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Current Hypertension Reports
Erschienen in: Current Hypertension Reports 6/2012

01.12.2012 | Mediators, Mechanisms, and Pathways in Tissue Injury (B Rothermel, Section Editor)

Mechanisms and Consequences of Inflammatory Signaling in the Myocardium

verfasst von: Jihyun Ahn, Jaetaek Kim

Erschienen in: Current Hypertension Reports | Ausgabe 6/2012

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Abstract

To further understand chronic heart disease, such as heart failure and cardiomyopathy, we must fully define signaling pathways within the myocardium. Recent studies suggest that some forms of heart disease are associated with a chronic low-grade inflammation that promotes adverse ventricular remodeling and correlates with disease progression. Several inflammatory mediators, including TNF-α, IL-1β, and IL-6, are involved in cardiac injury subsequent to myocardial ischemia and reperfusion, sepsis, viral myocarditis, and transplant rejection. Once activated, components of the inflammatory response can have both beneficial and deleterious effects on the heart. In this review, we discuss the complex inflammatory signaling pathways in the myocardium and potential therapeutic implications.
Literatur
1.
Fang J, Mensah GA, Croft JB, et al. Heart failure-related hospitalization in the U.S., 1979 to 2004. J Am Coll Cardiol. 2008;52:428–34.PubMedCrossRef
2.
Schocken DD, Benjamin EJ, Fonarow GC, et al. Prevention of heart failure: a scientific statement from the American Heart Association Councils on Epidemiology and Prevention, Clinical Cardiology, Cardiovascular Nursing, and High Blood Pressure Research; Quality of Care and Outcomes Research Interdisciplinary Working Group; and Functional Genomics and Translational Biology Interdisciplinary Working Group. Circulation. 2008;117:2544–65.PubMedCrossRef
3.
Velagaleti RS, Pencina MJ, Murabito JM, et al. Long-term trends in the incidence of heart failure after myocardial infarction. Circulation. 2008;118:2057–62.PubMedCrossRef
4.
Kalogeropoulos AP, Georgiopoulou VV, Butler J. From risk factors to structural heart disease: the role of inflammation. Heart Fail Clin. 2012;8:113–23.PubMedCrossRef
5.
•• Marchant D, Boyd J, Lin D, et al. Inflammation in myocardial diseases. Circ Res. 2012;110:126–44. This article addresses the specific pathways and mechanisms contributing to cardiac dysfunction in four classic settings marked by inflammation: ischemia-reperfusion injury, sepsis, myocarditis, and transplant rejection. PubMedCrossRef
6.
Hohensinner PJ, Niessner A, Huber K, et al. Inflammation and cardiac outcome. Curr Opin Infect Dis. 2011;24:259–64.PubMedCrossRef
7.
•• Mann DL. The emerging role of innate immunity in the heart and vascular system: for whom the cell tolls. Circ Res. 2011;108:1133–45. This article reviews the biology of innate immune signaling in the heart, suggesting that the innate immune system is involved in the pathogenesis of atherosclerosis, acute coronary syndromes, stroke, viral myocarditis, sepsis, ischemia/reperfusion injury, and heart failure. PubMedCrossRef
8.
Heymans S, Hirsch E, Anker SD, et al. Inflammation as a therapeutic target in heart failure? A scientific statement from the translational research committee of the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail. 2009;11:119–29.PubMedCrossRef
9.
Mohammed SF, Storlie JR, Oehler EA, et al. Variable phenotype in murine transverse aortic constriction. Cardiovasc Pathol. 2012;21:188–98.PubMedCrossRef
10.
• Kolattukudy PE, Niu J. Inflammation, endoplasmic reticulum stress, autophagy, and the monocyte chemoattractant protein-1/CCR2 pathway. Circ Res. 2012;110:174–89. This article reviews the role of ER stress and inflammation, with an emphasis on newly discovered roles for the chemokine monocyte chemoattractant protein-1 (MCP-1) and its downstream effector and novel zinc finger protein, MCP-1-induced protein. PubMedCrossRef
11.
