Gender Disparities in Statin Prescriptions in People With HIV With Low/Moderate to High Cardiovascular Risk.

The REPRIEVE trial suggests that primary cardiovascular disease (CVD) prevention could be considered among people with HIV at low CVD risk. We found cisgender women with low/moderate and high CVD risk are less likely to receive statins than cisgender men. Efforts are needed to guarantee equal access to statin-based CVD prevention.

Assessment of prescription pattern and impact of statin in lipid profile among ischemic heart disease patients.

BACKGROUND: Analysis of prescription patterns and lipid profiles can play a crucial role in rational drug use and patient safety. This study aimed to analyze the prescription pattern and impact of statin in lipid profile among ischemic heart disease (IHD) patients. MATERIALS AND METHODS: A prospective observational study was conducted for 7 months in the cardiology department. IHD patients above 18 years and undergoing statin therapy for at least 3 months were enrolled. Patients with elevated liver enzymes and unfit for statin therapy, pregnant women, psychiatry patients, and critically ill subjects were excluded. RESULTS: Of the total participants, 214 (71.8%) were males and 84 (28.2%) were females, with a mean age of 62.55 ± 9.56 years. The most common age group diagnosed with IHD was between 60 and 69 years. Hypertension was observed in 64.4% of the patients, while diabetes was present in 55.7% as the most commonly associated comorbidities. The majority of patients (75.8%) received atorvastatin. The prescription pattern for various drug classes included proton pump inhibitors (93%), antiplatelet agents (82.2%), statins (82.2%), nitrates (60.4%), beta-blockers (34.6%), diuretics (16.8%), biguanides (17.4%), and insulin (15.1%). After 3 months of statin therapy, a statistically significant change was observed in the lipid profile (P < 0.001). CONCLUSION: Statin agents were the most frequently prescribed class of drugs, followed by antiplatelets. Significant improvements were observed in the lipid profile after a 3-month course of statin therapy. Effective therapeutic monitoring can significantly impact a positive health outcome in patients.

Preliminary results on temporal evolution and clinical implications of atherosclerotic plaque in branch atheromatous disease after statin treatment.

Background: Branch atheromatous disease (BAD) is a primary cause of early neurological deterioration (END) in penetrating artery occlusion, leading to poor functional outcomes. While it has been proposed to classify BAD under large artery atherosclerosis, uncertainty exists regarding the optimal treatment strategy, including cholesterol-lowering targets. Objectives: We aimed to assess the clinical implications and temporal changes of atherosclerotic plaques before and after high-intensity statin treatment. Design: This is a high-resolution vessel-wall imaging sub-analysis of the trial of Statin and Dual Antiplatelet Therapy in Preventing Early Neurological Deterioration in Branch Atheromatous Disease (SATBRAD). Methods: In this prospective, single-group cohort study, participants in the treatment arm of the SATBRAD trial received early dual antiplatelet therapy and high-intensity statin treatment. The majority of these participants subsequently underwent high-resolution vessel-wall magnetic resonance imaging (MRI). Those with atheromatous plaques in the parent artery continued high-intensity statin treatment for 6 months, followed by a repeat MRI to monitor plaque changes. Results: There were 57 patients who underwent vessel-wall imaging and 24 exhibited contrast-enhanced plaques. Patients with contrast-enhanced plaques showed higher rates of END (29.2% vs 6.1%, p = 0.027), perfusion defects (62.5% vs 24.2%, p = 0.004), and lower rates of good outcomes at 3 months (50.0% vs 81.8%, p = 0.011). After adjusting for confounding factors, contrast-enhanced plaque had a negative impact on achieving a good outcome at 3 months (adjusted odds ratio = 0.04; 95% confidence interval = <0.01-0.60). Following high-intensity statin treatment in 36 patients, there was a notable reduction in stenosis (33.7% vs 29.3%, p = 0.005) and contrast-enhanced plaque volume (16.3 vs 11.6 mm3, p = 0.015). Conclusion: The study highlighted the association between contrast-enhanced atherosclerotic plaques, END, and poor functional outcomes, with high-intensity treatment leading to plaque volume reduction. These results underscore the shared pathology between BAD and intracranial atherosclerosis, emphasizing the necessity for further research and tailored treatment strategies for BAD. Trial registration: ClinicalTrials.gov; Identifier: NCT04824911 (https://clinicaltrials.gov/study/NCT04824911).

