Skip to main content
Erschienen in: Current Heart Failure Reports 1/2010

01.03.2010

Galectin-3 in Cardiac Remodeling and Heart Failure

verfasst von: Rudolf A. de Boer, Lili Yu, Dirk J. van Veldhuisen

Erschienen in: Current Heart Failure Reports | Ausgabe 1/2010

Einloggen, um Zugang zu erhalten

Abstract

Galectin-3 is a member of the galectin family, which consists of animal lectins that bind β-galactosides. Recently, a role for galectin-3 in the pathophysiology of heart failure has been suggested. It was observed that galectin-3 is specifically upregulated in decompensated heart failure compared with compensated heart failure in animal models of heart failure. This has been associated with activation of fibroblasts and macrophages, which are a hallmark of cardiac remodeling. Therefore, galectin-3 may be a culprit biomarker in heart failure. Initial clinical observations indicate that galectin-3 may be a useful biomarker for decompensated heart failure, with incremental value over well-used “pressure-dependent” biomarkers, such as B-type natriuretic peptide. Future studies should focus on galectin-3 biology to better address the usefulness of galectin-3 as a biomarker and probe the usefulness of anti-galectin-3 therapy in treating heart failure.
Literatur
1.
Zurück zum Zitat Barondes SH, Cooper DNW, Gitt MA, Leffler H: Galectins: structure and function of a large family of animal lectins. J Biol Chem 1994, 269:20807–20810.PubMed Barondes SH, Cooper DNW, Gitt MA, Leffler H: Galectins: structure and function of a large family of animal lectins. J Biol Chem 1994, 269:20807–20810.PubMed
2.
Zurück zum Zitat Cooper DN: Galectinomics: finding themes in complexity. Biochim Biophys Acta 2002, 1572:209–231.PubMedCrossRef Cooper DN: Galectinomics: finding themes in complexity. Biochim Biophys Acta 2002, 1572:209–231.PubMedCrossRef
3.
Zurück zum Zitat Wang JL, Laing JG, Anderson RL: Lectins in the cell nucleus. Glycobiology 1991, 3:243–252.CrossRef Wang JL, Laing JG, Anderson RL: Lectins in the cell nucleus. Glycobiology 1991, 3:243–252.CrossRef
4.
Zurück zum Zitat •• Yang RY, Rabinovich GA, Liu FT: Galectins: structure, function and therapeutic potential. Expert Rev Mol Med 2008, 13:e17–e39. This excellent review article provides insight regarding galectin biology.CrossRef •• Yang RY, Rabinovich GA, Liu FT: Galectins: structure, function and therapeutic potential. Expert Rev Mol Med 2008, 13:e17–e39. This excellent review article provides insight regarding galectin biology.CrossRef
5.
Zurück zum Zitat Elola MT, Wolfenstein-Todel C, Troncoso MF, et al.: Galectins: matricellular glycan-binding proteins linking cell adhesion, migration, and survival. Cell Mol Life Sci 2007, 64:1679–1700.PubMedCrossRef Elola MT, Wolfenstein-Todel C, Troncoso MF, et al.: Galectins: matricellular glycan-binding proteins linking cell adhesion, migration, and survival. Cell Mol Life Sci 2007, 64:1679–1700.PubMedCrossRef
6.
Zurück zum Zitat Liu FT, Patterson RJ, Wang JL: Intracellular functions of galectins. Biochim Biophys Acta 2002, 1572:263–273.PubMedCrossRef Liu FT, Patterson RJ, Wang JL: Intracellular functions of galectins. Biochim Biophys Acta 2002, 1572:263–273.PubMedCrossRef
7.
Zurück zum Zitat Wang JL, Laing JG, Anderson RL: Lectins in the cell nucleus. Glycobiology 1991, 3:243–252.CrossRef Wang JL, Laing JG, Anderson RL: Lectins in the cell nucleus. Glycobiology 1991, 3:243–252.CrossRef
8.
Zurück zum Zitat Hughes RC: Mac-2: a versatile galactose-binding protein of mammalian tissues. Glycobiology 1994, 4:5–12.PubMedCrossRef Hughes RC: Mac-2: a versatile galactose-binding protein of mammalian tissues. Glycobiology 1994, 4:5–12.PubMedCrossRef
9.
Zurück zum Zitat Birdsall B, Feeney J, Burdett IDJ, et al.: NMR solution studies of hamster galectin-3 and electron microscopic visualization of surface-adsorbed complexes: evidence for interactions between the N-and C-terminal domains. Biochemistry 2001, 40:4859–4866.PubMedCrossRef Birdsall B, Feeney J, Burdett IDJ, et al.: NMR solution studies of hamster galectin-3 and electron microscopic visualization of surface-adsorbed complexes: evidence for interactions between the N-and C-terminal domains. Biochemistry 2001, 40:4859–4866.PubMedCrossRef
10.
