Patients Receiving Statin Therapy Research Articles

Incremental Lowering of Low-Density Lipoprotein Cholesterol With Ezetimibe 20 mg vs 10 mg Daily in Patients Receiving Concomitant Statin Therapy

BackgroundEzetimibe is typically administered at a dose of 10 mg daily, with few reports of use at other doses. We compared plasma concentrations of low-density lipoprotein (LDL) cholesterol and other lipid variables in patients with dyslipidemia who were receiving ezetimibe 10 mg and then 20 mg daily. MethodsA retrospective chart review identified 27 patients who received ezetimibe 10 mg and then 20 mg daily at different times; 15 participants were receiving stable statin therapy and 12 were not receiving concomitant statins. Plasma concentrations of lipids, creatine kinase (CK), and aspartate transaminase (AST) were determined. Plasma concentrations of ezetimibe and ezetimibe glucuronide were measured in a second group of patients. ResultsPatients taking statins and ezetimibe 20 mg had further reductions in total and LDL cholesterol of 7.1% and 10.3%, respectively (both P < 0.05) than did those receiving the 10-mg dose. No difference between 20-mg and 10-mg dosing was seen among patients not receiving statins. Plasma concentrations of ezetimibe and its active metabolite were about 2-fold higher (P < 0.05) in patients taking ezetimibe 20 mg than in those receiving 10 mg daily. All patients tolerated ezetimibe 20 mg without side effects. ConclusionsEzetimibe 20 mg daily reduced total and LDL cholesterol further in patients receiving statin therapy compared with 10 mg daily. Prospective studies are required to show whether the higher plasma levels of ezetimibe and its active metabolite in patients taking the 20-mg dose have any detrimental effects. Increasing the ezetimibe dose to 20 mg daily might be an interesting potential approach for patients who fail to reach lipid targets on ezetimibe 10 mg daily along with maximally tolerated doses of statin.

AMG145, a Monoclonal Antibody Against Proprotein Convertase Subtilisin Kexin Type 9, Significantly Reduces Lipoprotein(a) in Hypercholesterolemic Patients Receiving Statin Therapy

Background— Lipoprotein(a) [Lp(a)] is an emerging risk factor for cardiovascular disease. Currently, there are few available therapies to lower Lp(a). We sought to evaluate the impact of AMG145, a monoclonal antibody against proprotein convertase subtilisin kexin type 9 (PCSK9), on Lp(a). Methods and Results— As part of the LDL-C Assessment With PCSK9 Monoclonal Antibody Inhibition Combined With Statin Therapy (LAPLACE)–Thrombolysis in Myocardial Infarction (TIMI) 57 trial, 631 patients with hypercholesterolemia receiving statin therapy were randomized to receive AMG145 at 1 of 3 different doses every 2 weeks or 1 of 3 different doses every 4 weeks versus placebo. Lp(a) and other lipid parameters were measured at baseline and at week 12. Compared with placebo, AMG145 70 mg, 105 mg, and 140 mg every 2 weeks reduced Lp(a) at 12 weeks by 18%, 32%, and 32%, respectively ( P &lt;0.001 for each dose versus placebo). Likewise, AMG145 280 mg, 350 mg, and 420 mg every 4 weeks reduced Lp(a) by 18%, 23%, and 23%, respectively ( P &lt;0.001 for each dose versus placebo). The reduction in Lp(a) correlated with the reduction in low-density lipoprotein cholesterol (ρ=0.33, P &lt;0.001). The effect of AMG145 on Lp(a) was consistent regardless of age, sex, race, history of diabetes mellitus, and background statin regimen. Patients with higher levels of Lp(a) at baseline had larger absolute reductions but comparatively smaller percent reductions in Lp(a) with AMG145 compared with those with lower baseline Lp(a) values. Conclusions— AMG145 significantly reduces Lp(a), by up to 32%, among subjects with hypercholesterolemia receiving statin therapy, offering an additional, complementary benefit beyond robust low-density lipoprotein cholesterol reduction with regard to a patient’s atherogenic lipid profile. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT01380730.

