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BackgroundAmong people with HIV (PWH), COVID-19 is common and potentially severe. We leveraged REPRIEVE (Randomized Trial to Prevent Vascular Events in HIV) to assess the effects of statin therapy for cardiovascular disease prevention on COVID-19 outcomes (incidence and serious cases) among a global cohort of PWH.MethodsCOVID-19 data collection was implemented April 2020 to capture events from January 2020. COVID-19 was defined by positive test result or clinical diagnosis and serious COVID-19 according to the International Conference on Harmonisation definition. Among participants in follow-up on 1 January 2020, Cox proportional hazards modeling was used to estimate the hazard ratio (HR) of COVID-19 (pitavastatin/placebo), stratified by Global Burden of Disease region. Modification of statin effect following COVID-19 vaccination was evaluated via interaction with time-updated vaccination status.ResultsAmong 6905 PWH, 32% were natal female and 41% were Black or African American. The median age was 53 years and the 10-year atherosclerotic cardiovascular disease risk score 4.5%. Statin therapy did not reduce COVID-19 incidence (HR, 1.05; 95% CI, .95-1.15) but appeared to reduce incidence of serious COVID-19 (HR, 0.75; 95% CI, .52-1.09). Among 1701 PWH with COVID-19, the relative risk (pitavastatin/placebo) for serious COVID-19 was 0.73 (95% CI, .52-1.03). The treatment effect size for serious COVID-19 fell within the hypothesized range, but the 95% CI crossed 1 given fewer-than-anticipated cases (117 vs 200). Furthermore, 83% reported COVID-19 vaccination by end of study, with a strong protective effect on serious COVID-19 (HR, 0.27; 95% CI, .14-.53; P < .0001). A protective statin effect was observed prior to vaccination.ConclusionsAmong PWH, statin therapy had no effect on COVID-19 incidence but showed potential to reduce risk of serious COVID-19 prior to COVID-19 vaccination.Clinical trials registrationNCT02344290 (ClinicalTrials.gov).

Background and purposeCerebral vasomotor reactivity (VMR) is vital for regulating brain blood flow and maintaining neurological function. Impaired cerebral VMR is linked to a higher risk of stroke and poor post-stroke outcomes. This study explores the relationship between statin treatment intensity and VMR in patients with ischemic stroke.MethodsSeventy-four consecutive patients (mean age 69.3 years, 59.4% male) with recent ischemic stroke were included. VMR levels were assessed 4 weeks after the index stroke using transcranial Doppler, measuring the breath-holding index (BHI) as an indicator of the percentage increase in middle cerebral artery blood flow (higher BHI signifies higher VMR). Multistep multivariable regression models, adjusted for demographic and cerebrovascular risk factors, were employed to examine the association between statin intensity treatment and BHI levels.ResultsForty-one patients (55%) received high-intensity statins. Patients receiving high-intensity statins exhibited a mean BHI of 0.85, whereas those on low-intensity statins had a mean BHI of 0.67 (mean difference 0.18, 95% confidence interval: 0.13-0.22, p-value.05). Furthermore, no significant association was found between baseline low-density lipoprotein (LDL) levels and BHI.ConclusionsHigh-intensity statin treatment post-ischemic stroke is linked to elevated VMR independent of demographic and clinical characteristics, including baseline LDL level. Further research is needed to explore statin therapy's impact on preserving brain vascular function beyond lipid-lowering effects.