Zurück zum Zitat Krześlak A, Lipińska A: Galectin-3 as a multifunctional protein. Cell Mol Biol Lett 2004, 9:305–328.PubMed Krześlak A, Lipińska A: Galectin-3 as a multifunctional protein. Cell Mol Biol Lett 2004, 9:305–328.PubMed
11.
Zurück zum Zitat Rosenberg I, Cherayil BJ, Isselbacher KJ, Pillai S: Mac-2-binding glycoproteins. Putative ligands for a cytosolic β-galactoside lectin. J Biol Chem 1991, 266:18731–18736. Rosenberg I, Cherayil BJ, Isselbacher KJ, Pillai S: Mac-2-binding glycoproteins. Putative ligands for a cytosolic β-galactoside lectin. J Biol Chem 1991, 266:18731–18736.
12.
Zurück zum Zitat Sato S, Hughes RC: Binding specificity of a baby hamster kidney lectin for H type I and II chains, polylactosamine glycans, and appropriately glycosylated forms of laminin and fibronectin. J Biol Chem 1992, 267:6983–6990.PubMed Sato S, Hughes RC: Binding specificity of a baby hamster kidney lectin for H type I and II chains, polylactosamine glycans, and appropriately glycosylated forms of laminin and fibronectin. J Biol Chem 1992, 267:6983–6990.PubMed
13.
Zurück zum Zitat Ochieng J, Furtak V, Lukyanov P: Extracellular functions of galectin-3. Glycoconj J 2004, 19:527–535.PubMedCrossRef Ochieng J, Furtak V, Lukyanov P: Extracellular functions of galectin-3. Glycoconj J 2004, 19:527–535.PubMedCrossRef
14.
Zurück zum Zitat Nakahara S, Oka N, Wang Y, et al.: Characterization of the nuclear import pathways of galectin-3. Cancer Res 2006, 66:9995–10006.PubMedCrossRef Nakahara S, Oka N, Wang Y, et al.: Characterization of the nuclear import pathways of galectin-3. Cancer Res 2006, 66:9995–10006.PubMedCrossRef
15.
Zurück zum Zitat Menon RP, Hughes RC: Determinants in the N-terminal domains of galectin-3 for secretion by a novel pathway circumventing the endoplasmic reticulum-Golgi complex. Eur J Biochem 1999, 264:569–576.PubMedCrossRef Menon RP, Hughes RC: Determinants in the N-terminal domains of galectin-3 for secretion by a novel pathway circumventing the endoplasmic reticulum-Golgi complex. Eur J Biochem 1999, 264:569–576.PubMedCrossRef
16.
Zurück zum Zitat Mehul B, Hughes RC: Plasma membrane targeting, vesicular budding and release of galectin 3 from the cytoplasm of mammalian cells during secretion. J Cell Sci 1997, 110:1169–1178.PubMed Mehul B, Hughes RC: Plasma membrane targeting, vesicular budding and release of galectin 3 from the cytoplasm of mammalian cells during secretion. J Cell Sci 1997, 110:1169–1178.PubMed
17.
Zurück zum Zitat Hughes RC: The galectin family of mammalian carbohydrate-binding molecules. Biochem Soc Transact 1997, 25:1194–1198. Hughes RC: The galectin family of mammalian carbohydrate-binding molecules. Biochem Soc Transact 1997, 25:1194–1198.
18.
Zurück zum Zitat Hughes RC: Secretion of the galectin family of mammalian carbohydrate-binding family proteins. Biochem Biophys Acta 1999, 1473:172–185.PubMedCrossRef Hughes RC: Secretion of the galectin family of mammalian carbohydrate-binding family proteins. Biochem Biophys Acta 1999, 1473:172–185.PubMedCrossRef
19.
Zurück zum Zitat Kim H, Lee J, Hyun JW, et al.: Expression and immunohistochemical localization of galectin-3 in various mouse tissues. Cell Biol Int 2007, 31:655–662.PubMedCrossRef Kim H, Lee J, Hyun JW, et al.: Expression and immunohistochemical localization of galectin-3 in various mouse tissues. Cell Biol Int 2007, 31:655–662.PubMedCrossRef
20.