On-treatment C-reactive protein and HDL cholesterol levels in patients at intermediate cardiovascular risk: Impact on carotid intima-media thickness

AimsStatin therapy is followed by reductions in carotid intima-media thickness (CIMT) and C-reactive protein (CRP) levels, but a significant number of treated patients still have increased CIMT. We investigated whether on-treatment levels of CRP are associated with CIMT in hypercholesterolemic patients receiving statin therapy. The influence of blood pressure and anti-hypertensive therapy on the association between CRP and CIMT was evaluated. Main methodsThe assessment of cardiovascular risk factors, CRP and CIMT, was performed in a cross-sectional study of 240 hypercholesterolemic patients at intermediate cardiovascular risk under statin therapy; 125 patients received only a statin (statin group) and 115 also anti-hypertensive therapy (combined therapy group). Key findingsLogarithmically transformed CRP (β=0.17, p=0.01) and HDL cholesterol levels (β=−0.27, p<0.001) were correlates of CIMT, irrespective of confounders. High CRP levels (>3mg/L) were associated with a 2.7-fold increased risk of having high CIMT (>1.25mm). High CIMT was present in a high percentage of patients not at target for cholesterol and blood pressure levels (61%). Patients in the statin group had lower Framingham risk and CIMT than those in the combined therapy group. In the statin group, logarithmically transformed CRP (β=0.28, p=0.004) and HDL cholesterol (β=−0.21, p=0.03) were associated with CIMT. In the combined therapy group, HDL cholesterol was the only significant CIMT correlate (β=−0.33, p=0.001). SignificanceOn-treatment CRP and HDL cholesterol levels are associated with CIMT among hypercholesterolemic patients under statin therapy. In patients receiving both statin and anti-hypertensive therapy, HDL cholesterol remains the main covariate of CIMT.

Statin Therapy Is Associated With Fewer Infections After Cardiac Operations

Statins interact with multiple pathways involved in infection. Therefore, we examined the association between preoperative statin therapy and infections after cardiac operations and assessed whether statin therapy was associated with lower infection-related mortality. From January 2005 to January 2011, 12,741 patients underwent cardiac operations. Endpoints were (1) postoperative infections and (2) mortality after an infectious complication. A propensity score was developed on the probability of patients receiving statin therapy; patients were matched in part on this score. A multivariable logistic model was developed to examine mortality. Survival of infected patients was estimated using Kaplan-Meier and multiphase hazard function methodology. A total of 6,113 patients (48%) were receiving statins and 6,628 (52%) were not. Five hundred fifteen patients had postoperative infections-260 (4.3%) in the statin group and 255 (3.8%) in the no-statin group. However, patients receiving statins were older with more comorbidities and less favorable operative characteristics. Among propensity-matched groups, postoperative infections were significantly lower in patients receiving statins (n = 102 [3.1%]) than in those who were not (n = 147 [4.5%]; p = 0.004). Among patients in whom infections developed, there was no significant difference in hospital mortality between the statin and no-statin groups either before or after propensity-score matching (odds ratio, 1.38; confidence limit [CL], 0.59, 3.22; p = 0.5). We observed a protective effect of statin therapy against the development of infections after cardiac operations, but not on mortality from these infections. Prospective investigations are needed to determine optimal dose and duration of statin therapy and their relationship to infectious complications.

