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PubMed2005

The influence of physicians' guideline compliance on patients' statin adherence: a retrospective cohort study.

BACKGROUND: National cholesterol management guidelines recommend regular follow-up of patients and annual lipid evaluations to promote adherence to statin therapy. OBJECTIVE: This study examined the relationship between primary care physicians' (PCPs') compliance with primary care guidelines and patients' adherence to statin therapy. METHODS: A retrospective cohort study was conducted among statin users aged > or = 50 years who had an assigned PCP at a Veterans Affairs Medical Center. The dependent variable was statin adherence by patients over 24 months. Computerized pharmacy, laboratory, and medical records were used to measure PCPs' compliance with 4 recommendations in national cholesterol management guidelines: (1) lipid-lowering drug (LLD) initiation; (2) 8-week follow-up visit after an initial LLD prescription; (3) 6- or 12-month follow-up visit for established LLD users; and (4) annual lipid evaluation. Multilevel, multivariable regression models were used to estimate the effects of PCPs' guideline compliance on patients' adherence while controlling for patients' demographic characteristics, comorbid conditions, and pharmacotherapy factors. RESULTS: The sample included 82 PCPs caring for 4707 patients. The mean statin adherence rate was 83.9%. An increase in the annual lipid evaluation rate resulted in an increase in patients' adherence (P = 0.037). Black race and higher statin dose negatively influenced patients' adherence (both, P < 0.001). The effects of PCPs' compliance rates were not homogeneous across race. Specifically, the 8-week follow-up visit rate after initial LLD prescription was significantly associated with improved statin adherence among the black subpopulation only. CONCLUSIONS: Patients' adherence to statin therapy was influenced by their PCPs' compliance with cholesterol management guidelines. Efforts should be made to align PCPs' practice with published guidelines for optimal statin therapy, especially for vulnerable subpopulations of patients.

Aged↗
PubMed2005

[Statins in patients with renal failure--the current therapeutic status].

Statins are the most frequently used lipid-lowering drugs in all cardiovascular disease. It has been postulated that also patients with renal failure and end-stage renal disease (ESRD) may benefit from statin therapy. Moreover, statins may exhibit additional inhibitory effects on the atherogenesis, such as a modulation of the immune system as triggered by oxidatively modified LDL and a reduction of the inflammatory marker C-reactive protein (CRP). Statins reduce inflammation, cell proliferation, which leads to a reduction in cellular damage. Those effects are probably independent of cholesterol levels. Limited data suggest that HMG-CoA reductase inhibitors (statins) may slow loss of renal function in individuals with chronic renal insufficiency. It is concluded on the basis of the CARE trial that pravastatin may slow renal function loss in individuals with moderate to severe kidney disease, especially those with proteinuria. Similar data were obtained from recently published HPS trial with simvastatin. These findings require confirmation by a large randomized trial conducted specifically in people with chronic renal insufficiency. Statins vary in their pharmacological profiles, leading to distinct levels of systemic exposure and capacities to penetrate skeletal myocytes. Pharmacokinetic interactions with certain agents increase the likelihood of statin-induced myopathy and, in exceedingly rare instances, potentially fatal rhabdomyolysis with myoglobinuria and renal failure, therefore two statins have been suggested for renal failure patients. These are the ones that are not metabolised by the cytochrome P450 3A4 system--fluvastatin and pravastatin. The article summarizes the current therapeutic status of statin use in renal failure patients.

Cytochrome P-450 CYP3A↗
PubMed2006

Presymptomatic neuromuscular disorders disclosed following statin treatment.

It is well recognized that statins affect muscular tissue adversely and that their use is associated with clinically important myositis, rhabdomyolysis, mild elevation of serum creatine kinase (CK) levels, myalgias, muscle weakness, muscle cramps, and persistent myalgias or serum CK level elevations after statin treatment is discontinued. The association between statins and the disclosure of presymptomatic metabolic myopathy is another underrated phenomenon related to statin therapy that was recently recognized in rare cases. The purpose of this report is to provide additional support for this association and to report other neuromuscular disorders that have also been seen following statin intake. The present case series illustrates that statins may act as unmasking agents in asymptomatic patients with a latent neuromuscular disorder. Thus, it may be postulated that statin intake may be a sufficient insult to precipitate neuromuscular symptoms and substantially increase muscle enzymes in presymptomatic patients with an abnormal neuromuscular substrate. In conclusion, muscular symptoms or increased serum CK levels persisting after statin treatment discontinuation should alert the clinician to pursue further diagnostic evaluations for the detection of potential underlying neuromuscular diseases.