Mitchell JA, Ryffel B, Quesniaux VF, et al. Role of pattern-recognition receptors in cardiovascular health and disease. Biochem Soc Trans. 2007;35:1449–52.PubMedCrossRef
12.
Takeuchi O, Akira S. Pattern recognition receptors and inflammation. Cell. 2010;140:805–20.PubMedCrossRef
13.
14.
Feng Y, Chao W. Toll-like receptors and myocardial inflammation. Int J Inflam. 2011;2011:170352.PubMed
15.
Chao W. Toll-like receptor signaling: a critical modulator of cell survival and ischemic injury in the heart. Am J Physiol Heart Circ Physiol. 2009;296:H1–12.PubMedCrossRef
16.
Antoniak S, Pawlinski R, Mackman N. Protease-activated receptors and myocardial infarction. IUBMB Life. 2011;63:383–9.PubMedCrossRef
17.
Sabri A, Muske G, Zhang H, et al. Signaling properties and functions of two distinct cardiomyocyte protease-activated receptors. Circ Res. 2000;86:1054–61.PubMedCrossRef
18.
Glembotski CC, Irons CE, Krown KA, et al. Myocardial α-thrombin receptor activation induces hypertrophy and increases atrial natriuretic factor gene expression. J Biol Chem. 1993;268:20646–52.PubMed
19.
Strande JL, Hsu A, Su J, et al. SCH 79797, a selective PAR1 antagonist, limits myocardial ischemia/reperfusion injury in rat hearts. Basic Res Cardiol. 2007;4:350–8.CrossRef
20.
Antoniak S, Rojas M, Spring D, et al. Protease-activated receptor 2 deficiency reduces cardiac ischemia/reperfusion injury. Arterioscler Thromb Vasc Biol. 2010;30:2136–42.PubMedCrossRef
21.
Napoli C, De Nigris F, Cicala C, et al. Protease-activated receptor-2 activation improves efficiency of experimental ischemic preconditioning. Am J Physiol Heart Circ Physiol. 2002;282:H2004–10.PubMed
22.
Barnes PJ, Karin M. Nuclear factor-κB: a pivotal transcription factor in chronic inflammatory diseases. N Engl J Med. 1997;336:1066–71.PubMedCrossRef
23.
Chen LW, Egan L, Li ZW, et al. The two faces of IKK and NF-κB inhibition: prevention of systemic inflammation but increased local injury following intestinal ischemia-reperfusion. Nat Med. 2003;9:575–81.PubMedCrossRef
24.
Mustapha S, Kirshner A, De Moissac D, et al. A direct requirement of nuclear factor-κB for suppression of apoptosis in ventricular myocytes. Am J Physiol Heart Circ Physiol. 2000;279:H939–45.PubMed
25.
Baetz D, Regula KM, Ens K, et al. Nuclear factor-κB-mediated cell survival involves transcriptional silencing of the mitochondrial death gene BNIP3 in ventricular myocytes. Circulation. 2005;112:3777–85.PubMedCrossRef
26.
Werner SL, Barken D, Hoffmann A. Stimulus specificity of gene expression programs determined by temporal control of IKK activity. Science. 2005;309:1857–61.PubMedCrossRef
27.
•• Gordon JW, Shaw JA, Kirshenbaum LA. Multiple facets of NF-κB in the heart: to be or not to NF-κB. Circ Res. 2011;108:1122–32. This study provides evidence of the duality of beneficial and deleterious effects of NF-κB in the heart such as potentially harmful inflammation as well as promoting cardiomyocyte survival. PubMedCrossRef
28.
•• Coggins M, Rosenzweig A. The fire within: cardiac inflammatory signaling in health and disease. Circ Res. 2012;110:116–25. This article introduces inflammatory pathways in the heart, as well as their interactions with signaling pathways regulating cell survival and metabolism. PubMedCrossRef
29.
