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PubMed2002

Statins in acute coronary syndromes.

The development of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors (statins) has been a very significant development in the management of coronary artery disease. Large prospective clinical trials have provided unequivocal evidence that cholesterol lowering therapy with statins reduces all-cause mortality in patients with coronary artery disease. There is now accumulating data indicating that statin treatment should be initiated early after an acute coronary syndrome. This body of evidence is based on large databases in which investigators compared outcomes among patients taking statins with those patients who were not prescribed cholesterol lowering therapy. Prospective, randomized, clinical trials also indicate that early statin therapy reduces recurrent ischemia. Finally, studies examining long-term compliance with statin therapy suggest increased adherence to therapy when statins are prescribed during the initial hospitalization for an acute coronary syndrome. In tandem with these clinical observations, there is a large body of scientific data that highlights many important cellular and molecular mechanisms through which statins may confer early benefit. These effects involve relatively rapid improvement in endothelial function, antiischemic, antithrombotic and antiinflammatory actions of statins.

Acute Disease↗
PubMed2005

National trends in statin use by coronary heart disease risk category.

BACKGROUND: Only limited research tracks United States trends in the use of statins recorded during outpatient visits, particularly use by patients at moderate to high cardiovascular risk. METHODS AND FINDINGS: Data collected between 1992 and 2002 in two federally administered surveys provided national estimates of statin use among ambulatory patients, stratified by coronary heart disease risk based on risk factor counting and clinical diagnoses. Statin use grew from 47% of all lipid-lowering medications in 1992 to 87% in 2002, with atorvastatin being the leading medication in 2002. Statin use by patients with hyperlipidemia, as recorded by the number of patient visits, increased significantly from 9% of patient visits in 1992 to 49% in 2000 but then declined to 36% in 2002. Absolute increases in the rate of statin use were greatest for high-risk patients, from 4% of patient visits in 1992 to 19% in 2002. Use among moderate-risk patients increased from 2% of patient visits in 1992 to 14% in 1999 but showed no continued growth subsequently. In 2002, 1 y after the release of the Adult Treatment Panel III recommendations, treatment gaps in statin use were detected for more than 50% of outpatient visits by moderate- and high-risk patients with reported hyperlipidemia. Lower statin use was independently associated with younger patient age, female gender, African American race (versus non-Hispanic white), and non-cardiologist care. CONCLUSION: Despite notable improvements in the past decade, clinical practice fails to institute recommended statin therapy during many ambulatory visits of patients at moderate-to-high cardiovascular risk. Innovative approaches are needed to promote appropriate, more aggressive statin use for eligible patients.

Adult↗
PubMed2006

Statins in the treatment of chronic heart failure: a systematic review.

BACKGROUND: The efficacy of statin therapy in patients with established chronic heart failure (CHF) is a subject of much debate. METHODS AND FINDINGS: We conducted three systematic literature searches to assess the evidence supporting the prescription of statins in CHF. First, we investigated the participation of CHF patients in randomized placebo-controlled clinical trials designed to evaluate the efficacy of statins in reducing major cardiovascular events and mortality. Second, we assessed the association between serum cholesterol and outcome in CHF. Finally, we evaluated the ability of statin treatment to modify surrogate endpoint parameters in CHF. Using validated search strategies, we systematically searched PubMed for our three queries. In addition, we searched the reference lists from eligible studies, used the "see related articles" feature for key publications in PubMed, consulted the Cochrane Library, and searched the ISI Web of Knowledge for papers citing key publications. Search 1 resulted in the retrieval of 47 placebo-controlled clinical statin trials involving more than 100,000 patients. CHF patients had, however, been systematically excluded from these trials. Search 2 resulted in the retrieval of eight studies assessing the relationship between cholesterol levels and outcome in CHF patients. Lower serum cholesterol was consistently associated with increased mortality. Search 3 resulted in the retrieval of 18 studies on the efficacy of statin treatment in CHF. On the whole, these studies reported favorable outcomes for almost all surrogate endpoints. CONCLUSIONS: Since CHF patients have been systematically excluded from randomized, controlled clinical cholesterol-lowering trials, the effect of statin therapy in these patients remains to be established. Currently, two large, randomized, placebo-controlled statin trials are under way to evaluate the efficacy of statin treatment in terms of reducing clinical endpoints in CHF patients in particular.

