Background: Cardiovascular (CV) disease is known as one of the major causes of death from disease worldwide. Statin therapy plays a pivotal role in atherosclerotic cardiovascular disease (ASCVD) lowering the LDL-cholesterol level effectively. The purpose of this study was to evaluate the association of the intensity of statin therapy in adult patients of Korea and the risk of ASCVD of the patient group. Methods: We used data from sample of patients from the Health Insurance Review and Assessment Service (HIRA-NPS-2018). We analyzed the patterns of prescribing statins including types of statin, statin intensity, and number of patients with ASCVD or risk of ASCVD. Results: 155,512 patients were included in the analysis, and 27,950 patients (18.0%) was over 75 years. High-intensity statin usage was increased in ASCVD patients compared with the low-intensity statin use. The OR (odds ratio) of high-intensity statin were increased in myocardial infarction patients compared with low-intensity statin use showing the highest OR; 12.40 (95% CI; 9.48-16.22). At patient groups of angina, ischemic heart disease and carotid disease, high-intensity statin prescription rate was increased compared with low-intensity statin. However, there was no statistical significance between both statin prescription rates in patients of peripheral arterial disease, abdominal aneurysm, diabetic mellitus and atherosclerosis. Conclusion: The statin prescription rate showed intensity increasing tendency according to the risk of ASCVD. More aggressive statin therapy might be beneficial for the ASCVD patients based on the recent guidelines of dyslipidemia.
Statin is commonly used for lowering cholesterols and can be myotoxic to cause drug-induced necrotizing myopathy. Statin-induced myopathy ranges from asymptomatic hyperCKemia to lethal rhabdomyolysis but is usually reversed by withdrawal of causative drugs. The patient in this study presented with statin-induced necrotizing myopathy, which was finally improved with immunosuppressive therapy, but not just with drug withdrawal. Since statin can induce myopathy through autoimmune processes, we should consider using immunomodulating agents in cases with statin-induced myopathy, which is refractory to drug withdrawal.
Kang, Min Sook;Yang, Hun Mo;Kang, Ja Young;Ryou, Sung Hee;Kang, Jung Sook
Nutrition Research and Practice
/
제6권5호
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pp.414-420
/
2012
Forty guinea pigs were divided into four groups and fed 0.04% cholesterol based control diet, plus 0.05% simvastatin, and statin plus 0.1% CoQ10 or 10% Ardisia Japonica Blume (AJB) leave powder for 4 weeks. Plasma total cholesterol levels decreased significantly in all groups fed the statin-containing diet compared with that in guinea pigs fed the control diet (P < 0.01). Plasma and liver triglycerides decreased significantly in the statin plus CoQ10 group compared with those in the control (both P < 0.05). Maximum platelet aggregation was significantly higher in the statin plus CoQ10 group than that in the other groups (P < 0.05). Na-K ATPase activity increased in the statin group and decreased in the statin plus CoQ10 group (P < 0.01). Na-K co-transport and Na passive transport decreased significantly in the control group compared with those in the other groups (both P < 0.05). Intracellular Na was highest in the statin group and lowest in the statin plus CoQ10 group and was correlated with Na-K ATPase activity. Thiobarbituric acid reactive substance production in platelet-rich plasma and liver tended to decrease in the statin plus CoQ10 group compared with those in the other groups. Plasma glutamic-pyruvic transaminase and glutamic-oxaloacetic transaminase increased significantly in the statin group compared with those in the control (P < 0.05). These result suggest that antioxidant rich AJB did not have positive effects on cardiovascular disease parameters. The statin plus CoQ10 seemed to decrease cholesterol more efficiently than that of statin alone.
Kim, Yang-Hee;Moon, Young-In;Kang, Young-Hee;Kang, Jung-Sook
Nutrition Research and Practice
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제1권4호
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pp.298-304
/
2007
This study was conducted to investigate the hypocholesterolemic effect of simvastatin (30 mg/kg BW) and antioxidant effect of coenzyme Q10 (CoQ10, 15 mg/kg BW) or green tea (5%) on erythrocyte Na leak, platelet aggregation and TBARS production in hypercholesterolemic rats treated with statin. Food efficiency ratio (FER, ADG/ADFI) was decreased in statin group and increased in green tea group, and the difference between these two groups was significant (p<0.05). Plasma total cholesterol was somewhat increased in all groups with statin compared with control. Plasma triglyceride was decreased in statin group and increased in groups of CoQ10 and green tea, and the difference between groups of statin and green tea was significant (p<0.05). Liver total cholesterol was not different between the control and statin group, but was significantly decreased in the group with green tea compared with other groups (p<0.05). Liver triglyceride was decreased in groups of statin and green tea compared with the control, and the difference between groups of the control and green tea was significant (p<0.05). Platelet aggregation of both the initial slope and the maximum was not significantly different, but the group with green tea tended to be higher in initial slope and lower in the maximum. Intracellular Na of group with green tea was significantly higher than the control or statin group (p<0.05). Na leak in intact cells was significantly decreased in the statin group compared with the control (p<0.05). Na leak in AAPH treated cells was also significantly reduced in the statin group compared with groups of the control and CoQ10 (p<0.05). TBARS production in platelet rich plasma was significantly decreased in the groups with CoQ10 and green tea compared with the control and statin groups (p<0.05). TBARS of liver was significantly decreased in the group with green tea compared with the statin group (p<0.05). In the present study, even a high dose of statin did not show a cholesterol lowering effect, therefore depletion of CoQ10 following statin treatment in rats is not clear. More clinical studies are needed for therapeutic use of CoQ10 as an antioxidant in prevention of degenerative diseases independent of statin therapy.
