Effects Of Statins Research Articles

The double-edged sword of statins in intracerebral hemorrhage patients: a systematic review and meta-analysis

BackgroundThis meta-analysis aimed to investigate the effect of statins on the prognosis of patients with intracerebral hemorrhage (ICH).MethodsWe conducted a systematic search using the keywords “statin” and “intracerebral hemorrhage” across four electronic databases (PubMed, Cochrane Library, Web of Science, and Embase) from their inception to October 31, 2023, to identify studies comparing the effects of statins on the prognosis of patients with ICH. The primary outcome was total mortality after ICH. This meta-analysis was registered online (PROSPERO ID: CRD42023493063).ResultsOur initial search identified 5,543 studies. After applying inclusion criteria, 30 studies with a total of 42,298 patients were included in the final analysis. Our meta-analysis showed that statins significantly reduced overall mortality in patients with ICH (OR: 0.61; 95% CI: 0.51–0.73; I2 = 87%; p < 0.01). Subgroup analyses further demonstrated lower mortality in ICH patients treated with statins compared to those not treated, including in the propensity score matching (PSM) group (OR: 0.59; 95% CI: 0.48–0.74; I2 = 90%; p < 0.01), the prospective cohort study (PCS) group (OR: 0.56; 95% CI: 0.40–0.77; I2 = 89%, p < 0.01), and the retrospective cohort study (RCS) group (OR: 0.64; 95% CI: 0.51–0.81; I2 = 87%, p < 0.01).ConclusionOur meta-analysis of 30 studies suggests that statin use may be associated with improved mortality and functional outcomes in patients with intracerebral hemorrhage (ICH).Systematic Review Registrationhttps://www.crd.york.ac.uk/PROSPERO/, CRD42023493063.

Lipid-Lowering and Antihypertensive Drugs on Aortic Disease Risk: Insights from Mendelian Randomization Analysis and Real-World Pharmacovigilance Data.

To assess the impact of lipid-lowering drugs (LLDs) and antihypertensive drugs on the risk of aortic diseases. Mendelian randomization was utilized to analyze data from 500,000 participants in the UK Biobank to evaluate the effects of statins, PCSK9 inhibitors (PCSK9i), beta-blockers, and calcium channel blockers on the risks of thoracic aortic aneurysm (TAA), abdominal aortic aneurysm (AAA), and aortic dissection (AD) using genetic variants as proxies. Real-world pharmacovigilance data from the FAERS database was used. PCSK9i and statins significantly reduced the risks of aortic aneurysms and AD, respectively. Furthermore, the two LLDs reduced the risk of aortic diseases through certain metabolites. Meanwhile, real-world pharmacovigilance reports also indicated a low incidence of aortic diseases with PCSK9i and statin treatment. LLDs, particularly statins and PCSK9i, significantly protect against aortic diseases, providing a scientific basis for preventing and treating aortic diseases.

Longitudinal association of statin treatment with insulin sensitivity and beta-cell function in the PROMISE cohort.

Statin treatment lowers low-density lipoprotein (LDL) cholesterol thereby reducing cardiovascular risk. Meta-analyses of clinical trials report a higher risk of new-onset type 2 diabetes with statins. Current clinical evidence regarding effects of statins on insulin sensitivity and beta-cell function is limited. We examined the effects of statin treatment on longitudinal changes in early risk phenotypes for type 2 diabetes. The PROMISE cohort is a longitudinal study of adults at-risk for type 2 diabetes. Data from baseline and 3 follow-up visits over 9 years were used to estimate insulin sensitivity (ISI, HOMA2-%S) and beta-cell function (IGI/IR, ISSI-2). Statin use was self-reported. Associations of statins with changes in metabolic markers were determined through Generalized Estimating Equations. Over 9 years, 169 of 498 participants (50 years, 74% female) received a statin, predominantly rosuvastatin and atorvastatin. Compared to no statin treatment, statin users had lower insulin sensitivity (5.32-6.36%) and beta-cell function (4.93-7.59%) (p<0.001) adjusting for metabolic risk factors. Rosuvastatin was associated with decreased insulin sensitivity and beta-cell function, while atorvastatin showed moderate inverse association with beta-cell function and insulin sensitivity. In females, statins reduced insulin sensitivity and beta-cell function, while in males only beta-cell function was altered. Statin treatment was associated with lowered insulin sensitivity and beta-cell function with potential differential effects among statin agents and the sexes.

