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PubMedDate not supplied

Statins and biomarkers in claudicants with peripheral arterial disease: cross-sectional study.

This exploratory substudy of The Iron (Fe) and Atherosclerosis Study (FeAST) compared baseline inflammatory markers, including cytokines, C-reactive protein (CRP), and ferritin, in subjects with peripheral arterial disease (PAD) taking statins with subjects with PAD who were not taking statins. Inflammatory markers in the serum of 47 subjects with PAD not taking statins and a healthy cohort of 21 medication-free men were compared with 53 PAD subjects taking statins at entry to the FeAST. Healthy subjects demonstrated lower levels of tumor necrosis factor (TNF)-R1, interleukin-6 (IL-6), and CRP. TNF-alpha R1 averaged 2.28 ng/mL versus 3.52 ng/mL, p = .0025; IL-6 averaged 4.24 pg/mL versus 16.61 pg/mL, p = .0008; and CRP averaged 0.58 mg/dL versus 0.92 mg/dL, p = .0192. A higher level of IL-6 was observed in PAD statin takers versus PAD subjects not taking statins: 19.47 pg/mL versus 13.24 pg/mL, p = .0455. As expected, total cholesterol and low-density lipoprotein levels were lower in the statin-treated group, p = .0006 and p = .0001, respectively. No significant differences in inflammatory cytokines were detected for varying doses of simvastatin. Additionally, no significant differences in inflammatory biomedical markers were found in subjects with PAD alone compared with those with concomitant coronary artery disease (CAD). Unexpectedly, serum inflammatory cytokine IL-6 levels were significantly higher in PAD subjects receiving statins. There was no difference in measured inflammatory markers in PAD subjects with concomitant CAD.

Aged↗
PubMedDate not supplied

[Some questions about statins].

More than ten years after the statins became available in therapeutics, some questions remain unanswered. What would be the populational impact if the results of clinical trials were applied to a country such as France? Is the extrapolation licit? Does the benefit of the statins actually exceed the risk? What is the relevant target population? Are statins more effective than agents acting on other cardiovascular risk factors? How efficient are the statins really? Are the statins effective in non-hypercholesterolaemic patients? What is the overall cost of the statins? Despite the fact that the statins are the drug of choice in many situations, it is still important for these questions to be answered before we accept the widespread use of statins in the general population, such as the large numbers of patients that the drug may be prescribed for in France.

Cardiovascular Diseases↗
PubMed2003

Use of statins in primary and secondary prevention of coronary heart disease and ischemic stroke. Meta-analysis of randomized trials.

OBJECTIVE: To estimate the relative risk reduction of the clinical outcomes (coronary events, strokes, cardiovascular, non-cardiovascular and all-cause mortality) associated with statin therapy in primary and secondary prevention. DATA SOURCES: A literature search of the Medline and Cohrane databases for articles published from 1985 to July 2002 was performed. The data on systematic reviews and preliminary reports were also included in this study. Primary and secondary prevention trials and regression trials were eligible. DATA EXTRACTION AND STATISTICAL METHOD: Data were extracted by 2 authors according to the defined inclusion criteria. Disagreements were resolved by consensus or by a third reviewer. Testing for heterogeneity was applied and on the basis of these results a fixed effect model or a random effect model was used for calculation of relative risk values (RR) and 95% confidence intervals (95% CI). Sensitivity analysis tested the impact of the individual study--duration of study, type of statin therapy and study size. The number of patients needed to treat was calculated as an absolute measure of clinical effectiveness of statin therapy when appropriate. RESULTS: Data from 15 trials with 63,410 participants and mean duration of treatment of 3.6 years, were included in this overview. Tests for heterogeneity showed that the variability between study estimates is sufficiently small to assume that they are estimating the same underlying treatment effect. Statin therapy was associated with a 22% reduction in total cholesterol, 29% reduction in LDL cholesterol, 12% reduction in triglycerides and 6% increase in HDL cholesterol. Overall (primary and secondary studies) statin therapy significantly reduces relative risk of coronary events (RR, 0.73, 95% CI, 0.68, 0.77, *p < 0.0001), relative risk of cardiovascular disease mortality (RR, 0.78, 95% CI, 0.73, 0.84, *p < 0.0001), relative risk of non-fatal stroke (RR, 0.74, 95% CI, 0.67, 0.82, *p < 0.0001), relative risk of total (fatal and non-fatal) stroke (RR, 0.77, 95% CI, 0.70, 0.84, *p < 0.001) and relative risk of all-cause death (RR, 0.85, 95% CI, 0.81, 0.89, *p < 0.0001). There was a slight and insignificant reduction of relative risk in non-cardiovascular mortality (RR, 0.94, 95% CI, 0.86, 1.03, p = 0.1677) and fatal strokes (RR, 0.86, 95% CI, 0.70, 1.07, p = 0.1912). Sensitivity analysis showed the robustness of our results for all outcomes. The results were not altered if an individual study was removed from meta-analysis. CONCLUSIONS: This overview indicates that statin treatment reduces the relative risk of occurrence of coronary events, cardiovascular disease mortality, non-fatal strokes and all-cause mortality. While secondary prevention with statins provides considerable improvement of cardiovascular morbidity/mortality, primary prevention with statins provides only small and clinically hardly relevant improvement of cardiovascular morbidity/mortality.