Biopsy↗
PubMed2005

Statin use and the risk of incident dementia: the Cardiovascular Health Study.

BACKGROUND: Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) reduce cardiovascular risk through mechanisms that might affect the development of dementia. OBJECTIVE: To evaluate whether statin use is associated with a lower risk of dementia compared with never use of lipid-lowering agents (LLAs). DESIGN: Cohort study of community-dwelling adults 65 years and older. The analysis included 2798 participants free of dementia at baseline. MAIN OUTCOME MEASURES: Using Cox proportional hazards regression analysis, we estimated the risk of incident all-cause and type-specific dementia associated with time-dependent statin therapy compared with never use of LLAs. The primary analyses incorporated a 1-year lag between exposure and outcome. Secondary analyses included the final year of exposure and modeled statin use as current use vs nonuse to simulate a case-control approach. RESULTS: Compared with never use of LLAs, ever use of statins was not associated with the risk of all-cause dementia (multivariable-adjusted hazard ratio [HR], 1.08; 95% confidence interval [CI], 0.77-1.52), Alzheimer disease alone (HR, 1.21; 95% CI, 0.76-1.91), mixed Alzheimer disease and vascular dementia (HR, 0.87; 95% CI, 0.44-1.72), or vascular dementia alone (HR, 1.36; 95% CI, 0.61-3.06). In contrast, in secondary analyses, current use of statins compared with nonuse of LLAs was associated with HRs of 0.69 (95% CI, 0.46-1.02) for all-cause dementia and 0.56 (95% CI, 0.35-0.92) for any Alzheimer disease. CONCLUSIONS: In this cohort study, statin therapy was not associated with a decreased risk of dementia. Methodological differences may explain why results of this cohort investigation differ from those of prior case-control studies. Additional investigation is needed to determine whether and for whom statin use may affect dementia risk.

Aged↗
PubMed2006

Achieving target cholesterol goals after stroke: is in-hospital statin initiation the key?

BACKGROUND: National advisories recommend statin therapy as an element of secondary prevention for patients with ischemic stroke or transient ischemic attack of atherosclerotic origin. Statins are of proven benefit in persons at high risk of vascular disease. OBJECTIVES: To evaluate the effects of in-hospital initiation of statins on 3-month treatment adherence rates and achievement of national guideline target cholesterol goals. METHODS: Data were collected in consecutively encountered patients with ischemic stroke or transient ischemic attack admitted to a university hospital stroke service beginning September 1, 2002. Patients were included in the study if they were not receiving a statin before admission and had an indication for statin therapy. Adherence to statin treatment and achievement of national guideline target cholesterol goals were assessed 3 months after discharge. RESULTS: From September 1, 2002, through April 30, 2005, 92 (17%) of 552 individuals met the study criteria. Hospital initiation of statin therapy yielded high rates of adherence (93% [86/92]), lowered mean low-density lipoprotein cholesterol levels from 120 to 78 mg/dL (3.1 to 2.0 mmol/L; P<.001), and increased the proportion of patients with low-density lipoprotein cholesterol levels lower than 100 mg/dL (2.6 mmol/L) from 36% to 88% (P<.001) at 3 months. CONCLUSIONS: Statin initiation during hospitalization for an ischemic cerebrovascular event is associated with high rates of adherence to treatment, lowering of low-density lipoprotein cholesterol levels, and higher rates of achieving national cholesterol guidelines.

Adult↗
PubMed2002

Statin inhibits leukocyte-endothelial interaction and prevents neuronal death induced by ischemia-reperfusion injury in the rat retina.

