Schlagen Frauenherzen anders? – Geschlechterunterschiede im Lipidmanagement DOI Creative Commons

Maximilian A. Muck,

Andrea Baessler

Deleted Journal, Journal Year: 2025, Volume and Issue: unknown

Published: March 10, 2025

Zusammenfassung Geschlechterspezifische Unterschiede im Lipidstoffwechsel sind vor allem hormonell bedingt. Frauen haben prämenopausal Vergleich zu Männern tendenziell günstigere Lipidwerte, wie höhere Konzentrationen an High-Density-Lipoprotein-Cholesterin (HDL-C) und niedrigere Low-Density-Lipoprotein-Cholesterin (LDL-C). Mit Beginn der Menopause verschlechtern sich diese Werte jedoch durch hormonelle Veränderungen, wodurch bei das Risiko für atherosklerotische Herz-Kreislauf-Erkrankungen erhöht. Trotz vergleichbarer Wirksamkeit lipidsenkender Therapien zeigen mehrere Studien einheitlich, dass seltener die empfohlenen LDL-C-Zielwerte erreichen. Besonders in klinischen Praxis bestehen große Diskrepanzen zwischen Leitlinienempfehlungen tatsächlicher Behandlung, Hochrisikopatientinnen. Verschiedene Barrieren tragen wesentlich dazu bei: Dazu gehören Unterschätzung des Risikos behandelnde Ärzte, ein zurückhaltenderes Verordnungsverhalten, eingeschränktes Bewusstsein Notwendigkeit einer Therapie Patientinnen sowie eine verminderte Medikamentenadhärenz. Letztere wird unter anderem stärkere Wahrnehmung von Nebenwirkungen Prävalenz Statinintoleranz beeinflusst. Die Betreuung spezialisierten Lipidzentren zeigt, viele schwer einstellbare Patienten, z. B. Patienten mit oder hohen LDL-C-Ausgangswerten, gezielter Nachsorge erfolgreich behandelt werden können. Neue pharmakologische Ansätze Kombinationstherapien ermöglichen es, Therapieziele Dennoch erreichen trotz solcher Maßnahmen ihre LDL-Zielwerte, was auf intensiverer geschlechtersensibler Strategien hinweist. Eine wirksame Lipidtherapie erfordert verstärkt den Einsatz Kombinationstherapien, regelmäßige Kontrollen enge Zusammenarbeit Patient Arzt. ist es entscheidend, Therapieadhärenz verbessern mögliche konsequent anzugehen, um kardiovaskuläre effektiv senken.

Lipoprotein(a) and cardiovascular disease DOI
Børge G. Nordestgaard, Anne Langsted

The Lancet, Journal Year: 2024, Volume and Issue: unknown

Published: Sept. 1, 2024

Language: Английский

Citations

21
High lipoprotein(a): Actionable strategies for risk assessment and mitigation DOI Creative Commons
Gissette Reyes‐Soffer, Calvin Yeang, Erin D. Michos

et al.

American Journal of Preventive Cardiology, Journal Year: 2024, Volume and Issue: 18, P. 100651 - 100651

Published: April 3, 2024

High levels of lipoprotein(a) [Lp(a)] are causal for atherosclerotic cardiovascular disease (ASCVD). Lp(a) is the most prevalent inherited dyslipidemia and strongest genetic ASCVD risk factor. This persists in presence at target, guideline-recommended, LDL-C adherence to lifestyle modifications. Epidemiological evidence supporting its role calcific aortic stenosis continues accumulate, although various facets regarding biology (genetics, pathophysiology, expression across race/ethnic groups) not yet fully understood. The evolving nature clinical guidelines consensus statements recommending universal measurements scientific data multiple states reinforce merit start population screening now. There a current gap implementation recommendations primary secondary (CVD) prevention those with high Lp(a), part due lack protocols management strategies. Importantly, targeted apolipoprotein(a) [apo(a)]-lowering therapies that reduce patients phase 3 development. review focuses on identification Lp(a). Specifically, we highlight value measuring use determining Lp(a)-associated CVD by providing actionable guidance, based knowledge, can be utilized now mitigate caused

Language: Английский

Citations

17
Advancements in risk stratification and management strategies in primary cardiovascular prevention DOI
Fotios Barkas, Yusuf Ziya Şener,

Pelin Golforoush

et al.