Aged↗
PubMed2004

Cholesterol-independent effects of statins and new therapeutic targets: ischemic stroke and dementia.

The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, or "statins", are used as cholesterol-lowering agents worldwide. Statins inhibit cholesterol biosynthesis, leading to enhanced uptake of low-density lipoprotein (LDL) from the circulation via LDL receptors. This strong cholesterol-lowering action contributes to the beneficial effects of statins. For example, large clinical trials have demonstrated that statins significantly reduce cardiovascular risk. Recent research has shown that statins have other multiple actions involved in endothelial function, cell proliferation, inflammatory response, immunological reactions, platelet function, and lipid oxidation. These "pleiotropic actions" of statins probably provide a significant contribution to the reduction of cardiovascular events. This review summarizes the pleiotropic actions of statins in both basic and clinical studies. It also considers the potential for statin therapy in the treatment of stroke and dementia.

Brain Ischemia↗
PubMed2005

Effect of statin on restenosis after radius stent implantation in patients with acute coronary syndrome.

Despite reports that statin treatment reduces the rate of coronary restenosis with a balloon expandable stent, there is no evidence that statins affect the incidence of restenosis with a self-expanding Radius stent. Ninety-five patients with acute coronary syndrome who had been implanted with a Radius stent were classified into two groups: those with hyperlipidemia and initial statin treatment (statin group, n = 38) and those without statin treatment (comparative group, n = 57). At six months after stent implantation, the rate of coronary restenosis was significantly lower in the statin group (10.5%) than control group (28.1%) (p = 0.033), while there were no differences in morphology, maximal inflation pressure or stent size between the two groups. Interestingly, there was no difference in the serum lipid profile between the two groups at the 6-month follow-up, although the statin group had a significantly lower rate of restenosis. In conclusion, initial statin therapy reduced the rate of coronary restenosis even when a Radius stent was implanted.

Acute Disease↗
PubMed2002

The effect of statins on mRNA levels of genes related to inflammation, coagulation, and vascular constriction in HUVEC. Human umbilical vein endothelial cells.

Large-scale clinical trials have demonstrated significant reductions in cardiovascular events following statin therapy. The observed benefit of statin therapy, however, may be greater in these trials than is to be expected from lowering lipid levels alone. In order to clarify the mechanism by which statins prevent cardiovascular events in vascular wall cells, we investigated the changes in gene expression profiles after incubation with atorvastatin or pitavastatin in cultured human umbilical vein endothelial cells using DNA microarrays. Statins affected the expression levels of genes involved in inflammation, coagulation, and vascular constriction. The mRNA levels for interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) decreased after statin treatment. Statins reduced mRNA levels of plasminogen activator inhibitor-1 (PAI-1) and increased the mRNA levels of thrombomodulin. Statins reduced the mRNA levels of endothelin-1 and increased the mRNA levels of nitric oxide synthase-3 (eNOS). These results show that, statins are clinically effective because of their ability to change the gene expression profile of endothelial cells thereby preventing vascular events.