BACKGROUND: Retinal ishchemia-induced neuronal death is believed to be a direct causal process in the development of many ocular diseases. The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, statin, is known to improve endothelial function in proinflammatory conditions. OBJECTIVE: To investigate the effects of statin on leukocyte accumulation during ischemia-reperfusion injury and on subsequent retinal damage. METHODS: Transient retinal ischemia was induced in Long-Evans rats for 60 minutes using temporal ligation of the optic nerve. Leukocyte-endothelial interactions in the postischemic retina were evaluated in vivo with a scanning laser ophthalmoscope. Statin was administered 5 minutes before the induction of retinal ischemia. P-selectin and intercellular adhesion molecule-1 (ICAM-1) gene expression in the postischemic retina were studied with the semiquantitative polymerase chain reaction. Histologic studies were carried out to evaluate retinal damage. RESULTS: The preadministration of statin attenuated the rolling and accumulation of leukocytes, decreased P-selectin and ICAM-1 expression, and reduced the number of apoptotic cells in the retina. Furthermore, histologic evaluation 168 hours after reperfusion showed that statin significantly diminished the resultant retinal tissue damage. The neuroprotective effect of statin was abolished when it was administered along with a nitric oxide synthase inhibitor, nitroglycerine-nitro-L-arginine methyl ester. CONCLUSION: Statin may exert neuroprotective effects by inhibiting leukocyte-endothelial interaction through the release of nitric oxide from the endothelium. CLINICAL RELEVANCE: As a result of its efficacy in preventing retinal neuronal death, statin may be developed into a novel therapeutic modality for many ocular ischemic diseases.

Acridine Orange↗
PubMed2004

Lipid-lowering therapy with statins in high-risk elderly patients: the treatment-risk paradox.

CONTEXT: The benefits of cardiovascular therapies such as statins for secondary prevention have been well documented, although they may not be optimally used in patients most likely to benefit. Ideally, aggressiveness in the use of these beneficial therapies should correlate with baseline cardiovascular risk. OBJECTIVE: To examine the association between physicians' treatment aggressiveness and baseline cardiovascular risk. DESIGN, SETTING, AND PATIENTS: Retrospective cohort study incorporating the use of multiple linked health care administrative databases covering more than 1.4 million elderly residents of Ontario. We included 396,077 patients aged 66 years or older who had a history of cardiovascular disease or diabetes while undergoing medical treatment and who were alive on April 1, 1998. Baseline cardiovascular risk was derived using a risk-adjustment index in which we modeled probability of death after 3 years of follow-up. MAIN OUTCOME MEASURE: Likelihood of statin use, stratified by baseline cardiovascular risk, after adjusting for age, sex, socioeconomic status, and rural or urban residence. RESULTS: Only 75,617 patients (19.1%) in this secondary prevention cohort were prescribed statins. In patients 66 to 74 years old, the adjusted probabilities of statin prescription were 37.7%, 26.7%, and 23.4% in the categories of low, intermediate, and high baseline risk, respectively. The likelihood of statin prescription was 6.4% lower (adjusted odds ratio, 0.94; 95% confidence interval, 0.93-0.95) for each year of increase in age and each 1% increase in predicted 3-year mortality risk. The influence of age also interacted synergistically with baseline risk on the prescription of statins (P<.001). CONCLUSIONS: We found that prescription of statins diminished progressively as baseline cardiovascular risk and future probability of death increased. Since the benefits of a therapy are dependent on the baseline risk, the maximum benefits of statins may not be fully realized until implementation of therapy includes patients at highest risk.

Aged↗
PubMed2006

Statin use and incident nuclear cataract.

