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Theranostics 2023Multigene mutations in colorectal cancer (CRC), including KRAS, BRAF, and p53, afford high metastatic ability and resistance to EGFR-targeting therapy. Understanding...
Multigene mutations in colorectal cancer (CRC), including KRAS, BRAF, and p53, afford high metastatic ability and resistance to EGFR-targeting therapy. Understanding the molecular mechanisms regulating anti-EGFR-resistant CRC metastasis can improve CRC therapy. This study aimed to investigate the effects of IL-8 and the activation of KRAS on reactive oxygen species (ROS) production and metastasis of hyperlipidemia-associated CRC harboring mutations of KRAS and p53. The cytokine array analysis determined the up-expression of secreted factors, including IL-8. The clinical relevance of the relationship between IL-8 and angiopoietin-like 4 (ANGPTL4) was examined in CRC patients from National Cheng Kung University Hospital and TCGA dataset. Expressions of IL-8, ANGPTL4, NADPH oxidase 4 (NOX4), and epithelial-mesenchymal transition (EMT) markers in free fatty acids (FFAs)-treated KRAS/p53 mutant CRC cells were determined. The hyperlipidemia-triggered metastatic ability of CRC cells under treatments of antioxidants, statin, and cetuximab or knockdown of IL-8, KRAS, and EGFR was evaluated in vitro and in vivo. In addition, the effects of antioxidants and depletion of IL-8 and KRAS on the correlation between ROS production and hyperlipidemia-promoted CRC metastasis were also clarified. In this study, we found that free fatty acids promoted KRAS/p53-mutant but not single-mutant or non-mutant CRC cell metastasis. IL-8, the most abundant secreted factor in KRAS/p53-mutant cells, was correlated with the upregulation of NOX4 expression and ROS production under oleic acid (OA)-treated conditions. In addition, the metastasis of KRAS/p53-mutant CRC relies on the ANGPTL4/IL-8/NOX4 axis and the activation of KRAS. The antioxidants and inactivation of KRAS also inhibited OA-induced EMT and metastasis. Although KRAS mediated EGF- and OA-promoted CRC cell invasion, the inhibition of EGFR did not affect OA-induced ANGPTL4/IL-8/NOX4 axis and CRC metastasis. The high-fat diet mice fed with vitamin E and statin or in IL-8-depleted cells significantly inhibited tumor extravasation and metastatic lung growth of CRC. The antioxidants, statins, and targeting IL-8 may provide better outcomes for treating metastatic CRC that harbors multigene mutations and anti-EGFR resistance.
Topics: Animals; Mice; Antibodies; Antioxidants; Colonic Neoplasms; Fatty Acids, Nonesterified; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Interleukin-8; Oleic Acids; Proto-Oncogene Proteins p21(ras); Reactive Oxygen Species; Tumor Suppressor Protein p53; Humans
PubMed: 37649607
DOI: 10.7150/thno.85855 -
Frontiers in Immunology 2023Atherosclerosis is a common cardiovascular disease caused by the abnormal expression of multiple factors and genes influenced by both environmental and genetic factors.... (Review)
Review
Atherosclerosis is a common cardiovascular disease caused by the abnormal expression of multiple factors and genes influenced by both environmental and genetic factors. The primary manifestation of atherosclerosis is plaque formation, which occurs when inflammatory cells consume excess lipids, affecting their retention and modification within the arterial intima. This triggers endothelial cell (EC) activation, immune cell infiltration, vascular smooth muscle cell (VSMC) proliferation and migration, foam cell formation, lipid streaks, and fibrous plaque development. These processes can lead to vascular wall sclerosis, lumen stenosis, and thrombosis. Immune cells, ECs, and VSMCs in atherosclerotic plaques undergo significant metabolic changes and inflammatory responses. The interaction of cytokines and chemokines secreted by these cells leads to the onset, progression, and regression of atherosclerosis. The regulation of cell- or cytokine-based immune responses is a novel therapeutic approach for atherosclerosis. Statins are currently the primary pharmacological agents utilised for managing unstable plaques owing to their ability to enhance endothelial function, regulate VSMC proliferation and apoptosis by reducing cholesterol levels, and mitigate the expression and activity of inflammatory cytokines. In this review, we provide an overview of the metabolic changes associated with atherosclerosis, describe the effects of inflammatory responses on atherosclerotic plaques, and discuss the mechanisms through which statins contribute to plaque stabilisation. Additionally, we examine the role of statins in combination with other drugs in the management of atherosclerosis.
