Beneficial Effects Of Statins Research Articles

Statin use and impact on tuberculosis risk

ABSTRACT Introduction: Tuberculosis, a chronic infection caused by Mycobacterium tuberculosis (MTB), is one of the 10 leading causes of death in the world. The current treatment is a combination antimicrobial therapy administered for 6–9 months. It is important to find therapeutic strategy to shorten the treatment during and strengthen the host immune response against MTB. Areas covered: There is evidence that MTB uses cholesterol in the host macrophage to infect and survive inside the host macrophage. Statins inhibit the synthesis of cholesterol and aid in reducing the levels of cholesterol in human, which have been associated with better outcome in infectious diseases. In this narrative review, we discuss recent studies that investigated the effects of statins on the prevention or treatment of TB infection. Expert opinion: The evaluation of the published evidence suggests that statins may be beneficial in the treatment of patients with TB infections. Future studies may focus not only on the beneficial effects of statins, but also on distinguishing the effects of different statins.

Beneficial Effect of Statins in COVID-19-Related Outcomes-Brief Report: A National Population-Based Cohort Study.

Although statins are widely prescribed lipid-lowering drugs, there are concerns about the safety of their use in the context of coronavirus disease 2019 (COVID-19), since statins increase the expression of ACE2 (angiotensin-converting enzyme 2). This study aimed to disclose the association between statins and 60-day COVID-19 mortality. Approach and Results: All patients hospitalized with laboratory-confirmed COVID-19 were enrolled in this study from January 19 to April 16, 2020, in Korea. We evaluated the association between the use of statins and COVID-19-related mortality in the overall and the nested 1:2 propensity score-matched study. Furthermore, a comparison of the hazard ratio for death was performed between COVID-19 patients and a retrospective cohort of patients hospitalized with pneumonia between January and June 2019 in Korea. The median age of the 10 448 COVID-19 patients was 45 years. Statins were prescribed in 533 (5.1%) patients. After adjusting for age, sex, and comorbidities, Cox regression showed a significant decrease in hazard ratio associated with the use of statins (hazard ratio, 0.637 [95% CI, 0.425-0.953]; P=0.0283). Moreover, on comparing the hazard ratio between COVID-19 patients and the retrospective cohort of hospitalized pneumonia patients, the use of statins showed similar benefits. The use of statins correlates significantly with lower mortality in patients with COVID-19, consistent with the findings in patients with pneumonia. Graphic Abstract: A graphic abstract is available for this article.

Post-operative Atrial Fibrillation at the Start of Atrial Fibrillation Burden

Atrial Fibrillation (AF) is the most common persistent arrhythmia with adverse clinical outcomes. AF ectopic firing and re-entry depends on several mechanisms: (1) ion channel dysfunction; (2) Ca2+-handling abnormalities; (3) structural remodelling; (4) autonomic neural dysregulation. The oxidized CAMKII enzyme pathway establishes a connexion between redox imbalance and the electrical and functional cardiomyocyte properties altered in AF patients. Postoperative atrial fibrillation (PoAF) is the most common complication after cardiac surgery and a subtype of AF, associated with increased time spent in the intensive care unit (ICU), in-hospital stay, stroke incidence and 30-day and long-term mortality. Recent studies have implicated oxidative stress in AF pathophysiology including mechanisms such as an imbalance in reactive oxygen species (ROS) production, decreased endothelial nitric oxide synthase (eNOS) activity and nitric oxide unavailability. Indeed, NADPH oxidase enzymes (NOX) are largely responsible for this imbalance, which is supported by the beneficial effect of statins in early atrium electrical remodelling. Epicardial adipose tissue has a direct contact with the myocardium, located between the myocardium and visceral pericardium, and it has been established a clinical relationship between EAT and the development of AF. In this review, we explore pathophysiological mechanisms of AF and POAF, as well as its implications for management.

