Non-statin Group Research Articles

Pravastatin treatment before coronary artery bypass grafting for reduction of postoperative atrial fibrillation

The aim of this observational study was to determine the incidence of atrial fibrillation (AF) after coronary artery bypass grafting (CABG) in patients with or without preoperative pravastatin treatment. Between January 2005 and December 2007, a total of 195 patients (39 women, mean age 66.5 +/- 10.2 years) who underwent CABG only were enrolled in this study. Patients were divided into three groups: nonstatin group (n = 111), atorvastatin group (n = 63), pravastatin group (n = 21). The endpoint of the study was the occurrence of new-onset AF during the first 14 days after CABG. Postoperative AF was less frequent in the pravastatin group (9.5%, 2/21 patients) than in the nonstatin group (34.2%, 38/111 patients; P = 0.0025) and the atorvastatin group (34.9%, 22/63 patients; P = 0.0257). C-reactive protein levels were lower in the pravastatin group 72 h after surgery (nonstatin vs. pravastatin, P = 0.0180; atorvastatin vs. pravastatin, P = 0.0383). The Kaplan-Meier analysis showed the protective effect of pravastatin against the risk of developing AF (nonstatin vs. pravastatin, P = 0.0369; atorvastatin vs. pravastatin, P = 0.0378). Multivariable analysis showed that pravastatin treatment conferred a reduced risk of AF (odds ratio 0.22, 95% confidence interval 0.05-0.92, P = 0.0172). Pravastatin treatment before CABG may decrease the incidence of postoperative AF.

Preoperative statin is associated with decreased operative mortality in high risk coronary artery bypass patients

BackgroundStatins are widely prescribed to patients with atherosclerosis. A retrospective database analysis was used to examine the role of preoperative statin use in hospital mortality, for patients undergoing isolated coronary artery bypass grafting (CABG.)MethodsThe study population comprised 2377 patients who had isolated CABG at Allegheny General Hospital between 2000 and 2004. Mean age of the patients was 65 ± 11 years (range 27 to 92 years). 1594 (67%) were male, 5% had previous open heart procedures, and 4% had emergency surgery. 1004 patients (42%) were being treated with a statin at the time of admission. Univariate, bivariate (Chi2, Fisher's Exact and Student's t-tests) and multivariate (stepwise linear regression) analyses were used to evaluate the association of statin use with mortality following CABG.ResultsAnnual prevalence of preoperative statin use was similar over the study period and averaged 40%. Preoperative clinical risk assessment demonstrated a 2% risk of mortality in both the statin and non-statin groups. Operative mortality was 2.4% for all patients, 1.7% for statin users and 2.8% for non-statin users (p < 0.07). Using multivariate analysis, lack of statin use was found to be an independent predictor of mortality in high-risk patients (n = 245, 12.9% vs. 5.6%, p < 0.05).ConclusionsBetween 2000 and 2004 less than 50% of patients at this institution were receiving statins before admission for isolated CABG. A retrospective analysis of this cohort provides evidence that preoperative statin use is associated with lower operative mortality in high-risk patients.

Effects of statins vs. non-statin lipid-lowering therapy on bone formation and bone mineral density biomarkers in patients with hyperlipidemia