Seo, Jeong-Hun;Chun, Kwang-Jin;Lee, Bong-Ki;Cho, Byung-Ryul;Ryu, Dong Ryeol
Journal of Cardiovascular Imaging
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제26권4호
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pp.229-237
/
2018
BACKGROUND: Statins are thought to have little effect on the progression of aortic stenosis, but the data on their role in patients with aortic valve sclerosis (AVS) are limited and inconsistent. METHODS: We retrospectively analyzed 541 consecutive patients (214 men, age: $70{\pm}11$ years) with AVS. Each patient underwent two or more electrocardiography examinations at least 6 months apart at Kangwon National University Hospital from August 2010 to August 2015. AVS is defined as irregular thickening of the leaflets, focal increases in echogenicity and minimal elevation of the peak aortic valve velocity (> 1.5 and < 2 m/s). The progression rate of AVS was expressed as the increase in peak velocity per year (m/s/yr). RESULTS: The mean follow-up duration was $24.9{\pm}13.3$ months in the statin-treated group and $24.1{\pm}12.4$ months in the non-statin-treated group (p = 0.460). There were no differences between the statin-treated and non-statin-treated groups in mean age, gender or smoking status. Relative to the non-statin-treated group, a higher number of patients in the statin-treated group had hypertension, diabetes, ischemic heart disease, and stroke. The progression rate of AVS did not differ between the statin-treated and non-statin-treated groups ($0.012{\pm}0.340m/s/yr$ vs. $0.014{\pm}0.245m/s/yr$, p = 0.956). Multivariate analysis showed initial peak aortic jet velocity was significantly associated with AVS progression (${\beta}=0.153$, p = 0.009). CONCLUSIONS: Our study demonstrated that statins had no effect on the progression of AVS. However, well-designed studies are needed to define the prognosis and management of AVS.
Statins are competitive inhibitors of hydroxy-3-methyl glutaryl coenzyme A (HMG-CoA) reductase and used most frequently to reduce plasma cholesterol levels and to decrease cardiovascular events. However, statins also have been reported to have undesirable side effects such as myotoxicity and hepatotoxicity associated with their intrinsic efficacy mechanisms. Clinical studies recurrently reported that statin therapy elevated the level of liver enzymes such as ALT and AST in patients suggesting possible liver toxicity due to statins. This observation has been drawn great attention since statins are the most prescribed drugs and statin-therapy was extended to a larger number of high-risk patients. Here we employed rat primary hepatocytes and microarray technique to understand underlying mechanism responsible for statin-induced liver toxicity on cell level. We isolated genes whose expressions were commonly modulated by statin treatments and examined their biological functions. It is of interest that those genes have function related to response to stress in particular immunity and defense in cells. Our study provided the basic information on cellular mechanism of statin-induced cytotoxicity and may serve for finding indicator genes of statin -induced toxicity in rat primary hepatocytes.
Objective: The aim of this study is to compare the clinical benefits between high-intensity and low-to moderate-intensity statin therapy in patients with acute myocardial infarction (AMI). Methods: A total of 1,230 patients in the Korea AMI Registry (KAMIR) were enrolled. Patients were divided into two groups according to the dosage of statin for the secondary prevention after AMI. The primary endpoint was composite of major adverse cardiac events (MACEs) including cardiac death, non-fatal MI, repeat revascularization during the 12 months of clinical follow-up. Result: The primary endpoint occurred in 101 patients (11.3%) from the low-to moderate-intensity statin group and 45 patients (13.4%) from the high-intensity statin group. The cumulative incidence of MACEs during 12-month follow-up was not significantly different between the two groups (p=0.323). After multi-variate analysis, MACEs-free survival rate was not significantly different between the two groups. Conclusion: High-intensity statin therapy did not show additional clinical benefit over low-to moderate-intensity statin therapy after AMI.