Atorvastatin↗
PubMed2002

Statin-associated myopathy with normal creatine kinase levels.

BACKGROUND: Muscle symptoms in patients who are treated with statins and have normal creatine kinase levels are not well understood. OBJECTIVE: To report biopsy-confirmed myopathy and normal creatine kinase levels associated with statin use. DESIGN: Case reports from preliminary analysis of an ongoing clinical trial. SETTING: Clinical research center in a community hospital. PATIENTS: Four patients with muscle symptoms that developed during statin therapy and reversed during placebo use. MEASUREMENTS: 1) Patients' ability to identify blinded statin therapy and 2) standard measures of functional capacity and muscle strength. RESULTS: All four patients repeatedly distinguished blinded statin therapy from placebo. Strength testing confirmed weakness during statin therapy that reversed during placebo use. Muscle biopsies showed evidence of mitochondrial dysfunction, including abnormally increased lipid stores, fibers that did not stain for cytochrome oxidase activity, and ragged red fibers. These findings reversed in the three patients who had repeated biopsy when they were not receiving statins. Creatine kinase levels were normal in all four patients despite the presence of significant myopathy. CONCLUSION: Some patients who develop muscle symptoms while receiving statin therapy have demonstrable weakness and histopathologic findings of myopathy despite normal serum creatine kinase levels.

Aged↗
PubMed1999

[Use of statins following myocardial infarction before and after the 4S study].

The 4S study was followed by guidelines for statin treatment of patients with manifest coronary heart disease recommending statins for patients with serum cholesterol above 5.5 mmol/l, age below 70 years, and more than three years life expectancy. The purpose of the present study was to investigate how these guidelines were implemented in clinical practice. A retrospective registration was conducted on two cohorts of patients; patients with myocardial infarction in 1994 (before 4S) (n = 101) and 1996 (n = 100). Risk factors for coronary diseases and the use of statins were registered from the patients records. No significant differences in risk factors between the two cohorts were observed. The proportion of patients given statins increased from 4% in 1994 to 40% in 1996, whereas 50% of patients with serum cholesterol above 5.5 mmol/l were given statins in 1996. Statin treatment was usually instituted during hospitalization. Awareness of actual prescription and handling of statin treatment, and adaption of knowledge from clinical studies to clinical practice is probably needed for further improvement of statin treatment.

Anticholesteremic Agents↗
PubMed1999

[The hyperlipidemias. Role of various statins].

MECHANISM OF ACTION: Statins act by competitive inhibition of HMG-CoA reductase, a key enzyme regulating cholesterol synthesis. Reduction in serum LDL, the crucial biological expression dependent on this mechanism, varies in intensity as a function of the type and of the dose of statin. PLEIOTROPIC EFFECTS: Besides their lipid lowering effect, statins have also been demonstrated to have pleiotropic effects mostly directly related to HMG-CoA reductase inhibition. CARDIOVASCULAR IMPACT: Several clinical studies investigating prevention of cardiovascular disease have established that statins decrease cardiovascular morbidity and mortality. Results have been very coherent for both primary and secondary prevention with statins. The cardiovascular benefit is most likely partly related to its pleiotropic effects, particularly those inducing a stabilization of the atheromatous plaques. INDICATIONS: Interventional studies have clearly established the role of statins in comparison with other lipid lowering agents for the prevention of cardiovascular events in most situations although a few therapeutic choices remain a subject of debate. Globally, the primary indications of statins are hypercholesterolemia and mixed hyperlipidemia with moderately elevated triglycerides. There are still some questions concerning the therapeutic goals of statin therapy.

Anticholesteremic Agents↗
PubMed2000

Pleiotropic effects of statins in atherosclerosis and diabetes.