Introduction The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, named statins, are well-established cholesterol-lowering drugs able to reduce cardiovascular risk in hypercholesterolemic patients. The possible effect of statin on bone tissue, so-called pleiotropic effects has received particular attention. Studies reported a positive effect of statin on bone tissue in both of animal and human study by enhancing the expression of the bone morphogenetic proteins (BMPs), in particular of BMP2, which in turn leads to osteoblast differentiation and bone formation including interfering with osteoclastic activity. In a systematic review, the lipophilic statin as simvastatin had positive effect to bone mineral density (BMD) better than the more hydrophilic statin such as atorvastatin and fluvastatin. This study was aimed to compare efficacy of medical therapy between HMG-CoA reductase inhibitor and non-HMG-CoA reductase inhibitor group to changing of bone mineral density and bone markers in the patients with hyperlipidemia. Materials and methods A prospective randomized control trial study enrolled the 212 hyperlipidemia with osteopenia patients to study in year 2006–2008. All subjects were randomized to 2 groups between statin and non-statin group; the patients were screened by inclusion criteria and measured in bone mineral density (BMD), bone marker and blood chemistry. All data were analyzed by difference of changing in bone marker and BMD between statin and non-statin groups using paired t test. Results The present study showed 212 hyperlipidemia with osteopenia patients of which 106 patients in statin group had mean age (63.17 ± 9.51 years) and the same number of patients in non-statin group had mean age (60.96 ± 8.9 years). All subjects were 63 patients in male and 149 patients in female. Difference of bone formation marker and BMD between after and before was significantly higher than in statin group and the difference of bone resorption marker was also significantly lower than in statin group. Conclusion The lipophilic statin as moderate to high dose of simvastatin had beneficial positive effect to increasing BMD and could be additive use for prevention of bone loss in hyperlipidemia patients.

Usual Dose of Simvastatin Does Not Inhibit Plaque Progression and Lumen Loss at the Peri-Stent Reference Segments after Bare-Metal Stent Implantation: A Serial Intravascular Ultrasound Analysis

Background/AimsThe aim of this study was to assess the effects of a usual dose of simvastatin (20 mg/day) on plaque regression and vascular remodeling at the peri-stent reference segments after bare-metal stent implantation.MethodsWe retrospectively investigated serial intravascular ultrasound (IVUS) findings in 380 peri-stent reference segments (184 proximal and 196 distal to the stent) in 196 patients (simvastatin group, n = 132 vs. non-statin group, n = 64). Quantitative volumetric IVUS analysis was performed in 5-mm vessel segments proximal and distal to the stent.ResultsIVUS follow-up was performed at a mean of 9.4 months after stenting (range, 5 to 19 months). No significant differences were observed in the changes in mean plaque plus media (P&M) area, mean lumen area, and mean external elastic membrane (EEM) area from post-stenting to follow-up at both proximal and distal edges between the simvastatin and non-statin group. Although lumen loss within the first 3 mm from each stent edge was primarily due to an increase in P&M area rather than a change in EEM area, and lumen loss beyond 3 mm from each stent edge was due to a combination of increased P&M area and decreased EEM area, no significant differences in changes were observed in P&M, EEM, and lumen area at every 1-mm subsegment between the simvastatin and non-statin group.ConclusionsA usual dose of simvastatin does not inhibit plaque progression and lumen loss and does not affect vascular remodeling in peri-stent reference segments in patients undergoing bare-metal stent implantation.

Effect of statins on erythropoietin responsiveness in Type 2-diabetic versus non-diabetic hemodialysis patients

This study investigated whether the antiinflammatory effect of statins improved erythropoietin responsiveness in hemodialysis patients. We also examined if Type 2 diabetes mellitus, which had been shown to increase erythropoietin resistance, affected this effect of statins. 103 patients were included in the cross-sectional study. Patients were stratified into statin and non-statin groups, and subgrouped based on the presence of Type 2 diabetes mellitus. Demographic, laboratory and other relevant data were analyzed by independent sample t-tests. The outcome of interest was erythropoietin dose. Two-way analysis of variance was used to determine the interaction between the use of statins and the presence of Type 2 diabetes mellitus. Of 103 patients, 34% were on statins and 38.8% were diabetic. The mean erythropoietin dose (units/kg per week) was significantly lower in the statin group (275.6 +/- 273.2, 449.5 +/- 555.9, p < 0.05). 20% of patients in the statin group required erythropoietin dose in excess of an epoetin equivalent of 500 units/kg per week, compared to 30.88% in the non-statin group. The mean C-reactive protein level (mg/l) was lower in the statin group, although there was no statistical significance (1.13 +/- 1.22, 1.77 +/- 2.43, p = 0.08). The two-way analysis of variance showed no interaction between the use of statins and the presence of Type 2 diabetes mellitus on erythropoietin dose. Our study demonstrated that hemodialysis patients who were on statins had a significantly lower erythropoietin requirement. This association is possibly due to the pleiotropic effect of statins.