Changes in atherosclerosis and its impact on health after statin treatment: what we learned from detailed vessel imaging in the SATBRAD trial Branch atheromatous disease (BAD) is a major cause of early worsening of stroke symptoms, leading to poor recovery. While some experts believe BAD should be treated like large artery disease, the best treatment approach, including cholesterol-lowering targets, remains unclear. This study aimed to assess how high-intensity statin treatment affects atherosclerotic plaques over time and its impact on patient health. Analyzing detailed vessel images from the SATBRAD trial, where patients received high-intensity statins and magnetic resonance imaging, revealed that 24 out of 57 patients had plaques that showed up clearly with contrast enhancement. These patients were more likely to experience early worsening of stroke symptoms and perfusion compromise and had poorer outcomes. After six months of high-intensity statin treatment, there was a significant reduction in plaque size and vessel narrowing. The study concluded that contrast-enhanced plaques are linked to worse early stroke symptoms and poor recovery, but high-intensity statin treatment can reduce plaque size, suggesting that BAD may share similarities with larger artery disease and highlighting the need for further research and tailored treatments for BAD.

Effects of Lipophilic Statins on Cell Viability and Tissue Factor Expression in Canine Haemangiosarcoma Cells.

Canine haemangiosarcoma (HSA) is a highly aggressive cancer often associated with coagulation abnormalities. Statins, inhibitors of 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMGCR) clinically prescribed for hypercholesterolemia, are also believed to possess antitumour and anticoagulant properties by inhibiting downstream Akt activation. Akt phosphorylation is involved in the mechanism of the antitumour and tissue factor (TF)-lowering effects of statins. In the present study, we aimed to investigate whether statins could inhibit cell viability while concurrently inducing anticoagulant properties by regulating the expression of TFs in canine HSA cells. Using reverse transcription-quantitative polymerase chain reaction (RT-qPCR), we initially exclusively detected HMGCR mRNA expression in canine HSA tissues and cell lines but not in normal cephalic vein and spleen tissues. Moreover, treatment with lipophilic statins, including atorvastatin, fluvastatin, and simvastatin, inhibited cell viability in a concentration-dependent manner and decreased TF expression both at the mRNA and protein levels, as evidenced by cell viability assays, RT-qPCR, and immunoblotting, respectively. Further investigation using cell viability assays and flow cytometry revealed that simvastatin decreased Akt phosphorylation, and MK-2206, a specific Akt inhibitor, mirrored the effect of simvastatin on cell viability and cell cycle arrest. However, MK-2206 exhibited different effects on TF expression depending on the cell type, indicating that Akt phosphorylation may not consistently regulate TF expression. Overall, this study provides insights into the potential therapeutic use of statins in targeting tumour growth and coagulation abnormalities in canine HSA. Further research is warranted to fully elucidate the underlying mechanisms and clinical applications of statins in canine HSA treatment.

Targeting ferroptosis for improved radiotherapy outcomes in HPV-negative head and neck squamous cell carcinoma.

To enhance the efficacy of radiotherapy (RT) in human papillomavirus (HPV)-negative head and neck squamous cell carcinoma (HNSCC), we explored targeting ferroptosis, a regulated cell death process. We developed a gene signature associated with ferroptosis using Cox proportional hazard modeling in HPV-negative HNSCC patients who underwent RT. This ferroptosis-related gene signature (FRGS) was a significant predictor of overall survival and recurrence-free survival in HPV-negative HNSCC patients who received RT. Subtype B of the FRGS, characterized by decreased expression of ferroptosis inducers [nuclear receptor coactivator 4 (NCOA4) and natural resistance-associated macrophage protein 2 homolog/divalent metal transporter 1 (NRAMP2/DMT1)] and increased expression of suppressors [phospholipid hydroperoxide glutathione peroxidase (GPX4) and ferritin heavy chain (FTH1)], was associated with poorer prognosis, potentially indicating the inhibition of ferroptosis. Furthermore, our in vitro and in vivo studies demonstrated that treatment with statins, such as atorvastatin and simvastatin, induced ferroptosis and sensitized radioresistant HNSCC cells to irradiation, improving radiosensitivity and potentially enhancing the response to RT. Additionally, in xenograft models, the combination of statins and RT led to a significant reduction in tumor initiation. These findings provide valuable insights for enhancing treatment and improving prognosis in HPV-negative HNSCC by targeting ferroptosis and utilizing statins to sensitize tumors to RT-induced cell death.