Statins-Their Effect on Lipoprotein(a) Levels.

Lipoprotein(a) (Lp(a)) serum concentration plays a crucial role as a risk factor in cardiovascular diseases and is gaining more and more attention. Patients with elevated lipoprotein(a) levels are often prescribed statins as they also have high concentrations of low-density lipoprotein cholesterol (LDL-C). Statins are drugs that successfully decrease LDL-C, but their effectiveness in Lp(a) levels reduction is uncertain. The aim of this study was to evaluate if statin therapy can affect Lp(a) concentration. A literature search on databases like PubMed, Oxford Academic, ScienceDirect, Embase, The Cochrane Library, Scopus, and Springer Link was conducted from 1 May to 10 August 2024 with the aim of finding studies concerning the effect of statins on Lp(a) levels. Only randomised control studies and studies with a placebo/comparator arm were included. For calculations, SPSS Statistics software version 29 was used. The risk of bias for this study was assessed using the revised Cochrane risk-of-bias tool for randomised trials. Overall, 43 studies (13,264 participants in study arms and 11,676 in control arms) were included in the analysis. The mean difference of absolute change in Lp(a) concentration for all 43 studies equaled 0.22 mg/dL and was not clinically significant. Egger's regression-based test resulted in no risk of bias in this study (p = 0.404). In conclusion, statin therapy does not significantly affect Lp(a) levels. Results of this work suggest that people with high Lp(a) levels will not change their Lp(a)-associated cardiovascular (CV) risk by statin administration.

Rho GTPases, a Potential Target for the Treatment of Neurodegenerative Disorders and the Neuroprotective Effect of Statins as a Rho GTPase Inhibitor

Rho GTPases, a Potential Target for the Treatment of Neurodegenerative Disorders and the Neuroprotective Effect of Statins as a Rho GTPase Inhibitor

Statin Use and the Risk of Graves' Orbitopathy: A Nationwide Population-Based Cohort Study.

Background: Statin use is reported to reduce the risk of Graves' orbitopathy (GO) in Western populations. However, study regarding the protective effect of statins against GO in Asians with Graves' disease (GD) is scarce. This study aims to investigate the efficacy of statins in preventing GO in Asian GD patients. Materials and Methods: This nationwide, population-based retrospective cohort study used data from beneficiaries aged >40 years diagnosed with GD from the National Health Insurance Research Database (NHIRD) from 2010 to 2020. The International Classification of Diseases codes, Anatomical Therapeutic Chemical codes, and the surgery/procedure codes derived from the NHIRD were used to obtain the information on GD, GO, and statin use. Propensity score (PS) analysis with matching and inverse probability of treatment weighting analysis (IPTW) was conducted to minimize confounding. The Kaplan-Meier survival analysis and multivariable Cox regression analysis were used to compare the risk of GO among statin users and nonusers. Results: The final analysis included 102,858 patients; 7,073 were statin users (62.9 ± 10.6 years, 29.7% male), and 95,785 were nonusers (53.6 ± 10.4 years, 25.7% male). The crude incidence rate of GO among statin users and nonusers was 5.00‰ versus 6.75‰ and 4.91‰ versus 5.15‰ for the overall population and population after PS matching method, respectively. The Cox regression analysis showed that statin users had a significantly lower risk of GO (adjusted hazard ratio [HR] after PS matching 0.79, 95% confidence interval [CI]: 0.63-0.99, p = 0.037; adjusted HR after IPTW method: 0.64, CI: 0.51-0.79, p < 0.001). The risk of GO was not different among users of different kinds of statins (i.e., atorvastatin, rosuvastatin, pitavastatin, and other statins) or among different intensities of statins (low-to-moderate intensity vs. high intensity). Conclusions: The use of statins in Asian GD patients was associated with a reduced risk of GO. In addition, the risk of developing GO among users of commonly prescribed statins or users of different intensities of statins was not significantly different.

