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PubMed2004

Statins and the myocardium.

Cardiac hypertrophy and heart failure are leading causes of morbidity and mortality worldwide. The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, or statins, have been shown to inhibit cardiac hypertrophy and improve symptoms of heart failure by cholesterol-independent mechanisms. Statins block the isoprenylation and function of members of the Rho GTPase family, such as Rac1 and RhoA. Because Rac1 is a requisite component of NADPH oxidase, which is a major source of reactive oxygen species in cardiovascular cells, the ability of statins to inhibit Rac1-mediated oxidative stress contributes importantly to their inhibitory effects on cardiac hypertrophy. Furthermore, inhibition of RhoA by statins leads to the activation of protein kinase B/Akt and upregulation of Type 3 nitric oxide synthase in the endothelium and the heart. This activation and upregulation results in increased angiogenesis and myocardial perfusion, decreased myocardial apoptosis, and improvement in endothelial and cardiac function. Because these effects of statins occur independent of cholesterol lowering, statins may have therapeutic benefits in nonhyperlipidemic patients with cardiac hypertrophy and heart failure.

Animals↗
PubMed2004

The pro- and antiangiogenic effects of statins.

Clinical studies indicate that 3-hydroxyl-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor (statin) therapy has a cardiovascular protective activity that may result from an improvement in endothelial function. Experimental studies have shown that statins protect against ischaemia-reperfusion injury of the heart and stimulate the growth of new blood vessels in ischemic limbs of normocholesterolemic animals. The mechanisms underlying these serum lipid-independent effects of statins are not completely understood, but there is increasing evidence that they improve endothelial function through molecular mechanisms that mediate an increase in endothelium-derived nitric oxide. Recent research has revealed a link between statins and the serine/threonine protein kinase Akt that regulates multiple angiogenic processes in endothelial cells, including the generation of nitrous oxide. In contrast to these data, it has also been reported that higher doses of statins inhibit endothelial cell migration and angiogenesis. Thus, further studies on the actions of statins may lead to the identification of new pharmacological targets for the control of blood vessel growth.

Animals↗
PubMed2004

Statins and cardiac allograft vasculopathy after heart transplantation.

Coronary artery disease in the transplanted heart, also known as cardiac allograft vasculopathy, is one of the major causes of mortality late after heart transplantation. There are multiple immune and nonimmune risk factors associated with this disease process, one of which is hyperlipidemia. Use of lipid-lowering agents, specifically 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) was initially reported to have outcomes benefit and possibly immunosuppressive effects in a single-center study of heart transplant recipients. Other subsequent studies have supported this beneficial effect. Hyperlipidemia is associated with immune activity, particularly with respect to oxidation-sensitive signaling pathways. By lowering lipids, statins can ameliorate this immune activity, but it has been a matter of contention as to whether statins have cholesterol-independent immune-modulating effects. In two recent papers, cholesterol-independent immune effects of statins have been reported, including repressed induction of major histocompatibility complex class II by interferon-gamma, and selective blocking of leukocyte function antigen 1, both of which reduce the activation of T lymphocytes. The clinical reports demonstrating outcomes benefits in heart transplant recipients and recent laboratory publications that report an immunomodulatory effect of statins provide a firm scientific rationale to support the routine use of statins in heart transplant patients.

Animals↗
PubMed2004

Statins in atherothrombosis.

Clinical studies have shown that hydroxy-methyl glutaryl coenzyme A reductase inhibitors (statins) may favorably affect atherothrombosis. In addition to their potent cholesterol-lowering properties, statins reduce atheroma progression as well as the incidence of acute thrombosis-related vascular events and their dreadful clinical consequences. Available data indicate that statins exert significant antithrombotic effects in clinical practice by reducing the occurrence of vascular atherothrombotic events, with a more prominent effect in high-risk patients. The mechanisms by which statins inhibit thrombosis have been extensively investigated, and several pathways appear to be involved. In particular, statins have been proposed to reduce platelet activation and to exert favorable effects on fibrinolysis, but no clear-cut conclusion can be drawn from available studies. Moreover, statins do not consistently influence fibrinogen or factor VII levels in plasma. In contrast, in vitro and in vivo data indicate that these compounds profoundly affect thrombin generation driven by tissue factor/factor VII pathway. In vitro studies indicate that this effect is not dependent on plasma cholesterol lowering but, rather, on the inhibition of isoprenoid biosynthesis. The relative contribution of reduced levels of prenylated proteins and of cholesterol pathway to the modulation of tissue factor expression is, however, hardly to be established in clinical settings.