Zurück zum Zitat Sharma UC, Pokharel S, van Brakel TJ, et al.: Galectin-3 marks activated macrophages in failure-prone hypertrophied hearts and contributes to cardiac dysfunction. Circulation 2004, 110:3121–3128.PubMedCrossRef Sharma UC, Pokharel S, van Brakel TJ, et al.: Galectin-3 marks activated macrophages in failure-prone hypertrophied hearts and contributes to cardiac dysfunction. Circulation 2004, 110:3121–3128.PubMedCrossRef
21.
Zurück zum Zitat Lee MA, Böhm M, Paul M, et al.: Physiological characterization of the hypertensive transgenic rat TGR(mREN2)27. Am J Physiol 1996, 270:E919–E929.PubMed Lee MA, Böhm M, Paul M, et al.: Physiological characterization of the hypertensive transgenic rat TGR(mREN2)27. Am J Physiol 1996, 270:E919–E929.PubMed
22.
Zurück zum Zitat de Boer RA, Pokharel S, Flesch M, et al.: Extracellular signal regulated kinase and SMAD signaling both mediate the angiotensin II driven progression towards overt heart failure in homozygous TGR(mRen2)27. J Mol Med 2004, 82:678–687.PubMedCrossRef de Boer RA, Pokharel S, Flesch M, et al.: Extracellular signal regulated kinase and SMAD signaling both mediate the angiotensin II driven progression towards overt heart failure in homozygous TGR(mRen2)27. J Mol Med 2004, 82:678–687.PubMedCrossRef
23.
Zurück zum Zitat Schroen B, Heymans S, Sharma U, et al.: Thrombospondin-2 is essential for myocardial matrix integrity: increased expression identifies failure-prone cardiac hypertrophy. Circ Res 2004, 95:515–522.PubMedCrossRef Schroen B, Heymans S, Sharma U, et al.: Thrombospondin-2 is essential for myocardial matrix integrity: increased expression identifies failure-prone cardiac hypertrophy. Circ Res 2004, 95:515–522.PubMedCrossRef
24.
Zurück zum Zitat Thandavarayan RA, Watanabe K, Ma M, et al.: 14-3-3 protein regulates Ask1 signaling and protects against diabetic cardiomyopathy. Biochem Pharmacol 2008, 75:1797–1806.PubMedCrossRef Thandavarayan RA, Watanabe K, Ma M, et al.: 14-3-3 protein regulates Ask1 signaling and protects against diabetic cardiomyopathy. Biochem Pharmacol 2008, 75:1797–1806.PubMedCrossRef
25.
Zurück zum Zitat Sharma U, Rhaleb NE, Pokharel S, et al.: Novel anti-inflammatory mechanisms of N-Acetyl-Ser-Asp-Lys-Pro in hypertension-induced target organ damage. Am J Physiol 2008, 294:H1226–H1232. Sharma U, Rhaleb NE, Pokharel S, et al.: Novel anti-inflammatory mechanisms of N-Acetyl-Ser-Asp-Lys-Pro in hypertension-induced target organ damage. Am J Physiol 2008, 294:H1226–H1232.
26.
Zurück zum Zitat • Liu YH, D’Ambrosio M, Liao TD, et al.: N-acetyl-seryl-aspartyl-lysyl-proline prevents cardiac remodeling and dysfunction induced by galectin-3, a mammalian adhesion/growth-regulatory lectin. Am J Physiol Heart Circ Physiol 2009, 296:H404–H412. This article evaluates anti-galectin-3 therapy and demonstrates how it may reverse adverse cardiac remodeling, providing support for the hypothesis that anti-galectin therapy may be feasible.PubMedCrossRef • Liu YH, D’Ambrosio M, Liao TD, et al.: N-acetyl-seryl-aspartyl-lysyl-proline prevents cardiac remodeling and dysfunction induced by galectin-3, a mammalian adhesion/growth-regulatory lectin. Am J Physiol Heart Circ Physiol 2009, 296:H404–H412. This article evaluates anti-galectin-3 therapy and demonstrates how it may reverse adverse cardiac remodeling, providing support for the hypothesis that anti-galectin therapy may be feasible.PubMedCrossRef
27.
Zurück zum Zitat Friedman SL: Molecular regulation of hepatic fibrosis, an integrated cellular response to tissue injury. J Biol Chem 2000, 275:2247–2250.PubMedCrossRef Friedman SL: Molecular regulation of hepatic fibrosis, an integrated cellular response to tissue injury. J Biol Chem 2000, 275:2247–2250.PubMedCrossRef
28.
Zurück zum Zitat Brown RD, Ambler SK, Mitchell MD, Long CS: The cardiac fibroblast: therapeutic target in myocardial remodeling and failure. Annu Rev Pharmacol Toxicol 2005, 45:657–687.PubMedCrossRef Brown RD, Ambler SK, Mitchell MD, Long CS: The cardiac fibroblast: therapeutic target in myocardial remodeling and failure. Annu Rev Pharmacol Toxicol 2005, 45:657–687.PubMedCrossRef
29.