Van der Heiden K, Cuhlmann S, le Luong A, et al. Role of nuclear factor κB in cardiovascular health and disease. Clin Sci (Lond). 2010;118:593–605.CrossRef
30.
Michel MC, Li Y, Heusch G. Mitogen-activated protein kinases in the heart. Naunyn Schmiedebergs Arch Pharmacol. 2001;363:245–66.PubMedCrossRef
31.
Demyanets S, Kaun C, Rychli K, et al. The inflammatory cytokine oncostatin M induces PAI-1 in human vascular smooth muscle cells in vitro via PI 3-kinase and ERK1/2-dependent pathways. Am J Physiol Heart Circ Physiol. 2007;293:H1962–8.PubMedCrossRef
32.
Heidbreder M, Naumann A, Tempel K, et al. Remote vs. ischaemic preconditioning: the differential role of mitogen-activated protein kinase pathways. Circ Res. 2008;78:108–15.
33.
Aoki H, Kang PM, Hampe J, et al. Direct activation of mitochondrial apoptosis machinery by c-Jun N-terminal kinase in adult cardiac myocytes. J Biol Chem. 2002;277:10244–50.PubMedCrossRef
34.
Remondino A, Kwon SH, Communal C, et al. β-adrenergic receptor-stimulated apoptosis in cardiac myocytes is mediated by reactive oxygen species/c-Jun NH2-terminal kinase-dependent activation of the mitochondrial pathway. Circ Res. 2003;92:136–8.PubMedCrossRef
35.
Andreka P, Zang J, Dougherty C, et al. Cytoprotection by Jun kinase during nitric oxide-induced cardiac myocyte apoptosis. Circ Res. 2001;88:305–12.PubMedCrossRef
36.
Dougherty CJ, Kubasiak LA, Prentice H, et al. Activation of c-Jun N-terminal kinase promotes survival of cardiac myocytes after oxidative stress. Biochem J. 2002;362:561–71.PubMedCrossRef
37.
Communal C, Colucci WS, Singh K. p38 mitogen-activated protein kinase pathway protects adult rat ventricular myocytes against β-adrenergic receptor-stimulated apoptosis. Evidence for Gi-dependent activation. J Biol Chem. 2000;275:19395–400.PubMedCrossRef
38.
Schneider S, Chen W, Hou J, et al. Inhibition of p38 MAPK α/β reduces ischemic injury and does not block protective effects of preconditioning. Am J Physiol Heart Circ Physiol. 2001;280:H499–508.PubMed
39.
Mascareno E, Dhar M, Siddiqui MA. Signal transduction and activator of transcription (STAT) protein-dependent activation of angiotensinogen promoter: a cellular signal for hypertrophy in cardiac muscle. Proc Natl Acad Sci U S A. 1998;95:5590–4.PubMedCrossRef
40.
Boengler K, Hilfiker-Kleiner D, Drexler H, et al. The myocardial JAK/STAT pathway: from protection to failure. Pharmacol Ther. 2008;120:172–85.PubMedCrossRef
41.
Fujio Y, Nguyen T, Wencker D, et al. Akt promotes survival of cardiomyocytes in vitro and protects against ischemia-reperfusion injury in mouse heart. Circulation. 2000;101:660–7.PubMedCrossRef
42.
Syed FM, Hahn HS, Odley A, et al. Proapoptotic effects of caspase-1/interleukin-converting enzyme dominate in myocardial ischemia. Circ Res. 2005;96:1103–9.PubMedCrossRef
43.
Tschopp J, Schroder K. NLRP3 inflammasome activation: The convergence of multiple signalling pathways on ROS production? Nat Rev Immunol. 2010;10:210–5.PubMedCrossRef
44.