Anticholesteremic Agents↗
PubMed2006

HMG-CoA reductase inhibitors (statins) might cause high elevations of creatine phosphokinase (CK) in patients with unnoticed hypothyroidism.

Serious side effects of statins, including severe myopathy and rhabdomyolysis, are rare but important in general practice. Hypothyroidism can cause secondary hypercholesterolemia and myopathy. There have been few reports on the risk of statins in patient with unnoticed hypothyroidism. We analyzed the characteristics of 77 patients with primary hypothyroidism in our hospital. Nine patients (11%) accidentally received statins in the treatment of hypercholesterolemia without diagnosis of hypothyroidism. In such patients, free T4 (FT4) levels were lower, and those of LDH, CK were higher than those in patients not receiving statins. In patients accidentally receiving statins, an inverse correlation between CK and FT4 could not be shown (which was recognized in patients not receiving them). Even after FT4 levels were matched, levels of CK were still higher in the patients accidentally receiving statins. Patients with high CK levels over 1000 U/L were 5 times more frequent (56%) in patients accidentally receiving statins than in those not receiving statins (11%). The present study confirms that statins enhances levels of CK in patients with hypothyroidism. We must not begin and continue to use these drugs without checking the possibility of hypothyroidism.

Aged↗
PubMed2004

Statin-associated peripheral neuropathy: review of the literature.

Various pharmacologic agents are available for the treatment of hypercholesterolemia, including 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, commonly referred to as statins, which offer favorable lipid-lowering effects and reductions in morbidity and mortality. Statins are usually better tolerated than other lipid-lowering agents and therefore have become a mainstay of treatment for hypercholesterolemia. However, recent case reports of peripheral neuropathy in patients treated with statins may have gone unnoticed by health care professionals. To evaluate the possible link between statins and peripheral neuropathy, literature searches using MEDLINE (January 1993--November 2003) and International Pharmaceutical Abstracts (January 1970--June 2002) were performed. Key search terms were statin, neuropathy, and HMG-CoA reductase inhibitors. Based on epidemiologic studies as well as case reports, a risk of peripheral neuropathy associated with statin use may exist; however, the risk appears to be minimal. On the other hand, the benefits of statins are firmly established. These findings should alert prescribers to a potential risk of peripheral neuropathy in patients receiving any of the statins; that is, statins should be considered the cause of peripheral neuropathy when other etiologies have been excluded.

Algorithms↗
PubMed2007

Effectiveness of statins in reducing the rate of severe sepsis: a retrospective evaluation.

STUDY OBJECTIVES: To determine whether use of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) is associated with a reduced rate of severe sepsis, and to further characterize the effect of statins on the frequency of organ dysfunction in patients with severe sepsis. DESIGN: Retrospective cohort study. SETTING: University-associated teaching hospital. PATIENTS: Fifty-three patients admitted with sepsis; 16 were receiving statins and 37 were not receiving statins (controls) before admission. MEASUREMENTS AND MAIN RESULTS: Patients were identified by the International Classification of Diseases, Ninth Revision, Clinical Modification codes. Patient demographics, vital signs, and laboratory values were collected from their electronic medical records. The primary end point was rate of severe sepsis, defined in accordance with guidelines from the American College of Chest Physicians and the Society of Critical Care Medicine. Secondary end points were in-hospital mortality rate and rate of five categories of organ dysfunction (cardiovascular, renal, pulmonary, hematologic, and metabolic). Preadmission statin therapy, compared with no statin therapy, was associated with a 30% lower rate of severe sepsis (56% vs 86%, p<0.02). In-hospital mortality was not significantly different between groups (38% vs 49%, p=0.33); however, the rate of cardiovascular dysfunction, defined as hypotension requiring vasopressor therapy, was significantly lower in the statin group (38% vs 73%, p<0.02). No significant differences in the other organ dysfunction categories were noted between groups. CONCLUSION: Statins appear to prevent sepsis from becoming severe, most notably through prevention of sepsis-induced hypotension. This potential role for statins in the prevention and treatment of severe sepsis should be further evaluated in a randomized controlled trial.