OBJECTIVE: To investigate the direct anti-atherosclerotic properties of statins. RESEARCH DESIGN AND METHODS: Using in vitro and ex vivo models, the effect of different statins on key events involved in atherogenesis has been investigated. We studied the ability of statins to modulate modified LDL-induced cholesterol esterification, metalloproteinase secretion by macrophages, and arterial myocyte migration and proliferation. The mechanisms underlying the inhibitory effect of statins have also been explored. Finally, the antiproliferative effect of sera from statin-treated patients has been confirmed in a cell culture system. RESULTS: Fluvastatin, simvastatin, lovastatin, atorvastatin, and cerivastatin, but not pravastatin, dose-dependently decrease smooth muscle cell (SMC) migration and proliferation. Moreover, statins are able to reduce cholesterol accumulation in macrophages in vitro by blocking cholesterol esterification and endocytosis of modified lipoproteins and matrix-degrading enzyme secretion. This in vitro inhibition was completely prevented by mevalonate and partially by all-trans farnesol and all-trans geranylgeraniol, confirming the specific role of isoprenoid metabolites (probably through prenylated protein[s]) in regulating these cellular events. The inhibitory effect of statins on SMC proliferation has been shown in different models of proliferating cells, such as cultured arterial myocytes and rapidly proliferating carotid and femoral intimal lesions in rabbits, independently of their ability to reduce plasma cholesterol. Finally, ex vivo studies showed that sera from fluvastatin-treated patients interfere with SMC proliferation. CONCLUSIONS: These results suggest that 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors exert a direct anti-atherosclerotic effect in the arterial wall, beyond their effects on plasma lipids that could translate into a more significant prevention of cardiovascular disease. These findings provide a basis for the beneficial effect of statins in clinical trials also involving diabetic patients--a population with a higher absolute risk of recurrent cardiovascular events.

Animals↗
PubMed2001

[Mechanisms of action of statins and their pleiotropic effects].

This brief review and update considers a few aspects of the mechanisms of action of statins, especially those related to some of the pleiotropic effects that have clinical relevance. The beneficial effect on endothelial dysfunction is a class effect that is related not only to the lowering of plasma LDL-cholesterol but also to a direct effect on nitric oxide (NO) production. It is an early and sustained effect, linked to oxidative processes, that deserves particular attention since endothelial dysfunction is intimately linked to atherogenesis. Awareness of the anti-inflammatory effect came about following the observation that statin administration in humans reduces markers of inflammation in the circulation. The importance of these observations is ascribable to the fact that atherosclerosis is an inflammatory disease, that the inflammatory process in a coronary artery is now measurable in vivo in humans, that it contributes to the progression and the destabilization of the plaque, and also, because statins exert a number of effects that tend to stabilize it. Statins, and particularly lipophilic statins, in general inhibit cell proliferation, seemingly by multifaceted mechanisms. These include inhibition of cell cycle progression, induction of apoptosis, reduction of cyclooxygenase-2 activity and an enhancement of angiogenesis. At the center of these mechanisms stands the ability to inhibit G protein prenylation through a reduction of farnesylation and geranylgeranylation. This effect has been used to show that statins are anticarcinogenic in vitro and in animals. The clinical relevance of such a property remains to be proven but is supported by promising observations in animals and in humans which are detailed in this review. Finally, the ability of lipophilic statins to increase the production of bone morphogenetic protein-2 (BMP-2), and to enhance osteogenesis in animals combined with the results of several clinical studies should stimulate physicians to seriously consider an eventual indication of statins for the treatment of osteoporosis.

Arteriosclerosis↗
PubMed2001

[Great discrepancies between European, Dutch and Belgian criteria for the use of statins in the prevention of primary cardiovascular disease in family practice].