Association Between Serum Levels of n-3 Polyunsaturated Fatty Acids and Coronary Plaque Detected by Coronary Computed Tomography Angiography in Patients Receiving Statin Therapy

Intensive lipid-lowering therapy with statins reduces cardiovascular events, but residual cardiovascular risks remain. Intake of n-3 polyunsaturated fatty acids (PUFAs) has been associated with cardiovascular events. We examined the relationships between serum n-3 PUFAs and coronary atherosclerotic findings on computed tomography angiography (CTA) in patients undergoing statin treatment. We enrolled 172 subjects (mean age: 68.2 years; 64% men) prior to statin treatment for 6 months. Serum PUFAs, including eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), and arachidonic acid, were measured. When the patients were divided into 2 groups according to the median EPA level (61.3 μg/ml), the low-EPA group showed higher incidences of 3-vessel plaque involvement (62% vs. 43%, P=0.015), noncalcified plaques (NCPs) (74% vs. 52%, P=0.0016), extensive NCPs (≥ 2 segments) (56% vs. 34%, P=0.0036), and high-risk plaques (minimum CT density <39 HU and remodeling index >1.05) (43% vs. 22%, P=0.0034). Multivariate analyses revealed that low EPA levels were an independent factor for these coronary plaque findings. The DHA levels were not independently associated with these findings. Low serum EPA level, but not serum DHA, is associated with the presence and extent of NCPs and high-risk plaques detected by coronary CTA in patients undergoing lipid-lowering therapy with statins.

Assessment of statin-associated muscle toxicity in Japan: a cohort study conducted using claims database and laboratory information

ObjectiveTo estimate the incidence of muscle toxicity in patients receiving statin therapy by examining study populations, drug exposure status and outcome definitions.DesignA retrospective cohort study.Setting16 medical facilities in Japan providing...

Dosage of statin, cardiovascular comorbidities, and risk of atrial fibrillation: A nationwide population-based cohort study

Statin has potential protective effects against atrial fibrillation. Clinically, there is a need to predict the atrial fibrillation protective effects in statin-treated patients. The purpose of this study was to investigate if cardiovascular co-morbidities or cumulative defined daily doses (cDDDs) of statin use could predict statin efficacy in atrial fibrillation prevention. Patients aged ≥ 50 years were identified from the Taiwan National Health Insurance Research Database. Medical records of 171,885 patients were used in this study, and 40,001 (23.3%) of the patients received statin therapy (≥ 28 cDDDs). Risk of new-onset atrial fibrillation in statin users and non-users (<28 cDDDs) was estimated. During the 9-year follow-up period, 6049 patients experienced new-onset atrial fibrillation. Overall, statin therapy reduced the risk of atrial fibrillation by 28% (adjusted hazard ratio [HR] 0.72; 95% CI 0.68 to 0.77). There was a dose-response relationship between statin use and the risk of atrial fibrillation. The adjusted HRs for atrial fibrillation were 1.04, 0.85, and 0.50 when cDDDs ranged from 28 to 90, 91 to 365, and more than 365, respectively. Subgroup analysis showed that statin use was more beneficial in patients with higher CHADS2 and CHA2DS2VASc scores than those with a score of 0 (P value for interaction<0.001). The therapy provided no obvious beneficial effect in those with a CHADS2 score of 0, a CHA2DS2VASc score of 0, or cDDDs less than 91. Statin therapy reduces the risk of new-onset atrial fibrillation in a dose-dependent manner, and is beneficial in patients with cardiovascular co-morbidities.

Statin pharmacogenomics: opportunities to improve patient outcomes and healthcare costs with genetic testing.

HMG-CoA reductase inhibitors, commonly known as statins, are some of the most widely prescribed medications worldwide and have been shown to be effective at lowering cholesterol in numerous long-term prospective trials, yet there are significant limitations to their use. First, patients receiving statin therapy have relatively low levels of medication adherence compared with other drug classes. Next, numerous statin formulations are available, each with its own unique safety and efficacy profile, and it may be unclear to prescribers which treatment is optimal for their patients. Finally, statins have class-wide side effects of myopathy and rhabdomyolysis that have resulted in a product recall and dosage limitations. Recent evidence suggests that two genomic markers, KIF6 and SLCO1B1, may inform the therapy choice of patients initiating statins. Given the prevalence of statin usage, their potential health advantages and their overall cost to the healthcare system, there could be significant clinical benefit from creating personalized treatment regimens. Ultimately, if this approach is effective it may encourage higher adoption of generic statins when appropriate, promote adherence, lower rates of myopathy, and overall achieve higher value cardiovascular care. This paper will review the evidence for personalized prescribing of statins via KIF6 and SLCO1B1 and consider some of the implications for testing these markers as part of routine clinical care.