2024 Egyptian consensus statement on the role of non-statin therapies for LDL cholesterol lowering in different patient risk categories.

BACKGROUND: The new millennium has witnessed increased understanding of cardiovascular (CV) risk factors and improvement in atherosclerotic cardiovascular disease (ASCVD) management. The role of LDL cholesterol and other atherogenic lipid particles in the development of atherosclerosis is now beyond doubt. MAIN BODY: Statins have been widely used and recommended in guidelines for preventing and managing ischemic events. However, statins have side effects, and many patients do not achieve their low-density lipoprotein cholesterol (LDL-C) goals. In recent years, non-statin lipid-lowering agents have gained increasing use as adjuncts to statins or as alternatives in patients who cannot tolerate statins. This consensus proposes a simple approach for initiating non-statin lipid-lowering therapy and provides evidence-based recommendations. Our key advancements include the identification of patients at extreme risk for CV events, the consideration of initial combination therapy of statin and ezetimibe in very high-risk and extreme-risk groups and the extended use of bempedoic acid in patients not reaching LDL-C targets especially in resource-limited settings. CONCLUSIONS: Overall, this consensus statement provides valuable insights into the expanding field of non-statin therapies and offers practical recommendations to enhance CV care, specifically focusing on improving LDL-C control in Egypt. While these recommendations hold promise, further research and real-world data are needed for validation and refinement.

Aggressive low-density lipoprotein (LDL) lowering for primary prevention: still an elusive goal.

Cardiovascular disease (CVD) is the leading cause of mortality globally. Low-density lipoprotein (LDL) plays an important role in CVD pathophysiology. Research has shown the safety and efficacy of keeping LDL at very low levels for CVD prevention. Therefore, experts recommend intense LDL-lowering approaches starting at young ages, promoting the mantras "the lower, the better" and "the earlier, the better." This commentary discusses the challenges regarding applying aggressive LDL-lowering approaches in the general population, including pharmacological efficacy and side effects, the cost-effectiveness of interventions, and patient adherence to treatment regimens.

Why make it if you can take it: review on extracellular cholesterol uptake and its importance in breast and ovarian cancers.

Cholesterol homeostasis is essential for healthy mammalian cells and dysregulation of cholesterol metabolism contributes to the pathogenesis of various diseases including cancer. Cancer cells are dependent on cholesterol. Malignant progression is associated with high cellular demand for cholesterol, and extracellular cholesterol uptake is often elevated in cancer cell to meet its metabolic needs. Tumors take up cholesterol from the blood stream through their vasculature. Breast cancer grows in, and ovarian cancer metastasizes into fatty tissue that provides them with an additional source of cholesterol. High levels of extracellular cholesterol are beneficial for tumors whose cancer cells master the uptake of extracellular cholesterol. In this review we concentrate on cholesterol uptake mechanisms, receptor-mediated endocytosis and macropinocytosis, and how these are utilized and manipulated by cancer cells to overcome their possible intrinsic or pharmacological limitations in cholesterol synthesis. We focus especially on the involvement of lysosomes in cholesterol uptake. Identifying the vulnerabilities of cholesterol metabolism and manipulating them could provide novel efficient therapeutic strategies for treatment of cancers that manifest dependency for extracellular cholesterol.

A Neuropathy Mimic: Statin-Induced Myopathy Presenting as Guillain-Barré Syndrome.