Topics: Humans; Plaque, Atherosclerotic; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Atherosclerosis; Apoptosis; Cytokines
PubMed: 38143759
DOI: 10.3389/fimmu.2023.1301051 -
Clinical Therapeutics Nov 2023Atherosclerotic cardiovascular disease (ASCVD) is the leading cause of death in women, yet it remains underdiagnosed, undertreated, and understudied in women compared... (Review)
Review
PURPOSE
Atherosclerotic cardiovascular disease (ASCVD) is the leading cause of death in women, yet it remains underdiagnosed, undertreated, and understudied in women compared with men. Although estrogen has provided observational evidence of cardioprotection, randomized controlled trials using hormone replacement therapy have generally produced unfavorable results.
METHODS
For this narrative review, a literature search was performed using the key words cardiovascular disease, women, and dyslipidemia in PubMed and Google Scholar with no date limitations. References within each article were also reviewed for additional relevant articles.
FINDINGS
Sex-specific risk factors and underrecognized conditions more predominant in women elevate ASCVD risk, creating further clinical challenges, such as the need for accurate risk stratification, compared with in men. Dyslipidemia frequently manifests or worsens during the menopausal transition. Therefore, identification during midlife and implementing lipid-lowering strategies to reduce ASCVD risk is imperative. Women have historically been poorly represented in cardiovascular (CV) outcome trials. However, more recent studies and meta-analyses have indicated that lipid-lowering therapies are equally effective in women and produce similar reductions in CV events and total mortality. Major cholesterol guidelines address many of the challenges that clinicians face when assessing ASCVD risk in women. Key points specific to women include obtaining a detailed history of pregnancy-related conditions, identification of common autoimmune disorders associated with systemic inflammation, and use of 10-year ASCVD risk calculators and imaging modalities (coronary artery calcium) to optimize ASCVD assessment. In terms of treatment, similar to men, women with existing ASCVD or high-risk primary prevention patients should be treated aggressively to achieve ≥50% LDL-C reductions and/or LDL-C goals as low as <55 mg/dL. Appropriate lipid-lowering therapies include high-intensity statins with or without ezetimibe and proprotein convertase subtilisin kexin/type 9 inhibitors. Women with lower ASCVD risk may be considered for low- to moderate-intensity statin therapy (approximately 30%-50% LDL-C reduction). All women, regardless of ASCVD risk category, should implement therapeutic lifestyle changes, which improve many common age-related cardiometabolic conditions.
IMPLICATIONS
Although ASCVD and current risk factor trends in women are concerning, numerous evidence-based approaches are available to protect women with ASCVD risk from life-changing CV events.
Topics: Male; Humans; Female; Anticholesteremic Agents; Cardiovascular Diseases; Cholesterol, LDL; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Atherosclerosis; Dyslipidemias
PubMed: 37770308
DOI: 10.1016/j.clinthera.2023.08.021 -
Frontiers in Endocrinology 2023Since the approval of the proprotein convertase subtilisin/kexin type 9 (PCSK9) monoclonal antibodies for marketing in 2015, PCSK9 inhibitors have attracted significant...
BACKGROUND
Since the approval of the proprotein convertase subtilisin/kexin type 9 (PCSK9) monoclonal antibodies for marketing in 2015, PCSK9 inhibitors have attracted significant interest in the field of cardiovascular endocrinology. A large number of clinical trials have confirmed the efficacy and safety of PCSK9 inhibitors in reducing cholesterol and the risk of cardiovascular events. No bibliometric analysis of PCSK9 inhibitors has been performed as of yet. This study aims to analyze the research trends and hotspots of PCSK9 inhibitors through bibliometric analysis.
METHODS
We searched the Web of Science Core Collection (WoSCC) database for PCSK9 inhibitor-related publications from 2007 to 2022. Data visualization analysis was performed using CiteSpace software. Microsoft Excel and Graphpad software were used for the drawing of some tables and figures.