Aged↗
PubMed2007

Effects of statins on cognitive function in patients with Alzheimer's disease in galantamine clinical trials.

BACKGROUND AND OBJECTIVE: A number of reports have been published on the possible involvement of changes in brain cholesterol metabolism in the origin of Alzheimer's disease (AD) and the potential for influencing these changes by administration of HMG-CoA reductase inhibitors ('statins'). The aim of this study was to evaluate a potential association between use of statins and maintenance of cognitive function in patients with AD in galantamine clinical trials. METHOD: A post hoc analysis was conducted on data pooled from three double-blind, placebo-controlled, clinical trials of galantamine in patients with AD. Patients were divided into four treatment groups: statin plus galantamine (n = 42), statin alone (n = 50), galantamine alone (n = 614) or neither galantamine nor statin (n = 619). RESULTS: Galantamine was associated with a significant beneficial effect on cognitive status (p < 0.001). The association of use of statins with changes in cognitive status was not significant (p = 0.083). There was no significant interaction between the effects on cognition of statins and galantamine (p = 0.183) and no statistically significant changes in adverse effect rates were observed. CONCLUSION: These findings suggest the need for larger long-term trials to confirm or refute possible effects of statins on cognitive function and the potential interaction of statins with acetylcholinesterase inhibitors in the treatment of AD.

Aged↗
PubMed2003

Cost effectiveness of statin therapy for the primary prevention of major coronary events in individuals with type 2 diabetes.

OBJECTIVE: To assess the cost and cost effectiveness of hydroxymethylglutaryl (HMG)-CoA reductase inhibitor (statin) therapy for the primary prevention of major coronary events in the U.S. population with diabetes and LDL cholesterol levels > or =100 mg/dl, especially in the population with LDL cholesterol levels 100-129 mg/dl. RESEARCH DESIGN AND METHODS: Analyses were performed using population estimates from National Health and Nutrition Examination Survey (NHANES)-III, cost estimates from a health system perspective, statin LDL-lowering effectiveness from pivotal clinical trials, and treatment effectiveness from the diabetic subgroup analysis of the Heart Protection Study. RESULTS: -There are approximately 8.2 million Americans with diabetes, LDL cholesterol levels > or =100 mg/dl, and no clinical evidence of cardiovascular disease. Each year, statin therapy could prevent approximately 71,000 major coronary events in this population. In the subgroup with LDL cholesterol levels 100-129 mg/dl, the annual cost of statin treatment ranges from 600 to 1,000 US dollars per subject. In the population with LDL cholesterol levels > or =130 mg/dl, the annual cost ranges from 700 to 2,100 US dollars. Annual incremental cost per subject, defined as the cost of statin treatment plus the cost of major coronary events with statin treatment minus the cost of major coronary events without statin treatment, ranges from 480 to 950 US dollars in the subgroup with LDL cholesterol levels 100-129 mg/dl and from 590 to 1,920 US dollars in the population with LDL cholesterol levels > or =130 mg/dl. CONCLUSIONS: Statin therapy for the primary prevention of major coronary events in subjects with type 2 diabetes and LDL cholesterol levels 100-129 mg/dl is affordable and cost effective relative to statin therapy in subjects with higher LDL cholesterol levels.

Atorvastatin↗
PubMedDate not supplied

[The statins: new properties]].