Statins are widely used to manage dyslipidemia and prevent cardiovascular diseases due to their effectiveness and general safety profile. However, they can sometimes cause severe muscle-related adverse effects, presenting diagnostic challenges when symptoms overlap with other conditions. This case report describes a middle-aged woman who presented to the emergency department with bilateral lower limb weakness, initially suggesting Guillain-Barré syndrome (GBS). Despite her history of low-grade fever and diarrhea, primary and secondary surveys, including electrocardiogram, blood gas analysis, and nerve conduction studies, showed no definitive signs of GBS. The patient had a recent history of percutaneous transluminal coronary angioplasty and was on dual antiplatelet therapy and rosuvastatin. Elevated creatine kinase levels and exclusion of other differential diagnoses led to the diagnosis of statin-induced myopathy, a rare but severe adverse effect of statins. The patient was treated with intravenous fluids, cessation of statins, and sessions of hemodialysis and plasmapheresis, resulting in significant improvement and eventual recovery of muscle power and neurological function. This case highlights the importance of recognizing statin-induced myopathy in patients with muscle weakness and emphasizes the need for thorough clinical evaluation to differentiate it from other conditions such as GBS. Further research is warranted to understand the pathophysiology of statin myopathy and identify at-risk populations.

Early statin use is associated with improved survival and cardiovascular outcomes in patients with atrial fibrillation and recent ischaemic stroke: A propensity-matched analysis of a global federated health database.

INTRODUCTION: Statins reduce recurrent stroke and cardiovascular events in patients with non-cardioembolic stroke. The benefits of statins in patients with AF and recent IS remain unclear. We aimed to investigate the benefits of statins in patients with AF and recent IS. PATIENTS AND METHODS: This retrospective, cohort study was conducted using deidentified electronic medical records within TriNetX platform. Patients with AF and recent IS, who received statins within 28 days of their index stroke were propensity score-matched with those who did not. Patients were followed up for up to 2 years. Primary outcomes were the 2-year risk of recurrent IS, all-cause mortality and the composite outcome of all-cause mortality, recurrent IS, transient ischaemic attack (TIA), and acute myocardial infarction (MI). Secondary outcomes were the 2-year risk of TIA, intracranial haemorrhage (ICH), acute MI, and hospital readmission. Cox regression analyses were used to calculate hazard ratios (HRs) with 95% confidence intervals (95%CI). RESULTS: Of 20,902 patients with AF and recent IS, 7500 (35.9%) received statins within 28 days of their stroke and 13,402 (64.1%) did not. 11,182 patients (mean age 73.7 ± 11.5; 5277 (47.2%) female) remained after propensity score matching. Patients who received early statins had significantly lower risk of recurrent IS (HR: 0.45, 95%CI: 0.41-0.48, p < 0.001), mortality (HR: 0.75, 95%CI: 0.66-0.84, p < 0.001), the composite outcome (HR: 0.48, 95%CI: 0.45-0.52, p < 0.001), TIA (HR: 0.37, 95%CI: 0.30-0.44, p < 0.001), ICH (HR: 0.59, 95%CI: 0.47-0.72, p < 0.001 ), acute MI (HR: 0.35, 95%CI: 0.30-0.42, p < 0.001) and hospital readmission (HR: 0.46, 95%CI: 0.42-0.50, <0.001). Beneficial effects of early statins were evident in the elderly, different ethnic groups, statin dose intensity, and AF subtypes, large vessel occlusion and embolic strokes and within the context of statin lipophilicity, optimal LDL-cholesterol levels, various cardiovascular comorbidities, treatment with intravenous thrombolysis or endovascular thrombectomy, and NIHSS 0-5 and NIHSS > 5 subgroups. DISCUSSION AND CONCLUSION: Patients with AF and recent IS, who received early statins, had a lower risk of recurrent stroke, death, and other cardiovascular outcomes including ICH, compared to those who did not.

Gender disparities in utilization of statins for low density lipoprotein management across the spectrum of atherosclerotic cardiovascular disease: Insights from the houston methodist cardiovascular disease learning health system registry.