Do statins influence platelet reactivity on acetylsalicylic acid therapy in patients with type 2 diabetes?

Type 2 diabetes (T2DM) patients are at increased risk of cardiovascular events despite long-term acetylsalicylic acid (ASA) therapy. This study was performed to establish the prevalence of high platelet reactivity (HPR) on ASA in T2DM and to identify its predictors. The study included 185 T2DM on chronic ASA therapy and to assess platelet reactivity during long-term ASA therapy, we applied the point-of-care method VerifyNow(®) aspirin test (Accumetrics, San Diego, CA, USA). Compared with the low platelet reactivity (LPR) group, patients with HPR had higher triglyceride levels (145 vs. 118 mg/dL, p = 0.041), were less frequently treated with statins (57.1% vs. 75.3%; p = 0.038) and tumor necrosis factor-alpha (TNF-α) concentrations were higher (2.15 vs. 1.74 pg/mL; p = 0.052). In a multivariate analysis only statin therapy (OR 0.375; 95% CI 0.15-0.91; P = 0.030) and lower concentrations of TNF-α (for each 1.0 pg/ml: or 1.3; 95% ci 1.00-1.72; p = 0.046) were predictive of LPR. Our study provides indirect evidence that the beneficial effect of statins on platelet activity may be related to their non-lipid-mediated, pleiotropic mechanisms of action. This might have been partly related to decreased platelet reactivity in patients receiving statin therapy. In our study in patients with T2DM, platelet reactivity on ASA therapy measured with VerifyNow(®) was associated with TNF-α concentrations and statin therapy. These results may imply a role for subclinical systemic inflammation and a beneficial effect of statins in the development of HPR in T2DM.

Effect of statin therapy on the progression of coronary atherosclerosis

BackgroundAn increasing number of authors employing intravascular ultrasound (IVUS) and virtual histology (VH-IVUS) have investigated the effect of statin use on plaque volume (PV) and plaque composition. However, inconsistent results have been reported. Therefore, we conducted a meta-analysis to determine the appropriate regimen of statins to effectively stabilize vulnerable coronary plaques.MethodsOnline electronic databases were carefully searched for all relevant studies. We compared mean values of PV and plaque composition between baseline and follow-up in patients receiving statin therapy. We pooled treatment effects and calculated mean differences (MD) with the 95% confidence interval (CI) using a random-effects model. By stratified analyses, we explored the influence of clinical presentation, dose and duration of statin treatment, and low-density lipoprotein-cholesterol (LDL-C) levels on the effects of statins.ResultsSeventeen studies involving 2,171 patients were analyzed. Statin therapy significantly decreased PV (−5.3 mm3; 95% CI: –3.3 mm3 to −7.2 mm3; P < 0.001), without heterogeneity. When considering the dose and duration of statins used, only subgroups employing a high dose and long duration demonstrated a significant reduction in PV (p < 0.001). A significant decrease in PV was noted if achieved LDL-C levels were <100 mg/dL (p < 0.001). Statin treatment could induce a twofold decrease in PV in patients with acute coronary syndrome (ACS) compared with that observed in patients with stable angina pectoris (SAP). A regressive trend was seen for necrotic core volume (MD: –2.1 mm3; 95% CI: –4.7 mm3 to 0.5 mm3, P = 0.11). However, statin use did not induce a significant change for fibrotic, fibro-fatty, or dense calcium compositions.ConclusionsOur meta-analysis demonstrated that statin therapy (especially that involving a high dose and long duration and achieving <100 mg/dL LDL-C levels) can significantly decrease PV in patients with SAP or ACS. These data suggested that statins can be used to reduce the atheroma burden for secondary prevention by appropriately selecting the statin regimen. No significant change in plaque composition was seen after statin therapy.

