seen. In conclusion, previous AF and nonuse of statins are significantly associated with AF after coronary artery bypass grafting. Statin use may be protective against AF after coronary artery bypass grafting, possibly due to alterations in the extracellular matrix and remodeling after coronary artery bypass grafting.

Aged↗
PubMed2006

Effects of statins on renal function after aortic cross clamping during major vascular surgery.

Ischemic reperfusion injury is an important cause of renal dysfunction after major vascular surgery and increases postoperative morbidity and mortality. The aim of the present study was to assess the effect of statins on renal function in patients at high risk for renal dysfunction, that is, those who underwent suprarenal aortic cross clamping-declamping. Seventy-seven patients (28 statin users, 57 men; mean age 69 +/- 8 years) with normal preoperative renal function requiring suprarenal aortic cross clamping-declamping during vascular surgery from 1995 to 2005 were studied. Creatinine levels were obtained before surgery and on days 1, 2, 3, 7, and 30 after surgery. An analysis-of-variance model for repeated measurements was applied to compare creatinine levels between statin users and nonusers, with adjustment for clamping time and blood loss. There were no differences in baseline clinical characteristics, preoperative creatinine levels (0.93 vs 0.96 mg/dl, p = 0.59), and glomerular filtration rate (79 vs 73 ml/min, p = 0.1). Postoperative creatinine levels during the 30 days after surgery were significantly lower in statin users than in nonusers (analysis-of-variance p <0.01, 1.17 vs 1.98 mg/dl). Postoperative hemodialysis was required (temporarily) in 7 patients (9.1%), all statin nonusers. These findings suggest an association between statin use and preserved renal function after suprarenal aortic clamping.

Aged↗
PubMed2006

Statin safety and drug interactions: clinical implications.

The risks of muscle adverse events related to use of the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, or statins, increase significantly with the addition of interacting drugs to a patient's therapy. The mechanism for most statin drug interactions involves the cytochrome P-450 system, which provides an indication of which drugs may interact. However, it is difficult to predict the probability of a drug interaction in a given patient because there are individual differences in sensitivity to increased statin drug levels. Drug metabolism studies show simvastatin and lovastatin to be especially sensitive to the inhibiting effects of other drugs on the cytochrome P-450 3A4 (CYP3A4) isoenzyme. Atorvastatin metabolism is less affected by inhibitors of this isoenzyme. Case reports, postmarketing surveillance, and clinical trial data demonstrate the clinical effect of CYP3A4 inhibitors on statins. Also, through possible inhibition of statin biliary excretion and glucuronidation, gemfibrozil given concomitantly with rosuvastatin, lovastatin, and simvastatin significantly increases the risk of myopathy and rhabdomyolysis, a potentially life-threatening consequence of statin drug interactions.

Cytochrome P-450 Enzyme System↗
PubMed2006

Statin safety: an appraisal from the adverse event reporting system.

The adverse event (AE) profiles of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor (statin) agents are of great interest, in particular the most recently approved statin, rosuvastatin. The forwarding of reports of AEs has been shown to be influenced by several reporting biases, including secular trend, the new drug reporting effect, product withdrawals, and publicity. Comparative assessments that use AE reporting rates are difficult to interpret under these circumstances, because such effects can themselves lead to marked increases in AE reporting. Consequently, many comparative reporting rate analyses are best carried out in conjunction with other metrics that put reporting burden into context, such as report proportion. All-AE reporting rates showed a temporal profile that resembled those of other statins when marketing cycle and secular trend were taken into account. A before-and-after cerivastatin withdrawal comparison showed a substantial increase in the reporting of AEs of interest for the statin class overall. Report proportion analyses indicated that the burden of rosuvastatin-associated AEs was similar to that for other statin agents. Analyses of monthly reporting rates showed that the reporting of rosuvastatin-associated rhabdomyolysis and renal failure have increased following AE-specific mass media publicity. Postrosuvastatin AE reporting patterns were comparable to those seen with other statins and did not resemble cerivastatin.

Adverse Drug Reaction Reporting Systems↗
PubMed2006

Relation of preprocedural statin therapy to in-hospital procedural complications following percutaneous coronary interventions in patients with hyperlipidemia.