Introduction: Lower statin utilization is reported among women compared to men, however large-scale studies evaluating gender disparities in LDL-C management in individuals with ASCVD and its subtypes remain limited, particularly across age and racial/ethnic subgroups. In this study, we address this knowledge gap using data from a large US healthcare system. Methods: All adult patients with established ASCVD in the Houston Methodist Learning Health System Registry during 2016-2022 were included. Statin use and dose were extracted from the database. The association between gender and statin utilization was evaluated using multivariate logistic regression analyses in patients with ASCVD overall, across ASCVD subtypes, and by age, racial/ethnic subgroups, and socioeconomic risk factors. Results: A total of 97,819 patients with prevalent ASCVD were included. Women with ASCVD had lower utilization of any statin (64.3% vs 72.6 %; p < 0.001) and high-intensity statin (29.8% vs 42.5 % p < 0.001) compared with men. In fully adjusted models, women had 40 % lower odds of any (adjusted odds ratio [aOR]:0.58, 95 % CI 0.57-0.60) and high-intensity statin use (aOR:0.59, 0.57-0.61) relative to men. Women were also less likely to have guideline-recommended LDL-C < 70 mg/dL (30.2% vs 42.7 %; p < 0.01). These differences persisted across age, racial/ethnic and socioeconomic subgroups. Conclusion: Significant gender disparities exist in contemporary lipid management among patients with ASCVD, with women being less likely to receive any and high-intensity statin and achieving guideline defined LDL-C goal compared with men across age and racial/ethnic subgroups. These disparities underscore the need to further understand potential socioeconomic drivers of the observed lower statin uptake in women.

Time difference for the presence of coronary calcium in those with and without coronary risk factors and statin use.

BACKGROUND: Coronary artery calcium (CAC) is a marker of subclinical atherosclerosis. We aimed to assess to what extent risk factors and statin use modify the time to occurrence of CAC. METHODS: The study population included 3484 patients who underwent CAC score measurements and CT angiography between January 2021 and March 2022. To assess to what extent risk factors and statin use modify the time to occurrence of CAC, a time difference for a 50% probability of having a non-zero CAC score between those with and without these factors was calculated. RESULTS: The mean age was 52.1 ± 10.9 years, and 43.1% of the population were women. Age was the most important factor for having non-zero CAC (z value 21.84, p-value <0.001). This is followed by male gender (Odds ratio [OR] and 95% CI 3.53 [2.96-4.21]; p < 0.001), and statin use (OR 3.09 [2.41-3.97], p < 0.001). A non-zero CAC develops on average 10.3 years earlier in men compared with women, and 9.1 years earlier in statin users compared with non-users. Diabetes mellitus, hypertension, and smoking were also associated with earlier occurrence of CAC score, but to a lower extent. CONCLUSION: Apart from age, male gender and statin use are the major factors for the occurrence of CAC and are associated with CAC occurrence 9-10 years earlier.

Statin-associated muscle symptoms: A comprehensive exploration of epidemiology, pathophysiology, diagnosis, and clinical management strategies.

Statins are the first line of treatment for both primary and secondary prevention of atherosclerotic cardiovascular disease. Despite the positive effects of statins on cardiovascular events, not all patients can use them at an optimized dose. The reason for this is the skeletal muscle side effects, termed statin-associated muscle symptoms (SAMS). Despite extensive research, the precise pathophysiology of SAMS remains unclear and multiple mechanisms may contribute to this phenomenon. Various therapeutic options are available for the management of SAMS, ranging from rechallenging with the same or a different statin to utilizing non-statin therapeutic alternatives in patients intolerant to statins. However, the lack of consensus on the definition of SAMS, the absence of a definitive diagnostic test, and lack of a universally accepted management algorithm pose a great challenge in dealing with this entity. This review aims to explore the various pathophysiological mechanisms involved in SAMS and understand the difference between self-limited toxic myopathy and immune-mediated myopathy requiring immunomodulatory therapy. The conundrum of statin withdrawal, tapering, and rechallenge in SAMS will also be explored in detail along with the newer non-statin therapies that are available.

Association of elevated baseline bilirubin caused by preadmission statin use with cardiovascular prognosis in patients undergoing elective percutaneous coronary intervention.