Impact of Metabolic Syndrome on Progression of Aortic Stenosis: Influence of Age and Statin Therapy

The aims of this study were to examine prospectively the relationship between metabolic syndrome (MetS) and aortic stenosis (AS) progression and to evaluate the effect of age and statin therapy on AS progression in patients with or without MetS. Despite the clear benefits of statin therapy in primary and secondary coronary heart disease prevention, several recent randomized trials have failed to demonstrate any significant effect of this class of drugs on the progression of AS. Previous retrospective studies have reported an association between MetS and faster AS progression. This predefined substudy included 243 of the 269 patients enrolled in the ASTRONOMER (AS Progression Observation: Measuring Effects of Rosuvastatin) trial. Follow-up was 3.4 ± 1.3 years. AS progression rate was measured by calculating the annualized increase in peak aortic jet velocity measured by Doppler echocardiography. Patients with MetS (27%) had faster stenosis progression (+0.25 ± 0.21 m/s/year vs. +0.19 ± 0.19 m/s/year, p = 0.03). Predictors of faster AS progression in multivariate analysis were older age (p = 0.01), higher degree of valve calcification (p = 0.01), higher peak aortic jet velocity at baseline (p = 0.007), and MetS (p = 0.005). Impact of MetS on AS progression was most significant in younger (< 57 years) patients (MetS: +0.24 ± 0.19 m/s/year vs. no MetS: +0.13 ± 0.18 m/s/year, p = 0.008) and among patients receiving statin therapy (+0.27 ± 0.23 m/s/year vs. +0.19 ± 0.18 m/s/year, p = 0.045). In multivariate analysis, the MetS-age interaction was significant (p = 0.01), but the MetS-statin use interaction was not. MetS was found to be a powerful and independent predictor of faster AS progression, with more pronounced impact in younger patients. These findings emphasize the importance of routinely identifying and treating MetS in AS patients. The apparent faster stenosis progression in the subset of normocholesterolemic patients with MetS receiving the statin will need to be confirmed by future studies.

Effects of statins on serum polyunsaturated fatty acids

I thank Dr. Berent and Dr. Sinzinger for thoughtful comments and appreciate their great interest in our study. Because baseline low-density lipoprotein (LDL) cholesterol was too high to achieve a level less than 100 mg/dl using low-potency statins, we used high-potency statins including atorvastatin, rosuvastatin, or pitavastatin for lipid-lowering therapy. Consequently, LDL cholesterol less than 100 mg/dl was achieved in 65 % of the patients. These high-potency statins are often called ‘‘strong statins’’ in the clinical setting [1, 2]. Because we used only highpotency statins in our study, the manuscript was entitled effects of lipid lowering therapy with ‘‘strong statin’’ on polyunsaturated fatty acid acids (PUFAs). I do not argue that only strong statins have the effects reducing n-3 PUFAs in proportion to the decrease in the LDL cholesterol. I agree with your suggestion that a higher dose of lowpotency statins may have the same effects. However, a previous study by Nakamura et al. [3] showed that lowpotency statins (pravastatin and simvastatin) decreased LDL cholesterol from 159 to 117 mg/dl, and increased arachidonic acid (AA) with no significant effects on eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). On the other hand, we demonstrated that highpotency statins decreased LDL cholesterol from 131 to 89 mg/dl, and decreased EPA and DHA with no significant effect on AA. There was an inconsistency of the results between the previous study using low-potency statins and our study using high-potency statins. Further studies are necessary to clarify whether the inconsistency results from the extent of LDL cholesterol lowering or the potency of statins. There was no wash out phase before the change from a low-potency statin to a high-potency statin. The presence of a wash out phase is helpful to clarify the effects of strong statins on PUFAs. However, it is not ethical in patients with coronary artery disease. This was why we did not make a wash out phase in our study. Statins cause stabilization and regression of plaque, as well as inhibiting adverse cardiovascular events through only LDL cholesterol lowering but also several pleiotropic effects. Statins are established drugs that should be prescribed in all patients with coronary artery disease regardless of LDL cholesterol level. The serious problem is the recurrence of adverse cardiovascular events in patients receiving statin therapy. I think that additional treatment with n-3 PUFAs may be a promising strategy especially in patients with a high risk of coronary artery disease.