CONTEXT: Statins are widely prescribed for their lipid-lowering effects but also have putative antioxidant properties. Oxidative stress is believed to play a role in the development of nuclear cataract, but little is known regarding the relationship of statin use and cataract incidence. OBJECTIVE: To evaluate the relationship of use of statins and incident cataract in adults in a midwestern community in the United States. DESIGN, SETTING, AND PARTICIPANTS: The Beaver Dam Eye Study, an observational, longitudinal, population-based study of age-related eye disease in Beaver Dam, Wis. There were 1299 persons who were seen at the third examination in 1998-2000, had gradable photographs in both eyes, and were deemed to be at risk of developing nuclear cataract within 5 years. MAIN OUTCOME MEASURE: Five-year incidence of cataract with respect to statin use. Cataracts were graded from photographs taken through the participant's dilated pupil. RESULTS: A total of 210 persons developed incident nuclear cataract in the interval from 1998-2000 to 2003-2005. Five-year incidence of nuclear cataract was 12.2% in statin users compared with 17.2% in nonusers (odds ratio [OR], 0.55; 95% confidence interval [CI], 0.36-0.84), controlling for age. When only never smokers without diabetes were assessed, the age-, lipid level-, and sex-adjusted OR was 0.40 (95% CI, 0.18-0.90). Five-year incidence of cortical cataract was 9.9% in statin users and 7.5% in nonusers (OR, 1.28; 95% CI, 0.79-2.08); posterior subcapsular cataract occurred in 3.0% of statin users and 3.4% of nonusers (OR, 0.82; 95% CI, 0.39-1.71). CONCLUSION: Statin use in a general population appears to be associated with lower risk of nuclear cataract, the most common type of age-related cataract.

Adult↗
PubMed1992

Modulation of nuclear statin expression in rat thyroid follicle cell following administration of thyroid stimulating hormone.

This study was designed to examine the state of proliferation in the rat thyrocyte following the administration of thyroid stimulating hormone (TSH). An immunohistochemical technique involving the use of a monoclonal antibody to statin, a nonproliferation-specific nuclear antigen, was developed to measure the subpopulation of cells that have ceased to divide. Following the random assignment of young male Sprague-Dawley rats into various groups, the rats in the control group received a single intraperitoneal (i-p) injection of normal saline, whereas the experimental groups received single i-p injections of TSH at doses of 0.25, 0.50, and 1.0 IU, respectively. All rats were subsequently sacrificed in groups of three at 1, 2, 4, and 24 hours. The statin antibody label was readily identified within the follicle cell nucleus. Results revealed a statistically significant transient decrease in the mean percent statin-positive nuclei in the TSH-treated groups. The time- and dose-dependent effect of TSH was maximal at 2 hours and no longer discernible at 24 hours. A second experiment involving the chronic administration of TSH (i-p 0.25 IU twice daily) resulted in a cumulative response with a statistically significant progressive decrease in the mean percent of statin-positive nuclei at 5 and 10 days, returning to near normal values 5 days following the cessation of treatment. Determination of the nuclear optical density of the statin reaction product by image analysis techniques revealed that a single injection of TSH resulted in a rapid disappearance of the statin nuclear protein. This result suggests that the disappearance of statin in the nucleus appears to reflect the event of cells leaving the nondividing quiescent state to resume the cell cycle traverse following the administration of TSH. The disappearance of statin appears as an early nuclear event that parallels the earliest known cytoplasmic pinocytotic response to TSH in the rat thyroid follicle cell.

Animals↗
PubMed2007

Effectiveness of two statin prescribing strategies with respect to adherence and cardiovascular outcomes: observational study.

BACKGROUND: There is considerable evidence that statins can reduce cardiovascular events. Currently high-risk patients are treated to a target cholesterol concentration. An alternative prescribing strategy (the 'fire-and-forget' approach) would instead deploy low-dose statins more widely. It has been suggested that for the same cost this approach might prevent more cardiovascular events. We have compared the treat-to-target and fire-and-forget statin prescribing strategies with respect to adherence and cardiovascular outcomes. METHODS: We used a population-based record-linkage database containing several data sets linked by a unique patient identifier. We identified two cohorts of patients. Patients in the treat-to-target cohort were prescribed a statin, and subsequent measurement of their cholesterol was followed by upward titration of their statin dose if necessary. Patients in the fire-and-forget cohort were prescribed a statin, but no further cholesterol measurement was observed during the follow-up period. FINDINGS: Adherence to statin treatment in patients treated to target was significantly better than in patients treated on a fire-and-forget basis (adjusted odds ratio 2.51, 95%CI 2.26-2.78). We found a lower cardiovascular disease (CVD) event rate in patients treated to target than in fire-and-forget patients (hazard ratio of CVD or cardiovascular death 0.41 (0.35-0.48) even after adjustment was made for adherence and baseline CVD risk). INTERPRETATION: Our findings suggest that adherence to statins is worse in patients treated on a fire-and-forget basis than in patients treated to a target cholesterol concentration, and that this prescribing strategy is associated with worse cardiovascular outcomes.