Long-term Safety of Testosterone and Growth Hormone Supplementation: A Retrospective Study of Metabolic, Cardiovascular, and Oncologic Outcomes

BackgroundClinical research into the effects of hormonal supplementation has tended to focus on beneficial changes in anthropometric measures. There are fewer data on long-term safety with extended hormonal supplementation.MethodsAs part of a retrospective database survey, clinical outcomes were tabulated among patients who received at least 1 year of testosterone and/or growth hormone (GH) supplementation. In patients who were treated for at least 2 years, changes in markers of glucose and lipid metabolism were analyzed with and without concomitant use of oral hypoglycemics and statins.ResultsIn 263 patients (mean age 56) treated for at least 2 years, the only statistically significant effect on markers of glucose metabolism was an increase in glycated hemoglobin (still within normal limits) in patients receiving GH alone or in combination with testosterone but without oral hypoglycemics; with or without hypoglycemics, insulin levels showed no significant change. The only significant effects on markers of lipid metabolism were decreases in total cholesterol and low-density lipoprotein (LDL) in patients receiving combined testosterone and GH without statins. Decreases in LDL were significant in both the statin and non-statin groups; decreases in triglycerides were significant only in the statin group. In 531 patients treated for at least 1 year (mean age 54), the overall incidence of adverse clinical outcomes (prostate disease, diabetes, cardiovascular disease, cancer) was 1.3%.ConclusionsIn this retrospective survey, extended testosterone and/or GH supplementation did not adversely affect metabolic markers or clinical outcomes.KeywordsSafety; Testosterone; Growth hormone; Supplementation

Effect of Statin on the Reference Segments after Bare-Metal Stent Implantation

Effect of Statin on the Reference Segments after Bare-Metal Stent Implantation

Arterial Remodeling in the Subclinical Carotid Artery Disease

We sought to identify clinical and/or plaque characteristics that affect atherosclerotic disease progression and arterial remodeling in the carotid artery with subclinical stenosis. Increasing severity of stenosis has been associated with a higher risk of stroke. Factors that drive subclinical lesions to become stenotic plaques remain ambiguous. Carotid magnetic resonance imaging (MRI) has been validated with histology to accurately quantify in vivo arterial morphology and plaque composition. A total of 67 asymptomatic participants with 16% to 49% carotid stenosis as demonstrated by duplex ultrasonography were imaged at 1.5-T with a carotid MRI protocol at baseline and at 18-month follow-up. Clinical and/or intra-arterial metrics with a significant association with change in plaque burden during multivariate analysis were evaluated for effects on lumen, wall, and total vessel volume. From multiple regression analysis, intraplaque hemorrhage (IPH) (p < 0.001) and statin therapy (p = 0.015) were identified as key determinants of change in plaque burden. The group with IPH compared with the group without IPH demonstrated luminal narrowing, with a mean +/- SD decrease in lumen volume (-24.9 +/- 21.1 mm(3)/year vs. -0.5 +/- 26.9 mm(3)/year; p = 0.005), a larger increase in wall volume (44.1 +/- 36.1 mm(3)/year vs. 0.8 +/- 34.5 mm(3)/year; p < 0.001), and no difference in total vessel volume (19.3 +/- 27.4 mm(3)/year vs. 0.4 +/- 42.4 mm(3)/year; p = 0.15). The nonstatin group compared with the statin group demonstrated outward remodeling, with an increase in wall volume (22.4 +/- 35.6 mm(3)/year(3)/year vs. 0.9 +/- 38.0 mm(3)/year; p = 0.026) and total vessel volume (19.2 +/- 36.9 mm(3)/year vs. -4.9 +/- 40.4 mm(3)/year; p = 0.019) and no difference in lumen volume (-5.8 +/- 26.6 mm(3)/year vs. -3.2 +/- 29.5 mm(3)/year; p = 0.72). IPH may represent an indication of accelerated plaque growth and impending luminal compromise in the subclinical carotid artery. Statin therapy may stabilize lesions by slowing or halting lesion progression. This phase of plaque stenosis (16% to 49%) may be a critical stage for intrinsic and extrinsic factors to affect the atherosclerotic disease process.