Kawaguchi M, Takahashi M, Hata T, et al. Inflammasome activation of cardiac fibroblasts is essential for myocardial ischemia/reperfusion injury. Circulation. 2011;123:594–604.PubMedCrossRef
45.
Palmer JN, Hartogensis WE, Patten M, et al. Interleukin-1β induces cardiac myocyte growth but inhibits cardiac fibroblast proliferation in culture. J Clin Invest. 1995;95:2555–64.PubMedCrossRef
46.
Van Tassell BW, Arena RA, Toldo S, et al. Enhanced interleukin-1 activity contributes to exercise intolerance in patients with systolic heart failure. PLoS One. 2012;7:e33438.PubMedCrossRef
47.
Kurdi M, Randon J, Cerutti C, et al. Increased expression of IL-6 and LIF in the hypertrophied left ventricle of TGR(mRen2)27 and SHR rats. Mol Cell Biochem. 2005;269:95–101.PubMedCrossRef
48.
Sano M, Fukuda K, Kodama H, et al. Interleukin-6 family of cytokines mediate angiotensin II-induced cardiac hypertrophy in rodent cardiomyocytes. J Biol Chem. 2000;275:29717–23.PubMedCrossRef
49.
50.
Lacey DL, Timms E, Tan HL, et al. Osteoprotegerin ligand is a cytokine that regulates osteoclast differentiation and activation. Cell. 1998;93:165–76.PubMedCrossRef
51.
Kim YM, Kim YM, Lee YM, et al. TNF-related activation-induced cytokine (TRANCE) induces angiogenesis through the activation of Src and phospholipase C (PLC) in human endothelial cells. J Biol Chem. 2002;277:6799–805.PubMedCrossRef
52.
Min JK, Kim YM, Kim SW, et al. TNF-related activation-induced cytokine enhances leukocyte adhesiveness: induction of ICAM-1 and VCAM-1 via TNF receptor-associated factor and protein kinase C-dependent NF-κB activation in endothelial cells. J Immunol. 2005;175:531–40.PubMed
53.
Min JK, Cho YL, Choi JH, et al. Receptor activator of nuclear factor (NF)-κB ligand (RANKL) increases vascular permeability: impaired permeability and angiogenesis in eNOS-deficient mice. Blood. 2007;109:1495–502.PubMedCrossRef
54.
Ueland T, Yndestad A, Øie E, et al. Dysregulated osteoprotegerin/RANK ligand/RANK axis in clinical and experimental heart failure. Circulation. 2005;111:2461–8.PubMedCrossRef
55.
Ock S, Ahn J, Lee SH, et al. Receptor activator of nuclear factor-κB ligand is a novel inducer of myocardial inflammation. Cardiovasc Res. 2012;94:105–14.PubMedCrossRef
56.
Niu J, Kolattukudy PE. Role of MCP-1 in cardiovascular disease: molecular mechanisms and clinical implications. Clin Sci (Lond). 2009;117:95–109.CrossRef
57.
Hayashidani S, Tsutsui H, Shiomi T, et al. Anti-monocyte chemoattractant protein-1 gene therapy attenuates left ventricular remodeling and failure after experimental myocardial infarction. Circulation. 2003;108:2134–40.PubMedCrossRef
58.
•• Frangogiannis NG. Regulation of the inflammatory response in cardiac repair. Circ Res. 2012;110:159–73. This review introduces recently identified endogenous inhibitors induced as part of the core inflammatory reaction that serve to reduce post-infarct inflammation. PubMedCrossRef
59.
Liehn EA, Postea O, Curaj A, et al. Repair after myocardial infarction, between fantasy and reality: the role of chemokines. J Am Coll Cardiol. 2011;58:2357–62.PubMedCrossRef
60.
Säemann MD, Haidinger M, Hecking M, et al. The multifunctional role of mTOR in innate immunity: implications for transplant immunity. Am J Transplant. 2009;9:2655–61.PubMedCrossRef
61.