Animals↗
PubMed2005

C-reactive protein levels and outcomes after statin therapy.

BACKGROUND: Statins lower the levels of low-density lipoprotein (LDL) cholesterol and C-reactive protein (CRP). Whether this latter property affects clinical outcomes is unknown. METHODS: We evaluated relationships between the LDL cholesterol and CRP levels achieved after treatment with 80 mg of atorvastatin or 40 mg of pravastatin per day and the risk of recurrent myocardial infarction or death from coronary causes among 3745 patients with acute coronary syndromes. RESULTS: Patients in whom statin therapy resulted in LDL cholesterol levels of less than 70 mg per deciliter (1.8 mmol per liter) had lower event rates than those with higher levels (2.7 vs. 4.0 events per 100 person-years, P=0.008). However, a virtually identical difference was observed between those who had CRP levels of less than 2 mg per liter after statin therapy and those who had higher levels (2.8 vs. 3.9 events per 100 person-years, P=0.006), an effect present at all levels of LDL cholesterol achieved. For patients with post-treatment LDL cholesterol levels of more than 70 mg per deciliter, the rates of recurrent events were 4.6 per 100 person-years among those with CRP levels of more than 2 mg per liter and 3.2 events per 100 person-years among those with CRP levels of less than 2 mg per liter; the respective rates among those with LDL cholesterol levels of less than 70 mg per deciliter were 3.1 and 2.4 events per 100 person-years (P<0.001). Although atorvastatin was more likely than pravastatin to result in low levels of LDL cholesterol and CRP, meeting these targets was more important in determining the outcomes than was the specific choice of therapy. Patients who had LDL cholesterol levels of less than 70 mg per deciliter and CRP levels of less than 1 mg per liter after statin therapy had the lowest rate of recurrent events (1.9 per 100 person-years). CONCLUSIONS: Patients who have low CRP levels after statin therapy have better clinical outcomes than those with higher CRP levels, regardless of the resultant level of LDL cholesterol. Strategies to lower cardiovascular risk with statins should include monitoring CRP as well as cholesterol.

Anticholesteremic Agents↗
PubMed2002

What do the statins tell us?

Until the recent introduction of the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), the potential effect of cholesterol lowering on the prevention of clinical manifestations of coronary disease was a matter of debate. In trials conducted before the introduction of statins, cholesterol levels were lowered, on average, by only approximately 10%, resulting in prevention of coronary events but with no effect on total mortality rates. However, statins have been able to reduce low-density lipoprotein cholesterol levels by a mean of roughly 28%, significantly decreasing both relative and absolute risk levels of coronary events and total mortality. These benefits have been demonstrated not only in middle-aged men but also in women and patients aged >65 years. Aggressive cholesterol lowering has also been shown to yield larger decreases in the incidence of subsequent coronary events than angioplasty, and to reduce the occurrence of such events in patients who have undergone coronary artery bypass graft surgery, which raises the question of whether these procedures should be relegated to symptom relief, with cholesterol lowering as the primary means of coronary heart disease event prevention. Statins, therefore, have unequivocally shown the importance of cholesterol lowering in the prevention of morbidity and mortality due to coronary disease. Ongoing research will elucidate the role of statin therapy in the prevention of strokes and in the treatment of patients aged >75 years, and future trials will be needed to evaluate the potential role of statins in primary prevention for younger populations who cannot control cholesterol with lifestyle changes.

Age Distribution↗
PubMed2003

Pretreatment with statins enhances myocardial protection during coronary revascularization.