Abstract 14687: Achieved Eicosapentaenoic Acid (EPA) Levels Predicts Regression of Coronary Plaque Volumes by Coronary Computed Tomography Angiography (CCTA) in the EVAPORATE Trial

Background: Despite the beneficial effects of statins on progression of coronary atherosclerosis and cardiovascular (CV) events, significant CV risk persists in patients with hypertriglyceridemia. In REDUCE-IT (Reduction of Cardiovascular Events with Icosapent Ethyl-Intervention Trial), icosapent ethyl (IPE) added to statins reduced initial and total CV events by 25% and 30%, but the mechanisms of benefit are unclear. In a follow-up analysis, degree of CV benefit from IPE was predominantly related to achieved serum EPA levels. Methods: EVAPORATE is a randomized, placebo-controlled trial, using CCTA to evaluate the effects of IPE as an adjunct to statins on coronary plaque volumes in a cohort with elevated triglycerides. Here, we present the 18-month, pre-specified secondary end-point analysis on association of achieved serum EPA levels, and change in coronary plaque volumes in the pooled cohort. Results: 80 patients were enrolled, and 68 completed the 18-month visit. Median (IQR) level of serum EPA for the pooled cohort was 20.6 (13.8) ug/ml at baseline and 25.3 (55.5) ug/ml at follow up. At 18 months, EPA levels > 26 ug/ml predicted regression of fibro-fatty plaque (logβ: - 0.75± 0.36), total non-calcified plaque (TNCP) (logβ: - 0.77± 0.33), and total plaque (TP) (logβ: - 0.63± 0.28) volumes (mm3), after adjustment for age, sex, diabetes, hypertension, and baseline TGL levels (p < 0.05 for all). Conclusions: Higher serum EPA levels predict regression of prognostically relevant coronary plaque volumes, TNCP, and TP on CCTA. This provides important mechanistic correlation to the CV benefits of IPE.

Measuring effects on intima-media thickness: an evaluation of rosuvastatin in Chinese subjects with subclinical atherosclerosis\u2014design, rationale, and methodology of the METEOR-China study

BackgroundThe beneficial effect of statins on atherosclerosis and cardiovascular outcomes has been well established. The Measuring Effects on intima media Thickness: an Evaluation Of Rosuvastatin (METEOR) global study demonstrated that a 2-year orally administered treatment with rosuvastatin 40 mg daily significantly slowed the progression of carotid intima-media thickness (CIMT) compared to placebo. The current METEOR-China study is designed to evaluate the effect of rosuvastatin 20 mg daily versus placebo on the progression of atherosclerosis measured by CIMT in asymptomatic Chinese subjects.MethodsThis is a phase 3, randomised, double-blind, placebo-controlled, multicentre parallel-group study. Asymptomatic Chinese subjects with a 10-year ischaemic cardiovascular disease (ICVD) risk < 10% will be recruited at 25 study sites. They will be treated with rosuvastatin 20 mg or placebo for 104 weeks. The primary endpoint is the annualised rate of change in CIMT measured by B-mode ultrasonography. Secondary endpoints include the annualised rate of change in CIMT at three different sections of the carotid artery and changes in the serum lipid profile. Safety parameters will also be assessed.ConclusionThe study will evaluate whether rosuvastatin 20 mg slows the progression of CIMT in asymptomatic Chinese subjects at low risk of ICVD.Trial registrationClinicalTrials.gov NCT02546323. Registered on September 10, 2015

Hepatocellular Carcinoma and Statins.

HMG-CoA reductase inhibitors (known as statins) are commonly prescribed worldwide for the management of coronary heart disease and the underlying dyslipidemia. This class of drugs has been shown to infer a significant decrease in the risk of cardiovascular morbidity and mortality. Only recently though have the beneficial effects of statins in other diseases such as non-alcoholic steatohepatitis been highlighted. Importantly, also, multiple studies have revealed that statin use was associated with lower cancer-associated mortality across multiple types of cancers. This work aims to review those studies with a particular focus on liver cancer. We also provide a review of the proposed mechanisms of action describing how statins can induce chemo-preventive and antitumor effects.

A clinical trial to evaluate the effect of statin use on lowering aldosterone levels