Weichhart T, Costantino G, Poglitsch M, et al. The TSC-mTOR signaling pathway regulates the innate inflammatory response. Immunity. 2008;29:565–77.PubMedCrossRef
62.
Song X, Kusakari Y, Xiao CY, et al. mTOR attenuates the inflammatory response in cardiomyocytes and prevents cardiac dysfunction in pathological hypertrophy. Am J Physiol Cell Physiol. 2010;299:C1256–66.PubMedCrossRef
63.
Deten A, Hölzl A, Leicht M, et al. Changes in extracellular matrix and in transforming growth factor beta isoforms after coronary artery ligation in rats. J Mol Cell Cardiol. 2001;33:1191–207.PubMedCrossRef
64.
Kuwahara F, Kai H, Tokuda K, et al. Transforming growth factor-β function blocking prevents myocardial fibrosis and diastolic dysfunction in pressure-overloaded rats. Circulation. 2002;106:130–5.PubMedCrossRef
65.
Sun Y. Myocardial repair/remodelling following infarction: roles of local factors. Cardiovasc Res. 2009;81:482–90.PubMedCrossRef
66.
Rosenkranz S. TGF-β1 and angiotensin networking in cardiac remodeling. Cardiovasc Res. 2004;63:423–32.PubMedCrossRef
67.
Chapman RE, Spinale FG. Extracellular protease activation and unraveling of the myocardial interstitium: critical steps toward clinical applications. Am J Physiol Heart Circ Physiol. 2004;286:H1–10.PubMedCrossRef
68.
Flores-Arredondo JH, García-Rivas G, Torre-Amione G. Immune modulation in heart failure: past challenges and future hopes. Curr Heart Fail Rep. 2011;8:28–37.PubMedCrossRef
69.
• Kempf T, Zarbock A, Vestweber D, et al. Anti-inflammatory mechanisms and therapeutic opportunities in myocardial infarct healing. J Mol Med (Berl). 2012;90:361–9. This article reviews anti-inflammatory and pro-inflammatory pathways during myocardial infarct healing. CrossRef
70.
Madias JE, Hood Jr WB. Effects of methylprednisolone on the ischemic damage in patients with acute myocardial infarction. Circulation. 1982;65:1106–13.PubMedCrossRef
71.
Mann DL, McMurray JJ, Packer M, et al. Targeted anticytokine therapy in patients with chronic heart failure: results of the Randomized Etanercept Worldwide Evaluation (RENEWAL). Circulation. 2004;109:1594–602.PubMedCrossRef
72.
Mann DL, Bozkurt B, Torreamione G, et al. Effect of the soluble TNF-antagonist etanercept on tumor necrosis factor bioactivity and stability. Clin Transl Sci. 2008;1:142–5.PubMedCrossRef
73.
Chung ES, Packer M, Lo KH, et al. Randomized, double-blind, placebo-controlled, pilot trial of infliximab, a chimeric monoclonal antibody to tumor necrosis factor-α, in patients with moderate-to-severe heart failure: results of the anti-TNF Therapy Against Congestive Heart Failure (ATTACH) trial. Circulation. 2003;107:3133–40.PubMedCrossRef
74.
Kotyla PJ, Owczarek A, Rakoczy J, et al. Infliximab treatment increases left ventricular ejection fraction in patients with rheumatoid arthritis: assessment of heart function by echocardiography, endothelin 1, interleukin 6, and NT-pro brain natriuretic peptide. J Rheumatol. 2012;39:701–6.PubMedCrossRef
75.
Shaw SM, Shah MK, Williams SG, et al. Immunological mechanisms of pentoxifylline in chronic heart failure. Eur J Heart Fail. 2009;11:113–8.PubMedCrossRef
76.