Bilirubin is widely recognized to possess antioxidant and anti-inflammatory characteristics. However, the relationship between bilirubin and coronary artery disease (CAD) remains controversial, particularly in individuals receiving Percutaneous Coronary Intervention (PCI). Given that statins may enhance the production of heme oxygenase-1 (HO-1) and bilirubin, we investigated the long-term cardiovascular prognostic role of bilirubin levels elevated by statin use in patients undergoing PCI. Data of 6945 subjects undergoing PCI were enrolled in this study. We divided the patients into two groups based on serum total bilirubin (TB) levels detected prior to PCI. The high TB group consisted of patients with serum TB values > 8.4 µmmol/L, while the low TB group consisted of patients with serum TB values ≤ 8.4 µmmol/L. The median follow-up time was 836 days. Cox proportional hazards models were performed to evaluate the hazard ratios (HRs) and 95% confidence interval (CI) for the incidence of major adverse cardiovascular event (MACE) associated with bilirubin levels. The association between TB levels and risk of MACE was significant [adjusted HR = 0.557, 95% CI (0.59-0.96), p = 0.020). Linear analysis was performed to determine the association between preadmission usage of statin and bilirubin level. The preadmission usage of statin independently linearly increases TB [adjusted-ß = 0.371, 95% CI (0.134-0.608), p = 0.002] and direct bilirubin (DB) [adjusted-ß = 0.411, 95% CI (0.300-0.522), p < 0.001). Mediation analysis demonstrated a direct protective role of preadmission statins treatment (ß = - 0.024, p < 0.01), TB (ß = - 0.003, p < 0.05) and DB (ß = - 0.009, p < 0.05). Furthermore, it was found that TB (4.0%) and DB (12.0%) mediated the relationship between preadmission statins therapy and MACE. Bilirubin has a protective effect against MACE. In patients with normal bilirubin level undergoing elective PCI, preadmission statin use elevated bilirubin levels, which were independently associated with a lower incidence of MACE over the long-term follow-up period.

Rosuvastatin-Induced Myopathy: A Case Series.

Statins are one of the most crucial drugs used for the prevention of atherosclerotic coronary artery disease. A wide spectrum of symptoms ranging from myalgia to symptoms of rhabdomyolysis with or without weakness of the upper and lower limbs are indicative of statin-induced rhabdomyolysis or myopathy. The current case series which represents three patients who developed statin-induced myopathy after starting rosuvastatin is one of a few if not the first case series. All three patients had recently started rosuvastatin 40mg once daily post-percutaneous transluminal coronary angioplasty (PTCA) for secondary prevention of atherosclerotic cardiovascular diseases (ASCVDs). Shortly after starting the medication, they were hospitalized due to bilateral lower limb pain and weakness. On further evaluation, they were diagnosed to have rosuvastatin-induced myopathy with acute kidney injury and/or liver injury. In all cases, myopathy, acute renal injury, and liver injury were caused by rosuvastatin, regardless of the presence of a vitamin D deficiency. Despite the documented risk of myopathy and renal toxicity associated with rosuvastatin, the drug remains highly popular worldwide in the modern period. Although all the cases discussed were successfully treated by stopping rosuvastatin and switching it with another class of lipid-lowering agent, it significantly increased morbidity and raised medical expenses. Hence, this case series not only adds to existing safety disputations associated with rosuvastatin but also calls for more pharmacovigilance when recommending this medication.

Short-Term and Long-Term Fluvastatin Inhibit Effects of Thrombospondin-1 on Human Vascular Smooth Muscle Cells.

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 TGFß2 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.

Lipid management strategies for diabetic patients align with an evidence-based guideline.