We investigated whether the observed protective effect of hyperlipidemia is stronger in patients who take statins and, if so, whether that effect is likely due to patient characteristics associated with statin use. In-hospital complications and long-term outcomes of patients with hyperlipidemia (cholesterol level > or = 240 mg/dl) undergoing percutaneous coronary interventions (PCI) on statins (group Ia, n = 2,052) and not on statins (group Ib, n = 1,650) were compared with 726 patients with lower cholesterol levels (group II). Despite a higher prevalence of co-morbidities and worse angiographic characteristics in patients with hyperlipidemia, patients in group Ia had significantly lower in-hospital mortality (0% vs 2% in the other 2 groups, p < 0.001), a lower increase in the postprocedure creatine kinase-MB fraction (14% vs 27% in group Ib and 28% in group II, p < 0.001), and fewer PCI complications (15% vs 30% in groups Ib and II, p < 0.001). After adjustment, patients in group Ia had a significant decrease in complications (odds ratio 0.72, 95% confidence interval 0.65 to 0.92, p = 0.009). In contrast, those in group Ib had outcomes similar to those of patients with lower cholesterol. After application of propensity analysis to adjust for the likelihood of receiving statins based on clinical, angiographic, and procedural characteristics, group Ia had fewer in-hospital complications (odds ratio 0.75, 95% confidence interval 0.62 to 0.90, p = 0.002) and lower in-hospital mortality (odds ratio 0.32, 95% confidence interval 0.12 to 0.84, p = 0.021). After successful PCI, overall survival after dismissal and survival free of myocardial infarction and target vessel revascularization were similar. In conclusion, hyperlipidemia per se is not associated with lower in-hospital complications after PCI. The benefit is largely limited to patients on statin treatment.

Aged↗
PubMed2006

Relation of serum total cholesterol, C-reactive protein levels, and statin therapy to survival in heart failure.

Although increased cholesterol levels predict mortality in patients with coronary artery disease, it is unclear whether hypercholesterolemia is associated with adverse survival in patients with heart failure. A cohort of subjects derived from the Intermountain Heart Collaborative Study Registry (1993 to 2003) who had ejection fractions < or = 40% or clinical diagnoses of heart failure and long-term follow-up for death were studied (n = 1,646). Total cholesterol (TC) was divided into quartiles: quartile 1, < 141.3 mg/dl; quartile 2, 141.3 to 167.9 mg/dl; quartile 3, 168.0 to 201.0 mg/dl; and quartile 4, > 201.0 mg/dl. Multivariate Cox regression models were used to evaluate the associations of cholesterol, statin therapy, and C-reactive protein to mortality. The mean age was 65.5 years; 65% of the subjects were men and 65% had coronary artery disease. Although 53% were using statins, statin use was not different across TC quartiles. Average time to death was 2.4 years (maximum 10). Mortality for quartile 4 versus quartile 1 was not different (hazard ratio [HR] 1.12, p = 0.52); mortality was reduced for quartile 3 versus quartile 1 (HR 0.66, p = 0.027) and tended to be reduced for quartile 2 versus quartile 1 (HR 0.77, p = 0.14). Subanalysis of patients not using statins (n = 737, death = 20.2%) found no association between TC and survival (for quartile 3 vs quartile 1, HR 0.97, p = 0.89), but for patients using statins (n = 848, death = 16.3%), the effect was even greater for quartile 3 versus quartile 1 (HR 0.40, p = 0.002) than in the overall population. Nonsurvivors had higher levels of C-reactive protein than survivors. In conclusion, elevated TC appears to be associated with improved survival. The effect was stronger in patients receiving statin therapy, but the cause of this differential effect is uncertain.

Aged↗
PubMed2006

Molecular basis of differences among statins and a comparison with antioxidant vitamins.

