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Association of Clinician Knowledge and Statin Beliefs With Statin Therapy Use and Lipid Levels (A Survey of US Practice in the PALM Registry).
Lowenstern, A, Navar, AM, Li, S, Virani, SS, Goldberg, AC, Louie, MJ, Lee, LV, Peterson, ED, Wang, TY
The American journal of cardiology. 2019;(7):1011-1018
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Abstract
Guideline implementation requires clinician knowledge but may be influenced by pre-existing beliefs and biases. We assessed the association of these clinician factors with lipid management following the release of the 2013 American College of Cardiology/American Heart Association cholesterol guidelines. In the PALM registry, 774 clinicians completed a survey to assess their knowledge of the 2013 American College of Cardiology/American Heart Association guidelines, belief in statin benefit, and statin safety concerns. The association of these factors with statin use, statin dosing, and low-density lipoprotein cholesterol (LDL-C) levels were assessed in the 6,839 patients treated by these clinicians between May and November 2015. Overall, 63.9% of clinicians responded to at least 3 out of 4 hypothetical scenarios in concordance with guideline recommendations (good tested knowledge), 88.4% reported belief in statin benefit, and 15.4% raised concerns about statin safety. Belief in statin benefit was more prevalent among cardiologists, who represented 48.8% of the clinicians surveyed, and concerns regarding statin safety were higher among noncardiologists and clinicians in an academic setting. Guideline knowledge was not associated with a difference in statin use (74.1% vs 73.8%, p = 0.84) and achievement of LDL-C level <100 mg/dl (54.7% vs 52.4%, p = 0.07). However, patients treated by clinicians who reported belief in statin benefit were more likely to receive guideline-recommended statin intensity (41.9% vs 36.9%, p = 0.03), whereas patients treated by clinicians expressing statin safety concerns were less likely receive statins of at least guideline-recommended intensity (36.8% vs 42.5%, p = 0.001) and to achieve an LDL-C <100 mg/dl (44.1% vs 56.1%, p <0.001); the latter persisted after multivariable adjustment (odds ratio 0.75, 95% confidence interval 0.63 to 0.89). In conclusion, clinician beliefs regarding benefits and risks of statins were significantly associated with guideline adherence and patients' achieved LDL-C levels, whereas clinician knowledge of guideline recommendations was not.
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Prescription of statins at discharge and 1-year risk of major clinical outcomes among acute coronary syndromes patients with extremely low LDL-cholesterol in clinical pathways for acute coronary syndromes studies.
Sun, Y, Xie, G, Patel, A, Li, S, Zhao, W, Yang, X, Wu, T, Li, M, Li, X, Du, X, et al
Clinical cardiology. 2018;(9):1192-1200
Abstract
OBJECTIVE The aim of this study was to investigate statin description on discharge and the benefit on the long-term outcomes in acute coronary syndromes (ACS) patients with very low baseline LDL-cholesterol (LDL-c). METHODS This is a post-hoc analysis of 3374 ACS patients who were discharged alive and had baseline LDL-c levels below 70 mg/dL (1.8 mmol/L). The propensity score of using statin was estimated with a multivariable Logistic model including patient's demography, social economic status, cardiovascular risk factors, subtype of the diagnosis, and treatments received during hospitalization and current LDL-c level. The risk of major adverse cardiovascular events (MACEs) was compared between patients received and not-received statin with Cox-regression models adjusting for the propensity score plus other factors. A sensitivity analysis was done in propensity score matched patients. RESULTS Compared with nonstatin group, the incidence of MACE at 12 months after discharge was lower in the statin group (11.1% vs 5.8%; P < 0.001). The propensity score plus other factors-adjusted hazard ratios for MACEs was significant (0.58; 95% CI: 0.39, 0.87). The effect showed a significant dose-response relationship (P for trend = 0.02). The results in analyses with propensity-score matched participants were in consistent with above findings. Analyses on total mortality in 12 months showed similar results. CONCLUSIONS Among ACS survivors with a very low baseline LDL-c, low to moderate intensity statin therapy was associated significantly with lower risk of MACEs and total mortality at 12 months. The results suggested that ACS survivors should take statin regardless of the baseline of LDL-c.
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Six-month adherence to Statin use and subsequent risk of major adverse cardiovascular events (MACE) in patients discharged with acute coronary syndromes.