RESULTS
A total of 1072 pieces of literature were retrieved between 2007 and 2022. The number of publications concerning PCSK9 inhibitors is growing annually. The top five countries with the most articles published were the United States, England, Canada, Italy, and France. Harvard University, Amgen, Brigham & Women's Hospital, Harvard Medical School, and Imperial College London are the five institutions with the highest output. The is the most popular journal in this field. The most frequently cited journal is the . As for authors, Sabatine MS and Giugliano RP from Brigham & Women's Hospital have the highest number of published articles. Amgen is the funding agency for most of the research. According to keyword analysis, "low density lipoprotein", "familial hypercholesterolemia", "PCSK9 inhibitor", "PCSK9", and "efficacy" are the five keywords with the highest frequency of co-occurrence.
CONCLUSION
The past 15 years have witnessed a rapid and fruitful development of PCSK9 inhibitors. The research trend and focus for PCSK9 inhibitors are from the mechanism of reducing low-density lipoprotein cholesterol to related clinical trials. Developed countries such as the United States have contributed prominently in this area. Coronary artery and inflammation are currently at the forefront of research in the field and are in an explosion period.
Topics: Female; Humans; United States; Proprotein Convertase 9; PCSK9 Inhibitors; Antibodies, Monoclonal, Humanized; Cholesterol, LDL; Enzyme Inhibitors; Bibliometrics
PubMed: 38093957
DOI: 10.3389/fendo.2023.1218968 -
BMJ Open Nov 2023Emergency percutaneous coronary intervention (PCI) can quickly restore myocardial perfusion after acute coronary syndrome. Whether and which lipid-lowering regimens are... (Meta-Analysis)
Meta-Analysis
Effectiveness of lipid-lowering therapy on mortality and major adverse cardiovascular event outcomes in patients undergoing percutaneous coronary intervention: a network meta-analysis of randomised controlled trials.
BACKGROUND
Emergency percutaneous coronary intervention (PCI) can quickly restore myocardial perfusion after acute coronary syndrome. Whether and which lipid-lowering regimens are effective in reducing major adverse cardiovascular events (MACEs) and mortality risk after PCI remain unclear.
OBJECTIVE
This study assessed the benefits of different lipid-lowering regimens on the risk of MACEs and mortality in the post-PCI population by network meta-analysis.
METHODS
Public databases, including PubMed, Embase and the Cochrane Library, were searched from inception to August 2022. Randomised controlled trials (RCTs) on lipid-lowering regimens in post-PCI populations were included and analysed. The outcomes were the incidence of all-cause mortality and MACEs, whether reported as dichotomous variables or as HRs.
RESULTS
Thirty-nine RCTs were included. For MACEs, alirocumab plus rosuvastatin (OR: 0.18; 95% CI: 0.07 to 0.44), evolocumab plus ezetimibe and statins (OR: 0.19; 95% CI: 0.06 to 0.59), eicosapentaenoic acid (EPA) plus pitavastatin (HR: 0.67; 95% CI: 0.49 to 0.96) and icosapent ethyl plus statins (HR: 0.73; 95% CI: 0.62 to 0.86) had significant advantages and relatively high rankings. For mortality, rosuvastatin (OR: 0.30; 95% CI: 0.11 to 0.84), ezetimibe plus statins (OR: 0.55; 95% CI: 0.43 to 0.89) and icosapent ethyl plus statins (OR: 0.66; 95% CI: 0.45 to 0.96) had significant advantages compared with the control.
CONCLUSION
EPA, especially icosapent ethyl, plus statins had a beneficial effect on reducing the risk of MACEs and mortality in post-PCI patients. Proprotein convertase subtilisin/kexin type-9 inhibitors plus statins were able to reduce the risk of MACEs, but the risk of mortality remained unclear.
PROSPERO REGISTRATION NUMBER
CRD42018099600.
Topics: Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Rosuvastatin Calcium; Network Meta-Analysis; Ezetimibe; Acute Coronary Syndrome; Percutaneous Coronary Intervention; Lipids
PubMed: 37967998
DOI: 10.1136/bmjopen-2022-070827 -
Atherosclerosis Dec 2023Among patients with prior myocardial infarction (MI), the risk of future ischaemic cardiovascular events is increased, and intensive lipid-lowering therapy (LLT) is... (Randomized Controlled Trial)
Randomized Controlled Trial
BACKGROUND AND AIMS
Among patients with prior myocardial infarction (MI), the risk of future ischaemic cardiovascular events is increased, and intensive lipid-lowering therapy (LLT) is indicated to achieve guideline-recommended low-density lipoprotein cholesterol (LDL-C) goals. Here, the efficacy and safety of inclisiran, a small interfering ribonucleic acid, were evaluated in patients with or without prior MI from the pooled ORION-10 and ORION-11 Phase 3 trials.