Study Design.: Retrospective cohort study. Objective.: To understand how preoperative LDL levels, statin intake, and fish oil intake affect rates of pseudarthrosis after single-level and multilevel ACDF. Summary of Background Data.: Anterior cervical discectomy and fusion (ACDF) is commonly performed to treat cervical degenerative diseases or injuries causing neck pain, myelopathy, and radiculopathy. Pseudarthrosis following ACDF can lead to persistent symptoms and may require revision surgery. No studies have explored the link between low-density lipoprotein (LDL) levels and statin or fish oil intake on pseudarthrosis in ACDF. Materials and Methods.: Patients undergoing ACDF were identified using TriNetX, a health care database with over 100 million patients. Pseudarthrosis rates following single-level and multilevel ACDF were compared between patients with high versus low LDL within one year before surgery. Pseudarthrosis rates were also compared between patients taking or not taking a statin as well as patients taking or not taking fish oil within six months before surgery. For all analyses, patients underwent propensity score matching in a 1:1 ratio based on relevant demographic factors and comorbidities. Results.: Patients with an LDL above 142 mg/dL, compared with below 66 mg/dL, had significantly higher rates of pseudarthrosis at six months, one year, and two years after single-level and multilevel ACDF. Patients not taking a statin or fish oil, compared with those taking a statin or fish oil, respectively, also had significantly higher rates of pseudarthrosis at all time points after multilevel ACDF, but not single-level ACDF. Conclusion.: Low LDL levels are associated with reduced rates of pseudarthrosis after single-level and multilevel ACDF. Statin and fish oil intake before surgery are also associated with reduced rates of pseudarthrosis after multilevel, but not single-level ACDF. These associations may be used for preoperative planning, patient optimization, and risk stratification. [ABSTRACT FROM AUTHOR]

Background: The effect of statins on the risk of dementia and Alzheimer's disease (AD) is unclear. Methods: We systematically searched EMBASE, Web of Science, PubMed, CENTRAL and ClinicalTrail.gov for cohort studies comparing incidence of new-onset dementia and AD between statin users and non-users. We applied the DerSimonian–Laird random effects method to pool hazard ratio (HR) with 95% confidence intervals (CI). Results: We included forty-two studies comprising 6,325,740 patients. Thirty-five cohort studies involving 6,306,043 participants were pooled and indicated that statin use was associated with a reduced risk of dementia (HR: 0.79, 95% CI: 0.71–0.88). Similarly, an analysis of 19 studies comprising 1,237,341 participants demonstrated a 29% decrease in the risk of AD among statin users (HR: 0.71, 95% CI: 0.60–0.85). In sensitivity analyses, diagnostic criteria for dementia/AD significantly affected the combined risk estimates. In subgroup analyses, compared to studies enrolling participants with a mean/median age over 70 years, those younger than 70 years exhibited greater efficacy of statins in preventing dementia (HR: 0.67, 95% CI: 0.56–0.81 vs HR: 0.86, 95% CI: 0.78–0.95; P = 0.02) and AD (HR: 0.47, 95% CI: 0.44–0.50 vs. HR: 0.81, 95% CI: 0.71–0.92; P < 0.01). Due to significant heterogeneity in the definitions of statin dosage and exposure duration, pooling the results was abandoned and most studies suggested that higher dosages and longer exposure duration of statins further reduce the risk of dementia and AD. Conclusion: Statin use is associated with a reduced incidence of dementia and AD, which might be modified by ages. [ABSTRACT FROM AUTHOR]

Background: Many studies recognize a close link between inflammation, cardiovascular disease (CVD), and oncological diseases. High-sensitivity C-reactive protein (hs-CRP), a marker of low-grade systemic inflammation, is a shared feature of these conditions. This retrospective study aims to assess the predictive value of hs-CRP for the development of cancer in patients with CVD. Methods: Analyzing data from 174 patients undergoing coronary angiography, we assessed hs-CRP levels and collected demographic, biological, and therapeutic data that could influence the studied parameters. Results: Only smoking and dyslipidemia correlated significantly with CRP levels (p = 0.018 and 0.049, respectively). However, hs-CRP did not predict cancer development (p = 0.52) but correlated with 1-year and follow-up mortality (p = 0.011 and 0.021, respectively). Antiplatelet and statin use was higher in the cancer-free group and associated with a lower probability of developing cancer (p < 0.001 and p = 0.009, respectively). Conclusions: While hs-CRP did not prove effective as a cancer predictor in our study, it correlated with all-cause mortality. Our findings suggest a potential protective effect of antiplatelet and statin treatments against cancer development, prompting further research to understand underlying processes and identify key factors in the pathophysiology of these diseases. [ABSTRACT FROM AUTHOR]