Impact of statin therapy on PSA kinetics during active surveillance of prostate cancer.

119 Background: Statin therapy has been associated with decreased serum PSA levels in men undergoing prostate cancer screening, lower rate of adverse pathologic features in radical prostatectomy specimens and decreased risk of biochemical recurrence following prostatectomy. Here we evaluate the impact of statin therapy on PSA kinetics during active surveillance of prostate cancer. Methods: A retrospective review of patients diagnosed with prostate cancer at our institution between the years 2000 and 2009 was performed. Patients undergoing at least 12 months of active surveillance were identified. PSA velocity and percentage change in PSA per year were compared between patients receiving and not receiving statin therapy during active surveillance. Subgroup analysis was performed on low risk patients (prebiopsy PSA &lt;10, Gleason score &lt;6, &lt;cT2). Results: We identified 81 patients meeting our inclusion criteria, 43% (35/81) were on statin therapy during active surveillance. Prebiopsy PSA was significantly lower in patients receiving statin therapy (6.0 ng/ml) compared to controls (8.3 ng/ml), p = 0.005. There was no difference in duration of active surveillance, PSA velocity, and percentage change in PSA per year based on statin use in all patients. When evaluating the 41 low risk patients, 54% (22/41) were on statin therapy. Prebiopsy PSA was lower in low risk patients receiving statin therapy (4.9 ng/ml) compared to controls (6.4 ng/ml), p= 0.055. PSA velocity was significantly lower in low risk patients (0.02 ng/ml/year) compared to low risk controls (0.89 ng/ml/year), p=0.024. Percentage change in PSA per year was significantly lower in low risk patients receiving statin therapy (-1.7%/year) compared to low risk controls (11.6%/year), p=0.05. The percentage of low risk patients receiving definitive therapy following a period of active surveillance on statin therapy was 9% (2/22)compared to 26% (5/19) in controls, p = 0.14. Conclusions: PSA kinetics during active surveillance appear to be significantly altered by statin therapy in low risk patients. Further evaluation of the impact of statin therapy on PSA kinetics and clinical outcomes of men undergoing active surveillance for prostate cancer are warranted.

Statin therapy and multiple sclerosis disability in a population-based cohort

Background: Axonal damage and inflammatory demyelination both occur in multiple sclerosis (MS). Some studies suggest that statins, through pleiotropic effects, reduce inflammatory episodes and protect neurons. However, other studies suggest statins have disparate impacts on these pathologic processes. Objective: The objective of this study was to assess disability progression in MS patients receiving statin therapy. Methods: We performed a retrospective medical record review of an established population-based MS prevalence cohort in Olmsted County, Minnesota, comparing disability progression between patients receiving statins and controls. Results: Duration of statin use ranged from 1.9 to 20.3 years with a mean and standard deviation of 6.8 ± 4 years. Years between assessments ranged from 0.6 to 8.2 (75% of patients having intervals >6.4 years). The median (interquartile range) absolute change of disability among the statin group was 0 (0 to +1), compared with +0.5 (0, +1) in the no-statin group. Distributions were not significantly different (p = 0.39). The mean (standard deviation) absolute change of disability scores among the statin group was +0.69 (+1.49), not significantly different from +0.61 (+1.31) in the no-statin group. Likewise, annualized disability scores did not differ significantly (p = 0.23). Eighteen (40%) patients worsened by 1.0 or more on Expanded Disability Status Scale (EDSS) in the statin group and 36 (40%) in the no-statin group (p = 0.85, chi-squared test). Conclusions: In this cohort, disability progression did not differ between those receiving statin therapy and controls. These findings support the hypothesis that statins, in doses currently prescribed for hyperlipidemia, do not affect the long-term course of MS.