Abstract 5622: Effectiveness of Hybrid Therapy With Warfarin and Statins to Reduce the Incidence of Ischemic Stroke in High-risk Patients With Atrial Fibrillation

Background HMG-CoA reductase inhibitor statins have been recently used to prevent ischemic stroke in patients with coronary artery disease. However, whether or not such statins truly reduce the risk of ischemic stroke in patients with atrial fibrillation (AF) remains to be clearly elucidated. Methods We performed a retrospective cohort study at 4 Japanese centers. The study sample consisted of a cohort of 1152 patients (mean age, 67±10 years; men, 64 %; 513 paroxysmal AF) who had documented AF on electrocardiograms before August 2002 and who also visited our hospitals after September 2002. The statin group consisted of 179 patients (16%). A cox proportional hazards analysis was performed to control for baseline differences. We assessed the incidence of ischemic stroke. Results During a follow-up of 61±23 months, 151 patients experienced ischemic stroke. Since the statin group had more risk factors for stroke, such as a history of congestive heart failure, hypertension and diabetes mellitus, than the non-statin group, the statin group had a higher CHADS2 score (congestive heart failure, hypertension, age, diabetes, stroke [doubled]) than the non-statin group (statin group 1.93±1.15 vs. non-statin group 1.42±1.19, p&lt;0.001). The incidence of ischemic stroke was similar in both groups (statin group 12.0% vs. non-statin group, 17.5%, P = 0.08). For patients with a CHADS2 score ranging from 2– 6 with concomitant warfarin use, however, ischemic stroke was significantly less frequent in the statin group (statin group 11.7% vs. non-statin group, 26.0%, P = 0.045) although the incidence of major bleeding was similar in both groups (statin group 14.4% vs. non-statin group, 21.1%, P = 0.508). After adjustment for differences in baseline clinical variables, statin use was significantly associated with the incidence of ischemic stroke (hazard ratio[HR], 0.43; 95% confidence interval[CI], 0.23 to 0.83; P = 0.012), Conclusions In comparison to warfarin alone, the hybrid therapy with warfarin and statin was therefore suggested to be more effective in high-risk patients with atrial fibrillation.

Pravastatin use and cancer risk: a meta‐analysis of individual patient data from long‐term prospective controlled trials in Japan

To assess the influence of pravastatin therapy on cancer morbidity and mortality by a meta-analysis of individual patient data (IPD) from three independent Japanese large-scale clinical trials. We conducted a meta-analysis of IPD collected from three large-scale prospective studies, the Management of Elevated Cholesterol in the Primary Prevention Group of Adult Japanese (MEGA) Study, Kyushu Lipid Intervention Study (KLIS), and Hokuriku Lipid Coronary Heart Disease Study-Pravastatin Atherosclerosis Trial (Holicos-PAT), which compared cardiovascular outcomes with pravastatin therapy and non-statin therapy in Japanese patients with hypercholesterolemia over a follow-up period of >or=4 years. The incidence of cancer or cancer death in the pravastatin and non-statin therapy groups was compared by multivariate Cox proportional hazard models stratified by trial. Subgroup analyses by sex and age were also conducted using the same methods. In a total of 13 724 patients (mean age, 58 years; women, 48%) included in the analyses, pravastatin was not associated with an increased risk of developing cancer (hazard ratio [HR], 0.99; 95% confidence interval [95%CI], 0.81-1.19). Similarly, pravastatin therapy did not statistically affect cancer death (HR, 0.86; 95%CI, 0.61-1.21). Moreover, in subgroups analyses, no influence was observed on cancer incidence or death in relation to sex and age. Pravastatin did not increase the rate of cancer incidence or cancer death in a large population of Japanese patients followed for >70,000 patient-years.