Background/Objectives: It has been shown that the use of statins in patients with type 2 diabetes mellitus (T2DM) worsens hyperglycemia and hemoglobin A1c levels but may help in the preservation of pancreatic β-cell function. The potential role of a high pancreatic fat fraction (PFF) in this process has not yet been clarified. This study aimed to investigate whether the liver fat fraction (LFF) and PFF in T2DM patients is affected by statin therapy. Methods: This cross-sectional study involved a total of 140 T2DM patients, including both those who were receiving (n = 70) and those who were not receiving (n = 70) statin therapy. The mapping of the LFF and PFF utilizing the IDEAL-IQ sequence was conducted in magnetic resonance imaging. Results: In T2DM patients who used statins, the median PFF was higher compared to those who did not use statins (8.4 vs. 6.2%, p = 0.021), while the median LFF was found to be similar (8.4 vs. 8.9, p = 0.572). Variations in PFF were associated with the use of various statins (non-statin group: 6.2 vs. atovastatin: 8.7 vs. rosuvastatin: 3.2 vs. pitavastatin: 9.2, p = 0.004). The multivariable regression analysis indicated that insulin usage decreased log(LFF) by a factor of 0.16-fold (ꞵ ± SE = −0.16 ± 0.05, p = 0.010), and rosuvastatin usage reduced log(PFF) by 0.16-fold (ꞵ ± SE = −0.16 ± 0.07, p = 0.025), irrespective of other risk factors. Furthermore, the use of atorvastatin (ꞵ ± SE = 0.17 ± 0.06, p = 0.011) and pitavastatin (ꞵ ± SE = 0.19 ± 0.07, p = 0.008) were independently associated with an increase in log(PFF). Conclusions: In patients with T2DM, statin use did not show a significant effect on the liver fat fraction, but it caused differences in the pancreatic fat fraction. The observation of a lower pancreatic fat fraction in patients taking a rosuvastatin and atorvastatin dose of 40 mg/day suggests that different types and doses of statins may have varying effects on pancreatic fat accumulation. [ABSTRACT FROM AUTHOR]

Background: This meta-analysis aimed to investigate the effect of statins on the prognosis of patients with intracerebral hemorrhage (ICH). Methods: We 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). Results: Our 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; I 2 = 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; I 2 = 90%; p < 0.01), the prospective cohort study (PCS) group (OR: 0.56; 95% CI: 0.40–0.77; I 2 = 89%, p < 0.01), and the retrospective cohort study (RCS) group (OR: 0.64; 95% CI: 0.51–0.81; I 2 = 87%, p < 0.01). Conclusion: Our 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 Registration: https://www.crd.york.ac.uk/PROSPERO/ , CRD42023493063. [ABSTRACT FROM AUTHOR]

Background Little is known about the potential benefits or harms of statins on physical function among people with human immunodeficiency virus (PWH). Methods REPRIEVE was a double-blind randomized controlled trial evaluating pitavastatin for primary prevention of major adverse cardiovascular events in PWH. Time to complete 10 chair rises, 4-m gait speed, grip strength, and a modified short physical performance test were assessed annually for up to 5 years in the ancillary study PREPARE and analyzed using linear mixed models. Findings Of 602 PWH, 52% were randomized to pitavastatin and 48% to placebo. Median age was 51 years; 18% were female at birth; 2% transgender; and 40% Black, and 18% Hispanic. Median PREPARE follow-up was 4.7 (4.3–5.0) years. Muscle symptoms (grade ≥3 or treatment-limiting) occurred in 5% of both groups. There was no evidence of decline in chair rise rate in either treatment group and no difference in the pitavastatin group compared to placebo (estimated difference −0.10 [95% confidence interval, −.30 to 0.10] rises/min/year; P =.31). Small declines over time were observed in other physical function tests in both treatment groups, with no apparent differences between groups. Interpretation We observed minimal declines in physical function over 5 years of follow-up among middle-aged PWH, with no differences among PWH randomized to pitavastatin compared to placebo. This finding, combined with low prevalence of myalgias, supports the long-term safety of statin therapy on physical function, when used for primary prevention of major adverse cardiovascular events among PWH. [ABSTRACT FROM AUTHOR]