OBJECTIVE: To determine the differences in prescribing advice for statines in primary cardiovascular prevention, applying different protocols, in a first-line setting. METHOD: In February-March 2000, at the general practice 'Medicine for the People' in Deurne-Antwerp, Belgium, all contacts with patients known with at least one cardiovascular risk factor and no signs of cardiovascular disease were included in the study. The absolute risk of developing cardiovascular disease in the next 10 years was calculated per patient according to the protocols of the 'European Society of Cardiology' (ESC) and the Dutch College of General Practitioners (NHG) and it was determined whether these protocols advised prescription of statines. It was also determined if the Belgian criteria for repayment of statines, developed by the Rijksinstituut voor Ziekte- en Invaliditeitsverzekering (RIZIV) were met. RESULTS: The study group comprised 143 patients with a mean age of 66 years, of which 51 (36%) were men. According to the RIZIV criteria 75 (52%) patients of these 143 were eligible for the repayment of statines. The NHG protocol advised to prescribe statines for 4 (3%) patients and the ESC protocol for 69 (48%) patients. Of the 75 patients who were considered for repayment, 34 (45%) according to the ESC protocol and 74 (99%) according to the NHG protocol did not need statines. Also, in the whole study population, 28 (20%) patients needed statines according to ESC and 3 (2%) patients according to NHG, but they could not get repayment for statines according to the RIZIV. The ESC protocol estimated the risk per patient on average 8.5% (95% confidence interval: 7.1-9.8; p < 0.0001) higher than the NHG protocol. CONCLUSION: The NHG protocol estimated the risk significantly and markedly lower than the European protocol, although they are both based on the same Framingham data. There also existed a weak concordance between both protocols. The RIZIV criteria were not 'evidence-based'. They incited to an irrational and wasting prescribing behaviour. There is a need for an integrated guideline for primary cardiovascular prevention and for the adjustment of the RIZIV criteria.

Aged↗
PubMed2001

[The promise of statins].

Statins, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, are a class of drugs with a potent lipid-lowering effect that have been shown to reduce LDL cholesterol by 35-45% at therapeutic doses. Recent trials have demonstrated that in subjects with coronary artery disease, an aggressive treatment with high doses of statins, which lowers LDL cholesterol below 100 mg/dl, can obtain better results in terms of reduction of cardiovascular events, compared to the currently used dosage of statins. The pharmacologic effect of statins is far beyond the mere reduction of LDL cholesterol, in that it has been demonstrated that they are able to inhibit the proliferation of smooth muscle cells and macrophages, to restore the endothelial activity, and to inhibit the inflammatory response of macrophages. These effects have been called "pleiotropic effects" of statins. These metabolic activities of statins play an important role in contrasting the inflammatory elements of the atherosclerotic plaque. The atherosclerotic plaque is formed by a lipid core and a fibrous cap. Smooth muscle cells, macrophages and T lymphocytes are present in the plaque, particularly in the fibrous cap. In stable plaques, smooth muscle cells produce extracellular matrix, i.e. collagen and elastin, which strengthens the fibrous cap. In the presence of inflammatory stimuli, primarily oxidized LDL, T lymphocytes activate macrophage and smooth muscle cells to secrete cytokines and proteolytic enzymes, the collagenolytic metalloproteases, that can weaken the extracellular matrix and rupture the fibrous cap. A local thrombotic mechanism starts in the ruptured plaque, promoted by the tissue factor released by macrophages in the lipid core of the plaque, which can propagate to the coronary lumen with total occlusion. Statins have been demonstrated to contrast the inflammatory activity of macrophages and smooth muscle cells, inducing smooth muscle cells to secrete extracellular matrix which strengthens the fibrous cap and prevents rupture. At present, the primary target of statins is LDL cholesterol reduction, but with additional effects on the inflammatory cell of the plaque with a reduction in macrophages and secretion of collagenolytic metalloproteases and reinforcing the fibrous skeleton of the plaque by increasing the content of interstitial collagen.

Anticholesteremic Agents↗
PubMedDate not supplied

[Postinfarction statins. An unquestionable benefit. A therapeutic strategy that can be improved].