Effect of Fibrates on Lipoprotein-associated Phospholipase A2 Mass and Activity: A Systematic Review and Meta-analysis of Controlled Clinical Trials.

In vascular tissue, macrophages and inflammatory cells produce the enzyme lipoprotein- associated phospholipase A2 (Lp-PLA2). Treatment with fibrates decreases Lp-PLA2 levels in individuals with obesity and metabolic syndrome; however, these findings have not been fully clarified. The goal of this study was to investigate the possible effects of fibrate therapy on Lp-PLA2 mass and activity through a meta-analysis of clinical trials. Web of Science, PubMed, Scopus, Google Scholar, and ClinicalTrials.gov databases were searched using MeSH terms and keywords. Randomized controlled trials (RCT) evaluating the effect of statins on Lp- PLA2 mass and/or activity were included in the meta-analysis. Quantitative data were analyzed using a random- effects model and the generic inverse variance method. The meta-analysis of 10 clinical trials indicated that fibrate treatment has no significant effect on Lp- PLA2 mass (fibrate vs. placebo/nothing = WMD: -3.29 ng/ml, 95% CI: -21.35, 14.78, p = 0.72; fibrate vs. active control = WMD: -1.08 ng/ml, 95% CI: -51.38, 49.22, p = 0.97); Lp-PLA2 activity (fibrate vs. active control = WMD: 0.84 nmol/ml/min, 95% CI: -0.17, 1.84, p = 0.10); HDL-LpPLA2 activity (fibrate vs. active control = WMD: 0.77 nmol/ml/min, 95% CI: -0.33, 1.88, p = 0.17); and secretory PLA2 (fibrate vs. active control = WMD: 0.37 ng/ml, 95% CI: -1.22, 1.97, p = 0.65). Also, the results of the sensitivity analysis were robust for all these parameters. In conclusion, fibrate therapy did not reduce the mass and activity of Lp-PLA2.

Statin therapy in ischemic stroke patients with atrial fibrillation: Efficacy and safety outcomes.

The efficacy and safety of statins for secondary prevention in patients who have experienced a cardioembolic stroke are not well-defined. However, previous observational data reported hyperlipidemia as a risk factor for both ischemic and bleeding complications in patients with AF and previous stroke. Based on these premises, we conducted a sub-analysis of the RAF and RAF-NOAC studies to evaluate the efficacy and safety of statins in secondary prevention in patients with acute ischemic stroke and AF. We combined patient data from the RAF and RAF-NOAC studies, prospective observational studies conducted across Stroke Units in Europe, the United States, and Asia from January 2012 to June 2016. We included consecutive patients with AF who suffered an acute ischemic stroke with a follow-up of 90 days. Our outcomes were the combined endpoint, including stroke, transient ischemic attack, systemic embolism, symptomatic intracerebral hemorrhage, and major extracranial bleeding. Furthermore, both ischemic and hemorrhagic outcomes were evaluated separately. A total of 1742 patients were included (46% male), and 898 (52%) received statins after the index event, of whom 436 (48.6%) were already taking statins before the index event, 462 (51.4%) started treatment after. At multivariable analysis, statin use was statistically associated with age (OR 0.92, 95% CI 0.97-0.99, p = 0.001), male sex (OR 1.35, 95% CI 1.07-1.70, p = 0.013), anticoagulation (OR 2.53, 95% CI 1.90-3.36, p < 0.0001), hyperlipidemia (OR 5.52, 95% CI 4.28-7.12, p < 0.0001), paroxysmal AF (OR 1.40, 95% CI 1.12-1.75, p = 0.003), leukoaraiosis (OR 1.39, 95% CI 1.11-1.75, p = 0.004) and heart failure (OR 0.72, 95% CI 0.53-0.98, p = 0.034). Statin use was not associated with the combined outcome event (OR 0.84, 95% CI 0.58-1.23, p = 0.3) and ischemic outcome event (OR 1.17, 95% CI 0.73-1.88, p = 0.5) while was associated with a lower risk of hemorrhagic outcome event (OR 0.51, 95% CI 0.28-0.91, p = 0.02). Statins protect cerebral arterial vessels (particularly small vessels) from subacute damage due to hypertension, diabetes, and other harmful agents (such as reactive oxygen species, proinflammatory cytokines, etc.) due to their systemic anti-inflammatory and endothelium-protective effects. Our data show that statins seem to protect against global bleeding events in cardioembolic stroke patients; this may be due to the pleiotropic effect of statins. More data are warranted to confirm these findings.

