Skip to main content
Hauptrubriken
CME Facharzt-Training Webinare Zeitschriften Bücher e.Medpedia Podcast
Service
Jobbörse Info & Hilfe
Fachgebiete
Anästhesiologie Allgemeinmedizin Arbeitsmedizin Augenheilkunde Chirurgie Dermatologie Gynäkologie und Geburtshilfe HNO Innere Medizin Kardiologie Neurologie Onkologie und Hämatologie Orthopädie und Unfallchirurgie Pädiatrie Pathologie Psychiatrie Radiologie Rechtsmedizin Urologie Zahnmedizin
Themen
Typ-2-Diabetes und Adipositas Klimawandel und Gesundheit Neues aus dem Markt COVID-19 Praxis und Beruf Seltene Erkrankungen GOÄ & EBM Panorama
Sammlungen
Kasuistiken Algorithmen & Infografiken Blickdiagnosen Arthropedia FlapFinder (für Dermatochirurgen) Videos Kongressberichterstattung Medizin für Apothekerinnen und Apotheker Für Ärztinnen und Ärzte in Weiterbildung Für Medizinstudierende

Live-Webinar "Urologie und Sexualmedizin in der Praxis"

Häufige urologisch-sexualmedizinische Themen in der Praxis sind das Thema des MMW-Webinars am 5. Juni von 17.30 bis 19 Uhr. Konkret geht es um die Frage, wann bei Harnwegsinfektionen auf Antibiotika verzichtet werden kann, und um ein Update zur Therapie von Libido- und Potenzstörungen des Mannes. Der dritte Vortrag behandelt sexuell übertragbare Krankheiten. Stellen Sie Ihre Fragen an die Experten und sammeln Sie 2 CME-Punkte. Jetzt gleich anmelden!
Erweiterte Suche
Anmelden
nach oben
Current Cardiology Reports
Erschienen in: Current Cardiology Reports 3/2024

10.02.2024 | Cardiac Biomarkers (AA Quyyumi, Section Editor)

Lysophosphatidic Acid-Mediated Inflammation at the Heart of Heart Failure

verfasst von: Rajesh Chaudhary, Tahra Suhan, Mahmud W. Tarhuni, Ahmed Abdel-Latif

Erschienen in: Current Cardiology Reports | Ausgabe 3/2024

Einloggen, um Zugang zu erhalten

Abstract

Purpose of Review

The primary aim of this review is to provide an in-depth examination of the role bioactive lipids—namely lysophosphatidic acid (LPA) and ceramides—play in inflammation-mediated cardiac remodeling during heart failure. With the global prevalence of heart failure on the rise, it is critical to understand the underlying molecular mechanisms contributing to its pathogenesis. Traditional studies have emphasized factors such as oxidative stress and neurohormonal activation, but emerging research has shed light on bioactive lipids as central mediators in heart failure pathology. By elucidating these intricacies, this review aims to:
  • Bridge the gap between basic research and clinical practice by highlighting clinically relevant pathways contributing to the pathogenesis and prognosis of heart failure.
  • Provide a foundation for the development of targeted therapies that could mitigate the effects of LPA and ceramides on heart failure.
  • Serve as a comprehensive resource for clinicians and researchers interested in the molecular biology of heart failure, aiding in better diagnostic and therapeutic decisions.

Recent Findings

Recent findings have shed light on the central role of bioactive lipids, specifically lysophosphatidic acid (LPA) and ceramides, in heart failure pathology. Traditional studies have emphasized factors such as hypoxia-mediated cardiomyocyte loss and neurohormonal activation in the development of heart failure. Emerging research has elucidated the intricacies of bioactive lipid-mediated inflammation in cardiac remodeling and the development of heart failure. Studies have shown that LPA and ceramides contribute to the pathogenesis of heart failure by promoting inflammation, fibrosis, and apoptosis in cardiac cells. Additionally, recent studies have identified potential targeted therapies that could mitigate the effects of bioactive lipids on heart failure, including LPA receptor antagonists and ceramide synthase inhibitors. These recent findings provide a promising avenue for the development of targeted therapies that could improve the diagnosis and treatment of heart failure.