The comparison of major statin trials with trials using either cholestyramine or ileal bypass has suggested that the reduction in coronary heart disease events for those patients receiving statin therapy largely result from their low density lipoprotein (LDL)-cholesterol lowering action. LDL-cholesterol lowering has several physiological consequences, including plaque stabilisation with a decrease in the inflammatory process, slowing of plaque progression, and improvement of endothelial function, as evidenced by the measurement of endothelial-dependent vasorelaxation in response to hyperhaemia or acetylcholine infusion. Statins lower C-reactive protein without any consistent effect on the other inflammation acute phase proteins. The cause and consequences of this effect are still debated. In order to explain why some statins can prevent coronary events within a few months, a direct effect of this therapy on thrombosis has also been advocated; however, the evaluation of statin antithrombotic effects in humans has produced conflicting results. By inhibiting L-mevalonic acid synthesis, statins also prevent the farnelysation of small-GTP binding proteins such as Rho and Ras. In vitro, and in animal models, the inhibition of Rho with statins results in a decrease in endothelial nitric oxide production, an inhibition of leucocyte adhesion on endothelium, decrease in PPAR alpha activation and high density lipoprotein (HDL) production by the hepatocyte, decrease in Ca2+ stores in vascular smooth cells, and a stimulation of vascular smooth muscle cell apoptosis. However, most of these effects were obtained with high statin concentrations. Further evidence is needed before a full assessment of the clinical importance of isoprenylation blockage with therapeutic concentrations of statins in humans can be made.

Animals↗
PubMed2002

Statin lipid-lowering therapy for acute myocardial infarction and unstable angina: efficacy and mechanism of benefit.

The use of statin agents in patients with acute coronary syndromes (ACSs) remains an area of intense clinical interest. Statin therapy has an established secondary preventive benefit in patients with coronary artery disease, and its extension to ACS seems logical. A number of observational studies have shown an association between initiation of statin therapy early in ACS and improved clinical outcome. Additionally, 4 randomized controlled trials have examined the use of statin therapy for ACS: the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) study, the Pravastatin Turkish Trial, the Fluvastatin on Risk Diminishing After Acute Myocardial Infarction (FLORIDA) study, and the Lipid-Coronary Artery Disease (L-CAD) study. Three of these trials showed a benefit with early initiation of statin therapy, whereas 1 trial demonstrated neither benefit nor harm. All the available trials lacked the power and design to sufficiently evaluate whether early initiation of statin therapy reduces mortality and reinfarction in patients with ACS. Four ongoing trials have been designed and sufficiently powered to determine whether statin therapy reduces the risk of death and reinfarction when initiated early in ACS treatment. A body of evidence suggests that the pleiotropic actions of statin agents might modulate benefit in ACS. This article summarizes the available data and provides a rationale for early initiation of statin therapy for patients with ACS.

Angina, Unstable↗
PubMed2005

The future of statins: Alzheimer's disease?

OBJECTIVES: To review available clinical trial data and discuss the potential role of statins on the development of Alzheimer's disease (AD). DATA SOURCES: Searches of PubMed and MEDLINE (1985-February 2005) were conducted. STUDY SELECTION AND DATA EXTRACTION: English language articles, review papers, and human studies with special emphasis on those dealing with statin use and AD. DATA SYNTHESIS: Early data from retrospective trials indicate that patients receiving statins have a reduced risk of developing AD. Two large published prospective clinical trials with cognition as secondary endpoint found that statins did not show any benefit compared with placebo. Only one of two more recent cohort community-based studies of statins found a lower risk of dementia and cognitive impairment. A small placebo-controlled pilot study reported that atorvastatin slows the progression of AD. Case reports indicate that in rare cases, statins may be associated with cognitive impairment. The results of ongoing placebo-controlled trials in patients with cognitive impairment should yield more definitive answers. CONCLUSION: Current literature is conflicting with regard to the neuroprotective effects of statins on cognitive impairment. A firm conclusion regarding the effects of cholesterol or statins on human brain and cognitive function has not been well established, and it is premature to recommend statins for prevention and/or treatment of AD.