Xie, G, Sun, Y, Myint, PK, Patel, A, Yang, X, Li, M, Li, X, Wu, T, Li, S, Gao, R, et al
Lipids in health and disease. 2017;(1):155
Abstract
BACKGROUND The evidence of adherence to statin decreasing risk of major adverse cardiovascular events (MACEs) is still lack among patients discharged with acute coronary syndrome (ACS). Our objective is to determine the relationship between six-month adherence to statins and subsequent risk of MACEs in patients discharged with ACS. METHODS Using two prospective registry cohorts (CPACS-1 and -2), we analyzed data from 12,516 consecutive patients with ACS who were prescribed statin at hospital discharge and survived beyond 6 months without recurrent myocardial infarction (MI) or stroke. Adherence to statin was defined as good (using statin at discharge and 6 months without declined dosage) and poor adherence groups (using statin at discharge but declining dosage or stopping at 6 months). We compared the hazard ratios of all-cause mortality and MACE in subsequent 6 months between groups, using Cox-regression models, adjusting for multiple potential confounders. RESULTS Seventy two percent of patients adhered to statin therapy at 6 months. The incident MACE in the poor adherence group was significantly higher than in good adherence group (2.7% vs. 1.8%, p = 0.002). Compared with poor adherence group, the good adherence group showed a 27% lower relative risk of MACE during the 6 month follow up (fully-adjusted hazard ratio (HR) = 0.73; 95%CI: 0.56-0.97). The protective effects of good adherence were similar in groups with different statin dose as well as groups by other baseline clinical characteristics and treatments (p > 0.05 for interaction). CONCLUSION Our study highlights the importance of adherence to statin therapy in prevention of MACE and clinicians should aim to achieve higher dosage if tolerable. CLINICAL TRIAL REGISTRATION CPACS2 was registered on URL: http://www.anzctr.org.au/default.aspx and unique identifier is ACTRN12609000491268 . CPACS1 was not a clinical trial and thus not registered.
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Association Between SLCO1B1 Gene T521C Polymorphism and Statin-Related Myopathy Risk: A Meta-Analysis of Case-Control Studies.
Hou, Q, Li, S, Li, L, Li, Y, Sun, X, Tian, H
Medicine. 2015;(37):e1268
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Abstract
Statin-related myopathy is an important adverse effect of statin which is classically unpredictable. The evidence of association between solute carrier organic anion transporter 1B1 (SLCO1B1) gene T521C polymorphism and statin-related myopathy risk remained controversial. This study aimed to investigate this genetic association. Databases of PubMed, EMBASE, Chinese Biomedical Literature Database (CBM), China National Knowledge Infrastructure (CNKI), Chinese Scientific Journals Database, and Wanfang Data were searched till June 17, 2015. Case-control studies investigating the association between SLCO1B1 gene T521C polymorphism and statin-related myopathy risk were included. The Newcastle-Ottawa Scale (NOS) was used for assessing the quality of included studies. Data were pooled by odds ratios (ORs) and their 95% confidence intervals (CIs). Nine studies with 1360 cases and 3082 controls were included. Cases of statin-related myopathy were found to be significantly associated with the variant C allele (TC + CC vs TT: OR = 2.09, 95% CI = 1.27-3.43, P = 0.003; C vs T: OR = 2.10, 95% CI = 1.43-3.09, P < 0.001), especially when statin-related myopathy was defined as an elevation of creatine kinase (CK) >10 times the upper limit of normal (ULN) or rhabdomyolysis (TC + CC vs TT: OR = 3.83, 95% CI = 1.41-10.39, P = 0.008; C vs T: OR = 2.94, 95% CI = 1.47-5.89, P = 0.002). When stratified by statin type, the association was significant in individuals receiving simvastatin (TC + CC vs TT: OR = 3.09, 95% CI = 1.64-5.85, P = 0.001; C vs T: OR = 3.00, 95% CI = 1.38-6.49, P = 0.005), but not in those receiving atorvastatin (TC + CC vs TT: OR = 1.31, 95% CI = 0.74-2.30, P = 0.35; C vs T: OR = 1.33, 95% CI = 0.57-3.12, P = 0.52). The available evidence suggests that SLCO1B1 gene T521C polymorphism is associated with an increased risk of statin-related myopathy, especially in individuals receiving simvastatin. Thus, a genetic test before initiation of statins may be meaningful for personalizing the treatment.