Summary

In this review, we highlight the pivotal role of inflammation induced by bioactive lipid signaling and its influence on the pathogenesis of heart failure. By critically assessing the existing literature, we provide a comprehensive resource for clinicians and researchers interested in the molecular mechanisms of heart failure. Our review aims to bridge the gap between basic research and clinical practice by providing actionable insights and a foundation for the development of targeted therapies that could mitigate the effects of bioactive lipids on heart failure. We hope that this review will aid in better diagnostic and therapeutic decisions, further advancing our collective understanding and management of heart failure.
Literatur
1.
Virani SS, et al. Heart disease and stroke statistics-2020 update: a report from the American Heart Association. Circulation. 2020;141(9):e139–596.PubMedCrossRef
2.
McDonagh TA, et al. focused update of the 2021 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J. 2023;2023.
3.
Tyminska A, et al. Ischemic cardiomyopathy versus non-ischemic dilated cardiomyopathy in patients with reduced ejection fraction- clinical characteristics and prognosis depending on heart failure etiology (data from European Society of Cardiology Heart Failure Registries). Biology (Basel). 2022;11(2).
4.
Zhu J, et al. The incidence of acute myocardial infarction in relation to overweight and obesity: a meta-analysis. Arch Med Sci. 2014;10(5):855–62.PubMedPubMedCentralCrossRef
5.
Rieckmann M, et al. Myocardial infarction triggers cardioprotective antigen-specific T helper cell responses. J Clin Invest. 2019;129(11):4922–36.PubMedPubMedCentralCrossRef
6.
Yue R, et al. NLRP3-mediated pyroptosis aggravates pressure overload-induced cardiac hypertrophy, fibrosis, and dysfunction in mice: cardioprotective role of irisin. Cell Death Discov. 2021;7(1):50.PubMedPubMedCentralCrossRef
7.
Xu S, et al. Excessive inflammation impairs heart regeneration in zebrafish breakdance mutant after cryoinjury. Fish Shellfish Immunol. 2019;89:117–26.PubMedCrossRef
8.
Lee JW, et al. Lysophosphatidic acid receptor 4 is transiently expressed during cardiac differentiation and critical for repair of the damaged heart. Mol Ther. 2021;29(3):1151–63.PubMedCrossRef
9.
Wang F, et al. LPA(3)-mediated lysophosphatidic acid signaling promotes postnatal heart regeneration in mice. Theranostics. 2020;10(24):10892–907.PubMedPubMedCentralCrossRef
10.
Yang J, et al. Lysophosphatidic acid is associated with cardiac dysfunction and hypertrophy by suppressing autophagy via the LPA3/AKT/mTOR pathway. Front Physiol. 2018;9:1315.PubMedPubMedCentralCrossRef
11.
Wen H, et al. Higher serum lysophosphatidic acids predict left ventricular reverse remodeling in pediatric dilated cardiomyopathy. Front Pediatr. 2021;9: 710720.PubMedPubMedCentralCrossRef
12.
Brown A, et al. Lysophosphatidic acid receptor mRNA levels in heart and white adipose tissue are associated with obesity in mice and humans. PLoS ONE. 2017;12(12): e0189402.PubMedPubMedCentralCrossRef
13.
14.
Berwick ML, et al. The role of ceramide 1-phosphate in inflammation, cellular proliferation, and wound healing. Adv Exp Med Biol. 2019;1159:65–77.PubMedCrossRef
15.
Geraldo LHM, et al. Role of lysophosphatidic acid and its receptors in health and disease: novel therapeutic strategies. Signal Transduct Target Ther. 2021;6(1):45.PubMedPubMedCentralCrossRef
16.
Tokumura A, et al. Identification of human plasma lysophospholipase D, a lysophosphatidic acid-producing enzyme, as autotaxin, a multifunctional phosphodiesterase. J Biol Chem. 2002;277(42):39436–42.PubMedCrossRef
17.
Spohr TC, et al. LPA-primed astrocytes induce axonal outgrowth of cortical progenitors by activating PKA signaling pathways and modulating extracellular matrix proteins. Front Cell Neurosci. 2014;8:296.PubMedPubMedCentralCrossRef
18.
Fukushima N, Weiner JA, Chun J. Lysophosphatidic acid (LPA) is a novel extracellular regulator of cortical neuroblast morphology. Dev Biol. 2000;228(1):6–1.PubMedCrossRef
19.
McIntyre TM, et al. Identification of an intracellular receptor for lysophosphatidic acid (LPA): LPA is a transcellular PPARgamma agonist. Proc Natl Acad Sci USA. 2003;100(1):131–6.PubMedCrossRef
20.