Cardiovascular Diseases↗
PubMed2007

Statins and biomarkers of inflammation.

Clinical and epidemiologic studies convincingly demonstrate that increased levels of low-density lipoprotein cholesterol promote premature atherosclerosis. Several large clinical trials have demonstrated that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) decrease cardiovascular events. The beneficial effects of statins may extend to mechanisms beyond cholesterol reduction. Evidence for the pleiotropic effects of statins is provided by recent clinical trials in which the benefit of statin drugs is manifest early in the course of lipid-lowering therapy, well before plaque regression could occur. Inflammation is pivotal in all stages of atherosclerosis, and C-reactive protein (CRP), the prototypic marker of inflammation, has emerged as a cardiovascular risk marker. Statins reduce CRP levels, and this reduction in most studies does not correlate to reduction in cholesterol. In addition, statins have beneficial effects on endothelial function, monocyte-macrophages, and platelets. In this review we discuss the role of inflammation in atherosclerosis, the role of CRP as a risk marker, the clinical evidence implicating the anti-inflammatory effects of statins, and the cellular and molecular basis underlying the anti-inflammatory effects of statins.

Biomarkers↗
PubMed2006

Review article: The role of statins in reducing perioperative cardiac risk: Physiologic and clinical perspectives.

PURPOSE: To review the pathobiology and clinical implications of coronary vulnerable atherosclerotic plaques (VAPs), to discuss the role of statin therapy in VAP stabilization, and the potential benefits of perioperative statin therapy (PST) in reducing perioperative risk of acute coronary syndromes (ACSs). SOURCE: MEDLINE search using "perioperative", "cardiac morbidity", "atherosclerosis", "vulnerable plaque", "statins" and combinations of these terms as keywords. The reference lists of relevant articles were further reviewed to identify additional citations. PRINCIPAL FINDINGS: The nonstenotic, yet rupture-prone VAP causes most myocardial infarctions (MIs) and other ACSs, both in the nonsurgical and surgical patients. Large clinical trials in both primary and secondary prevention and in patients with ACSs have demonstrated that statin therapy will reduce cardiovascular morbidity and mortality across a broad spectrum of patient subgroups. These trials also suggest, and laboratory investigations establish, that statins possess favourable vascular effects independent of cholesterol reduction. Statins appear to interfere specifically with the pathophysiologic mechanisms implicated in atherothrombotic disease. Statins reduce vascular inflammation, improve endothelial function, stabilize VAPs, and reduce platelet aggregability and thrombus formation. Recent studies have shown that PST is associated with a reduced incidence of perioperative and long-term cardiovascular complications in high-risk patients. Combined therapy with statins and ss-blockers is a conceptually valid strategy targeting critical steps in the pathogenesis of an ACS. CONCLUSION: Emerging evidence for the efficacy and safety of PST is promising, especially when combined with ss-blocker therapy in patients at highest risk. Confirmation of this early evidence awaits the results of ongoing and future prospective randomized controlled trials.

Anticholesteremic Agents↗
PubMed2006

Preprocedural statin therapy reduces the risk and extent of cardiac biomarker release following percutaneous coronary intervention.

This study evaluates the association between statin therapy in patients treated by percutaneous coronary intervention (PCI) for stable angina pectoris and postinterventional myocardial injury with subsequent long-term clinical outcome. Prospectively collected data on 400 consecutive patients with stable angina pectoris or evidence of inducible myocardial ischemia were analyzed. The incidence of myocardial infarction based on postinterventional release of troponin I>1.5 ng/ml was 12% in the statin pretreated patients and 20% in those not pretreated with statin therapy (P=0.04, odds ratio 1.84, 95% confidence interval 1.06-3.21). Of the patients experiencing a post-PCI troponin elevation>1.5 ng/ml, those pretreated with a statin pre-PCI had a lesser troponin elevation compared with those not receiving a statin pre-PCI (median: 2.9 ng/ml [1.9-11.5] vs 5.0 ng/ml [3.1-8.8]; P<0.001). In the multivariate model, preprocedural statin therapy was identified as the only independent negative predictor of procedure-related myocardial necrosis based on postprocedural troponin elevation. In the 21-month follow-up period, statin pretreated patients were observed to have fewer deaths, revascularizations, or myocardial infarction; however, this difference was not statistically significant. These results suggest that pretreatment with statins in patients undergoing PCI for stable angina pectoris reduces the risk and extent of procedure-related myocardial injury measured by troponin release.