Statins for the Prevention and Treatment of Infections

Emerging epidemiological evidence suggests that statin use may reduce the risk of infections and infection-related complications. Our objective was to examine the association between statin use and the risk of infections and related outcomes. We searched several electronic databases from inception through December 2007 for randomized trials and cohort studies that examined the association between statin use and the risk or outcome of infections. Data on study characteristics, measurement of statin use, outcomes (adjusted for potential confounders), and quality assessment were extracted. Sixteen cohorts were eligible and differed in representativeness, outcome assessment, and comparability of exposed (statin) and unexposed (nonstatin) groups. Nine cohorts addressed the role of statins in treating infections: bacteremia (n = 3), pneumonia (n = 3), sepsis (n = 2), and bacterial infection (n = 1). The pooled adjusted effect estimate was 0.55 (95% confidence interval, 0.36-0.83; I(2) = 76.5%) in favor of statins. Seven cohorts addressed infection prevention in patients with vascular diseases (n = 3), chronic kidney disease (n = 1), diabetes (n = 1), intensive care unit-acquired infections (n = 1), and in general practice (n = 1). The pooled effect estimate was 0.57 (95% confidence interval, 0.43-0.75; I(2) = 82%) in favor of statin use; there was some evidence of publication bias for this analysis (Egger test; P = .07). Meta-regression did not identify potential effect modifiers that explain the between-study heterogeneity. Results for our meta-analysis suggest that statin use may be associated with a beneficial effect in treating and preventing different infections. Given the presence of heterogeneity and publication bias, there is a need for randomized trials to confirm the benefit of statin use in this context.

Statin therapy and serum transaminases among a cohort of HCV-infected veterans.

We sought to determine the effect of statin therapy on serum AST and ALT levels in a cohort of HCV-infected veterans with well-characterized liver disease. We examined liver biopsy records of consecutive HCV-infected patients and identified 20 patients who were prescribed statins. We matched them on age, stage of fibrosis, and time between HCV diagnosis and statin start dates with up to four HCV-infected patients who did not use statins. ALT and AST values from up to four time points within 1 year of follow-up were abstracted from the medical record. We compared median ALT and AST levels using Wilcoxon-Mann-Whitney tests and assessed changes in ALT and AST over time between the statin and non-statin groups using a non-parametric repeated measures ANOVA model, adjusting for the matching factors, receipt of HCV treatment, BMI, and diabetes. Patients prescribed statins had higher median BMIs, were more likely to have diabetes, and had higher total cholesterol levels. Median baseline ALT levels were higher among those prescribed statins (P = 0.04) while median baseline AST levels were lower among statin users (P = 0.03). From baseline to follow-up, the median decreases in both ALT (-13.5 vs. -4.0) and AST (-4.5 vs. -0.5) were significantly larger among statin users compared to non-statin users (P = 0.03 and P = 0.0007, respectively) even after adjustment. Among HCV-infected patients AST and ALT levels for those prescribed statins decreased over a 6 to 12-month follow-up period compared to patients not taking statins.

Aggressive statin therapy in multicenter and effectiveness for the reduction of intra-myocardial damage caused by non-ST elevation acute coronary syndrome: AMERICA study