Statins and the incidence of post-stroke depression: a systematic review and meta-analysis.

Post-stroke depression (PSD) can lead to poorer functional outcomes and prognosis. Brain inflammation is a risk factor for PSD. Statins might be beneficial due to their anti-inflammatory properties. Different studies have yielded varying results regarding the effects of statins. Therefore, this meta-analysis aims to clarify the effect of statins on PSD. Objectives: To evaluate the relationship between PSD and the use of statins. Data Sources: Databases including PubMed, Web of Science, Embase, and Cochrane Library. Eligibility Criteria: Original observational cohort studies. Participants: Patients with ischemic stroke. Interventions: Use of statins. Appraisal and Synthesis Methods: Forest plot to display pooled results; I 2 test to evaluate heterogeneity. Of the 37 studies selected, four were eligible. The four studies included 93,893 patients (with statins: 45,598) and more than 17,470 PSD patients. The mean age ranged from 62.1 to 70.8 years. The percentage of female participants ranged from 42.1% to 57.9%. For PSD in different regions, the pooled OR for all regions using random-effects methods was 1.21 (95% CI: 0.44-3.33). The pooled OR for Asian populations was 1.42 (95% CI: 0.37-5.40), and for European populations, it was 0.76 (95% CI: 0.73-0.78). The pooled OR for all regions using fixed-effects methods was 0.84 (95% CI: 0.81-0.86). The pooled OR for Asian populations was 2.62 (95% CI: 2.34-2.93). Depending on the pooling method used, statin use in Asia either increased or had no relationship with PSD. For European patients, statin use reduced the incidence of PSD.

Effect of statins and antihyperglycemics on chronic kidney disease in patients with type 2 diabetes mellitus: a retrospective cohort study with a 12-year follow-up.

Chronic Kidney Disease (CKD) represents a significant worldwide health challenge, with far-reaching implications for both patients and healthcare systems. This study aimed to identify the incidence of CKD at stages 3-5, analyzed the impact of statin and other antihyperglycemic interventions, on the CKD progression in individuals with T2DM. This was a single-center retrospective cohort study based on data derived from electronic medical records (EMR) of UAE populations with diabetes mellitus, registered at outpatient clinics at Tawam Hospital in Al Ain, UAE, between January 2011 and December 2021. T2DM patients aged ≥ 18 years who had serum HbA1c level ≥ 6.5% and using one of the statin therapies were inclusion criteria. Patients with T1DM, who had undergone permanent renal replacement therapy, with under 1 year of follow-up and missing or incomplete data were excluded from the study. The collected data encompassed socio-demographics, detailed medical history, anthropometric measurements, laboratory analyses, clinical parameters, disease characteristics, and medications. Our study included a cohort of 1,003 individuals. We observed 388 subjects developed CKD stages 3-5 across an average monitoring duration of 11.7 years. This resulted in a cumulative incidence of 38.7%, translating to an incidence rate of 38 cases per 1000 person-years. There was a statistically significant difference in the cumulative incidence of CKD stages 3 ± 5 according to statin therapy (P = 0.047). High intensity statin users are more likely to develop a CKD stage 3-5 compared to low/moderate intensity users and to no statin users respectively (44.3% vs 37.9%), (44.3% vs 30.9%). Conversely, the use of Biguanides was associated with a decreased probability of CKD progression (37.9% vs. 52.8%; P = 0.001), whereas Insulin users demonstrated a heightened risk (54.2% vs. 34.1%; P < 0.001). The findings emphasise the pivotal role of personalised treatment strategies, particularly concerning statin therapy and other medications, in populations at high risk.

Effects Of Statins On Outcomes After Cardiac Transplantation: A Systematic Review And Meta-analysis Of Published Studies.

Effects Of Statins On Outcomes After Cardiac Transplantation: A Systematic Review And Meta-analysis Of Published Studies.