OBJECTIVE: This experimental study was undertaken to determine whether pretreatment with statins would enhance myocardial protection and minimize ischemic injury during revascularization of acutely ischemic myocardium. METHODS: In 20 pigs the second and third diagonal arteries were occluded for 90 minutes, followed by 45 minutes of blood cardioplegic arrest and 180 minutes of reperfusion. Ten pigs received atorvastatin (40 mg orally every day) for 21 days before surgical intervention; 10 others received no statins. Ischemic damage was assessed on the basis of the need for cardioversions for ventricular arrhythmias, regional wall-motion scores (4 = normal to -1 = dyskinesia) were determined by means of 2-dimensional echocardiography, endothelial function was assessed on the basis of bradykinin-induced coronary artery relaxation, and infarct size was calculated by determining the area of necrosis to the area of risk by means of histochemical staining. Results are given as means +/- SE. RESULTS: Statin-treated animals required fewer cardioversions (0.11 +/- 0.01 vs 2.87 +/- 0.20, P =.0001), had improved wall-motion scores (2.81 +/- 0.10 vs 1.52 +/- 0.08, P =.01), had lower infarct size (21% +/- 2% vs 41% +/- 2%, P =.0001), and had more complete coronary artery relaxation (34% +/- 5% vs 8% +/- 4%, P =.01). Total serum cholesterol levels were similar between the groups (62 +/- 5 mg/dL for statin-treated animals vs 68 +/- 5 mg/dL for non-statin-treated animals, P =.30). CONCLUSIONS: Pretreatment with statins enhances myocardial protection during revascularization by means of mechanisms that are independent of their cholesterol-lowering properties.

Animals↗
PubMed2002

Early initiation of treatment with statins in acute coronary syndromes.

Statins may act rapidly to reverse abnormalities of the arterial wall that may predispose to recurrent ischemic events after acute coronary syndromes. Such abnormalities are endothelial dysfunction, a local inflammatory response. and an exaggerated thrombogenic tendency. In one study almost 20,000 patients with first myocardial infarction were studied with regard to statin treatment (28%) or not. Baseline characteristics were adjusted using multivariate regression analysis including propensity analysis. One year mortality was 3.7/5.0% in statin/not statin groups, respectively, P = 0.001, relative risk 0.75. In another study of more than 20,000 patients, 18% were prescribed statin after an acute coronary syndrome and followed for six months. Propensity analysis was performed in this study as well. Deaths in statin/not statin groups were 1.7/3.5%, P<0.0001, relative risk 0.48. In the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL), a double-blind randomized, placebo-controlled intervention study, 3086 patient with acute non-Q-wave coronary syndromes were allocated immediately in hospital to receive atorvastatin 80 mg daily or placebo for four months. No lower limit for plasma LDL cholesterol was used. Primary endpoint was time to first occurrence of death, non-fatal myocardial infarction, cardiac arrest, and worsening angina with objective evidence of ischemia. This was significantly reduced compared to the placebo group by 2.4% (14.8 versus 17.2%, relative risk 0.84, P= 0.048). Atorvastatin also reduced significantly fatal or non-fatal strokes. Possible mechanisms behind these acute beneficial effects are discussed. The studies highlight the importance of treatment with a statin in the early management of acute coronary syndromes and the need to incorporate this therapeutic strategy in national guidelines and treatment recommendations.

Angina, Unstable↗
PubMedDate not supplied

Stroke prevention and statin treatment.

Randomized trials with statins have shown a modest but significant absolute reduction in the incidence of stroke in patients with a previous myocardial infarction. The reasons for the positive statin effect on stroke endpoint are unclear, because a link between serum cholesterol level and stroke never has been established. However, positive results of statin trials were mainly obtained in patients with an average or a low serum cholesterol level. Statins have a good overall safety profile. Statins reduced stroke incidence in high-risk (mainly coronary heart disease, diabetics, and hypertensives) population even with a normal baseline blood cholesterol level. In patients with prior strokes, statins reduce the incidence of coronary events, but it is not yet proven if drugs of this class actually reduce the incidence of recurrent strokes in terms of secondary prevention.

Clinical Trials as Topic↗
PubMed1985

Rapid disappearance of statin, a nonproliferating and senescent cell-specific protein, upon reentering the process of cell cycling.