Atherosclerosis, Journal Year: 2024, Volume and Issue: 395, P. 117579 - 117579

Published: May 15, 2024

Language: Английский

Citations

16
Apolipoprotein B-containing lipoproteins in atherogenesis DOI
Jan Borén,

Chris J. Packard,

Christoph J. Binder

et al.

Nature Reviews Cardiology, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 2, 2025

Language: Английский

Citations

2
Therapeutic Potential of Lipoprotein(a) Inhibitors DOI Creative Commons
Stephen J. Nicholls

Drugs, Journal Year: 2024, Volume and Issue: 84(6), P. 637 - 643

Published: June 1, 2024

Increasing evidence has implicated lipoprotein(a) [Lp(a)] in the causality of atherosclerosis and calcific aortic stenosis. This stimulated immense interest developing novel approaches to integrating Lp(a) into setting cardiovascular prevention. Current guidelines advocate universal measurement levels, with potential influence risk assessment triage higher-risk patients use more intensive preventive therapies. In parallel, considerable activity been undertaken develop therapeutics achieve selective substantial reductions levels. Early studies antisense oligonucleotides (e.g., mipomersen, pelacarsen), RNA interference olpasiran, zerlasiran, lepodisiran) small molecule inhibitors muvalaplin) have demonstrated effective lowering good tolerability. These agents are moving forward clinical development, order determine whether reduces risk. The results these transform our approach prevention disease.

Language: Английский

Citations

14
Oral Muvalaplin for Lowering of Lipoprotein(a) DOI
Stephen J. Nicholls, Wei Ni,

Grace M. Rhodes

et al.

JAMA, Journal Year: 2024, Volume and Issue: unknown

Published: Nov. 18, 2024

Importance Muvalaplin inhibits lipoprotein(a) formation. A 14-day phase 1 study demonstrated that muvalaplin was well tolerated and reduced levels up to 65%. The effect of longer administration on in individuals at high cardiovascular risk remains uncertain. Objectives To determine the assess safety tolerability. Design, Setting, Participants Phase 2, placebo-controlled, randomized, double-blind trial enrolling 233 participants with concentrations 175 nmol/L or greater atherosclerotic disease, diabetes, familial hypercholesterolemia 43 sites Asia, Europe, Australia, Brazil, United States between December 10, 2022, November 22, 2023. Interventions were randomized receive orally administered dosages 10 mg/d (n = 34), 60 64), 240 68) placebo 67) for 12 weeks. Main Outcomes Measures primary end point placebo-adjusted percentage change from baseline molar concentration week 12, using an assay measure intact a traditional apolipoprotein(a)-based assay. Secondary points included apolipoprotein B high-sensitivity C-reactive protein. Results median age 66 years; 33% female; 27% identified as Asian, 4% Black, 66% White. resulted reductions 47.6% (95% CI, 35.1%-57.7%), 81.7% 78.1%-84.6%), 85.8% 83.1%-88.0%) 10-mg/d, 60-mg/d, 240-mg/d dosages, respectively, 40.4% 28.3%-50.5%), 70.0% 65.0%-74.2%), 68.9% 63.8%-73.3%) Dose-dependent observed 8.9% −2.2% 18.8%), 13.1% 4.4%-20.9%), 16.1% 7.8%-23.7%) mg/d, respectively. No protein observed. tolerability concerns any dosage. Conclusions Relevance measured assays tolerated. events requires further investigation. Trial Registration ClinicalTrials.gov Identifier: NCT05563246

Language: Английский

Citations

12
A Comprehensive Review of the Genetics of Dyslipidemias and Risk of Atherosclerotic Cardiovascular Disease DOI Open Access