Statin Use is Associated with Decreased Venous Thromboembolism Events Following Total Hip Arthroplasty: A Matched Retrospective Cohort Study.

Despite advances in surgical techniques and postoperative prophylactic protocols, venous thromboembolism (VTE) events remain an important source of morbidity following total hip arthroplasty (THA). Prior research in cardiology and other surgical fields has suggested that statin medications may have a protective effect against VTE. Our study aimed to: 1) Assess if preoperative statin use was associated with decreased rates of VTE following THA, and 2) conduct a subgroup analysis of statin intensity and VTE events. A total of 1,154 patients who had preoperative statin use for at least four weeks before surgery and who underwent primary THA at a large, urban academic center between January 1, 2012, and June 1, 2023, were identified. The 90-day postoperative VTE events, deep vein thrombosis (DVT), pulmonary embolism (PE), emergency department (ED) visits, reoperations, and readmission rates were collected from institutional coding software. Mortality rate in the 90-day postoperative period was also measured. Propensity matching was used to control for demographics and selected comorbidities. Preoperative statin use was associated with significantly lower rates of 90-day VTE events (Statin: 0.43% versus No-Statin: 1.13%, P = 0.047). There were no significant differences in 90-day PE, DVT, ED visit, readmission, or reoperation rates. There were no deaths within 90 days of THA in either group. Subgroup analysis of statin intensity revealed no significant differences in any outcomes measured between high-intensity, medium-intensity, and low-intensity statin groups. Preoperative statin use is associated with significantly lower rates of VTE events in the 90-day postoperative period following THA. Further research into the effect of statins on post-THA VTE is warranted.

β-Caryophyllene and Statins in Bone Fracture Healing - A Narrative Review.

Bone fractures are a leading cause of morbidity and healthcare expenditure globally. The complex healing process involves inflammation, cartilage formation, mineralization, and bone remodeling. Current treatments like immobilization, surgery, and bone grafting, though effective, pose significant challenges, such as prolonged recovery and high costs. Emerging therapies such as biological agents, pharmacological treatments, and physical stimulation techniques are also associated with high costs, side effects, and practical applicability limitations. There is a critical need for alternative therapies that are cost-effective, safe, and easy to use. Recent studies suggest the potential of β-caryophyllene (BCP) and statins in promoting bone healing. BCP, a naturally occurring anti-inflammatory and antioxidant compound found in essential oils, enhances osteoblast activity and inhibits osteoclastogenesis. Statins, known for their cholesterol-lowering effects, also promote bone formation and reduce bone resorption through multiple biochemical pathways. Both BCP and statins have shown promising results in preclinical studies, enhancing bone density and promoting fracture healing. This review explores the individual and potential synergistic effects of BCP and statins on bone fracture healing. It highlights the complementary mechanisms of these agents: BCP's anti-inflammatory and osteogenic properties and statins' ability to inhibit osteoclast activity and promote angiogenesis. Combining BCP and statins could offer a multifaceted approach to enhance fracture healing, reduce complications, and improve patient outcomes. While individual effects are supported preclinically, further studies investigating synergies, formulations, and clinical translation are needed to develop this promising novel therapeutic approach for improving fracture repair outcomes.

Differential effects of statins on the anti-dyskinetic activity of sub-anesthetic ketamine.

Sub-anesthetic ketamine has been demonstrated to reduce abnormal involuntary movements (AIMs) in preclinical models of L-DOPA-induced dyskinesia (LID) and retrospective Parkinson's disease (PD) case reports. In this study, we examined the effects on LID of two different statins alone and in combination with ketamine in unilateral 6-hydroxydopamine-lesioned male rats, the standard model for preclinical LID studies. Ketamine attenuated the development of AIMs, while the non-polar lovastatin only showed anti-dyskinetic activity early in the priming period but did not prevent the development of LID, and the polar pravastatin showed no anti-dyskinetic activity. Furthermore, our main result is that pravastatin blocked the long-term neuroplastic anti-dyskinetic effects of ketamine, while lovastatin did not. This study shows two different statins affect LID and the anti-dyskinetic activity of ketamine differentially, pointing to an important drug interaction. The results further inform and support ongoing clinical testing of sub-anesthetic ketamine to treat LID in individuals with PD.