Statin, a 57,000-D protein characteristically found in nonreplicating cells, was identified by a monoclonal antibody produced by hybridomas established from mice injected with extracts of in vitro aged human fibroblasts (Wang, E., 1985, J. Cell Biol., 100:545-551). Fluorescence staining with the antibody shows that the expression of statin disappears upon reinitiation of the process for cell replication. The rapid de-expression is observed in fibroblasts involved in the in vitro wound-healing process, as well as in cells that have been subcultured after trypsinization and replated from a confluent culture. Kinetic analysis shows that 50% of the cell population lose their statin expression at 12 h after replating, before the actual events of mitosis. Immunogold labeling with highly purified antibodies localizes the protein at the nuclear envelope in nonreplicating cells, but not in their replicating counterparts. Immunoblotting analysis confirms the disappearance of statin in cells that have reentered the cycling process. Using the technique of flow cytometry to examine the large number of nonreplicating fibroblasts in confluent cultures, we have found that statin is mostly expressed in those cells showing the least amount of DNA content, whose growth is blocked at the G0/G1 stage of the cell cycle. This close correlation is rapidly altered once the cells are released from the confluent state. These results suggest that the expression of statin may be regulated by a fine mechanism controlling the transition from the nonreplicating to the replicating state, and that the protein is structurally associated with the nuclear envelope.

Aged↗
PubMed2004

Statins inhibit HIV-1 infection by down-regulating Rho activity.

Human immunodeficiency virus (HIV)-1 infectivity requires actin-dependent clustering of host lipid raft-associated receptors, a process that might be linked to Rho guanosine triphosphatase (GTPase) activation. Rho GTPase activity can be negatively regulated by statins, a family of drugs used to treat hypercholesterolemia in man. Statins mediate inhibition of Rho GTPases by impeding prenylation of small G proteins through blockade of 3-hydroxy-3-methylglutaryl coenzyme A reductase. We show that statins decreased viral load and increased CD4+ cell counts in acute infection models and in chronically HIV-1-infected patients. Viral entry and exit was reduced in statin-treated cells, and inhibition was blocked by the addition of l-mevalonate or of geranylgeranylpyrophosphate, but not by cholesterol. Cell treatment with a geranylgeranyl transferase inhibitor, but not a farnesyl transferase inhibitor, specifically inhibited entry of HIV-1-pseudotyped viruses. Statins blocked Rho-A activation induced by HIV-1 binding to target cells, and expression of the dominant negative mutant RhoN19 inhibited HIV-1 envelope fusion with target cell membranes, reducing cell infection rates. We suggest that statins have direct anti-HIV-1 effects by targeting Rho.

Acquired Immunodeficiency Syndrome↗
PubMed2001

The effect of statins on mortality in patients with bacteremia.

The statins, inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, act to regulate the biosynthesis of cholesterol. Statins also deplete nonsterol cholesterol precursors, the isoprenoids, which are necessary for prenylation of critical membrane proteins that regulate cellular communication, including the inflammatory response. In a retrospective review of 388 bacteremic infections due to aerobic gram-negative bacilli and Staphylococcus aureus, there was a significant reduction in both overall (6% vs. 28%; P=.002) and attributable (3% vs. 20%; P=.010) mortality among patients taking statins compared with patients not taking statins. This reduction in mortality persisted in a multivariate analysis (odds ratio, 7.6; 95% confidence interval, 1.01-57.5). Among the statin group, diabetes, hypertension, and coronary artery disease were more prevalent (P<.001), and there were more skin and soft tissue infections identified as sources of bacteremia (P=.008). These data suggest a potential clinical role of statins in bacteremic infection; however, the mechanism by which mortality is reduced remains undefined.

Bacteremia↗
PubMed2006

Adherence to evidence-based statin guidelines reduces the risk of hospitalizations for acute myocardial infarction by 40%: a cohort study.

AIMS: To investigate the 'real world' effectiveness of robust statin therapy, focusing on the effect of dose and early treatment discontinuation on the risk of hospitalization for acute myocardial infarction (AMI). METHODS AND RESULTS: In the PHARMO database, including among others drug-dispensing and hospital discharge records for more than two million subjects in the Netherlands, 59,094 new users of statins in the period 1 January 1991 until 31 December 2004, >or=18 years of age were identified. In these patients, exposure to statins, both in terms of persistence and dose, was determined over the first two treatment years. To determine the risk for AMI, patients were followed from this 2-year time point until the first hospital admission for AMI, death, or end of the study period. A total of 31,557 patients (53%) discontinued statin use within 2 years; 20 883 patients (35%) were persistent users with an average equipotent dose>or=4. A 30% reduction in risk of hospitalization for AMI with persistent statin use was observed. The protective effect increased with a higher dose (20 and 40% risk reduction with an equipotent dose or=4, respectively). CONCLUSION: These results show that statins are suboptimally used in real life for having the maximum benefit in terms of preventing AMI.