Journal Article↗
PubMed2001

Drug interactions of the statins and consequences for drug selection.

Cholesterol-lowering drugs such as HMG-CoA reductase inhibitors ("statins") are increasingly used in hypercholesterolemic patients who suffer from multiple concomitant diseases, and are therefore taking multiple drugs. The statins do not differ in their mechanism of action (pharmacodynamics), but there are differences in the affinity to the target enzyme as well as differences in pharmacokinetic properties, which need to be considered when choosing a statin for a specific patient. The most critical side effect of statins is development of myopathy, which becomes evident as muscle pain, weakness, and elevation of serum creatine kinase activity. The incidence of myopathy is usually low. However, myopathy and rhabdomyolysis are more frequent when statins are combined with other drugs that inhibit cytochrome P450-dependent metabolism of statins in the liver (e.g., itraconazole, erythromycin). Drug interactions can thus significantly increase the risk associated with statin therapy. Oral bioavailability of the statins varies considerably. Besides the absolute rate of oral bioavailability, it is important to know the relative difference between intestinal absorption rate and rate of oral bioavailability in order to assess the potential for drug-drug interactions. Statins that are not metabolized by a single cytochrome P450 isoenzyme, and have a high bioavailability, are the least prone to drug interactions.

Anticholesteremic Agents↗
PubMed2005

Analysis of the global RNA expression profiles of skeletal muscle cells treated with statins.

The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) are the most effective drugs for hypercholesteloremia. However, a significant side effect of statin treatment is rhabdomyolysis. In order to study the effect of statins in skeletal muscle cells, we used a DNA microarray analysis to investigate the changes in gene expression profiles brought about by statins in two skeletal muscle cell lines, namely, differentiated rat L6 myotubes and a human skeletal muscle cell line (hSkMC). In both cell lines, the statins (atorvastatin, cerivastatin and pitavastatin) induced the expression of four genes, which relate to cholesterol metabolism, namely, HMG-CoA synthase 1, HMG-CoA reductase, farnesyl diphosphate synthase and isopentenyl-diphosphate delta isomerase. Statin inhibited the synthesis of cholesterol at least five times more effectively in hSkMCs than in the hepatocytes. In addition, unlike in osteoblasts or coronary artery smooth muscle cells, statins upregulated the mRNA expression of cholesterol-associated enzymes in hSkMCs. These results provide basic information on skeletal muscle cells treated with statins and indicate that the cells are sensitive to the inhibition of HMG-CoA reductase, which may be related to the pathogenesis of muscle damage in statin therapy.

Animals↗
PubMed1999

Lipophilic statins induce apoptosis of human vascular smooth muscle cells.

BACKGROUND: The accumulation of vascular smooth muscle cells (VSMC) in the intima is an early feature of atherosclerosis that results from a balance of migration from the media, proliferation, and eventual death (including programmed cell death) of VSMC. Several reports have described that HMG-CoA reductase inhibitors (statins) attenuate both the migration and proliferation of VSMC. However, the potential effect of statins on VSMC programmed cell death has received little attention. METHODS: Human and rat VSMC were incubated with different concentration of statins in the presence of fetal bovine serum as a survival factor. The presence of apoptosis was evaluated by morphological criteria, flow cytometry and DNA electrophoresis. RESULTS: Lipophilic statins induced, in a dose-dependent manner the appearance of VSMC apoptosis. The effect of statins was fully reversed by mevalonate, farnesylpyrophosphate, and geranylgeranypyrophosphate, but not by cholesterol or other mevalonate metabolites, suggesting a role for isoprenoids in VSMC apoptosis. In addition, the induction of apoptosis by statins was associated with the inhibition of prenylation of Rho B. CONCLUSIONS: The present results suggest that protein prenylation inhibition by statins may be involved in statin-induced VSMC apoptosis. These data provide a new potential mechanism by which statins may modulate the evolution of atherosclerotic lesions.