Choi JW, et al. LPA receptors: subtypes and biological actions. Annu Rev Pharmacol Toxicol. 2010;50:157–86.PubMedCrossRef
21.
Ray R, et al. Lysophosphatidic acid-RAGE axis promotes lung and mammary oncogenesis via protein kinase B and regulating tumor microenvironment. Cell Commun Signal. 2020;18(1):170.PubMedPubMedCentralCrossRef
22.
Li N, et al. Lysophosphatidic acid enhances human umbilical cord mesenchymal stem cell viability without differentiation via LPA receptor mediating manner. Apoptosis. 2017;22(10):1296–309.PubMedPubMedCentralCrossRef
23.
Tigyi G, et al. Revisiting the role of lysophosphatidic acid in stem cell biology. Exp Biol Med (Maywood). 2021;246(16):1802–9.PubMedCrossRef
24.
Pan X, et al. Lysophosphatidic acid may be a novel biomarker for early acute aortic dissection. Front Surg. 2021;8: 789992.PubMedCrossRef
25.
Axelsson Raja A, et al. Ablation of lysophosphatidic acid receptor 1 attenuates hypertrophic cardiomyopathy in a mouse model. Proc Natl Acad Sci USA. 2022;119(28): e2204174119.PubMedPubMedCentralCrossRef
26.
Wu L, et al. Lysophosphatidic acid mediates fibrosis in injured joints by regulating collagen type I biosynthesis. Osteoarthritis Cartilage. 2015;23(2):308–18.PubMedCrossRef
27.
Cao P, et al. Autocrine lysophosphatidic acid signaling activates beta-catenin and promotes lung allograft fibrosis. J Clin Invest. 2017;127(4):1517–30.PubMedPubMedCentralCrossRef
28.
Tang N, et al. Lysophosphatidic acid accelerates lung fibrosis by inducing differentiation of mesenchymal stem cells into myofibroblasts. J Cell Mol Med. 2014;18(1):156–69.PubMedCrossRef
29.
Bot M, et al. Lysophosphatidic acid triggers mast cell-driven atherosclerotic plaque destabilization by increasing vascular inflammation. J Lipid Res. 2013;54(5):1265–74.PubMedPubMedCentralCrossRef
30.
Kritikou E, et al. Inhibition of lysophosphatidic acid receptors 1 and 3 attenuates atherosclerosis development in LDL-receptor deficient mice. Sci Rep. 2016;6:37585.PubMedPubMedCentralCrossRef
31.
Aldi S, et al. Integrated human evaluation of the lysophosphatidic acid pathway as a novel therapeutic target in atherosclerosis. Mol Ther Methods Clin Dev. 2018;10:17–28.PubMedPubMedCentralCrossRef
32.
Nathan S, et al. CREB-dependent LPA-induced signaling initiates a pro-fibrotic feedback loop between small airway basal cells and fibroblasts. Respir Res. 2021;22(1):97.PubMedPubMedCentralCrossRef
33.
• Decato BE, et al. LPA(1) antagonist BMS-986020 changes collagen dynamics and exerts antifibrotic effects in vitro and in patients with idiopathic pulmonary fibrosis. Respir Res. 2022;23(1):61. Decato et al. studied the antifibrotic effects of the LPA1 antagonist BMS-986020 in idiopathic pulmonary fibrosis (IPF), a disease with limited treatment options. This research is groundbreaking because it not only highlights the potential of targeting the LPA-LPA1 pathway in IPF treatment, but also extends our understanding of the disease's mechanisms, particularly in relation to collagen turnover, that can have a therapeutic potential in number of other disease conditions where fibrosis is one of the hallmark of disease including heart failure.
34.
Palmer SM, et al. Randomized, double-blind, placebo-controlled, phase 2 trial of BMS-986020, a lysophosphatidic acid receptor antagonist for the treatment of idiopathic pulmonary fibrosis. Chest. 2018;154(5):1061–9.PubMedCrossRef
35.
Corte TJ, et al. Phase 2 trial design of BMS-986278, a lysophosphatidic acid receptor 1 (LPA(1)) antagonist, in patients with idiopathic pulmonary fibrosis (IPF) or progressive fibrotic interstitial lung disease (PF-ILD). BMJ Open Respir Res. 2021;8(1).
36.
37.
Mozaffarian D, et al. Heart disease and stroke statistics–2015 update: a report from the American Heart Association. Circulation. 2015;131(4):e29–32.PubMed
38.
Zouggari Y, et al. B lymphocytes trigger monocyte mobilization and impair heart function after acute myocardial infarction. Nat Med. 2013;19(10):1273–80.PubMedPubMedCentralCrossRef
39.
Abo-Aly M, et al. Prognostic significance of activated monocytes in patients with ST-elevation myocardial infarction. Int J Mol Sci. 2023;24(14).
40.
Maekawa Y, et al. Prognostic significance of peripheral monocytosis after reperfused acute myocardial infarction:a possible role for left ventricular remodeling. J Am Coll Cardiol. 2002;39(2):241–6.PubMedCrossRef