Adult↗
PubMed2003

Statin therapy in patients with coronary artery disease improves the impaired endothelial progenitor cell differentiation into cardiomyogenic cells.

Human endothelial progenitor cells (EPCs) can differentiate into cardiomyogenic cells in vitro. We tested the effects of statin therapy on the differentiation rate of EPCs from patients with coronary artery disease (CAD), who may benefit from autologous cell therapy.EPCs from 3 age-matched groups were tested: No CAD (n = 13), CAD patients with (n = 10) or without (n = 16) statin therapy. From 4 CAD patients, EPCs were tested before and after 4 weeks of therapy with 20 mg atorvastatin. After 6 days of co-culture with rat neonatal cardiomyocytes, EPC differentiation was quantified by immunostaining for alpha-sarcomeric actinin flow cytometry analysis. After 6 days of co-culture, the percentage of -sarcomeric actinin-positive EPCs was significantly (p = 0.014) higher in EPCs from adults without CAD (8.07% +/- 1.48% of EPCs) compared to EPCs from CAD patients without statin (3.56% +/- 0.72%). Importantly, patients with statin therapy revealed significantly higher numbers of alpha-sarcomeric actinin-positive EPCs (6.36% +/- 0.69%, p = 0.01) compared to CAD patients without statin. In addition, statin therapy resulted in a significant (p = 0.017) increase of EPC differentiation in all 4 CAD patients investigated before and 4 weeks after statin therapy. The survival of EPCs did not differ between the different groups suggesting that the regulation of EPC differentiation is not secondary to altered EPC survival. In vitro, EPC treatment with 0.1 micro M atorvastatin did not affect EPC differentiation (116.15% +/- 49.11% of control).EPCs from patients with CAD display impaired differentiation into cardiomyogenic cells. This defect can be improved by in vivo, statin therapy.

Adult↗
PubMed1986

Disappearance of statin, a protein marker for non-proliferating and senescent cells, following serum-stimulated cell cycle entry.

Statin, a protein of 57,000 D, is present in the nuclei of quiescent or senescent fibroblasts (Wang, E, J cell biol 100 (1985) 545), but is absent in their young replicating counterparts. Immunohistochemical survey of a variety of tissues demonstrates that the presence of statin is a marker for cells that are no longer involved in proliferation, i.e. those cells that are terminally differentiated. Statin expression was examined by immunofluorescence microscopy in serum-starved cultures whose replication had been reinitiated by raising the serum concentration from 0.5 to 10%. Prior to serum addition, more than 85% of the cells stained positively for statin. After stimulation with serum, the expression of statin disappeared rapidly within the first 12-14 h. On the other hand, an increase in the level of DNA synthesis, signifying entry into S phase, was observed initially at 18 h after serum stimulation, and reached maximal levels 6 h later. Immunoprecipitation of statin derived from cells harvested at different intervals after serum stimulation revealed that the level of statin synthesis was reduced by 4 h and was hardly detectable at 8 h. These results demonstrate that the synthesis of statin occurs primarily when cells are in a quiescent state, and declines rapidly when cells are induced to proliferate; this decline precedes the transition from G1 to S phase.

Cell Cycle Proteins↗
PubMed2004

Statin therapy is associated with lower mortality among patients with severe heart failure.