Animals↗
PubMed2004

Atorvastatin: gold standard for prophylaxis of myocardial ischemia and stroke - comparison of the clinical benefit of statins on the basis of randomized controlled endpoint studies.

AIM: of this study was to compare the clinical benefit - reduction of heart attacks, strokes or deaths - of the different statins applying the results of randomized controlled endpoint studies. - METHOD: We analyzed 11 published randomized controlled endpoint studies statin-to-placebo looking for the cardiovasculoprotective benefit of the 5 statins (atorvastatin, fluvastatin, lovastatin, pravastatin, simvastatin) tested: AFCAPS/TexCAPS, ASCOT, CARE, FLORIDA, HPS, PROSPER, LIPID, LIPS, MIRACL, 4S, WOSCOPS. - RESULTS: 1. Statins produced substantial benefit for the patients, reducing the rate of cardiovascular morbidity and mortality. 2. This benefit was independent of the patient's initial cholesterol or LDL-cholesterol concentrations and could also be demonstrated in patients who had average or low cholesterol levels. 3. Men and women showed a comparable benefit from statin treatment, elderly patients a little more than younger patients. 4. The statins did not have like effects. There were clear differences in potency as well as in the interval between initiation of treatment and the onset of clinical benefit. 5. Estimating 5 years of treatment, cardiac morbidity decreased with atorvastatin up to 44 %, with pravastatin up to 36 %, with fluva- or simvastatin up to 32 % and with lovastatin up to 24 %, approximately. 6. Estimating 5 years of treatment, morbidity of suffering from stroke decreased with atorvastatin up to 41 %, with simvastatin up to 34 % and with pravastatin up to 31 %, approximately. For fluva- and lovastatin there are no comparable data. Within the first 16 weeks of treatment following an acute coronary syndrome relative risk for suffering a non-lethal stroke was reduced with atorvastatin 80 mg/day up to 59 % compared to placebo, the relative risk for stroke up to 50 %. 7. The fastest onset of clinical benefit - reduction of fatal and non-fatal cardiovascular events, hospitalization and necessity of invasive interventions - was demonstrated by treatment with atorvastatin (rapid, within some weeks), followed by lovastatin (after one year), fluva-, prava- and simvastatin (after 11/2 - 2 years). 8. These results were achieved with atorvastatin 10 mg/day (80 mg/day used in MIRACL), lovastatin 20 to 40 mg/day (caused by dosage titration), pravastatin 40 mg/day, simvastatin 20 to 80 mg/day (caused by dosage titration) or fluvastatin 80 mg/day. 9. The advantage of atorvastatin may be due to its ability to reduce cardiovascular disease by stopping the growth of plaques in artery walls. 10. Atorvastatin was the most powerful compound in the group of statins, improving patients' health and expectation of life. - CONCLUSIONS: The authors of the studies agree, that patients at risk for cardiovascular diseases should be treated with a statin irrespective of initial cholesterol concentrations, sex or age. If an acute cardiovascular event has happened, statin treatment should be initiated early to improve the prognosis of these patients at high risk, independent from initial LDL cholesterol values. - Summing-up of these 11 trials, the best results and the greatest benefit for the patients were achieved with atorvastatin, which might be considered to be the gold standard for prophylaxis of cardiac ischemia and stroke.

Anticholesteremic Agents↗
PubMedDate not supplied

Frequency of statin use in type 2 diabetics having macrovascular disease- at a Tertiary Care Hospital of Karachi.