41.
42.
43.
44.
Shen JL, Xie XJ. Insight into the pro-inflammatory and profibrotic role of macrophage in heart failure with preserved ejection fraction. J Cardiovasc Pharmacol. 2020;76(3):276–85.PubMedCrossRef
45.
Yasuda D, et al. Lysophosphatidic acid-induced YAP/TAZ activation promotes developmental angiogenesis by repressing Notch ligand Dll4. J Clin Invest. 2019;129(10):4332–49.PubMedPubMedCentralCrossRef
46.
Pei J, et al. LPA(2) Contributes to vascular endothelium homeostasis and cardiac remodeling after myocardial infarction. Circ Res. 2022;131(5):388–93.PubMedCrossRef
47.
Chen X, et al. Serum lysophosphatidic acid concentrations measured by dot immunogold filtration assay in patients with acute myocardial infarction. Scand J Clin Lab Invest. 2003;63(7–8):497–503.PubMedCrossRef
48.
•• Tripathi H, et al. Autotaxin inhibition reduces cardiac inflammation and mitigates adverse cardiac remodeling after myocardial infarction. J Mol Cell Cardiol. 2020;149:95-1. The study by Tripathi et al. uncovers the pivotal role of autotaxin inhibition in reducing cardiac inflammation and adverse remodeling after myocardial infarction, offering a novel therapeutic approach for heart disease. This research is important in cardiac research as it underscores the fact that targeting the ATX/LPA signaling nexus can significantly improve cardiac recovery and function post-infarction, a major advancement in treating heart failure.
49.
Murphy AJ, et al. ApoE regulates hematopoietic stem cell proliferation, monocytosis, and monocyte accumulation in atherosclerotic lesions in mice. J Clin Invest. 2011;121(10):4138–49.PubMedPubMedCentralCrossRef
50.
•• Tripathi H, et al. Myeloid-Specific Deletion of Lipid Plpp3 (Phosphate Phosphatase 3) Increases Cardiac Inflammation After Myocardial Infarction. Arterioscler Thromb Vasc Biol. 2023;43(2):379-81. Tripathi et al and coauthors examined the role of lipid phosphate phosphatase 3 (LPP3) in myeolid cells in cardiac inflammation after myocardial infarction. The studies used loss of function genetic animal model that confirmed that deletion of LPP3 results in unopposed lysophosphatidic acid signaling which exacerbates post-myocardial infarction inflammation. The heightened inflammation in LPP3 cKO mice results in worsening cardiac function and larger scar size after ischemic injury.
51.
Sokolowska E, Blachnio-Zabielska A. The role of ceramides in insulin resistance. Front Endocrinol (Lausanne). 2019;10:577.PubMedCrossRef
52.
Lee SY, et al. Cardiomyocyte specific deficiency of serine palmitoyltransferase subunit 2 reduces ceramide but leads to cardiac dysfunction. J Biol Chem. 2012;287(22):18429–39.PubMedPubMedCentralCrossRef
53.
54.
Ji R, et al. Increased de novo ceramide synthesis and accumulation in failing myocardium. JCI Insight. 2017;2(14).
55.
Hilvo M, et al. Prediction of residual risk by ceramide-phospholipid score in patients with stable coronary heart disease on optimal medical therapy. J Am Heart Assoc. 2020;9(10): e015258.PubMedPubMedCentralCrossRef
56.
Mantovani A, Dugo C. Ceramides and risk of major adverse cardiovascular events: a meta-analysis of longitudinal studies. J Clin Lipidol. 2020;14(2):176–85.PubMedCrossRef
57.
Havulinna AS, et al. Circulating ceramides predict cardiovascular outcomes in the population-based FINRISK 2002 cohort. Arterioscler Thromb Vasc Biol. 2016;36(12):2424–30.PubMedCrossRef
58.
Nwabuo CC, et al. Association of circulating ceramides with cardiac structure and function in the community: the framingham heart study. J Am Heart Assoc. 2019;8(19): e013050.PubMedPubMedCentralCrossRef
59.
60.
Chun L, et al. Inhibition of ceramide synthesis reverses endothelial dysfunction and atherosclerosis in streptozotocin-induced diabetic rats. Diabetes Res Clin Pract. 2011;93(1):77–85.PubMedCrossRef
61.
Cantalupo A, et al. Endothelial sphingolipid de novo synthesis controls blood pressure by regulating signal transduction and NO via ceramide. Hypertension. 2020;75(5):1279–88.PubMedCrossRef
62.
Zhang DX, Zou AP, Li PL. Ceramide-induced activation of NADPH oxidase and endothelial dysfunction in small coronary arteries. Am J Physiol Heart Circ Physiol. 2003;284(2):H605–12.PubMedCrossRef