Metastasis is a leading cause of mortality in breast cancer, as metastatic disease is often aggressive and resistant to conventional treatments. Cancer cells that spread to distant organs can enter a dormant phase for extended periods, sometimes years or decades. During this dormant phase, cancer cells avoid immune and pharmacological response. Thus, new approaches are needed to prevent these disseminated cells from becoming lethal cancers. Statins are known inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase that have been extensively used in patients with cardiovascular diseases to lower cholesterol. However, recent research has demonstrated their potential in anticancer therapies. Epidemiological evidence suggests that statins are associated with a reduction in breast cancer-specific mortality, although they do not appear to affect the incidence of primary tumors. In this review, we discuss the role of statins in metastasis and dormancy, their cytocidal and cytostatic effects and their interactions with different cell types in the tumor microenvironment. The exact mechanisms by which statins reduce mortality without influencing primary tumor growth remain unclear, also warranting further investigation into their potential role in metastasis and tumor dormancy, which could ultimately help patients to improve survival and quality of life. [ABSTRACT FROM AUTHOR]

Supplemental Digital Content is Available in the Text. Background: Evidence-based guidelines recommend statins as first-line therapy to reduce the risk of cardiovascular events in patients with cardiovascular disease and/or diabetes. The Centers for Medicare and Medicaid Services assess compliance with these guidelines through performance and process quality measures. Purpose: To describe innovative practices to address statin use care gaps, to identify successes and challenges of a pharmacist-led statin initiative, and share quality improvement opportunities related to statin quality metrics. Methods: A retrospective review was conducted in 2023 of patients enrolled in Medicare Advantage value-based care contracts in a large health system. The primary outcome measures were the percentage of patients identified with statin care gaps who met the criteria for statin treatment and the percentage of patients who accepted pharmacist-led recommendations to initiate statin therapy. Outcomes were analyzed using descriptive statistics. Results: Among those with statin care gaps, 42% met criteria for pharmacist-led statin initiation. Of those who met criteria, 22% accepted pharmacist's recommendation to initiate statin therapy. Conclusions: Pharmacist-led statin initiation is effective; however, systematic barriers remain to improve statin quality performance. These results can help others adopt innovative practices that target statin care gaps and assess opportunities for quality improvement. [ABSTRACT FROM AUTHOR]

Background: Despite the advent of new pharmacotherapies, statins remain a cornerstone in the secondary prevention of myocardial infarction (MI). However, the cardiac adverse events (AEs) linked to statins are not well-documented. Aim: This pharmacovigilance study used data from the FDA Adverse Event Reporting System (FAERS) to investigate the association between statin use and cardiac AEs in MI patients. Method: Reports from the FAERS database (2004–2023) identifying statins as the primary suspect in MI patients were analyzed. The study evaluated seven types of statins: atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin, and simvastatin. Disproportionality analysis using four major indices, Reporting Odds Ratio (ROR), Proportional Reporting Ratio (PRR), Bayesian Confidence Propagation Neural Network (BCPNN), and Multi-Item Gamma-Poisson Shrinker (MGPS), was conducted to detect signals of statin-related cardiac AEs. Results: Of the 20,346,289 reports reviewed, 150 identified statins as the primary suspect drug in MI patients. The most common cardiac AEs were recurrent MI (50 reports), acute MI (14 reports), followed by tachycardia (10), angina pectoris (8), coronary artery occlusion (6), cardiac failure (6), and arrhythmia (6). The analysis revealed no significant signals of statin-induced cardiac AEs. Conclusion: The findings confirm that statin use in MI patients does not significantly increase the risk of cardiac adverse effects, supporting their safety profile in this context. [ABSTRACT FROM AUTHOR]

Introduction: Lipid-lowering therapies are well established for the treatment of cardiovascular disease (CVD). Historically monotherapy studies have been performed, but the introduction of statins has led to these drugs being recognized as baseline therapies and to the investigation of combination therapy of both older and newer medications with them. Areas covered: Surrogate marker studies have shown additive effects on LDL-C, triglycerides and HDL-C of combination therapies with statins and these have extended to lipoprotein (a). Imaging studies have often shown benefits paralleling lipid studies. However, outcome studies have failed to show added benefits with niacin or fibrates while confirming the benefits of ezetimibe, bempedoic acid and proprotein convertase subtilisin kexin-9 (PCSK-9) inhibitors and icosapent ethyl. Expert opinion: Combination therapy for LDL-C in dual combinations is well validated. Data for intervention on triglycerides is limited to icosapent ethyl, but this may exert effects independent of lipids. New drugs targeting triglycerides through apolipoprotein C3 and angiopoietin-like peptides are in development. Studies on combination therapy raising HDL-C have generally disappointed, though cholesterol ester transfer protein (CETP) inhibition remains a target. Lipoprotein (a) is recognized as a CVD risk factor and effective therapies are in development but results on CVD events are lacking. [ABSTRACT FROM AUTHOR]