BACKGROUND: Diabetes mellitus (DM) increases the risk of cardiovascular diseases (CVD) significantly. Statins are recommended for all diabetic patients aged ≥ 40 years to alleviate this risk. OBJECTIVES: This study aimed to determine the status of the implementation of the recommendations of lipid management strategies for diabetic patients. METHODS: In this cross-sectional study, 500 patients with DM, aged ≥ 40 referring to a public pharmacy with at least one diabetic medication in their prescription, were enrolled. Patients' demographics, lipid panel data, medications, personal and family history of atherosclerotic cardiovascular disease (ASCVD), and risk factors for ASCVD were documented. The appropriateness of stain dosing intensity was judged based on the American Diabetes Association (ADA) guideline. RESULTS: The mean ± SD of the age of patients was 61.39 ± 10.49 years. Among patients, 238 (47.6) were men. More than half of the patients were subject to receiving primary prevention (59.8%, n = 299). For 80.8% (n = 404) of patients, a statin, most frequently atorvastatin (61.8%), was prescribed. The appropriate statin dose based on the guideline for 470 patients (94%), was high-intensity statin. In 70.6% (n = 353) of patients, lipid management was not in accordance with the guideline. Patients with ASCVD were more likely to receive the statins and the appropriate doses compared to patients without ASCVD (p-value < 0.001). CONCLUSION: Despite a relatively high percentage of patients who received statins, the lipid management in most patients was not in accordance with the guideline. The profound problem was the suboptimal dosage of statins. Investigating the reasons and barriers of the appropriate management can be helpful. Additionally, since patients without ASCVD who should receive statins for primary prevention were significantly less likely to receive statins and evidence-based doses, more attention is needed for this population.

Sex specific analysis of patients with and without reported statin intolerance referred to a specialized outpatient lipid clinic.

BACKGROUND: Lowering LDL-cholesterol is a fundamental goal for both primary and secondary prevention of atherosclerotic cardiovascular diseases. Our study aims to analyse potential sex disparities regarding the tolerability and effectiveness of lipid-lowering therapy in patients with and without reported statin intolerance who are being treated at a lipid-outpatient clinic. METHODS: From 2017 to 2022, n = 1062 patients (n = 612 men, n = 450 women) at high-risk were referred to our lipid-outpatient clinic because of difficulties in lipid control by primary healthcare providers. The main therapeutic objective was to optimize lipid-lowering therapy according to current treatment guidelines. RESULTS: Patients presented with high LDL-C baseline levels (4.97 ± 1.81 mmol/l (192 ± 70 mg/dL) in men and 5.46 ± 2.04 mmol/l (211 ± 79 mg/dL) in women). Intolerance towards statins was reported more frequently by women (48.2%) than by men (38.9%, p = 0.004). LDL-C continuously decreased with individual treatment adjustments across follow-up visits. In total, treatment goals (LDL < 1.4 mmol/l (< 55 mg/dl) or < 1.8 mmol/l (< 70 mg/dl)) were accomplished in 75.8% of men and 55.5% of women after the last follow-up visit (p < 0.0001). In men, these data are almost identical in subjects with statin intolerance. In contrast, treatment goals were reached less frequently in women with statin intolerance compared to women tolerant to statin therapy. CONCLUSION: Even if treated in a specialized lipid clinic, women are less likely to reach their target LDL-C than men, particularly when statin intolerant. Nevertheless, many patients with statin intolerance can be successfully treated using oral combination and PCSK9 inhibitor therapy. However, ongoing follow-up care to monitor progress and to adjust treatment plans is necessary to reach this goal.

We investigated patients at high cardiovascular risk who were referred to our specialized lipid outpatient clinic because of elevated lipid levels and difficulties in lipid-lowering treatment in the primary care setting. The primary goal of such a clinic is to help patients to achieve optimal lipid levels through personalized treatment plans. We focused on prescription behavior and differences in treatment tolerability and effectiveness between men and women.A large proportion of patients (more frequently women (48.2%) than men (38.9%)) reported intolerance towards statins and most patients' LDL-cholesterol levels were far away from treatment goals. However, when treated at a specialized lipid clinic providing ongoing follow-up care to monitor progress and to adjust treatment plans if necessary, many of those patients were able to tolerate lipid lowering medication to achieve better lipid control and to maintain their lipid levels within target ranges.However, women were less likely to reach LDL-cholesterol treatment targets compared to men, especially if they reported intolerance towards statins. Ongoing follow-up care to monitor progress and to adjust treatment plans is necessary to reach treatment goals.