BACKGROUND: During the last two decades with the introduction of statins large reductions in cholesterol concentrations were easily and safely achievable and this led to studies that demonstrated benefits of statin use. But only fewer than one fourth of adults with coronary heart disease were receiving lipid-lowering drugs in a cross sectional health survey done in England. Thus this study was designed to evaluate the frequency of statin use in type 2 Pakistani diabetic subjects with macrovascular disease attending a tertiary care unit in Karachi, Pakistan. METHODS: Records of type 2 diabetic subjects coming to the outpatient department of Baqai Institute of Diabetology and Endocrinology from September 1996 to December 2001 was analyzed for their anthropometric and biochemical characteristics. Patients having any macrovascular disease were identified and frequency of statin use by these subjects was studied. RESULTS: Out of a total of 2152 patients 502 (252 males, 250 females) having macrovascular disease were identified. Only 16.5% of them (44 males, 39 females) were taking statins. Use of statins was higher amongst those who had angina (20%) or myocardial infarction (17%) compared to those who had stroke (10%). Sixty two percent of the users while 52% of the non-users had elevated blood cholesterol. CONCLUSION: Frequency of statin use in the subjects studied was much lower than was warranted with respect to their disease status. Presence of elevated blood cholesterol despite using statins suggested inappropriate treatment in these subjects. Further studies are required to identify the factors leading to low use of statins in type 2 diabetic subjects with macrovascular symptoms.

Age Distribution↗
PubMed2005

Combined treatment with statin and angiotensin-receptor blocker after stenting as a useful strategy for prevention of coronary restenosis.

OBJECTIVES: 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) enhances the inhibitory effects of angiotensin-receptor blocker (ARB) on vascular neointimal formation in mice. The present case-control study investigated the efficacy of combined treatment with statin and ARB for preventing restenosis in patients with coronary artery disease. METHODS: We examined 210 patients with angina pectoris undergoing elective coronary stenting for de novo lesions of native coronary arteries. All enrolled patients received aspirin and ticlopidine. The subjects included patients who received no statin (control group, n = 137) or started statin treatment (statin group, n = 73) with or without ARB treatment after stenting. RESULTS: The rate of restenosis at 6 months after stent implantation in the statin group (19%) was significantly lower than that in the control group (32%). The restenosis rate in self-expanding Radius stents. (23%) was significantly lower than that in balloon-expandable Velocity stents (42%) independent of statin treatment. Patients treated with statins and ARBs were least likely [odds ratio (95% confidence interval): 0.30 (0.12-0.74)] to develop coronary restenosis, as assessed by multiple logistic regression analysis. CONCLUSIONS: These findings indicate that combined treatment with statin and ARB after stenting is a useful strategy for the prevention of coronary restenosis.

Aged↗
PubMed2005

Adherence to statins, beta-blockers and angiotensin-converting enzyme inhibitors following a first cardiovascular event: a retrospective cohort study.

BACKGROUND: Population studies of statin adherence are generally restricted to one to two years of follow-up and do not analyze adherence to other drugs. OBJECTIVES: To report long-term adherence rates for statins, angiotensin-converting enzyme (ACE) inhibitors and beta-blockers in patients who recently experienced a first cardiovascular event. METHODS: Linked administrative databases in the province of Saskatchewan were used in this retrospective cohort study. Eligible patients received a new statin prescription within one year of their first cardiovascular event between 1994 and 2001. Adherence to statins, beta-blockers and ACE inhibitors was assessed from the first statin prescription to a subsequent cardiovascular event. RESULTS: Of 1221 eligible patients, the proportion of patients adherent to statin medications dropped to 60.3% at one year and 48.8% at five years. The decline in the proportion of adherent patients was most notable during the first two years (100% to 53.7%). Several factors were associated with statin adherence, including age (P = 0.012), number of physician service days (P = 0.037), chronic disease score (P = 0.032), beta-blocker adherence (P < 0.001) and ACE inhibitor adherence (P < 0.001). Adherence to beta-blockers and ACE inhibitors was very similar to adherence to statin medications at each year of follow-up. CONCLUSIONS: Patients who exhibit optimal adherence over one to two years after their initial cardiovascular event generally remain adherent over subsequent years. Also, adherence to beta-blockers and ACE inhibitors is significantly associated with statin adherence in a subset of patients; however, overall adherence to all three drugs was similarly poor.

Adrenergic beta-Antagonists↗