Bahrmann P, Hengst UM, Richartz BM, et al. Pentoxifylline in ischemic, hypertensive and idiopathic-dilated cardiomyopathy: effects on left-ventricular function, inflammatory cytokines and symptoms. Eur J Heart Fail. 2004;6:195–201.PubMedCrossRef
77.
Nussinovitch U, Shoenfeld Y. Intravenous immunoglobulin—indications and mechanisms in cardiovascular diseases. Autoimmun Rev. 2008;7:445–52.PubMedCrossRef
78.
Suri V, Varma S, Joshi K, et al. Lupus myocarditis: marked improvement in cardiac function after intravenous immunoglobulin therapy. Rheumatol Int. 2010;30:1503–5.PubMedCrossRef
79.
McNamara DM, Holubkov R, Starling RC, et al. Controlled trial of intravenous immune globulin in recent-onset dilated cardiomyopathy. Circulation. 2001;103:2254–9.PubMedCrossRef
80.
Földes G, von Haehling S, Okonko DO, et al. Fluvastatin reduces increased blood monocyte Toll-like receptor 4 expression in whole blood from patients with chronic heart failure. Int J Cardiol. 2008;124:80–5.PubMedCrossRef
81.
Yang J, Zhang XD, Yang J, et al. The cardioprotective effect of fluvastatin on ischemic injury via down-regulation of toll-like receptor 4. Mol Biol Rep. 2011;38:3037–44.PubMedCrossRef
82.
Okopien B, Kowalski J, Krysiak R, et al. Monocyte suppressing action of fenofibrate. Pharmacol Rep. 2005;57:367–72.PubMed
83.
Huang WP, Yin WH, Chen JW, et al. Fenofibrate attenuates endothelial monocyte adhesion in chronic heart failure: an in vitro study. Eur J Clin Invest. 2009;39:775–83.PubMedCrossRef
84.
Liu H, Li W, Gu W, et al. Immunoregulatory effects of carvedilol on rat experimental autoimmune myocarditis. Scand J Immunol. 2010;71:38–44.PubMedCrossRef
85.
Satoh M, Ishikawa Y, Minami Y, et al. Eplerenone inhibits tumour necrosis factor α shedding process by tumour necrosis factor α converting enzyme in monocytes from patients with congestive heart failure. Heart. 2006;92:979–80.PubMedCrossRef
86.
Frangogiannis NG, Dewald O, Xia Y, et al. Critical role of monocyte chemoattractant protein-1/CC chemokine ligand 2 in the pathogenesis of ischemic cardiomyopathy. Circulation. 2007;115:584–92.PubMedCrossRef
87.
Gilbert J, Lekstrom-Himes J, Donaldson D, et al. Effect of CC chemokine receptor 2 CCR2 blockade on serum C-reactive protein in individuals at atherosclerotic risk and with a single nucleotide polymorphism of the monocyte chemoattractant protein-1 promoter region. Am J Cardiol. 2011;107:906–11.PubMedCrossRef
88.
Arefieva TI, Krasnikova TL, Potekhina AV, et al. Synthetic peptide fragment (65–76) of monocyte chemotactic protein-1 (MCP-1) inhibits MCP-1 binding to heparin and possesses anti-inflammatory activity in stable angina patients after coronary stenting. Inflamm Res. 2011;60:955–64.PubMedCrossRef
89.
Aukrust P, Gullestad L, Ueland T, et al. Inflammatory and anti-inflammatory cytokines in chronic heart failure: potential therapeutic implications. Ann Med. 2005;37:74–85.PubMedCrossRef
Metadaten
Titel
Mechanisms and Consequences of Inflammatory Signaling in the Myocardium
verfasst von
Jihyun Ahn
Jaetaek Kim
Publikationsdatum
01.12.2012
Verlag
Current Science Inc.
Erschienen in
Current Hypertension Reports / Ausgabe 6/2012
Print ISSN: 1522-6417
Elektronische ISSN: 1534-3111
DOI
https://doi.org/10.1007/s11906-012-0309-0

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