Background: Proprotein convertase subtilisin/kexin type 9 inhibitors effectively reduce LDL cholesterol and adverse cardiovascular events with a safety profile comparable to a placebo. Limited real-world data exists on their effectiveness in different patient groups. This study evaluated evolocumab's efficacy and safety in hypercholesteremia patients with and without diabetes. Method: In a large tertiary hospital in Saudi Arabia, patients aged 18 and above who initiated evolocumab therapy were screened for eligibility between January 2017 and July 2023. All patients who had been on maximally tolerated statin and ezetimibe therapy for at least 4 months before starting evolocumab were included. The included participants were then divided into diabetic and non-diabetic groups and assessed for evolocumab's efficacy and safety. Efficacy was measured by LDL-C reduction and target achievement, while safety was assessed by examining glycemic control changes, new-onset diabetes (NOD) and hepatic enzyme levels. Data analysis included descriptive and comparative methods, with significance set at p < 0.05. Results: A total of 151 patients were included, with an average age of 51.77 years. The majority of patients were male (67.6%) and obese (81.5%). Around 55% had diabetes, and 63% had established atherosclerotic cardiovascular disease at baseline. During a mean follow-up period of 13.17 months, the average reduction in LDL-C from baseline was − 34.21, − 28.66, and − 39.61% for the overall cohort, non-diabetic patients, and diabetic patients, respectively. In the overall cohort, 34.4 and 24.5% reached the target LDL-C levels of less than 1.4 mmol/L (55 mg/dL) and less than 1.8 mmol/L (70 mg/dL), respectively. Worsening of glycemic control (HbA1C increase > 0.5) was observed in 25.83% of the overall cohort, 16.18% of non-diabetics, and 33.74% of diabetics. An HbA1C increase > 1 was observed in 13.25% of the overall cohort, 2.94% in non-diabetics and 21.69% in diabetics. Five patients (3.3%) developed NOD. Conclusion: The study demonstrated that the addition of evolocumab to maximally tolerated statin and ezetimibe therapy reduced LDL-C levels but with a smaller average reduction and a lower proportion of patients achieving recommended LDL-C targets than in landmark clinical trials. Additionally, there was a potential negative effect on glycemic control, warranting further investigation. [ABSTRACT FROM AUTHOR]

Introduction: Vascular smooth muscle cells are important in intimal hyperplasia. Thrombospondin-1 is a matricellular protein involved in the vascular injury response. Statins are cholesterol lowering drugs that have beneficial cardiovascular effects. Statis have been shown to inhibit smooth muscle migration through the mevalonate pathway. This effect is thought to be mediated by small G protein Ras and Rho turnover which requires many hours. While many patients undergoing treatment for vascular disease are on statins, many are not. Thus immediate pretreatment with statins before surgery may be beneficial. We hypothesized that statins have effects independent of the mevalonate pathway and thus have an immediate effect. Methods: Human vascular smooth muscle cells were pretreated for 20 h (long-term) or 20 min (short-term) with fluvastatin, or mevalonolactone plus fluvastatin. Thrombospondin-1-induced migration, activation of p42/p44 extracellular signal-regulated kinase, c-Src, focal adhesion kinase and PI3 kinase was determined. The effect of fluvastatin on thrombospondin-1-induced expression of THBS1, FOS, HAS2 and TGFB2 was examined. Results: Both treatments inhibited thrombospondin-1-induced chemotaxis back to the control group. Mevalonolactone reversed the long-term statin effect by increasing migration but had no effect on the short-term statin response. p42/p44 extracellular signal-regulated kinase was activated by thrombospondin-1 and both treatments augmented activation. Neither treatment affected c-Src activity, but both inhibited focal adhesion kinase and PI3 kinase activity. Only long-term statin treatment inhibited THBS1 expression while both treatments inhibited FOS and TGFB2 expression. Neither treatment affected HAS2. FOS knockdown inhibited thrombospondin-1-induced HAS2 but not TGFβ2 gene expression. Conclusion: Long-term fluvastatin inhibited thrombospondin-1-induced chemotaxis through the mevalonate pathway while short-term fluvastatin inhibited chemotaxis through an alternate mechanism. Short-term stains have immediate effects independent of the mevalonate pathway. Acute local treatment with statins followed by longer term therapy may limit the vascular response to injury. [ABSTRACT FROM AUTHOR]