Zurück zum Zitat de Cavanagh EM, Ferder M, Inserra F, Ferder L: Angiotensin II, mitochondria, cytoskeletal, and extracellular matrix connections: an integrating viewpoint. Am J Physiol Heart Circ Physiol 2009, 296:H550–H558.PubMedCrossRef de Cavanagh EM, Ferder M, Inserra F, Ferder L: Angiotensin II, mitochondria, cytoskeletal, and extracellular matrix connections: an integrating viewpoint. Am J Physiol Heart Circ Physiol 2009, 296:H550–H558.PubMedCrossRef
30.
Zurück zum Zitat Hsu DK, Dowling CA, Jeng KC, et al.: Galectin-3 expression is induced in cirrhotic liver and hepatocellular carcinoma. Int J Cancer 1999, 81:519–526.PubMedCrossRef Hsu DK, Dowling CA, Jeng KC, et al.: Galectin-3 expression is induced in cirrhotic liver and hepatocellular carcinoma. Int J Cancer 1999, 81:519–526.PubMedCrossRef
31.
Zurück zum Zitat Henderson NC, Mackinnon AC, Farnworth SL, et al.: Galectin-3 regulates myofibroblast activation and hepatic fibrosis. Proc Natl Acad Sci USA 2006, 103:5060–5065.PubMedCrossRef Henderson NC, Mackinnon AC, Farnworth SL, et al.: Galectin-3 regulates myofibroblast activation and hepatic fibrosis. Proc Natl Acad Sci USA 2006, 103:5060–5065.PubMedCrossRef
32.
Zurück zum Zitat Nishi Y, Sano H, Kawashima T, et al.: Role of galectin-3 in human pulmonary fibrosis. Allergol Int 2007, 56:57–65.PubMedCrossRef Nishi Y, Sano H, Kawashima T, et al.: Role of galectin-3 in human pulmonary fibrosis. Allergol Int 2007, 56:57–65.PubMedCrossRef
33.
Zurück zum Zitat Wang L, Friess H, Zhu Z, et al.: Galectin-1 and galectin-3 in chronic pancreatitis. Lab Invest 2000, 80:1223–1241.CrossRef Wang L, Friess H, Zhu Z, et al.: Galectin-1 and galectin-3 in chronic pancreatitis. Lab Invest 2000, 80:1223–1241.CrossRef
34.
Zurück zum Zitat Sasaki S, Bao Q, Hughes RC: Galectin-3 modulates rat mesangial cell proliferation and matrix synthesis during experimental glomerulonephritis induced by anti-Thy1.1 antibodies. J Pathol 1999, 187:481–489.PubMedCrossRef Sasaki S, Bao Q, Hughes RC: Galectin-3 modulates rat mesangial cell proliferation and matrix synthesis during experimental glomerulonephritis induced by anti-Thy1.1 antibodies. J Pathol 1999, 187:481–489.PubMedCrossRef
35.
Zurück zum Zitat • Henderson NC, Mackinnon AC, Farnworth SL, et al.: Galectin-3 expression and secretion links macrophages to the promotion of renal fibrosis. Am J Pathol 2008, 172:288–298. This experimental study underscores the pivotal role of galectin-3 in the fibrosis process. Employing galectin-3 deficient mice, the authors show that galectin-3 regulates renal fibrosis.PubMedCrossRef • Henderson NC, Mackinnon AC, Farnworth SL, et al.: Galectin-3 expression and secretion links macrophages to the promotion of renal fibrosis. Am J Pathol 2008, 172:288–298. This experimental study underscores the pivotal role of galectin-3 in the fibrosis process. Employing galectin-3 deficient mice, the authors show that galectin-3 regulates renal fibrosis.PubMedCrossRef
36.
Zurück zum Zitat Eis V, Luckow B, Vielhauer V, et al.: Chemokine receptor CCR1 but not CCR5 mediates leukocyte recruitment and subsequent renal fibrosis after unilateral ureteral obstruction. J Am Soc Nephrol 2004, 15:337–347.PubMedCrossRef Eis V, Luckow B, Vielhauer V, et al.: Chemokine receptor CCR1 but not CCR5 mediates leukocyte recruitment and subsequent renal fibrosis after unilateral ureteral obstruction. J Am Soc Nephrol 2004, 15:337–347.PubMedCrossRef
37.
