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      Statin therapy for preventing cardiovascular diseases in patients treated with tacrolimus after kidney transplantation

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          Abstract

          Background

          Lipid abnormalities are prevalent in tacrolimus-treated patients. The aim of the study was to evaluate the preventive effects of statin therapy on major adverse cardiovascular events (MACE) in patients treated with tacrolimus-based immunosuppression after kidney transplantation (KT), and to identify the risk factors.

          Methods

          This observational cohort study included adult patients who underwent KT and were treated with tacrolimus. Patients who received any lipid-lowering agents except statins, or had a history of immunosuppressant use before transplantation were excluded. The primary outcome was the adjusted risk of the first occurrence of MACE. The secondary outcomes included the risk of individual cardiovascular disease (CVD) and changes in cholesterol level. Subgroup analyses were performed in the statin-user group according to the dosage and/or type of statin.

          Results

          Compared with the control group (n=73), the statin-users (n=92) had a significantly reduced risk of MACE (adjusted HR, 0.31; 95% CI, 0.13–0.74). In the Cox regression analysis, old age, history of CVD, and comorbid hypertension were identified as independent factors associated with increased MACE. The total cholesterol levels were not significantly different between the two groups. Subjects with higher cumulative defined daily dose of statins had significantly lower risks of MACE.

          Conclusion

          Statin therapy in patients treated with tacrolimus after KT significantly lowered the risk of MACE. Long-term statin therapy is clearly indicated in older kidney transplant recipients for secondary prevention.

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          Most cited references 37

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          High-dose atorvastatin vs usual-dose simvastatin for secondary prevention after myocardial infarction: the IDEAL study: a randomized controlled trial.

          Evidence suggests that more intensive lowering of low-density lipoprotein cholesterol (LDL-C) than is commonly applied clinically will provide further benefit in stable coronary artery disease. To compare the effects of 2 strategies of lipid lowering on the risk of cardiovascular disease among patients with a previous myocardial infarction (MI). The IDEAL study, a prospective, randomized, open-label, blinded end-point evaluation trial conducted at 190 ambulatory cardiology care and specialist practices in northern Europe between March 1999 and March 2005 with a median follow-up of 4.8 years, which enrolled 8888 patients aged 80 years or younger with a history of acute MI. Patients were randomly assigned to receive a high dose of atorvastatin (80 mg/d; n = 4439), or usual-dose simvastatin (20 mg/d; n = 4449). Occurrence of a major coronary event, defined as coronary death, confirmed nonfatal acute MI, or cardiac arrest with resuscitation. During treatment, mean LDL-C levels were 104 (SE, 0.3) mg/dL in the simvastatin group and 81 (SE, 0.3) mg/dL in the atorvastatin group. A major coronary event occurred in 463 simvastatin patients (10.4%) and in 411 atorvastatin patients (9.3%) (hazard ratio [HR], 0.89; 95% CI, 0.78-1.01; P = .07). Nonfatal acute MI occurred in 321 (7.2%) and 267 (6.0%) in the 2 groups (HR, 0.83; 95% CI, 0.71-0.98; P = .02), but no differences were seen in the 2 other components of the primary end point. Major cardiovascular events occurred in 608 and 533 in the 2 groups, respectively (HR, 0.87; 95% CI, 0.77-0.98; P = .02). Occurrence of any coronary event was reported in 1059 simvastatin and 898 atorvastatin patients (HR, 0.84; 95% CI, 0.76-0.91; P<.001). Noncardiovascular death occurred in 156 (3.5%) and 143 (3.2%) in the 2 groups (HR, 0.92; 95% CI, 0.73-1.15; P = .47). Death from any cause occurred in 374 (8.4%) in the simvastatin group and 366 (8.2%) in the atorvastatin group (HR, 0.98; 95% CI, 0.85-1.13; P = .81). Patients in the atorvastatin group had higher rates of drug discontinuation due to nonserious adverse events; transaminase elevation resulted in 43 (1.0%) vs 5 (0.1%) withdrawals (P<.001). Serious myopathy and rhabdomyolysis were rare in both groups. In this study of patients with previous MI, intensive lowering of LDL-C did not result in a significant reduction in the primary outcome of major coronary events, but did reduce the risk of other composite secondary end points and nonfatal acute MI. There were no differences in cardiovascular or all-cause mortality. Patients with MI may benefit from intensive lowering of LDL-C without an increase in noncardiovascular mortality or other serious adverse reactions.Trial Registration ClinicalTrials.gov Identifier: NCT00159835.
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            Accelerated atherosclerosis in prolonged maintenance hemodialysis.

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              Use of statins and the risk of death in patients with prostate cancer.

              To determine whether the use of statins after prostate cancer diagnosis is associated with a decreased risk of cancer-related mortality and all-cause mortality and to assess whether this association is modified by prediagnostic use of statins. A cohort of 11,772 men newly diagnosed with nonmetastatic prostate cancer between April 1, 1998, and December 31, 2009, followed until October 1, 2012, was identified using a large population-based electronic database from the United Kingdom. Time-dependent Cox proportional hazards models were used to estimate adjusted hazard ratios (HRs) with 95% CIs of mortality outcomes associated with postdiagnostic use of statins, lagged by 1 year to account for latency considerations and to minimize reverse causality, and considering effect modification by prediagnostic use of statins. During a mean follow-up time of 4.4 years (standard deviation, 2.9 years), 3,499 deaths occurred, including 1,791 from prostate cancer. Postdiagnostic use of statins was associated with a decreased risk of prostate cancer mortality (HR, 0.76; 95% CI, 0.66 to 0.88) and all-cause mortality (HR, 0.86; 95% CI, 0.78 to 0.95). These decreased risks of prostate cancer mortality and all-cause mortality were more pronounced in patients who also used statins before diagnosis (HR, 0.55; 95% CI, 0.41 to 0.74; and HR, 0.66; 95% CI, 0.53 to 0.81, respectively), with weaker effects in patients who initiated the treatment only after diagnosis (HR, 0.82; 95% CI, 0.71 to 0.96; and HR, 0.91; 95% CI, 0.82 to 1.01, respectively). Overall, the use of statins after diagnosis was associated with a decreased risk in prostate cancer mortality. However, this effect was stronger in patients who also used statins before diagnosis.
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                Author and article information

                Journal
                Ther Clin Risk Manag
                Ther Clin Risk Manag
                Therapeutics and Clinical Risk Management
                Therapeutics and Clinical Risk Management
                Dove Medical Press
                1176-6336
                1178-203X
                2017
                21 November 2017
                : 13
                : 1513-1520
                Affiliations
                [1 ]Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul
                [2 ]Department of Pharmacy, Asan Medical Center, Seoul
                [3 ]Department of Internal Medicine, Seoul National University Hospital, Seoul
                [4 ]College of Medicine, Seoul National University, Seoul, Republic of Korea
                Author notes
                Correspondence: Jung Mi Oh; In-Wha Kim, College of Pharmacy, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul 08826, Republic of Korea, Tel +82 2 880 7997; +82 2 880 7736, Fax +82 2 766 9560; +82 2 882 9560, Email jmoh@ 123456snu.ac.kr ; iwkim2@ 123456hanmail.net
                [*]

                These authors contributed equally to this work

                Article
                tcrm-13-1513
                10.2147/TCRM.S147327
                5701562
                © 2017 Han et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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                Original Research

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