Coenzyme Q10 (CoQ10) plays a crucial role in facilitating electron transport during oxidative phosphorylation, thus contributing to cellular energy production. Statin treatment causes a decrease in CoQ10 levels in muscle tissue as well as in serum, which may contribute to the musculoskeletal side effects. Therefore, we aimed to assess the effect of newly initiated statin treatment on serum CoQ10 levels after acute ST-elevation myocardial infarction (STEMI) and the correlation of CoQ10 levels with key biomarkers of subclinical or clinically overt myopathy. In this study, we enrolled 67 non-diabetic, statin-naïve early-onset STEMI patients with preserved renal function. Plasma CoQ10 level was determined by ultra-high-performance liquid chromatography–tandem mass spectrometry (UPLC/MS-MS), while the myopathy marker serum fatty acid-binding protein 3 (FABP3) level was measured with enzyme-linked immunosorbent assay (ELISA) at hospital admission and after 3 months of statin treatment. The treatment significantly decreased the plasma CoQ10 (by 43%) and FABP3 levels (by 79%) as well as total cholesterol, low-density lipoprotein cholesterol (LDL-C), apolipoprotein B100 (ApoB100), and oxidized LDL (oxLDL) levels. The change in CoQ10 level showed significant positive correlations with the changes in total cholesterol, LDL-C, ApoB100, and oxLDL levels, while it did not correlate with the change in FABP3 level. Our results prove the CoQ10-reducing effect of statin treatment and demonstrate its lipid-lowering efficacy but contradict the role of CoQ10 reduction in statin-induced myopathy. [ABSTRACT FROM AUTHOR]

Purpose: Previous studies implied that different types of statins may pose divergent impacts on the risk of glaucoma onset. This study aimed to comprehensively evaluate the effects of various statins on the risk of glaucoma occurrence. Methods: PubMed, Cochrane CENTRAL, Embase, and Web of Science were searched from February 1994 to February 2024. We included studies that investigated the effects of various types of statins, fibrates, ezetimibe, cholestyramine, niacin, PCSK9 inhibitors, omega-3 fatty acids, and any cholesterol-lowering medications on glaucoma onset or progression. The revised Cochrane risk-of-bias tool for randomized trials (RoB 2.0) and the Risk Of Bias In Non-randomized Studies—of Interventions (ROBINS-1) tool were used to assess the quality of randomized controlled trials (RCTs) and non-RCTs, respectively. The frequentist network meta-analysis framework was utilized to evaluate the comparative effectiveness, with the random effects model applied. Results: This network meta-analysis comprised 12 studies, encompassing 262,217 individuals and including cholesterol-lowering medications such as statins, fibrates, ezetimibe, cholestyramine, niacin, and omega-3 fatty acids. Our findings demonstrate that comparing to the placebo, rosuvastatin (risk ratio [RR], 1.23; 95% confidence interval [CI], 1.03 to 1.46), simvastatin (RR, 1.21; 95% CI, 1.02 to 1.43), and pravastatin (RR, 1.20; 95% CI, 1.01 to 1.43) increased the risk of glaucoma onset with statistical significance. Conclusion: Rosuvastatin, simvastatin, and pravastatin were each associated with a significantly increased risk of glaucoma onset. We advise medical practitioners to exercise caution when prescribing these specific statins for patients who are at risk of developing glaucoma. Key messages: What is known Previous studies have suggested a link between statins and the risk of developing glaucoma. However, there is still ongoing debate regarding the specific effects of each type of statin on the onset of glaucoma. What is new This network meta-analysis comprehensively evaluated the effects of various statins on the risk of glaucoma onset. Rosuvastatin, simvastatin, and pravastatin were associated with a significantly increased risk of glaucoma onset. [ABSTRACT FROM AUTHOR]