BackgroundStatins are the first-line pharmaceutical agent in the management of hypercholesterolemia and cardiovascular (CV) risk reduction, and the most commonly prescribed class of drugs worldwide. Studies describing CV risk reduction independent of LDL-cholesterol lowering have evoked an interest in the pleiotropic mechanisms of statins’ benefits. We recently demonstrated that administration of statins in animal models lowers aldosterone levels and observed an association between statin use and reduced aldosterone levels in two human cohorts, with lipophilic statins displaying a greater effect than hydrophilic statins. Therefore, we designed a randomized, placebo-controlled, double-blinded intervention study to assess whether statin treatment lowers aldosterone in a type-dependent manner in humans, with simvastatin (lipophilic) showing a greater effect than pravastatin (hydrophilic).Methods/designOne hundred five healthy participants will be recruited from the general population to enroll in a 12-week, randomized, placebo-controlled, double-blinded, 3-arm clinical trial. Ninety participants are anticipated to complete the protocol. After baseline assessment of aldosterone levels, participants will be randomized to daily simvastatin, pravastatin, or placebo. Aldosterone levels will be assessed after 2 days on study drug and again after 6 weeks and 12 weeks on study drug. Prior to each aldosterone assessment, participants will consume an isocaloric sodium and potassium-controlled run-in diet for 5 days. Assessments will occur on an inpatient research unit to control for diurnal, fasting, and posture conditions. The primary outcome will compare 12-week angiotensin II-stimulated serum aldosterone by study drug. Secondary outcomes will compare baseline and 12-week 24-h urine aldosterone by study drug.DiscussionResults from this rigorous study design should provide strong support that statins lower aldosterone levels in humans. These results may explain some of the beneficial effects of statins that are not attributed to the LDL-lowering effect of this important class of medications. Results would demonstrate that statin lipophilicity is an important attribute in lowering aldosterone levels. The outcomes of this program will have implications for the design of studies involving statin medications, as well as for the differential use of classes of statins.Trial registrationClinicalTrials.gov; NCT02871687; First Posted August 18, 2016.

Are statins toxic or safe for kidney diseases? An updated mini-review study

Statins, as the most important cholesterol-lowering agents, inhibit the production of blood cholesterol by blocking an enzyme called the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-COA) reductase. Statins have beneficial effects in some tissues during various injuries. Recent evidence suggests that unlike the beneficial effects of statins, administration of high doses of these drugs may increase renal impairment, although more research is needed in this regard. Therefore, this study aimed to evaluate the possible effect of different doses of statins on the morphology and function of the kidney tubular cells.

Liver stiffness across different chronic liver disease under therapy with statin in a real life cohort.

Statins have been associated with improved clinical outcomes in patients with viral hepatitis and after variceal bleeding. Still, the clinical benefit of statins is not well defined for different liver diseases. Moreover, associations between statin use and liver stiffness as well as event free survival have not been established. Liver stiffness was evaluated in 6490 patients with liver disease (January 2012 till December 2016). Two hundred thirty-four of those received statin therapy, 468 controls without statins were selected by a 1:2 case by case matching using age, sex, underlying liver disease and BMI. Statins were given to 234 patients with chronic virus hepatitis (n = 104), nonalcoholic fatty liver disease (n = 52), autoimmune liver disease including autoimmune hepatitis, primary biliary cholangitis and primary sclerosing cholangitis (n = 31) and hepatitis of unknown origin (n = 47). Follow-up data were available for 96 and 119 pairs (mean follow-up 2 years). Statin users showed reduced inflammatory activity. Elevated liver enzymes were reported in 57% of statin-treated compared with 70% of controls (mean alanine aminotransferase level 53 vs. 74 U/l; P < 0.001). Statin use was well tolerated in this cohort. Mean liver stiffness values were 10.7 kPa (SEM 0.7) and 15.5 kPa (SEM 0.7) accordingly (P < 0.0001). Decompensation was less likely to occur in the statin group, both groups do not defer in the incidence of liver tumor occurrence, transplantation or death (odds ratio = 1, P = nonsignificant). Use of statins was well tolerated irrespective of liver disease. Statin users showed reduced hepatic inflammatory activity, less severe markers of liver stiffness and portal hypertension. There might be a beneficial effect of statin on the risk to experience hepatic decompensation.

Endothelial Dysfunction in Dyslipidaemia: Molecular Mechanisms and Clinical Implications.