Atherosclerotic disease is etiopathogenically related to the presence of hypercholesterolemia. Physicians have never had until now a generation of lipid-lowering drugs with a comparable degree of efficacy, potency and safety as statins. The most explored field with statins has been the post myocardial infarction period, since this type of patients is at high risk of new cardiovascular events and, as a consequence, can obtain a marked benefit from intervention. Accordingly, three large-scale clinical trials with statins have conclusively demonstrated a significant reduction in cardiovascular events and in mortality after myocardial infarction. Nevertheless, although there is convincing evidence that statins should be implemented after myocardial infarction, there are still a number of relevant questions open and under study. The first of them is the value of the so-called pleiotropic properties of statins (additional properties independent from cholesterol lowering), so important for plaque stabilization. In addition, there is uncertainty about how early treatment with statins has to be started after the acute phase. Another point we do not know is the goal of lipid intervention (the level of total or LDL-cholesterol to be achieved). In fact, there is still a debate on whether patients with average levels of cholesterol or even with low levels are to treated. Finally, but related to the previous question, it would be very interesting to determine whether high doses of statins, are necessary or can low doses be equally efficacious. In conclusion, statins are a landmark in cholesterol-lowering interventions after myocardial infarction. Probably, the majority of survivors should be treated. At present, active research is focused on delineating more precisely the manner in which these drugs are to be used to prolong life in these patients.

Cardiovascular Diseases↗
PubMed2002

Preclinical pharmacokinetics of statins.

This review summarizes the pharmacokinetic properties of HMG-CoA reductase inhibitors (or statins) reported in animals. Lovastatin and simvastatin are administered as lactone prodrugs in contrast to other statins, which are generally formulated in the pharmacological active hydroxy acid form. Pharmacokinetics vary with the statin and animal species considered. Oral absorption is rapid and the bioavailability low due to an extensive first-pass metabolism. Pitavastatin is the exception, with high bioavailability in all species except monkeys (80% vs. 18%). Plasma protein binding is high for all statins (> 95%) except pravastatin (60%). Regardless of the dosing schedule (single or multiple), animal species and statin, the highest tissue levels are found in the liver--the target organ. Elimination is rapid with metabolism being the main elimination route for all statins, except for pitavastatin, which is only slightly metabolized, and pravastatin, which aside from metabolism is also eliminated by renal excretion. Statins undergo enterohepatic circulation and are recovered mainly in feces via bile, the extent of which is species-dependent. Metabolism varies with the statin and animal species, particularly the beta-oxidation of the dihydroxy heptanoic side chain that occurs primarily in rodents.

Absorption↗
PubMed1992

Statin, a protein specifically present in nonproliferating cells, is a phosphoprotein and forms a complex with a 45-kilodalton serine/threonine kinase.

The protein statin is found in nuclei of nonproliferating cells. Here we report that statin is a phosphoprotein, phosphorylated at serine residues in cultured cells. During immunoprecipitation with anti-statin (S44) antibody, a 45-kDa protein co-precipitates with the 57-kDa statin. In vitro kinase assays demonstrate that the S44 immunoprecipitates can phosphorylate, besides statin, immunoglobulins, enolase, and casein, at either serine or serine/threonine residues. Kinase assays with immunoprecipitated proteins performed on casein- or enolase-impregnated gels show that these substrates are phosphorylated by the 45-kDa (p45) protein. When the S44 immunoprecipitates from human cultured fibroblasts with different in vitro life-spans were compared, the p45 kinase activity was present only in young nongrowing and senescent cells, but not in young growing ones. In other cell cultures, the kinase is detected only in protein complexes precipitated from quiescent 3T3 cells, but not from cycling 3T3 cells or from transformed human glioma (U251-4) cells. Cell fractionation studies, indicating that the phosphorylating activity of S44 immunoprecipitates correlates both qualitatively and quantitatively with the amount of statin present, provide strong evidence that in vivo statin is specifically associated with the p45 kinase. These results suggest that the nonproliferation-specific nature of statin is indeed related to the phosphorylated property of this protein and maybe contributed by the associated kinase.