Background/Objectives: Psoriasis is a chronic inflammatory disease that significantly impacts physical and emotional health. Statins, primarily used as lipid-lowering drugs, have also demonstrated anti-inflammatory effects. While some studies suggest that statins may improve psoriasis symptoms, the findings have been inconsistent. This study aims to investigate the association between prior statin use and the onset of psoriasis in a Korean population, focusing on individuals with dyslipidemia to minimize confounding factors. Methods: Using the Korean Health Insurance database (2002–2019), a nationwide nested case-control study was conducted, enrolling 8285 participants with psoriasis and 33,140 controls, matched 1:4 for sex, age, residence, and income through propensity scoring. Results: Adjusted odds ratios revealed significantly lower risks of psoriasis among short-term statin users (OR = 0.70, 95% CI = 0.66–0.74) and long-term users (OR = 0.77, 95% CI = 0.73–0.82) than in nonusers. This trend was consistent for both lipophilic and hydrophilic statins, and across subgroup analyses. Conclusions: These findings suggest that statins may reduce the incidence of psoriasis. However, further research is needed to assess their effects on psoriasis progression and severity. [ABSTRACT FROM AUTHOR]

Optimal medical therapy (OMT) is a modifiable factor that decreases mortality and cardiovascular events in patients with severe peripheral arterial disease. We hypothesized that preintervention OMT would be associated with improved 1-year reintervention and major adverse limb event (MALE) rates after elective endovascular revascularization for intermittent claudication (IC). Using the Vascular Quality Initiative (2010-2020), we identified patients with IC undergoing elective endovascular, hybrid, and open surgical interventions. Preoperative antiplatelet, statin, and nonsmoking status defined OMT components and created three groups: complete (all components), partial (1-2 components), and no OMT. The primary outcome was 1-year reintervention. Secondary outcomes included MALE and factors associated with OMT usage. Multivariable logistic regression generated adjusted odds ratios (aOR). There were 39,088 patients (14,907 [38.1%] complete, 22,054 [56.4%)] partial, 2127 [5.4%] no OMT) who met our criteria. Patients with any OMT were more frequently older with more cardiovascular diseases and diabetes (P <.0001). Patients without OMT were more likely to be Black or with Medicare or Medicaid (P <.05). Observed 1-year reintervention (5.3% complete OMT, 6.1% partial OMT, 8.3% no OMT; P <.001) and MALE (5.6% complete OMT, 6.3% partial OMT, 8.8% no OMT; P <.001) were decreased by partial or complete OMT compared with no OMT. Complete OMT significantly decreased the adjusted odds of reintervention and MALE by 28% (aOR, 0.72, 95% confidence interval [95% CI], 0.59-0.88) and 30% (aOR, 0.70; 95% CI, 0.58-0.85), respectively, compared with no OMT. Partial OMT decrease the adjusted odds of reintervention and MALE by 24% (aOR, 0.76; 95% CI, 0.63-0.92) and 26% (aOR, 0.74; 95% CI, 0.62-0.89), respectively. Preintervention OMT is an underused, modifiable risk factor associated with improved 1-year reintervention and MALE. Vascular surgeons are uniquely positioned to initiate and maintain OMT in patients with IC before revascularization to optimize patient outcomes. [ABSTRACT FROM AUTHOR]

Aims Low levels of LDL cholesterol may be associated with risk of infectious disease. We tested the hypothesis that low LDL cholesterol due to genetic variation in the LDLR , PCSK9 , and HMGCR genes and a polygenic LDL cholesterol score is associated with risk of infectious diseases in the general population. Methods and results Using observational and Mendelian randomization designs, we examined associations of low plasma LDL cholesterol with risk of bacterial and viral infections in 119 805 individuals from the Copenhagen General Population Study/Copenhagen City Heart Study, 468 701 from the UK Biobank, and up to 376 773 from the FinnGen Research Project. Observationally, low LDL cholesterol concentrations were associated with risk of hospitalization for both bacterial and viral infections. In genetic analyses, a 1 mmol/L lower LDL cholesterol was associated with lower plasma PCSK9 {−0.55 nmol/L [95% confidence interval (CI): −1.06 to −0.05]; P = 0.03}, leucocyte count [−0.42 × 109/L (−0.61 to −0.24); P < 0.001], and high-sensitivity C-reactive protein [−0.44 mg/L (−0.79 to −0.09); P = 0.014]. Using an LDLR , HMGCR , and PCSK9 score, a 1 mmol/L lower LDL cholesterol was associated with risk ratios of 0.91 (95% CI: 0.86–0.97; P = 0.002) for unspecified bacterial infection, of 0.92 (0.87–0.97; P = 0.004) for diarrhoeal disease, and of 1.15 (1.03–1.29; P = 0.012) for unspecified viral infections and 1.64 (1.13–2.39; P = 0.009) for HIV/AIDS. Using a polygenic LDL cholesterol score largely showed similar results and in addition a lower risk of 0.85 (0.76–0.96; P = 0.006) for bacterial pneumonia and 0.91 (0.82–0.99; P = 0.035) for sepsis. Conclusion Genetically low LDL cholesterol concentrations were associated with lower concentration of markers of inflammation; lower risk of hospitalization for unspecified bacterial infections, infectious diarrhoeal diseases, bacterial pneumonia, and sepsis; and higher risk of viral infections and HIV/AIDS. [ABSTRACT FROM AUTHOR]