METHODS
Patients (n = 2636) were randomised 1:1 to receive 284 mg inclisiran (300 mg inclisiran sodium) or placebo on Day 1, Day 90, and 6-monthly thereafter over 18 months, along with background oral LLT, including statins. Of these, 1643 (62.3%) patients had an MI prior to randomisation, stratified as recent (>3 months to <1 year) or remote (≥1 year), and 993 (37.7%) patients were without a prior MI. The percentage change in LDL-C from baseline and safety were assessed.
RESULTS
Baseline characteristics were well balanced across the treatment arms and MI strata. The mean (95% confidence interval) placebo-corrected LDL-C reductions from baseline to Day 510 with inclisiran were 52.6% (40.1, 65.1), 50.4% (47.0, 53.8), and 51.6% (47.4, 55.9) for recent, remote, and no prior MI, respectively. Corresponding time-adjusted LDL-C reductions were 50.0% (41.4, 58.7), 52.2% (49.8, 54.7), and 51.2% (48.1, 54.2). In each MI stratum, treatment-emergent adverse events (TEAEs) at the injection site (all mild to moderate) were observed more in inclisiran-treated patients than placebo, without an excess of other TEAEs.
CONCLUSIONS
Inclisiran provided effective and consistent LDL-C lowering, irrespective of MI status.
Topics: Humans; Cholesterol, LDL; Myocardial Infarction; RNA, Small Interfering; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Anticholesteremic Agents; Proprotein Convertase 9
PubMed: 38016401
DOI: 10.1016/j.atherosclerosis.2023.117354 -
Journal of the American Heart... Dec 2023Establishing the sex-specific efficacy of cardiovascular medications is pivotal to evidence-based clinical practice, potentially closing the gender gap in longevity....
BACKGROUND
Establishing the sex-specific efficacy of cardiovascular medications is pivotal to evidence-based clinical practice, potentially closing the gender gap in longevity. Trials large enough to establish sex differences are unavailable. This study evaluated sex-specific effects of commonly prescribed cardiovascular medications on lifespan.
METHODS AND RESULTS
In a two-sample Mendelian randomization study, established genetic variants mimicking effects of lipid-lowering drugs, antihypertensives, and diabetes drugs were applied to genetic associations with lifespan proxied by UK Biobank maternal (n=412 937) and paternal (n=415 311) attained age. Estimates were obtained using inverse variance weighting, with sensitivity analyses where possible. For lipid-lowering drugs, genetically mimicked PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibitors were associated with longer lifespan, particularly in men (2.39 years per SD low-density lipoprotein cholesterol reduction [95% CI, 0.42-4.36], for interaction=0.14). Genetically mimicked treatments targeting , , or possibly were associated with longer lifespan in both sexes. For antihypertensives, genetically mimicked β-blockers and calcium channel blockers were associated with longer lifespan, particularly in men ( for interaction=0.17 for β-blockers and 0.31 for calcium channel blockers). For diabetes drugs, genetically mimicked metformin was associated with longer lifespan in both sexes. No associations were found for genetically mimicked statins, ezetimibe, or angiotensin-converting enzyme inhibitors.
CONCLUSIONS
PCSK9 inhibitors, β-blockers, and calcium channel blockers may prolong lifespan in the general population, particularly men. Treatments targeting , , or and metformin may be relevant to both sexes. Whether other null findings are attributable to lack of efficacy requires investigation. Further investigation of repurposing should be conducted.
Topics: Humans; Male; Female; Proprotein Convertase 9; Calcium Channel Blockers; Antihypertensive Agents; Mendelian Randomization Analysis; Longevity; Cholesterol, LDL; Hypolipidemic Agents; Cardiovascular Agents; Metformin; Diabetes Mellitus
PubMed: 38108247
DOI: 10.1161/JAHA.123.030943 -
The Journal of Antimicrobial... Dec 2023Global emergence of rapidly developing resistance to multiple antifungal drugs and high mortality pose challenges to the treatment of invasive Candida auris infections....
BACKGROUND
Global emergence of rapidly developing resistance to multiple antifungal drugs and high mortality pose challenges to the treatment of invasive Candida auris infections. New therapeutic approaches are needed, such as repurposing drugs including combination with antifungals. Statins have been reported to exert antifungal effects against various Candida species.