Although all statin drugs lower levels of circulating low-density lipoprotein cholesterol by inhibiting 3-hydroxy-3-methylglutaryl coenzyme A, molecular differences among statins affect their metabolism, solubility, and intramembrane localization, which in turn is likely to influence their efficacy and safety. In addition, these properties may have a differential impact on the pleiotropic effects of statins, including their ability to improve endothelial function and to affect proliferation and apoptosis in vascular tissues. Many pleiotropic effects of statins appear to be due to inhibition of small guanosine triphosphate-binding proteins and/or restoration of nitric oxide bioavailability, and atorvastatin metabolites may also directly protect vascular tissues from oxidative damage. The possibility of cardiovascular benefits from antioxidant effects of atorvastatin metabolites contrasts with the lack of benefits seen in most studies of antioxidant vitamins. This article reviews some of the differences in pleiotropic effects of statins and assesses the contribution of their solubility and membrane localization as the possible basis for these differences. In addition, the possibility that statin benefits on stroke reflect pleiotropic effects is reviewed. Finally, possible reasons for differences between the effects of atorvastatin metabolites and antioxidant vitamins are considered.

Antioxidants↗
PubMed2004

Association between long-term statin use and mortality after successful abdominal aortic aneurysm surgery.

PURPOSE: To assess the potential long-term beneficial effects of statin use after successful abdominal aortic surgery. METHODS: Between 1991 and 2001, 570 patients underwent abdominal aortic aneurysm repair at the Erasmus Medical Center. Of the 519 patients (91%) who survived surgery beyond 30 days, 510 (98%) were followed for a median of 4.7 years (interquartile range, 2.7 to 7.3 years). These patients were evaluated for use of statins and beta-blockers, and for clinical risk factors (e.g., advanced age; prior myocardial infarction; diabetes mellitus; renal dysfunction; chronic pulmonary disease; history of heart failure, stroke, or angina), and their association with all-cause and cardiovascular mortality. RESULTS: A total of 205 patients (40%) died during follow-up; 140 due to cardiovascular causes. The incidence of all-cause (18% [27/154] vs. 50% [178/356], P <0.001) and cardiovascular (11% [17/154] vs. 34% [122/356], P <0.001) mortality was significantly lower in statin users than in nonstatin users. After adjusting for clinical risk factors and beta-blocker use, the association between statin use and reduced all-cause (hazard ratio [HR] = 0.4; 95% confidence interval [CI]: 0.3 to 0.6; P <0.001) and cardiovascular (HR = 0.3; 95% CI: 0.2 to 0.6; P <0.001) mortality persisted. Beta-blocker use was also associated with a significant reduction in all-cause (HR = 0.6; 95% CI: 0.5 to 0.9; P = 0.003) and cardiovascular (HR = 0.7; 95% CI: 0.4 to 0.9; P = 0.03) mortality. There was no evidence of an association between statin use and all-cause and cardiovascular mortality according to beta-blocker use or clinical risk factors. CONCLUSION: Long-term statin use is associated with reduced all-cause and cardiovascular mortality irrespective of clinical risk factors and beta-blocker use.

Adrenergic beta-Antagonists↗
PubMed2004

Statin-induced immunomodulatory effects on human T cells in vivo.

Statins are widely used for treatment of hypercholesterolemia. Recent experimental studies revealed that these drugs also exert anti-inflammatory effects. The aim of this study was to assess immunomodulatory effects of statins in humans in vivo. Twenty-seven healthy volunteers were analyzed for serum cytokines and acute phase proteins, HLA-DR and CD38 expression on T cells and superantigen-mediated T cell activation ex vivo before and after 14 days of statin treatment. First, simvastatin 40 mg was compared to atorvastatin 20 mg. Second, two different doses of simvastatin (20 and 40 mg) were tested. Atorvastatin treatment led to a significant down-regulation of HLA-DR and the CD38 activation marker on peripheral T cells, whereas simvastatin up-regulated both of these molecules. In contrast, superantigen-mediated T cell activation was inhibited by simvastatin and enhanced by atorvastatin. No significant effect of statin treatment on inflammatory serum markers was detected. Thus, immunomodulatory effects of statins on human T cells are first demonstrated in vivo and are differentially induced by two different statins: atorvastatin led to a major histocompatibility class II (MHC II) antigens down-regulation and may therefore be investigated for treatment of chronic transplant rejection; simvastatin inhibited superantigen-mediated T cell activation, which might explain reduced mortality of simvastatin-treated patients with staphylococcal bacteremia.

ADP-ribosyl Cyclase↗