3T3 Cells↗
PubMed2004

Statin prescribing in Australia: socioeconomic and sex differences. A cross-sectional study.

OBJECTIVE: To assess if there are any differences in statin prescribing across Australia by socioeconomic status or sex and to relate prescribing rates to coronary heart disease (CHD) mortality rates. DESIGN: Cross-sectional study using data on statin prescribing by age, sex and patient postcode for the period May to December 2002. SETTING AND PARTICIPANTS: The Australian population, stratified by sex and quintile of Index of Relative Socio-Economic Disadvantage (IRSD). MAIN OUTCOME MEASURES: Age-standardised rates of statin scripts per 1000 population per month for each sex and IRSD quintile. RESULTS: 9.1 million prescriptions for statins were supplied between May and December 2002, for a total cost of 570 million dollars. The age-standardised rates for statin prescribing in women varied from 56.9 (95% CI, 56.6-57.2) scripts per 1000 population per month in the most disadvantaged socioeconomic quintile through 53.4 (95% CI, 53.0-53.7), 50.3 (95% CI, 50.0-50.6), 48.4 (95% CI, 48.1-48.7) to 46.3 (95% CI, 46.0-46.6) in the least disadvantaged quintile. For men the figures were 52.6 (95% CI, 52.3-52.9), 50.9 (95% CI, 50.6-51.2), 48.8 (95% CI, 48.6-49.1), 47.7 (95% CI, 47.4-47.9), and 51.9 (95% CI, 51.6-52.2). There was a significant linear association between statin prescribing and CHD mortality by quintile of socioeconomic disadvantage in women (weighted least squares slope, 0.380; 95% CI, 0.366 to 0.395; P < 0.0001), but not in men (slope, -0.002; 95% CI, -0.010 to 0.006; P = 0.65). CONCLUSIONS: Our results suggest that in men there is either overprescribing of statins in the highest socioeconomic quintile or underprescribing in the lowest. Furthermore, contrary to expectation, women - relative to men - are prescribed statins at higher rates at lower levels of risk (using CHD deaths as a proxy measure of risk).

Adult↗
PubMed2004

Pharmacoutilization of statin therapy after acute myocardial infarction. A real practice analysis based on administrative data.

BACKGROUND: Despite randomized and controlled trials indicating continuous treatment with statin therapy as a factor in reducing morbidity and mortality after acute myocardial infarction, records reveal a high percentage of patients at risk who are either not receiving treatment or being treated inadequately. METHODS: An administrative database kept by the Local Health Unit of Ravenna and listing patient baseline characteristics, drug prescriptions and hospital admissions was used to perform: 1) an analysis of patients discharged alive from hospital each year between 1996 and 2000 with a diagnosis of acute myocardial infarction, and 2) a retrospective cohort study of drug utilization, and particularly the use of statins, year by year. All prescriptions for statins filled in the 6 months after hospital discharge were considered and used to classify patients in terms of their exposure to statin therapy and of their pharmacoutilization. RESULTS: A total of 2265 subjects were enrolled (446 in 1996, 440 in 1997, 443 in 1998, 443 in 1999, and 493 in 2000). The percentage of patients treated with statins increased each year (from 22.6% in 1996 to 43.8% in 2000) as did the percentage of adequately dosed patients (from 4.3% in 1996 to 23.9% in 2000). The overall cost of dispensed statins amounted to 10,610 euros in 1996 and 45,102 euros in 2000. The proportion of cost for statins accountable to adequately dosed patients ranged from 36.4% in 1996 to 77.4% in 2000. The average cost per adequately dosed patient ranged from 203.40 euros in 1996 to 296.00 euros in 2000 and increased year by year. CONCLUSIONS: Pharmacoutilization of statin therapy was found to be unsatisfactory in each study year. Interestingly, however, the trend indicated by the study suggests increasing percentages of patients being exposed to the treatment, and of adequately dosed patients. These results may be attributed to a greater awareness of the need for proper treatment, and may be considered as reflecting a significant improvement in drug management.

Adult↗