Pleiotropic Effect of Statins: Beyond Cholesterol Reduction

Pleiotropic Effect of Statins: Beyond Cholesterol Reduction

Personalized statin therapy: Targeting metabolic processes to modulate the therapeutic and adverse effects of statins.

Statins are widely used for treating lipid disorders and cardiovascular diseases. However, the therapeutic efficiency and adverse effects of statins vary among different patients, which numerous clinical and epidemiological studies have attributed to genetic polymorphisms in statin-metabolizing enzymes and transport proteins. The metabolic processes of statins are relatively complex, involving spontaneous or enzyme-catalyzed interconversion between more toxic lactone metabolites and active acid forms in the liver and bloodstream, influenced by multiple factors, including the expression levels of many metabolic enzymes and transporters. Addressing the variable statin therapeutic outcomes is a pressing clinical challenge. Transcription factors and epigenetic modifications regulate the metabolic enzymes and transporters involved in statin metabolism and disposition and, therefore, hold promise as 'personalized' targets for achieving optimized statin therapy. In this review, we explore the potential for customizing therapy by targeting the metabolism of statin medications. The biochemical bases of adverse reactions to statin drugs and their correlation with polymorphisms in metabolic enzymes and transporters are summarized. Next, we mainly focus on the regulatory roles of transcription factors and epigenetic modifications in regulating the gene expression of statin biochemical machinery. The recommendations for future therapies are finally proposed by targeting the central regulatory factors of statin metabolism.

Impact of dyslipidemia and lipid-lowering therapy with statins in patients with neuroendocrine tumors.

Dyslipidemia is a potential unfavorable prognostic factor in neuroendocrine tumors (NETs); conversely, statins proved to have antiproliferative effects in NET cell lines and could be a helpful therapeutic strategy for these patients. The main objective of this observational cohort retrospective study is to explore the associations between dyslipidemia and NET progression and evaluate the potential influence of statins in this context. 393 patients with histologically confirmed gastroenteropancreatic or bronchopulmonary NETs from six Italian centres didicated to NET diagnosis and therapy were included. The cohort included 123 patients with dyslipidemia, 81 of which were taking statins. Clinicopathological data, including patient demographics, tumor characteristics, and treatment details as well as the prevalence, timing of dyslipidemia and hypolipemic therapy were collected. The main outcome measure used is progression-free survival (PFS). Among the 393 patients, 123 (31.3%) had dyslipidemia. Statins were used by 81 (65.8%) dyslipidemic patients, mostly atorvastatin. Median PFS was 87 months overall, 124 months in non-dyslipidemic patients, and 72 months in dyslipidemic patients (p = .268). Dyslipidemic patients on statins had a significantly better median PFS (108 months) than those not on statins (26 months; p = .024). Recurrence-free survival(RFS) was also evaluated, but no significant differences were found. In conclusion, while PFS was lower in dyslipidemic patients compared to non-dyslipidemic patients, the difference was not statistically significant. Statin therapy was associated with improved PFS among dyslipidemic patients, suggesting a potential antiproliferative effect of statins in NETs. These findings warrant further investigation to substantiate the role of statins in the management of NETs.

Inclisiran as a siRNA Inhibitor of Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9); Past, Present, and Future.

Reducing low-density lipoprotein cholesterol (LDL-C) levels has been shown to reduce the risk of developing atherosclerotic cardiovascular disease (ASCVD). Statins are the foundation of LDL-C lowering therapy with other non-statin agents used in circumstances where goal LDL-C levels are not reached or owing to intolerance to adverse effects of statins. In 2003, the discovery of the role of the proprotein convertase subtilisin/kexin type 9 (PCSK9) system in promoting elevated LDL-C levels led to new avenues of drug development to achieve target LDL-C. In 2021, inclisiran, a small interfering ribonucleic acid (siRNA) molecule targeting PCSK9 was approved by the Food and Drug Administration (FDA). Inclisiran has demonstrated effective reductions of LDL-C, such as in the large phase-3 ORION-9, ORION-10, and ORION-11 trials in which it achieved LDL-C reductions of 39.7%, 52.3%, and 49.9%, respectively. This review discusses the current clinical evidence and ongoing clinical studies of inclisiran as well as analyzes other areas of PCSK9 inhibition development.