Adult↗
PubMed2006

Effect of statin treatment on renal function and serum uric acid levels and their relation to vascular events in patients with coronary heart disease and metabolic syndrome: a subgroup analysis of the GREek Atorvastatin and Coronary heart disease Evaluation (GREACE) Study.

BACKGROUND: Metabolic syndrome (MetS) is associated with increased risk for both vascular and chronic kidney disease. Whether statins ameliorate these risks is not established. METHODS: This post hoc analysis of the GREek Atorvastatin and Coronary heart disease (CHD). Evaluation (GREACE) examines the effect of statins on estimated glomerular filtration rate (e-GFR) and serum uric acid (SUA) levels and their relation to vascular events in CHD patients with MetS. MetS patients were divided into two groups: Group A (n = 365) received lifestyle advice, target-driven treatment with statins (mainly atorvastatin) and treatment for hypertension and elevated glucose. Group B (n = 347) received the same except for statins. Patients without MetS were divided into those who received treatment similar to Group A and Group B [Groups C (n = 504) and D (n = 384), respectively]. All patients were followed for 3 years. RESULTS: A total of 12.1% of patients in Group A experienced a vascular event vs 28% in Group B; risk ratio (RR) 0.43, 95% confidence interval (CI) 0.20-0.64, P < 0.0001, while in those without MetS (Group C vs Group D), the respective RR was 0.59, 95% CI 0.41-0.79, P < 0.0001. In Group A, e-GFR increased by 13.7% and SUA levels fell by 8.9%, while in Group B e-GFR was reduced by 5.8% and SUA increased by 4.3% (P < 0.005). Stepwise regression analysis showed that these changes were independently related to vascular events. CONCLUSION: Among CHD patients, those with MetS benefited more from statin treatment than those without MetS. This benefit could be partially attributed to favourable changes in e-GFR and SUA levels probably induced by statin treatment.

Aged↗
PubMed2002

Costs of aspirin and statins in general practice.

BACKGROUND: Aspirin and statins are the two drugs most commonly indicated for secondary prevention of atherosclerotic disease in the UK. Statin treatment, which is more expensive, is under-prescribed. AIM: To assess the expenditure in Greater Manchester general practices on aspirin and statins. DESIGN: Survey of general practice records. METHODS: Practice registers were searched for patients receiving regular prescriptions for aspirin. For each patient, the next patient of the same sex, aged within +/- 5 years, not on aspirin, acted as a control. Details of all medications were recorded. In a sub-study, records of 100 patients on aspirin were studied to determine indications for aspirin prescription. RESULTS: There were 1003 (511 men, 492 women) in each group; mean age was 70 years in both groups. In the sub-study, 79% of patients received aspirin for established vascular disease, 9% for hypertension, 5% for diabetes mellitus, 5% for unknown reasons and 2% for arthritis. Of the patients on aspirin, 67% received dispersible aspirin 75 mg/day. The rest were on higher doses (10%) or on more expensive preparations (22%), costing up to 22.4 p/day. The mean daily cost of aspirin was 1.7p. Dyspepsia treatment was received by 266 patients and 194 controls (p<0.001). There was a wide range of dyspepsia medications (10-306p/day), averaging in the groups as a whole 15.5p/day in patients and 12.5p/day in controls. Of the patients on aspirin, 28% received statins, compared to 4% of controls. Mean daily expenditure on statins in patients was 23.4p. CONCLUSION: Assuming the difference in the use of medication for dyspepsia between patients and controls was due to aspirin, the full cost of aspirin treatment was 4.7p/day. Statins were probably under-prescribed in aspirin-takers, many of whom would have been at high CHD risk.

Aged↗
PubMed2000

Evidence that luteinizing hormone-releasing hormone statin from ovine rete testis fluid is immunologically related to alphaC inhibin.