While preprocedural statin treatment for acute coronary syndrome (ACS) is widely regarded as beneficial, there has been no prospective randomized multicenter trial of patients with non-ST elevation ACS in the Japanese population to examine the efficacy of preprocedural aggressive statin use. The aim of this study was to confirm this effect by prospective randomized multicenter design. Fifty patients who presented with non-ST elevation ACS were enrolled, and randomly assigned to aggressive statin administration before percutaneous coronary intervention (PCI). Troponin-T (TnT), creatine phosphokinase (CK), CK-myocardial band (CK-MB), high-sense C-reactive protein (hs-CRP), and brain natriuretic peptide (BNP) were measured at baseline and/ or after procedure. Three days after PCI, the statin group had significantly less CK elevation compared with the nonstatin group (84+/-17 IU/l versus 180+/-68 IU/l, respectively, p = 0.02). CK-MB elevation also tended to be lower in the statin group than in the nonstatin group (3.2+/-1.9 versus. 7.0+/-3.0, respectively, p = 0.07), as was BNP level (3.2+/-1.9 versus 7.0+/-3.0 pg/ml, respectively, p = 0.07). The change of serum LDL cholesterol was significantly correlated with CK (p = 0.01) and TnT (p = 0.02) at 1 day after PCI. Aggressive statin usage before PCI to Japanese patients with non-ST elevation ACS appears to reduce myocardial damage after procedure. The degree of serum lipid level reduction may reflect the vulnerability of atheromatous plaques that could cause cardiac damage after PCI.

Intravesical Bacille Calmette-Guérin Therapy for Non-Muscle-Invasive Bladder Cancer: Effects of Concurrent Statin Therapy

Recent studies provide conflicting evidence about the association of statin use and decreased efficacy of intravesical bacille Calmette-Guérin (BCG) therapy for bladder cancer. Because statin drugs have immunomodulatory properties that could reduce the effectiveness of BCG, we investigated whether concurrent use of statin drugs was associated with worsened clinical outcomes in patients undergoing BCG treatment for non-muscle-invasive bladder cancer. We retrospectively analyzed records of 120 patients undergoing BCG treatment during 1997 through 2007 at a single Department of Veterans Affairs Medical Center. Tumor-progression events, total recurrences, disease-specific and overall mortality were the outcomes relative to statin use. Fisher's exact, Student's t-tests, and logistic regression were used to compare the groups. Among the 90 evaluable patients, there were no significant differences between groups with regard to tumor grade and stage distribution or smoking status. Statins were used during BCG therapy by 47.8% of patients. Comparing patients with no use versus use of statins, 8.5% versus 11.6% had local tumor progression (p = 0.44); 10.6% versus 9.3% underwent cystectomy, chemotherapy, or radiation therapy (p = 0.56); and metastatic disease developed in 6.7% versus 11.6% (p = 0.33). Of the 27 patients who died of any cause, 12.5% (2 of 16) versus 27.3% (3 of 11) in the nonstatin versus statin groups, respectively, died of disease (p = 0.32). Concurrent statin use was not associated with adverse outcomes for patients undergoing BCG treatment for bladder cancer. While statins have a plausible biologic mechanism to reduce BCG efficacy, no differences were seen in this small pilot study.

Reduction in Mortality Associated with Statin Therapy in Patients with Severe Sepsis

To evaluate the effect of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) on mortality in patients with severe sepsis. Retrospective cohort study. Intensive care unit (ICU) of an academic medical center. One hundred eighty-eight patients aged 40 years or older with a diagnosis of severe sepsis and an ICU stay between January 1, 2005, and December 31, 2006. Patient demographic data, statin use, and Acute Physiology and Chronic Health Evaluation (APACHE) II scores at the time of sepsis diagnosis were collected from the patient database. We used a multivariable logistic regression model to evaluate the association between statin use and in-hospital all-cause mortality after controlling for age, sex, and severity of illness. Of the 188 patients who met our inclusion criteria, 60 (32%) had statin exposure. Patients receiving statins were similar in age, sex, and APACHE II scores to those not receiving statins. In the univariable comparison, the statin group had a 35% relative reduction in mortality compared with the nonstatin group (mortality rate 31.7% vs 48.4%, p=0.040). Most of the mortality reduction attributed to statins occurred in patients with APACHE II scores higher than 24 (mortality rate 32.3% vs 57.5%, p=0.031), with a minimal mortality difference in patients with APACHE II scores of 24 or lower (31% vs 36.4%, p=0.810). In the multivariable regression model, statin use had a protective effect (odds ratio [OR] 0.42, 95% confidence interval [CI] 0.21-0.84, p=0.014), whereas increasing age (OR 1.03, 95% CI 1.01-1.06, p=0.013) and higher APACHE II score (OR 1.11, 95% CI 1.05-1.18, p=0.001) were associated with increased mortality. The use of statins was associated with a protective effect in patients with severe sepsis, as demonstrated by a significant reduction in mortality compared with patients not receiving statins.