OBJECTIVES
Our study investigated potential synergy between the statins (rosuvastatin and fluvastatin) and azoles (voriconazole, posaconazole and isavuconazole) on clinical isolates of C. auris.
METHODS
Twenty-one clinical isolates of C. auris were obtained. Chequerboard assays based on the CLSI broth microdilution method were used to assess synergy based on FIC index (FICI) calculations of MICs of individual drugs and in combinations.
RESULTS
Single drug geometric mean (GM) MICs of fluvastatin and rosuvastatin were ≥128 mg/L in all 21 isolates. GM (range) MICs of posaconazole, voriconazole and isavuconazole were 0.259 (0.016-1 mg/L), 0.469 (0.016-2 mg/L) and 0.085 (0.004-1 mg/L), respectively. Combination of azoles with fluvastatin showed synergy in 70%-90% of C. auris isolates. In particular, voriconazole/fluvastatin resulted in 16-fold reduction in voriconazole MIC and synergy in 14/21 (67%) isolates. Posaconazole/fluvastatin resulted in 8-fold reduction in posaconazole MIC and synergy in 19/21 (90%) isolates.Combining rosuvastatin with the azoles also showed synergy against C. auris in 40%-60% of the isolates and additive effect in 40%-50%. None of the combinations was antagonistic.
CONCLUSIONS
Our results provide a rationale for pursuing in vivo synergy tests as well as clinical studies to explore tolerability, treatment outcomes, optimal dose and exposure targets.
Topics: Antifungal Agents; Voriconazole; Candida auris; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Fluvastatin; Rosuvastatin Calcium; Azoles; Microbial Sensitivity Tests; Drug Resistance, Fungal
PubMed: 37823357
DOI: 10.1093/jac/dkad303 -
The Lancet. Diabetes & Endocrinology May 2024Previous meta-analyses of summary data from randomised controlled trials have shown that statin therapy increases the risk of diabetes, but less is known about the size... (Meta-Analysis)
Meta-Analysis
Effects of statin therapy on diagnoses of new-onset diabetes and worsening glycaemia in large-scale randomised blinded statin trials: an individual participant data meta-analysis.
BACKGROUND
Previous meta-analyses of summary data from randomised controlled trials have shown that statin therapy increases the risk of diabetes, but less is known about the size or timing of this effect, or who is at greatest risk. We aimed to address these gaps in knowledge through analysis of individual participant data from large, long-term, randomised, double-blind trials of statin therapy.
METHODS
We conducted a meta-analysis of individual participant data from randomised controlled trials of statin therapy that participated in the CTT Collaboration. All double-blind randomised controlled trials of statin therapy of at least 2 years' scheduled duration and with at least 1000 participants were eligible for inclusion in this meta-analysis. All recorded diabetes-related adverse events, treatments, and measures of glycaemia were sought from eligible trials. Meta-analyses assessed the effects of allocation to statin therapy on new-onset diabetes (defined by diabetes-related adverse events, use of new glucose-lowering medications, glucose concentrations, or HbA values) and on worsening glycaemia in people with diabetes (defined by complications of glucose control, increased use of glucose-lowering medication, or HbA increase of ≥0·5%). Standard inverse-variance-weighted meta-analyses of the effects on these outcomes were conducted according to a prespecified protocol.
FINDINGS
Of the trials participating in the CTT Collaboration, 19 trials compared statin versus placebo (123 940 participants, 25 701 [21%] with diabetes; median follow-up of 4·3 years), and four trials compared more versus less intensive statin therapy (30 724 participants, 5340 [17%] with diabetes, median follow-up of 4·9 years). Compared with placebo, allocation to low-intensity or moderate-intensity statin therapy resulted in a 10% proportional increase in new-onset diabetes (2420 of 39 179 participants assigned to receive a statin [1·3% per year] vs 2214 of 39 266 participants assigned to receive placebo [1·2% per year]; rate ratio [RR] 1·10, 95% CI 1·04-1·16), and allocation to high-intensity statin therapy resulted in a 36% proportional increase (1221 of 9935 participants assigned to receive a statin [4·8% per year] vs 905 of 9859 participants assigned to receive placebo [3·5% per year]; 1·36, 1·25-1·48). For each trial, the rate of new-onset diabetes among participants allocated to receive placebo depended mostly on the proportion of participants who had at least one follow-up HbA measurement; this proportion was much higher in the high-intensity than the low-intensity or moderate-intensity trials. Consequently, the main determinant of the magnitude of the absolute excesses in the two types of trial was the extent of HbA measurement rather than the proportional increase in risk associated with statin therapy. In participants without baseline diabetes, mean glucose increased by 0·04 mmol/L with both low-intensity or moderate-intensity (95% CI 0·03-0·05) and high-intensity statins (0·02-0·06), and mean HbA increased by 0·06% (0·00-0·12) with low-intensity or moderate-intensity statins and 0·08% (0·07-0·09) with high-intensity statins. Among those with a baseline measure of glycaemia, approximately 62% of new-onset diabetes cases were among participants who were already in the top quarter of the baseline distribution. The relative effects of statin therapy on new-onset diabetes were similar among different types of participants and over time. Among participants with baseline diabetes, the RRs for worsening glycaemia were 1·10 (1·06-1·14) for low-intensity or moderate-intensity statin therapy and 1·24 (1·06-1·44) for high-intensity statin therapy compared with placebo.