The endothelium consists of a monolayer of Endothelial Cells (ECs) which form the inner cellular lining of veins, arteries, capillaries and lymphatic vessels. ECs interact with the blood and lymph. The endothelium fulfils functions such as vasodilatation, regulation of adhesion, infiltration of leukocytes, inhibition of platelet adhesion, vessel remodeling and lipoprotein metabolism. ECs synthesize and release compounds such as Nitric Oxide (NO), metabolites of arachidonic acid, Reactive Oxygen Species (ROS) and enzymes that degrade the extracellular matrix. Endothelial dysfunction represents a phenotype prone to atherogenesis and may be used as a marker of atherosclerotic risk. Such dysfunction includes impaired synthesis and availability of NO and an imbalance in the relative contribution of endothelialderived relaxing factors and contracting factors such as endothelin-1 and angiotensin. This dysfunction appears before the earliest anatomic evidence of atherosclerosis and could be an important initial step in further development of atherosclerosis. Endothelial dysfunction was historically treated with vitamin C supplementation and L-arginine supplementation. Short term improvement of the expression of adhesion molecule and endothelial function during antioxidant therapy has been observed. Statins are used in the treatment of hyperlipidaemia, a risk factor for cardiovascular disease. Future studies should focus on identifying the mechanisms involved in the beneficial effects of statins on the endothelium. This may help develop drugs specifically aimed at endothelial dysfunction.

Use of Statins in COVID-19 Treatment: Multiple Pathways but Minimal Evidence

Coronavirus disease-2019(COVID-19) is an emerging viral infection of public importance and it is caused by a beta coronavirus called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). So far, it has affected about 15 million individuals and over 600 000 patients have died from it. The virus is novel and there is no approved specific therapy for the infection. This has led to the trial of different drugs to reduce the morbidity and mortality of the infection. Statins are primarily used to lower cholesterol. They also have other pleiotropic effects such as anti-inflammatory, anti-thrombotic, immunomodulatory and antiviral effects. Coincidentally, the processes that statins antagonize are the mechanisms underlying the pathogenesis of COVID-19. Therefore, it has been suggested that statins should be considered as an adjunct in the treatment of COVID-19. In the new era of evidence-based medicine, there is a need to examine the level of evidence available to support the clinically beneficial effect of statins in COVID-19 treatment. This literature review explores the strength and volume of evidence for the usage of statins in COVID-19. However, as at the time of writing this review, the evidence base is very scanty. The most quoted evidence available is a retrospective study which is a low level of evidence. Therefore, it can be concluded that there are various mechanisms identified by which statins could be useful in the treatment of COVID-19. However, the evidence for their recommendation as adjuncts for COVID-19 treatment is very weak.

Beneficial effect of statin on preventing contrast-induced acute kidney injury in patients with renal insufficiency: A meta-analysis.

Renal insufficiency is an important predictor of contrast-induced acute kidney injury (CI-AKI). We performed a meta-analysis to examine the effects of short-term statin therapy on the incidence of CI-AKI, particularly in patients with renal insufficiency. A systematic search was conducted to retrieve randomized controlled trials (RCTs) that investigated the impact of statin pretreatment before administration of contrast media on the development of CI-AKI in patients with mild to moderate renal insufficiency. The primary outcome was development of CI-AKI. The secondary outcome was the incidence ofacute kidney injury requiring hemodialysis. Data analysis from 8 RCTs, which included a total of 2313 subjects in the statin-treated group and 2322 in the control group, showed that statin pretreatment was associated with significant reduction of the risk of CI-AKI (relative risk [RR] = 0.59; 95% confidential interval [CI] 0.44-0.79; P = .0003, I = 0%). A beneficial effect of statin on preventing CI-AKI was consistent, regardless of the dose of statin and use of N-acetylcysteine. In subgroup analysis based on baseline estimated glomerular filtration rate (eGFR), patients with baseline eGFR <60 mL/min/1.73 m (RR = 0.63; 95% CI 0.41-0.98; P = .04, I = 0%) and 30 < eGFR < 90 mL/min/1.73 m (RR = 0.56; 95% CI 0.39-0.82; P = .003, I = 0%) showed significant reduction of risk of CI-AKI. Statin pretreatment is effective at preventing CI-AKI and should be considered in patients with preexisting renal insufficiency.

Statins Induce a DAF-16/Foxo-dependent Longevity Phenotype via JNK-1 through Mevalonate Depletion in C. elegans.