Purpose: An integrative literature review was done to identify the best interventions for older adults with dyslipidemia in an effort to promote nursing involvement in the prevention of statin-induced symptoms (SIS). Such awareness could increase the capacity of interventions by geriatric nurses using evidence-based practices in the reassessment of statin therapy. Methods: CINAHL, Pubmed, and ProQuest were searched using these terms: dyslipidemia in, elderly, statins, adverse effects, and quality of life. Eleven articles fitting the inclusion criteria were identified and analyzed. Results: The findings indicate no evidence for the benefit of statin therapy for morbidity/mortality in a high-risk primary prevention set-up, specifically in the elderly population. Although SIS prevails among older adults, there are limited data that confidently support this observation along with nursing interventions specifically for the geriatric nursing community. Conclusion: Future research is necessary to shift nursing intervention with statin users (specifically in older adults) from an illness-based intervention to a preventive care plan to provide optimal care based on evidence. It is essential to involve self-reporting, cooperation, and communication with health care professionals, specifically with geriatric nurses. Additional studies are needed to further direct practice interventions in elderly statin users.
Objective : Endovascular mechanical thrombectomy (MT) has been regarded as one of the standard treatments for acute ischemic stroke caused by large vessel occlusion. Despite the wide use of stent retrievers for MT, arterial intimal damage caused when deployed stent is pulled has been a certain disadvantage. We hypothesized that statin could protect and stabilize vessel damage after endovascular MT using a stent retriever. In this animal study, we observed the protective effects of the statins towards MT-induced vessel wall injury. Methods : Twenty-eight carotid arteries of fourteen rabbits were used in the experiments with MT using stent retriever. We divided the rabbits into four groups as follows : group 1, negative control; group 2, positive control; group 3, statin before MT; and group 4, statin after MT. After MT procedures, we harvested the carotid arteries and performed histomorphological and immunohistochemical analyses. Results : In histomorphological analysis with hematoxylin and eosin and Masson's trichrome stain, significant intimal thickening (p<0.05) was observed in the positive control (group 2), compared to in the negative control (group 1). Intimal thickening was improved in the statin-administered groups (groups 3 and 4 vs. group 2, p<0.05). We also observed that statin administration after MT (group 4) resulted in a more effective decrease in intimal thickness than statin administration before MT (group 3) (p<0.05). We performed immunohistochemical analysis with the antibodies for tumor necrosis factor-alpha (TNF-α), cluster of differentiation (CD)11b, and CD163. In contrast to the negative control (group 1), the stained percentage areas of all immunological markers were markedly increased in the positive control (group 2) (p<0.05). Based on statin administration, the percentage area of TNF-α staining was significantly reduced (p<0.05) in group 3, compared to the positive control group (group 2). However, significant differences were not observed for CD11b and CD163 staining. In group 4, no significant differences were observed for TNF-α, CD11b, and CD163 staining (p≥0.05). The differences in the percentage areas of the different markers between the statin-administered groups (groups 3 and 4) were also not revealed. Conclusion : We presented that statin administration before and after MT exerted protective effects towards vessel wall injury. The efficacy of statins was greater post-administration than pre-administration. Thus, statin administration in routine prescriptions in the peri-procedural period is strongly advised.
Objective: Dyslipidemia is recognized as a prominent risk factor for cardiovascular and cerebrovascular diseases but it is manageable through therapeutic and lifestyle intervention. Interpreting the latest guidelines is essential for an application of recommendation from guidelines into clinical practice. Therefore, this study aimed to compare the most recent guidelines on dyslipidemia treatment recommendations in Korea and USA. Methods: This study analyzed and compared 2015 Korean guidelines for the management of dyslipidemia, 2013 American College of Cardiology/American Heart Association (ACC/AHA) guideline and 2016 supportive guidelines from ACC. Results: A comparison was made focused on the following: target patients based on cardiovascular risk assessment, target goal, and treatment strategies including statin and non-statin therapies. Four target patient groups by risk were suggested in 2015 Korean guideline and cardiovascular risk factors were also considered for initiation of lipid lowering therapy. Titrated statin regimen was recommended by Korean guideline to reach LDL cholesterol and non-HDL cholesterol target level. In 2013 ACC/AHA guideline, four statin benefit group was introduced considering ASCVD risk and high intensity statin or intermediate intensity statin use were recommended without dose titration. 2016 update was to support non-statin therapy based on updated evidence and new consideration of ezetimibe, PCSK9-inhibitor and bile acid sequestrant was brought up. Conclusion: Guidelines are continuously updating as new and important clinical data are constantly released along with the advent of newly approved drugs for lipid disorder. This article provides resources that facilitates uptake of these recommendations into clinical practice.
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