INTERPRETATION
Statins cause a moderate dose-dependent increase in new diagnoses of diabetes that is consistent with a small upwards shift in glycaemia, with the majority of new diagnoses of diabetes occurring in people with baseline glycaemic markers that are close to the diagnostic threshold for diabetes. Importantly, however, any theoretical adverse effects of statins on cardiovascular risk that might arise from these small increases in glycaemia (or, indeed, from any other mechanism) are already accounted for in the overall reduction in cardiovascular risk that is seen with statin therapy in these trials. These findings should further inform clinical guidelines regarding clinical management of people taking statin therapy.
FUNDING
British Heart Foundation, UK Medical Research Council, and Australian National Health and Medical Research Council.
Topics: Aged; Female; Humans; Male; Middle Aged; Blood Glucose; Diabetes Mellitus; Diabetes Mellitus, Type 2; Double-Blind Method; Glycated Hemoglobin; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Randomized Controlled Trials as Topic
PubMed: 38554713
DOI: 10.1016/S2213-8587(24)00040-8 -
Canadian Family Physician Medecin de... Oct 2023To update the 2015 clinical practice guideline and provide a simplified approach to lipid management in the prevention of cardiovascular disease (CVD) for primary care.
OBJECTIVE
To update the 2015 clinical practice guideline and provide a simplified approach to lipid management in the prevention of cardiovascular disease (CVD) for primary care.
METHODS
Following the Institute of Medicine's , a multidisciplinary, pan-Canadian guideline panel was formed. This panel was represented by primary care providers, free from conflicts of interest with industry, and included the patient perspective. A separate scientific evidence team performed evidence reviews on statins, ezetimibe, proprotein convertase subtilisin-kexin type 9 inhibitors, fibrates, bile acid sequestrants, niacin, and omega-3 supplements (docosahexaenoic acid with eicosapentaenoic acid [EPA] or EPA ethyl ester alone [icosapent]), as well as on 11 supplemental questions. Recommendations were finalized by the guideline panel through use of the Grading of Recommendations Assessment, Development and Evaluation methodology.
RECOMMENDATIONS
All recommendations are presented in a patient-centred manner designed with the needs of family physicians and other primary care providers in mind. Many recommendations are similar to those published in 2015. Statins remain first-line therapy for both primary and secondary CVD prevention, and the Mediterranean diet and physical activity are recommended to reduce cardiovascular risk (primary and secondary prevention). The guideline panel recommended against using lipoprotein a, apolipoprotein B, or coronary artery calcium levels when assessing cardiovascular risk, and recommended against targeting specific lipid levels. The team also reviewed new evidence pertaining to omega-3 fatty acids (including EPA ethyl ester [icosapent]) and proprotein convertase subtilisin-kexin type 9 inhibitors, and outlined when to engage in informed shared decision making with patients on interventions to lower cardiovascular risk.
CONCLUSION
These updated evidence-based guidelines provide a simplified approach to lipid management for the prevention and management of CVD. These guidelines were created by and for primary health care professionals and their patients.
Topics: Humans; Cardiovascular Diseases; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Anticholesteremic Agents; Eicosapentaenoic Acid; Canada; Proprotein Convertases; Primary Health Care; Subtilisins; Esters; Primary Prevention
PubMed: 37833089
DOI: 10.46747/cfp.6910675