Effect of Statins on the Prognosis After Thoracic Endovascular Aortic Repair for Patients With Acute Type B Aortic Dissection.

To analyze the clinical efficacy of long-term statin therapy following thoracic endovascular aortic repair (TEVAR) in patients with acute type B aortic dissection (ATBAD). We retrospectively analyzed data from 645 patients treated between January 2005 and June 2022, dividing them into Statin Group (n=330) and Non-statin Group (n=315) based on whether they received long-term postoperative statin therapy. Patients were further categorized based on median admission low-density lipoprotein cholesterol (LDL-C) levels into High and Low LDL-C Groups to assess the effect of statins on the prognosis of ATBAD patients after TEVAR. The cohort had an average age of 53.44±11.42 years old, and 81.71% were male. Statin therapy significantly reduced occurrences of all-cause death (3.03% vs 8.57%, p=0.002) and aorta-related death (0.91% vs 3.81%, p=0.015), particularly in patients with high admission LDL-C levels. In addition, patients with statin therapy had a lower incidence of aorta-related adverse events (ARAE) (4.24% vs 11.11%, p=0.001). Kaplan-Meier analysis indicated statins reduced 5-year cumulative incidence rates of all-cause death and ARAE (all Log-rank p<0.05). These trends were sustained after adjustment. Multivariate Cox analysis confirmed that statin therapy was associated with reduced risks of all-cause and aorta-related deaths, as well as ARAE. Long-term statin therapy appears to decrease the risk of all-cause and aorta-related death in ATBAD patients after TEVAR, particularly patients with high admission LDL-C levels. Patients with lower LDL-C levels at admission have a reduction of aorta-related death in the follow-up period. Statin therapy also was associated with a lower incidence of ARAE in follow-up. These findings suggest that statins might be crucial in improving long-term outcomes in this patient population. Long-term statin therapy administered to patients with acute type B aortic dissection (ATBAD) following thoracic endovascular aortic repair (TEVAR) demonstrates a substantial reduction in both all-cause and aorta-related mortality. Notably, this therapeutic benefit is most evident in patients presenting with elevated low-density lipoprotein cholesterol (LDL-C) levels at admission. Furthermore, statin therapy is associated with a decreased incidence of aorta-related adverse events during follow-up. These findings underscore the pivotal role of statin therapy in enhancing long-term clinical outcomes for ATBAD patients undergoing TEVAR, thereby contributing to improved patient care and prognosis.

Regulatory effects of statins on CCL2/CCR2 axis in cardiovascular diseases: new insight into pleiotropic effects of statins

BackgroundHMG-CoA reductase inhibitors are well-known medications in the treatment of cardiovascular disorders due to their pleiotropic and lipid-lowering properties. Herein, we reviewed the effects of statins on the CCL2/CCR2 axis.MethodScopus and Pubmed databases were systematically searched using the following keywords:” Hydroxymethylglutaryl CoA Reductase Inhibitors”,” HMG-CoA Reductase Inhibitors”,” Statins”, “CCL2, Chemokine”, “Monocyte Chemoattractant Protein-1” and “Chemokine (C-C Motif) Ligand 2”. Evidence investigating the role of statin on MCP-1 in CVD was identified and bibliographies were completely evaluated to gather further related studies.ResultsThe anti-inflammatory effects of statins on the CCL2/CCR2 pathway have been widely investigated. Despite inconclusive results, a great body of research supports the regulatory roles of statins on this pathway due to their pleiotropic effects. By disrupting the CCL2/CCR2 axis, statins attenuate the infiltration of monocytes and macrophages into the zone of inflammation and hence down-regulate the inflammatory cascades in various CVDs including atherosclerosis, cardiac remodeling, and stroke, among others.ConclusionCCL2 plays a major role in the pathogenesis of cardiovascular disorders. Down-regulation of CCL2 is proposed as one of the pleiotropic properties of statins. However, more investigations are required to elucidate which statin in what dose exerts a more potent effect on CCL2/CCR2 pathway.