Experimental considerations suggest both potential harm and benefit from statin therapy in patients with severe heart failure. However, relations of statin therapy with clinical outcomes in severe heart failure are not well established. Using data from the Prospective Randomized Amlodipine Survival Evaluation (PRAISE) trial, we evaluated associations of statin therapy with total mortality among 1,153 patients with severe heart failure (ejection fraction <30% and New York Heart Association class IIIB or IV symptoms) of ischemic and nonischemic etiologies. Statin therapy was administered to 134 patients (12%) during the study period. Over a 1.3-year mean follow-up, there were 413 deaths (29 deaths/100 person-years). Adjusting for age, gender, diabetes, smoking, heart failure etiology, ejection fraction, and New York Heart Association class, statin therapy was associated with a 62% lower risk of death (hazard ratio 0.38, 95% confidence interval 0.23 to 0.65), or 1 fewer death/5 patients taking statin therapy for 1 year. This association was not greatly altered by additional adjustment for a variety of other patient characteristics, including serum cholesterol levels. After propensity score analyses, statin therapy was still associated with a 48% lower risk of death (hazard ratio 0.52, 95% confidence interval 0.30 to 0.89). Although this observational study does not prove causality, further investigation of potential benefits of statins in patients with severe heart failure appears warranted.

Aged↗
PubMed2004

Effect of statin therapy prior to elective percutaneous coronary intervention on frequency of periprocedural myocardial injury.

This study evaluated whether pretreatment with statins was associated with a decreased incidence of periprocedural myocardial injury. Periprocedural myocardial injury occurs after percutaneous coronary intervention (PCI) and is associated with adverse outcomes. The pleiotropic properties of statins stabilize plaque and decrease the inflammatory milieu of atherosclerotic lesions. Accordingly, we hypothesized that preprocedural statin therapy would decrease periprocedural myocardial injury. We enrolled 425 patients who underwent successful PCI. The control arm (n = 150) included patients not on statin therapy at the time of PCI, and the statin arm (n = 275) included patients who were taking statin medication before PCI. All patients had serial enzymes measured, including creatine kinase (CK), CK-MB, and troponin I. The incidence of increased levels of CK and CK-MB >3 times normal and the absolute increase in CK and troponin I were compared between groups. The control arm had significantly higher periprocedural levels of CK. In the control group, 6% of patients had CK increases >3 times the upper limit of normal compared with 1.8% in the statin group (p = 0.02). The control arm had a higher frequency of CK-MB increases >3 times the upper limit of normal (7.3% vs 2.2%, p = 0.01). There was a trend toward higher levels of troponin I in the control group (3.21 vs 1.85 ng/ml, p = 0.06). Thus, statin therapy before elective PCI was associated with lower levels of periprocedural CK.

Aged↗
PubMed2005

The case for intensive statin therapy after acute coronary syndromes.

Acute coronary syndromes (ACS) consist of unstable angina or acute myocardial infarction and are associated with a high risk of early recurrent ischemic events. Revascularization procedures do not modify underlying pathophysiology and only modestly reduce early ischemic events after an index episode of ACS. Although statins improve dyslipidemia and cardiovascular risk over the long term, efforts to identify new ACS treatments are focusing on the ability of statins to modify the arterial wall-blood interface and reduce the risk of early recurrent ischemic events. Statins have been shown to reduce circulating markers of inflammation within days of an acute ischemic event. Short-term statin therapy also has been associated with improved coronary endothelial function, reversal of prothrombotic states, and reduction in atherosclerotic plaque volume. Findings from 6 randomized, controlled intervention trials were evaluated to determine if risk reduction is associated with the intensity of statin therapy. In addition, the predictive ability of baseline lipid levels and inflammatory markers were examined. High-intensity statin therapy (atorvastatin 80 mg) reduced early recurrent ischemic events after ACS compared with moderate-intensity treatment (eg, pravastatin 40 mg) or placebo. Moderate-intensity regimens (simvastatin 40 mg, pravastatin 20 to 40 mg, fluvastatin 80 mg, cerivastatin 0.4 mg) provided minimal benefit compared with placebo. Although there was no apparent relation between low-density lipoprotein (LDL) cholesterol levels before or during randomized treatment and short-term (4-month) risk of recurrent events, the degree of LDL cholesterol reduction with statin treatment after ACS may be related to longer-term event reduction. Moreover, evidence suggests that anti-inflammatory effects of high-intensity statin treatment are associated with clinical benefit.

Humans↗