Comment on “Statin administration did not influence the progression of lung injury or associated organ failures in a cohort of patients with acute lung injury”

Preclinical studies suggest that HMG-CoA reductase inhibitors (statins) may attenuate organ dysfunction. We evaluated whether statins are associated with attenuation of lung injury and prevention of associated organ failure in patients with ALI/ARDS. From a database of patients with ALI/ARDS, we determined the presence and timing of statin administration. Main outcome measures were the development and progression of pulmonary and nonpulmonary organ failures as assessed by changes in PaO2/FiO2 ratio and Sequential Organ Failure Assessment score (SOFA) between days 1 and 7 after the onset of ALI/ARDS. Secondary outcomes included ventilator free days, ICU and hospital mortality, and lengths of ICU and hospital stay. From 178 patients with ALI/ARDS, 45 (25%) received statin therapy. From day 1 to day 7, the statin group showed less improvement in their PaO2/FiO2 ratio (27 vs. 55, P = 0.042). Ventilator free days (median 21 vs. 16 days, P = 0.158), development or progression of organ failures (median ΔSOFA 1 vs. 2, P = 0.275), ICU mortality (20% vs. 23%, P = 0.643), and hospital mortality (27 vs. 37%, P = 0.207) were not significantly different in the statin and non-statin groups. After adjustment for baseline characteristics and propensity for statin administration, there were no differences in ICU or hospital lengths of stay. In this retrospective cohort study, statin use was not associated with improved outcome in patients with ALI/ARDS. We were unable to find evidence for protection against pulmonary or nonpulmonary organ dysfunction.

Atorvastatin might improve ventricular electrostability and decelerate the deterioration of renal function in patients with heart failure and diabetes mellitus

Previous studies suggested that statins have pleiotropic effects, such as improvements in endothelial function, as well as anti-inflammatory, anti-proliferative, and anti-oxidative effects. These effects might benefit patients with heart failure. In those patients, statins relieved symptoms, decreased the frequency of hospitalization, suppressed neurohumoral activation, and improved cardiac function. However, it remains unknown how statins impact pathophysiology of heart failure with diabetes mellitus. The aim of this study was to investigate the effects of atorvastatin on pathophysiology of heart failure with diabetes mellitus. We enrolled retrospectively 128 patients with heart failure with diabetes mellitus who were admitted from January 2003 to December 2005. Among these patients, 80 received atorvastatin (statin group) and the remaining patients served as controls (non-statin group). At study entry, there were no significant differences in the patient profiles between the two groups except for the low-density lipoprotein cholesterol level being higher in the statin group. After the follow-up period of two years, the frequency of re-hospitalization, brain natriuretic peptide, premature ventricular contractions, Lown grade, and deterioration of glomerular filtration rate were significantly less in the statin group. Atorvastatin might benefit patients with heart failure and diabetes mellitus by improving ventricular electrical stability and decelerating deterioration of renal function.

Statin administration did not influence the progression of lung injury or associated organ failures in a cohort of patients with acute lung injury