63.
Zheng T, et al. Sphingomyelinase and ceramide analogs induce contraction and rises in [Ca(2+)](i) in canine cerebral vascular muscle. Am J Physiol Heart Circ Physiol. 2000;278(5):H1421–8.PubMedCrossRef
64.
Li H, et al. Dual effect of ceramide on human endothelial cells: induction of oxidative stress and transcriptional upregulation of endothelial nitric oxide synthase. Circulation. 2002;106(17):2250–6.PubMedCrossRef
65.
Zhang QJ, et al. Ceramide mediates vascular dysfunction in diet-induced obesity by PP2A-mediated dephosphorylation of the eNOS-Akt complex. Diabetes. 2012;61(7):1848–59.PubMedPubMedCentralCrossRef
66.
Bharath LP, et al. Ceramide-initiated protein phosphatase 2A activation contributes to arterial dysfunction in vivo. Diabetes. 2015;64(11):3914–26.PubMedPubMedCentralCrossRef
67.
Wretlind A, et al. Ceramides are decreased after liraglutide treatment in people with type 2 diabetes: a post hoc analysis of two randomized clinical trials. Lipids Health Dis. 2023;22(1):160.PubMedPubMedCentralCrossRef
68.
Presa N, et al. Regulation of cell migration and inflammation by ceramide 1-phosphate. Biochim Biophys Acta. 2016;1861(5):402–9.PubMedCrossRef
69.
Arana L, et al. Ceramide 1-phosphate induces macrophage chemoattractant protein-1 release: involvement in ceramide 1-phosphate-stimulated cell migration. Am J Physiol Endocrinol Metab. 2013;304(11):E1213–26.PubMedCrossRef
70.
Gomez-Munoz A, et al. New insights on the role of ceramide 1-phosphate in inflammation. Biochim Biophys Acta. 2013;1831(6):1060–6.PubMedCrossRef
71.
Hotamisligil GS, et al. Increased adipose tissue expression of tumor necrosis factor-alpha in human obesity and insulin resistance. J Clin Invest. 1995;95(5):2409–15.PubMedPubMedCentralCrossRef
72.
Ahmad R, et al. The synergy between palmitate and TNF-alpha for CCL2 production is dependent on the TRIF/IRF3 pathway: implications for metabolic inflammation. J Immunol. 2018;200(10):3599–611.PubMedPubMedCentralCrossRef
73.
Wouters K, et al. Circulating classical monocytes are associated with CD11c(+) macrophages in human visceral adipose tissue. Sci Rep. 2017;7:42665.PubMedPubMedCentralCrossRef
74.
75.
76.
Yamamoto T, Sano M. Deranged myocardial fatty acid metabolism in heart failure. Int J Mol Sci. 2022;23(2).
77.
Datta Chaudhuri R, et al. Cardiac-specific overexpression of HIF-1alpha during acute myocardial infarction ameliorates cardiomyocyte apoptosis via differential regulation of hypoxia-inducible pro-apoptotic and anti-oxidative genes. Biochem Biophys Res Commun. 2021;537:100–8.PubMedCrossRef
78.
Bonney S, et al. Cardiac Per2 functions as novel link between fatty acid metabolism and myocardial inflammation during ischemia and reperfusion injury of the heart. PLoS ONE. 2013;8(8): e71493.PubMedPubMedCentralCrossRef
79.
80.
Li C, et al. HIF1alpha-dependent glycolysis promotes macrophage functional activities in protecting against bacterial and fungal infection. Sci Rep. 2018;8(1):3603.PubMedPubMedCentralCrossRef
81.
82.
83.
Higgins DF, et al. Hypoxia promotes fibrogenesis in vivo via HIF-1 stimulation of epithelial-to-mesenchymal transition. J Clin Invest. 2007;117(12):3810–20.PubMedPubMedCentral
84.
Epstein Shochet G, et al. Hypoxia inducible factor 1A supports a pro-fibrotic phenotype loop in idiopathic pulmonary fibrosis. Int J Mol Sci. 2021;22(7).
85.
Wang P, et al. Disruption of adipocyte HIF-1alpha improves atherosclerosis through the inhibition of ceramide generation. Acta Pharm Sin B. 2022;12(4):1899–912.PubMedCrossRef
86.
Hadas Y, et al. Altering sphingolipid metabolism attenuates cell death and inflammatory response after myocardial infarction. Circulation. 2020;141(11):916–30.PubMedPubMedCentralCrossRef
87.
Al-Rashed F, et al. Neutral sphingomyelinase 2 regulates inflammatory responses in monocytes/macrophages induced by TNF-alpha. Sci Rep. 2020;10(1):16802.PubMedPubMedCentralCrossRef
Metadaten
Titel
Lysophosphatidic Acid-Mediated Inflammation at the Heart of Heart Failure
verfasst von
Rajesh Chaudhary
Tahra Suhan
Mahmud W. Tarhuni
Ahmed Abdel-Latif
Publikationsdatum
10.02.2024
Verlag
Springer US
Erschienen in
Current Cardiology Reports / Ausgabe 3/2024
Print ISSN: 1523-3782
Elektronische ISSN: 1534-3170
DOI
https://doi.org/10.1007/s11886-024-02023-8