Sleep is a fundamental phenomenon that helps maintain normal physiological processes. Conversely, sleep disorders, usually presented as insomnia, are a common public health problem that can lead to multiple pathophysiological changes in humans, including lipid metabolic abnormality. Interestingly, several previous studies have examined the potential relation of insomnia to metabolic syndrome and hyperlipidemia and found that insomnia was associated with elevated plasma cholesterol and triglyceride concentrations. This review summarizes evidence regarding the linkage between insomnia and lipid abnormalities. Moreover, the underlying physiologic mechanisms linking insomnia to lipid abnormalities are systemically discussed. Finally, issues with lipid-lowering drugs and the risk of insomnia are also presented. This knowledge can improve our understanding of the pathophysiological features of insomnia, which may help to prevent and treat insomnia-induced dyslipidemia clinically. [ABSTRACT FROM AUTHOR]

Purpose of Review: Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common chronic liver disease, characterized by hepatic steatosis with at least one cardiometabolic risk factor. Patients with MASLD are at increased risk for the occurrence of cardiovascular events. Within this review article, we aimed to provide an update on the pathophysiology of MASLD, its interplay with cardiovascular disease, and current treatment strategies. Recent Findings: Given their high burden of cardiovascular comorbidities, patients with MASLD or MASH should undergo regular cardiovascular risk assessment using established risk models. In the absence of liver-specific therapies, therapeutic strategies should focus on improving cardiometabolic risk factors. Patients require a multimodal and multi-stakeholder treatment approach, including optimization of lifestyle, dysglycemia, obesity, and dyslipidemia. Statin treatment represents a safe and effective but often underused therapy in the management of at-risk patients with MASLD and MASH. Novel promising approaches include the use of GLP-1 receptor agonists, especially in, but not limited to, patients with cardiovascular disease and obesity. Summary: Patients with MASLD and MASH are at high cardiovascular risk requiring a multi-modal therapeutic approach including regular cardiovascular risk assessment, as well as lifestyle and pharmacological interventions. Statin therapy represents an inexpensive, safe and effective therapy across the spectrum of non-alcohol related steatotic liver diseases without major safety concerns. More prospective, randomized trials in patients with MASLD and MASH are needed. [ABSTRACT FROM AUTHOR]

Abstract Low-density lipoprotein cholesterol (LDL-C) is an important factor in the development of cardiovascular disease, making its management a key aspect of cardiovascular health. While high-dose statin therapy is often recommended for LDL-C reduction, careful consideration is needed due to patient-specific factors and potential side effects. This study aimed to develop a machine learning (ML) model to estimate the likelihood of achieving target LDL-C levels in patients hospitalized for coronary artery disease and treated with moderate-dose statins. The predictive performance of three ML models, including Extreme Gradient Boosting (XGBoost), Random Forest, and Logistic Regression, was evaluated using electronic medical records from the Asan Medical Center in Seoul across six performance metrics. Additionally, all three models achieved an average AUROC of 0.695 despite reducing features by over 43%. SHAP analysis was conducted to identify key features influencing model predictions, aiming insights into patient characteristics associated with achieving LDL-C targets. This study suggests that ML-based approaches may help identify patients likely to benefit from moderate-dose statins, potentially supporting personalized treatment strategies and clinical decision-making for LDL-C management.