Preclinical studies suggest that HMG-CoA reductase inhibitors (statins) may attenuate organ dysfunction. We evaluated whether statins are associated with attenuation of lung injury and prevention of associated organ failure in patients with ALI/ARDS. From a database of patients with ALI/ARDS, we determined the presence and timing of statin administration. Main outcome measures were the development and progression of pulmonary and nonpulmonary organ failures as assessed by changes in PaO(2)/FiO(2) ratio and Sequential Organ Failure Assessment score (SOFA) between days 1 and 7 after the onset of ALI/ARDS. Secondary outcomes included ventilator free days, ICU and hospital mortality, and lengths of ICU and hospital stay. From 178 patients with ALI/ARDS, 45 (25%) received statin therapy. From day 1 to day 7, the statin group showed less improvement in their PaO(2)/FiO(2) ratio (27 vs. 55, P = 0.042). Ventilator free days (median 21 vs. 16 days, P = 0.158), development or progression of organ failures (median DeltaSOFA 1 vs. 2, P = 0.275), ICU mortality (20% vs. 23%, P = 0.643), and hospital mortality (27 vs. 37%, P = 0.207) were not significantly different in the statin and non-statin groups. After adjustment for baseline characteristics and propensity for statin administration, there were no differences in ICU or hospital lengths of stay. In this retrospective cohort study, statin use was not associated with improved outcome in patients with ALI/ARDS. We were unable to find evidence for protection against pulmonary or nonpulmonary organ dysfunction.

Low Incidence of Cardiac Events in Statin-Administered Patients in CAG Study

The effect of statins in preventing cardiac events in Japanese coronary artery disease (CAD) patients was studied in a retrospective investigation of 148 patients diagnosed with CAD by coronary angiography (CAG). Sixty-five patients received statins within 2 weeks after CAG, and 83 patients did not receive statins after CAG. In the statin group, total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) were reduced significantly with statin administration (p<0.01). In the non-statin group, baseline levels of TC, LDL-C and high-density lipoprotein cholesterol were not changed significantly at the end of the follow-up period. As for the effect of statin in preventing cardiac events, the incidence of cardiac events was significantly lower (p<0.0003) in the statin group (n=5: 8%) than in the non-statin group (n=28: 34%). In subanalysis of 37 patients whose TC at the time of initial CAG was less than 200 mg/dL, none of the statin group (n=17) suffered a cardiac event. This was significantly lower than the incidence of cardiac events in the non-statin group (n=5: 25%; p<0.05). The present study demonstrated that lowering LDL-C of Japanese CAD patients by statin administration is effective to prevent cardiac events, particularly, a second percutaneous coronary intervention (PCI) for restenosis of a coronary artery following the initial PCI whether or not these patients had hypercholesterolemia.

Impact of long-term statin treatment on coronary plaque composition at angiographically severe lesions: A nonrandomized study of the history of long-term statin treatment before coronary angioplasty

Background: Studies have found an association between treatment with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (“statins”) and reductions in procedure-related complications in percutaneous coronary intervention (PCI). Objective: This study investigated the effects of long-term statin treatment before elective PCI on coronary plaque composition at the angiographically severe target stenotic lesions. Methods: This nonrandomized, observational study was conducted at Nagoya University Hospital, Nagoya, Japan. Data were collected from the electronic medical records of patients with stable angina pectoris who underwent PCI guided by intravascular ultrasound (IVUS). Patients were stratified into 2 groups: those who received long-term statin treatment for ≥6 months before PCI (statin group) and those who did not (nonstatin group). The tissue characteristics of the coronary plaque at each target stenotic site were analyzed using 3-dimensional integrated backscatter IVUS immediately before PCI. Results: Data from 100 patients were included (91 men, 9 women; mean [SD] age, 67 [10] years; statin group, 44 patients; nonstatin group, 56). The clinical characteristics of the 2 groups were not significantly different, with the exception of the prevalence of hyperlipidemia (statin vs nonstatin, 100% vs 51.8%; P < 0.001). There were no significant between-group differences in serum lipid profiles. The statin group had a significantly greater mean (SD) percentage decrease in lipid volume (28.7% [10.0%] vs 34.7% [9.8%]; P = 0.003) and a significantly greater increase in fibrous volume (66.5% [8.5%] vs 60.9% [8.6%]; P = 0.001) compared with the nonstatin group. Conclusion: This study found a significant difference in lipid and fibrous volumes in angiographically severe coronary stenotic lesions in these patients with stable angina who received long-term statin treatment before PCI versus those who did not.