Weitere Artikel der Ausgabe 3/2024

Current Cardiology Reports 3/2024 Zur Ausgabe

Women and Cardiovascular Health (N Goldberg and S Lewis, Section Editors)

Spontaneous Coronary Artery Dissection (SCAD) from an Interventionalist Perspective

Cardiometabolic Disease (DM and CV) (CJ Lavie, Section Editor)

Worth Their Weight? An Update on New and Emerging Pharmacologic Agents for Obesity and Their Potential Role for Persons with Cardiac Conditions

Cardiometabolic Disease (DM and CV) (CJ Lavie, Section Editor)

Nutritional Aspects to Cardiovascular Diseases and Type 2 Diabetes Mellitus

Cardiovascular Genomics (KG Aragam, Section Editor)

The Expansion of Genetic Testing in Cardiovascular Medicine: Preparing the Cardiology Community for the Changing Landscape

Congenital Heart Disease (RA Krasuski and G Fleming, Section Editors)

Understanding the Genetic and Non-genetic Interconnections in the Aetiology of Isolated Congenital Heart Disease: An Updated Review: Part 1

Echocardiography (JM Gardin and AH Waller, Section Editors)

Echogenomics: Echocardiography in Heritable Aortopathies

Neu im Fachgebiet Kardiologie

Nach Herzinfarkt mit Typ-1-Diabetes schlechtere Karten als mit Typ 2?

29.05.2024 Herzinfarkt Nachrichten

Bei Menschen mit Typ-2-Diabetes sind die Chancen, einen Myokardinfarkt zu überleben, in den letzten 15 Jahren deutlich gestiegen – nicht jedoch bei Betroffenen mit Typ 1.

Erhöhtes Risiko fürs Herz unter Checkpointhemmer-Therapie

28.05.2024 Nebenwirkungen der Krebstherapie Nachrichten

Kardiotoxische Nebenwirkungen einer Therapie mit Immuncheckpointhemmern mögen selten sein – wenn sie aber auftreten, wird es für Patienten oft lebensgefährlich. Voruntersuchung und Monitoring sind daher obligat.

GLP-1-Agonisten können Fortschreiten diabetischer Retinopathie begünstigen

24.05.2024 Diabetische Retinopathie Nachrichten

Möglicherweise hängt es von der Art der Diabetesmedikamente ab, wie hoch das Risiko der Betroffenen ist, dass sich sehkraftgefährdende Komplikationen verschlimmern.

TAVI versus Klappenchirurgie: Neue Vergleichsstudie sorgt für Erstaunen

21.05.2024 TAVI Nachrichten

Bei schwerer Aortenstenose und obstruktiver KHK empfehlen die Leitlinien derzeit eine chirurgische Kombi-Behandlung aus Klappenersatz plus Bypass-OP. Diese Empfehlung wird allerdings jetzt durch eine aktuelle Studie infrage gestellt – mit überraschender Deutlichkeit.

Update Kardiologie

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.

Newsletter bestellen