Statins belong to the most pre-scribed cholesterol lowering drugs in western countries. Their competitive inhibition of the HMG-CoA reductase causes a reduction in the mevalonate pool, resulting in reduced cholesterol biosynthesis, impaired protein prenylation and glycosylation. Recently, a cohort study showed a decreased mortality rate in humans between age 78-90 going along with statin therapy, which is independent of blood cholesterol levels. As C. elegans harbors the mevalonate pathway, but is cholesterol-auxotroph, it is particularly suitable to study cholesterol-independent effects of statins on aging-associated phenotypes. Here, we show that low doses of lovastatin or a mild HMG-CoA reductase knockdown via hmgr-1(RNAi) in C. elegans substantially attenuate aging pigment accumulation, which is a well-established surrogate marker for biological age. Consistently, for two statins we found dosages, which prolonged the lifespan of C. elegans. Together with an observed reduced fertility, slower developmental timing and thermal stress resistance this complex of outcomes point to the involvement of DAF-16/hFOXO3a, the master regulator of stress resistance and longevity. Accordingly, prolonged low-dose statin exposure leads to an increased expression of jnk-1, a known activator of DAF-16. Moreover, the beneficial effects of statins on aging pigments and lifespan depend on DAF-16 and JNK-1, as shown in epistasis analyses. These effects can be reverted by mevalonate supplementation. In conclusion, we describe a lifespan extension in C. elegans, which is conferred via two well-conserved stress-related factors (JNK-1, DAF-16) and results from mevalonate depletion.

Clinical Benefit of Statins in Korean Patients with Acute Myocardial Infarction: Experience of the Korea Acute Myocardial Infarction Registry.

Statins (3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor) are among the most important medications for treating patients with acute myocardial infarction (AMI). Herein, we review the clinical benefit and future scope of statin therapy in Korean patients with AMI from the experience of the Korea AMI Registry. Statins are effective and safe in AMI patients, even in those with very low low-density lipoprotein cholesterol (LDL-C). Peri-procedural statin treatment could reduce the incidence of early stent thrombosis in patients with AMI after percutaneous coronary intervention. Reduction of high sensitivity C-reactive protein levels in patients with AMI plays an important role in the beneficial effect of statins on regression and compositional change of coronary plaques. Obtaining ≥50% reduction in LDL-C is associated with better clinical outcomes after AMI, whereas achieving <70 mg/dL LDL-C is not. Statin therapy has positive effects on clinical outcomes in patients with cardiogenic shock, ischemic heart failure, chronic kidney disease, and vasospasm. The combination of high-dose statin plus N-acetyl cysteine is associated with lower incidence of contrast-induced nephropathy in patients who underwent primary percutaneous coronary intervention. Moderate-intensity pitavastatin therapy is associated with a lower incidence of new-onset diabetes mellitus in patients with AMI and has similar clinical outcomes to moderate-intensity atorvastatin and rosuvastatin therapy. Future studies are required to assess the optimal intensity and LDL-C target concerning statin therapy, and the implementation of guidelines based cholesterol lowering practice in Korean patients with AMI.

Allergic asthma aggravated atherosclerosis increases cholesterol biosynthesis and foam cell formation in apolipoprotein E-deficient mice

Several studies have demonstrated that allergic asthma can induce atherosclerosis formation in mice. Moreover, allergic asthma and atherosclerosis have been shown to be strongly associated with dyslipidemia. In this study, we investigated the underlying mechanism of allergic asthma-aggravated atherosclerosis-induced cholesterol metabolism disorder in asthmatic apoE−/- mice. We found that allergic asthma increased the expression of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) in the liver and CD36 in the aorta during the acute and advanced stages of atherosclerosis, respectively. These results indicate that cholesterol biosynthesis is increased during acute atherosclerosis and cholesterol uptake and foam cell formation is increased during advanced atherosclerosis. Simvastatin administration significantly ameliorated the aortic root lesion size of asthmatic mice and significantly decreased HMGCR and CD36 expression. However, the expression of the low-density lipoprotein receptor and ATP-binding cassette transporter A1 was markedly increased, indicating that the beneficial effect of statins in allergic asthma and coronary artery disease was mediated, at least in part, by decreasing cholesterol biosynthesis and foam cell formation. In conclusion, allergic asthma aggravates atherosclerosis by regulating cholesterol metabolism in apoE−/- mice. Allergic asthma selectively promotes cholesterol biosynthesis in acute atherosclerosis and increases foam cell formation in advanced atherosclerosis.