Megan Kalwick,

Mendel Roth

Nutrients, Journal Year: 2025, Volume and Issue: 17(4), P. 659 - 659

Published: Feb. 12, 2025

Dyslipidemias are often diagnosed based on an individual's lipid panel that may or not include Lp(a) apoB. But these values alone omit key information can underestimate risk and misdiagnose disease, which leads to imprecise medical therapies reduce efficacy with unnecessary adverse events. For example, knowing whether dyslipidemia is monogenic granularly inform create opportunities for precision therapeutics. This review explores the canonical non-canonical causes of dyslipidemias how they impact atherosclerotic cardiovascular disease (ASCVD) risk. emphasizes multitude genetic cause primary hypercholesterolemia, hypertriglyceridemia, low elevated high-density lipoprotein (HDL)-cholesterol levels. Within each sections, this will explore evidence linking conditions ASCVD Where applicable, summarize approved a particular condition.

Language: Английский

Citations

1
Discordance Analyses Comparing LDL Cholesterol, Non-HDL Cholesterol, and Apolipoprotein B for Cardiovascular Risk Estimation DOI

Camilla Ditlev Lindhardt Johannesen,

Martin Bødtker Mortensen, Børge G. Nordestgaard

et al.

Atherosclerosis, Journal Year: 2025, Volume and Issue: 403, P. 119139 - 119139

Published: Feb. 18, 2025

Language: Английский

Citations

1
The Interplay Between Immunity, Inflammation and Endothelial Dysfunction DOI Open Access
Ying Jie Chee, Rinkoo Dalan, Christine Cheung

et al.

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(4), P. 1708 - 1708

Published: Feb. 17, 2025

The endothelium is pivotal in multiple physiological processes, such as maintaining vascular homeostasis, metabolism, platelet function, and oxidative stress. Emerging evidence the past decade highlighted immunomodulatory function of endothelium, serving a link between innate, adaptive immunity inflammation. This review examines regulation immune-inflammatory axis by discusses immune functions, explores pathophysiological processes leading to endothelial dysfunction various metabolic disturbances, including hyperglycemia, obesity, hypertension, dyslipidaemia. final section focuses on novel, repurposed, emerging therapeutic targets that address dysfunction.

Language: Английский

Citations

1
The Effects of Colchicine on Lipoprotein(a) and Oxidized Phospholipid Associated Cardiovascular Disease Risk DOI
Niekbachsh Mohammadnia, Amber van Broekhoven, Willem A. Bax

et al.

European Journal of Preventive Cardiology, Journal Year: 2024, Volume and Issue: unknown

Published: Oct. 30, 2024

Abstract Aims Inflammatory lipoprotein(a) [Lp(a)] and oxidized phospholipids (OxPLs) on lipoproteins convey residual cardiovascular disease risk. The low-dose colchicine 2 (LoDoCo2) trial showed that reduced the risk of events occurring standard therapies in patients with chronic coronary syndrome (CCS). We explored effects Lp(a)- lipoprotein-associated a LoDoCo2 biomarker subpopulation. Methods results Lipoprotein(a) OxPLs apolipoprotein(a) [OxPL-apo(a)] apolipoprotein B-100 (OxPL-apoB) levels were determined population (n = 1777). Cox regression analysis was used to compare primary endpoint, consisting myocardial infarction, ischaemic stroke, or ischaemia-driven revascularization by levels. Interactions between treatment, Lp(a), OxPL evaluated. Lipoprotein(a), OxPL-apo(a), OxPL-apoB similar placebo groups. Consistent reduction observed those Lp(a) < 125 nmol/L ≥125 highest OxPL-apo(a) tertile compared lowest (Pinteraction 0.92 0.66). absolute for ≥ appeared higher (4.4% vs. 2.4%). A treatment interaction found 0.04). Conclusion In CCS, reduces without elevated but benefits nmol/L. Patients experienced greater benefit colchicine, suggesting may be more effective subjects heightened oxidation-driven inflammation.

Language: Английский

Citations

6