Mechanisms of statin-induced myalgia assessed by physiogenomic associations

ObjectiveWe investigated genetic variants predictive of muscular side effects in patients treated with statins. We utilized a physiogenomic approach to prototype a multi-gene panel correlated with statin-induced myalgia. BackgroundStatin-induced myalgia occurs in ∼10% of lipid clinic outpatients. Its clinical manifestation may depend in part upon gene variation from patient to patient. MethodsWe genotyped 793 patients (377 with myalgia and 416 without) undergoing statin therapy at four U.S. outpatient clinic sites to evaluate 31 candidate genes from the literature for their association with statin-induced common myalgia. ResultsThree previously hypothesized candidate genes were validated: COQ2 (rs4693570) encoding para-hydroxybenzoate-polyprenyltransferase, which participates in the biosynthesis of coenzyme Q10 (p<0.000041); ATP2B1 (rs17381194) which encodes a calcium transporting ATPase involved in calcium homeostasis (p<0.00079); and DMPK (rs672348) which encodes a protein kinase implicated in myotonic dystrophy (p<0.0016). ConclusionsThe candidate genes COQ2, ATP2B1, and DMPK, representing pathways involved in myocellular energy transfer, calcium homeostasis, and myotonic dystonia, respectively, were validated as markers for the common myalgia observed in patients receiving statin therapy. The three genes integrated into a physiogenomic predictive system could be relevant to myalgia diagnosis and prognosis in clinical practice.

Succinylcholine Should Be Avoided in Patients on Statin Therapy

This article has been selected for the ANESTHESIOLOGY CME Program. Learning objectives and disclosure and ordering information can be found in the CME section at the front of this issue.

Prevalence and Risk Distribution of Residual Dyslipidemia in Statin-Treated Patients in Greece

Many statin-treated patients are not achieving treatment goals and are at risk of cardiovascular (CV) disease. We report the results of patients enrolled in an observational study in Greece, which estimated the residual lipid abnormalities in statin-treated patients. Low-density lipoprotein cholesterol (LDL-c), high-density lipoprotein cholesterol (HDL-c), and triglyceride concentrations were recorded in patients receiving statin therapy for ≥ 3 months, classified by CV risk according to European Society of Cardiology guidelines. Sixty-three percent of statin-treated patients had an LDL-c not at goal. Low-risk patients were more likely to have an LDL-c not at goal compared with high-risk patients (67.3% vs 61.0%, respectively). They were also less likely to have low HDL-c levels and elevated triglyceride levels compared with high-risk patients. Smoking and sedentary lifestyle were not associated with dyslipidemia in this population. Approximately two thirds of statin-treated patients in Greece are not reaching target/normal lipid levels and could benefit from improved lipid management.

Clinical Benefit of Statin Pretreatment in Patients Undergoing Percutaneous Coronary Intervention