Antioxidatant Effect of Atorvastatin and Rosuvastatin in Hyperlipidemic Patients: A Randomized Controlled Trial

Introduction: Hyperlipidemia is a major risk for the development of atherosclerosis leading to cardiovascular complications. Atorvastatin and rosuvastatin are two widely used important members of the HMG-CoA reductase inhibitor (statins). The beneficial effects of statins on clinical events also involve lipid-independent mechanisms which include improvement of oxidative stress status.&#x0D; Objective: To compare the antioxidative effect of atorvastatin and rosuvastatin in patients with hyperlipidemia.&#x0D; Materials and Methods: A prospective randomized single-center analytic study was carried out in Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka from March 2016 to August 2017 on 52 hyperlipidemic patients. After randomization patients were assigned to atorvastatin 10 mg or rosuvastatin 5 mg daily for 8 weeks. Blood was collected at baseline and after the intervention to measure plasma malondialdehyde (MDA), erythrocyte reduced glutathione (GSH) (as biomarkers of oxidative stress) and serum lipid profile.&#x0D; Results: The baseline characteristics of patients treated with atorvastatin and rosuvastatin were almost identical. The level of plasma MDA in atorvastatin (1.35 ± 0.94 to 0.97± 0.64) and rosuvastatin (1.56±0.69 to 0.98±0.38) group was significantly reduced after intervention (28.15%, p&lt;0.05 and 37.18%, p&lt;0.001 respectively) but no statistically significant difference (p&gt;0.05) was observed between the two statin-treated groups. Erythrocyte GSH level was increased after intervention in both atorvastatin (2.43±2.90 to 4.14 ± 4.87) group (70.37%, p&lt;0.01) and rosuvastatin (2.76±3.80 to 8.36±12.93) group (202.90%, p&lt;0.01), which was statistically significant. No significant difference was observed between the two groups (p&gt;0.05). Both atorvastatin and rosuvastatin significantly improved serum lipid profile.&#x0D; Conclusion: Both atorvastatin and rosuvastatin significantly improved oxidative stress status in hyperlipidemic patients but no significant change was observed between the two statin-treated groups.&#x0D; Journal of Armed Forces Medical College Bangladesh Vol.14(1) 2018: 54-58

SP561Biomarkers for targeting beneficial effects of statin in hemodialysis patients

SP561Biomarkers for targeting beneficial effects of statin in hemodialysis patients

STATIN THERAPY AMONG CHRONIC KIDNEY DISEASE PATIENTS PRESENTING WITH ACUTE CORONARY SYNDROME

Beneficial effect of statins has been well validated for primary and secondary prevention of cardiovascular disease, however, they are underused among patients with chronic kidney disease (CKD). All patients with acute coronary syndrome (ACS) enrolled in the ACS Israeli Survey (ACSIS) between the

Liver-Related Effects of Statin Use in Patients with Primary Sclerosing Cholangitis

Recent studies suggest beneficial effects of statins on chronic liver diseases and show associations with reduced risks for hepatic decompensation and

Comparison Between Atorvastatin and Rosuvastatin on Anti- Thrombogenic Effect in Patients with Hyperlipidemia

Background: Atorvastatin and rosuvastatin are two widely used HMG-CoA reductase inhibitors (statins). These are used as lipid-lowering drugs to reduce atherosclerosis-induced cardiovascular events. The beneficial effects of statins also involve some lipid-independent mechanisms which include modification of thrombus formation and degradation, alteration in inflammatory response, plaque stabilization and improvement of endothelial function.Objective: To compare antithrombogenic effect of atorvastatin and rosuvastatin in patients with hyperlipidemia.Materials and Methods: A prospective, open-labeled, interventional, randomized and single-center study was carried out in Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka from March, 2016 to August, 2017 on 52 hyperlipidemic patients. After randomization patients were assigned to atorvastatin 10 mg or rosuvastatin 5 mg daily for 8 weeks. Blood was collected at baseline and after intervention to measure platelet count, prothrombin time (PT) and serum lipid profile.Results: The baseline characteristics of patients treated with atorvastatin and rosuvastatin were almost identical. The platelet count in atorvastatin group was reduced after intervention (2.30%, p=0.463) which was not significant but in rosuvastatin group platelet count reduced significantly (12.33%, p=0.021) after intervention. There was no statistically significant difference (p=0.187) between the two statin treated groups. PT was increased significantly after intervention in both atorvastatin group (31.44%, p&lt;0.001) and in rosuvastatin group (31.93%, p=0.003), which was statistically significant. No significant difference was observed between the two groups (p=0.573). Both atorvastatin and rosuvastatin significantly improved serum lipid profile.Conclusion: The present study reveals that rosuvastatin reduced thrombogenesis more effectively than atorvastatin in hyperlipidemic patients.J Enam Med Col 2018; 8(3): 153-158