LHRH Statin is a putative gonadal protein that increases the interval between two consecutive LHRH pulses. The present work was aimed at analyzing the immunological homology between LHRH Statin and the N-terminal region of the alphaC subunit of inhibin. Thus, rete testis fluid (RTF) proteins were purified by immunoaffinity chromatography using antibodies against residues 1-7 plus 7-30 (experiment 1, A-fractions) and 14-28 of the alphaC inhibin subunit (experiment 2, B-fractions), and the LHRH Statin activity of the fractions was examined by intracerebroventricular administration in castrated rams followed by RIA of plasma LH levels in 15-min blood samples. Fractions that bound to the immunoaffinity column with low affinity were eluted with 0.5 M NaCl, pH 7.4 (-F2); then highly bound fractions were eluted sequentially in acidic (pH 2.5, -F3) followed by basic conditions (pH 11.5, -F4). In experiment 1, RTF (40 microg, n = 4) and highly bound fractions (A-F3, 30 ng, n = 8, 150 ng, n = 3; A-F4, 120 ng, n = 5) decreased LH mean plasma levels between 4 and 6 h after injection by 39%, 29%, 43%, and 37%, respectively (P<0.001 to 0.01), while the weakly bound fractions (A-F2, 180 ng, n = 4) and albumin control (40 microg, n = 4) had no activity. In experiment 2, RTF (100 microg, n = 4) and B-F3 (100 ng, n = 3) decreased plasma LH levels by 48% and 38%, respectively (P<0.001 to 0.05), whereas B-F4 (100 ng, n = 4) and albumin control (100 microg, n = 4) had no effect. A fraction obtained from B-F3 by gel filtration had significant LHRH Statin activity (63%, n = 6, P<0.001). PAGE with colloidal gold staining revealed 3 high molecular weight bands and 5 low molecular weight bands in B-F3. The 3 high molecular weight bands were shown to belong to the clusterin family and did not appear to have LHRH Statin activity. The 5 low molecular weight bands were all labeled by anti-alphaC inhibin antibodies. Collectively, these results strongly suggest that LHRH Statin has some homology with the 14-28 alphaC inhibin sequence.

Animals↗
PubMed2005

Statins in the prevention of perioperative cardiovascular complications.

PURPOSE OF REVIEW: This is a review of recent experimental and clinical evidence for the use of perioperative statins to reduce cardiovascular complications. RECENT FINDINGS: Clinical trials have demonstrated an improved survival of statin users in the perioperative period. This beneficial effect of statins is ascribed to the non-lipid lowering effect to stabilize vulnerable plaques, thereby preventing myocardial ischaemia and infarction. The proposed mechanism of this cardioprotective effect is by the anti-inflammatory properties of statins. The fear of adverse perioperative effects of statin use, i.e. rhabdomyolysis, has not been confirmed in clinical studies. SUMMARY: The anti-inflammatory properties of statins appear to have an important effect on coronary plaque stabilization in the perioperative setting, resulting in a reduction in perioperative cardiovascular complications.

Journal Article↗
PubMed2002

Statin use and the risk of breast and prostate cancer.

BACKGROUND: Laboratory data suggest that the cholesterol-lowering "statin" drugs may have chemopreventive potential against cancer at various sites, including breast and prostate. However, in one trial of pravastatin there was a significant excess of breast cancer in the treatment group. In the present study, we assessed the relation of statin use to the risk of breast and prostate cancer in our hospital-based Case-Control Surveillance Study of Drugs and Serious Illnesses. METHODS: Cases were 1,132 women with breast cancer and 1,009 men with prostate cancer; controls were 1,331 women and 1,387 men admitted for conditions unrelated to statin use. We used multivariate unconditional logistic regression models to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for use of statins compared with no use. RESULTS: The OR for breast cancer among statin users was 1.5 (95% CI = 1.0-2.3), largely accounted for by an OR of 1.8 (95% CI = 0.9-3.6) among cases with carcinoma in situ. Among invasive cases, the OR was 1.2 (95% CI = 0.7-2.0). The odds ratio for prostate cancer overall was 1.2 (95% CI = 0.8-1.7), and it was 1.4 (95% CI = 0.7-2.5) for Stage A. CONCLUSIONS: The data from the present study do not support a protective effect of statins against breast or prostate cancer. Detection bias is a possible explanation for the higher ORs observed for carcinoma in situ or early-stage cancer as compared with more invasive cancer.

Aged↗