Background— Previous studies suggested that statin pretreatment reduces cardiac events in patients undergoing percutaneous coronary intervention. However, most data were observational, and single randomized trials included limited numbers of patients. Methods and Results— We performed a collaborative meta-analysis using individual patient data from 13 randomized studies in which 3341 patients received either high-dose statin (n=1692) or no statin/low-dose statin (n=1649) before percutaneous coronary intervention, with all patients receiving statin therapy after intervention. Occurrence of periprocedural myocardial infarction, defined as postintervention creatine kinase–MB increase ≥3 times the upper limit of normal, and 30-day major adverse cardiac events (death, myocardial infarction, target-vessel revascularization) was evaluated. Incidence of periprocedural myocardial infarction was 7.0% in the high-dose statin versus 11.9% in the control group, which corresponds to a 44% risk reduction in the active-treatment arm (odds ratio by fixed-effects model 0.56, 95% confidence interval, 0.44 to 0.71, P &lt;0.00001). The rate of major adverse cardiac events at 30 days was significantly lower in the high-dose statin group (7.4% versus 12.6%, a 44% risk reduction; P &lt;0.00001), and 1-month major adverse cardiac events, excluding periprocedural events, were also reduced (0.6% versus 1.4%; P =0.05). The benefit of high-dose statins was realized irrespective of clinical presentation ( P for interaction=0.43) and was maintained across various subgroups but appeared greater in the subgroup with elevated baseline C-reactive protein levels (n=734; 68% risk reduction for periprocedural myocardial infarction versus 31% in those 1861 patients with normal CRP; P for quantitative interaction=0.025). Conclusions— High-dose statin pretreatment leads to a significant reduction in periprocedural myocardial infarction and 30-day adverse events in patients undergoing percutaneous coronary intervention. This strategy should be considered in all patients with planned percutaneous coronary intervention.

Prevalencia y características de la dislipemia en pacientes en prevención primaria y secundaria tratados con estatinas en España. Estudio DYSIS-España

Introduction and objectives Patients at high risk of suffering cardiovascular events require medical treatment to optimize their lipid profile. The present analysis evaluates the lipid profiles among Spanish patients receiving statin therapy in the international DYSIS study. Methods DYSIS is a multinational cross-sectional study carried out in Canada and Europe (n = 22,063). In Spain, 3710 patients treated with statin therapy for at least 3 months were included. We compared data relating to demographic parameters and cardiovascular risk profile. Results Complete lipid profiles of 3617 patients were recorded. Regarding the high cardiovascular risk patients with complete lipid profiles (n = 2273), 78.9% had a disorder in at least one of the three main lipid parameters: low-density lipoprotein cholesterol (LDLc), high-density lipoprotein cholesterol (HDLc) and/or triglycerides. LDLc was not within target levels in 61.4% of these high risk patients; HDLc was abnormal in 25.3%, and triglycerides were elevated in 37.8%. Overall, LDLc was outside the target range in 63.1%, and 20.7% (n = 668) of those treated with statins were normal for all parameters. Conclusions Most patients in this study who received statin therapy, particularly those at high cardiovascular risk, were not at the normal lipid parameter levels according to cardiovascular guidelines. Although it is necessary to wait for the final results of current studies on the use of combined lipid-modifying treatments, the management of lipid levels in Spain still has potential for improvement. Full English text available from: www.revespcardiol.org

Prevalence and Characteristics of Lipid Abnormalities in Patients Treated With Statins in Primary and Secondary Prevention in Spain. DYSIS-Spain Study

Introduction and objectives Patients at high risk of suffering cardiovascular events require medical treatment to optimize their lipid profile. The present analysis evaluates the lipid profiles among Spanish patients receiving statin therapy in the international DYSIS study. Methods DYSIS is a multinational cross-sectional study carried out in Canada and Europe (n = 22,063). In Spain, 3710 patients treated with statin therapy for at least 3 months were included. We compared data relating to demographic parameters and cardiovascular risk profile. Results Complete lipid profiles of 3617 patients were recorded. Regarding the high cardiovascular risk patients with complete lipid profiles (n = 2273), 78.9% had a disorder in at least one of the three main lipid parameters: low-density lipoprotein cholesterol (LDLc), high-density lipoprotein cholesterol (HDLc) and/or triglycerides. LDLc was not within target levels in 61.4% of these high risk patients; HDLc was abnormal in 25.3%, and triglycerides were elevated in 37.8%. Overall, LDLc was outside the target range in 63.1%, and 20.7% (n = 668) of those treated with statins were normal for all parameters. Conclusions Most patients in this study who received statin therapy, particularly those at high cardiovascular risk, were not at the normal lipid parameter levels according to cardiovascular guidelines. Although it is necessary to wait for the final results of current studies on the use of combined lipid-modifying treatments, the management of lipid levels in Spain still has potential for improvement.