Zurück zum Zitat Vlassara H, Li YM, Imani F, et al.: Identification of galectin-3 as a high-affinity binding protein for advanced glycation end products (AGE): a new member of the AGE-receptor complex. Mol Med 1995, 1:634–646.PubMed Vlassara H, Li YM, Imani F, et al.: Identification of galectin-3 as a high-affinity binding protein for advanced glycation end products (AGE): a new member of the AGE-receptor complex. Mol Med 1995, 1:634–646.PubMed
38.
Zurück zum Zitat Hartog JW, Voors AA, Bakker SJ, et al.: Advanced glycation end-products (AGEs) and heart failure: pathophysiology and clinical implications. Eur J Heart Fail 2007, 9:1146–1155.PubMedCrossRef Hartog JW, Voors AA, Bakker SJ, et al.: Advanced glycation end-products (AGEs) and heart failure: pathophysiology and clinical implications. Eur J Heart Fail 2007, 9:1146–1155.PubMedCrossRef
39.
Zurück zum Zitat Iacobini C, Oddi G, Menini S, et al.: Development of age-dependent glomerular lesions in galectin-3/AGE-receptor-3 knockout mice. Am J Physiol 2005, 289:F611–F621.CrossRef Iacobini C, Oddi G, Menini S, et al.: Development of age-dependent glomerular lesions in galectin-3/AGE-receptor-3 knockout mice. Am J Physiol 2005, 289:F611–F621.CrossRef
40.
Zurück zum Zitat Iacobini C, Menini S, Oddi G, et al.: Galectin-3/AGE-receptor 3 knockout mice show accelerated AGE-induced glomerular injury: evidence for a protective role of galectin-3 as an AGE receptor. FASEB J 2004, 18:1773–1775.PubMed Iacobini C, Menini S, Oddi G, et al.: Galectin-3/AGE-receptor 3 knockout mice show accelerated AGE-induced glomerular injury: evidence for a protective role of galectin-3 as an AGE receptor. FASEB J 2004, 18:1773–1775.PubMed
41.
42.
Zurück zum Zitat Reifenberg K, Lehr HA, Torzewski M, et al.: Interferon-gamma induces chronic active myocarditis and cardiomyopathy in transgenic mice. Am J Pathol 2007, 171:463–472.PubMedCrossRef Reifenberg K, Lehr HA, Torzewski M, et al.: Interferon-gamma induces chronic active myocarditis and cardiomyopathy in transgenic mice. Am J Pathol 2007, 171:463–472.PubMedCrossRef
43.
Zurück zum Zitat van Kimmenade RR, Januzzi JL Jr, Ellinor PT, et al.: Utility of aminoterminal pro-brain natriuretic peptide, galectin-3, and apelin for the evaluation of patients with acute heart failure. J Am Coll Cardiol 2006, 48:1217–1224.PubMedCrossRef van Kimmenade RR, Januzzi JL Jr, Ellinor PT, et al.: Utility of aminoterminal pro-brain natriuretic peptide, galectin-3, and apelin for the evaluation of patients with acute heart failure. J Am Coll Cardiol 2006, 48:1217–1224.PubMedCrossRef
44.
Zurück zum Zitat Milting H, Ellinghaus P, Seewald M, et al.: Plasma biomarkers of myocardial fibrosis and remodeling in terminal heart failure patients supported by mechanical circulatory support devices. J Heart Lung Transplant 2008, 27:589–596.PubMedCrossRef Milting H, Ellinghaus P, Seewald M, et al.: Plasma biomarkers of myocardial fibrosis and remodeling in terminal heart failure patients supported by mechanical circulatory support devices. J Heart Lung Transplant 2008, 27:589–596.PubMedCrossRef
45.
Zurück zum Zitat Lin YH, Lin LY, Wu YW, et al.: The relationship between serum galectin-3 and serum markers of cardiac extracellular matrix turnover in heart failure patients. Clin Chim Acta 2009, 409:96–99.PubMedCrossRef Lin YH, Lin LY, Wu YW, et al.: The relationship between serum galectin-3 and serum markers of cardiac extracellular matrix turnover in heart failure patients. Clin Chim Acta 2009, 409:96–99.PubMedCrossRef
46.
Zurück zum Zitat • de Boer RA, Voors AA, Muntendam P, et al.: Galectin-3: a novel mediator of heart failure development and progression. Eur J Heart Fail 2009, 11:811–817. This article provides a complete overview of the potential role of galectin-3 in the pathophysiology of heart failure.PubMedCrossRef • de Boer RA, Voors AA, Muntendam P, et al.: Galectin-3: a novel mediator of heart failure development and progression. Eur J Heart Fail 2009, 11:811–817. This article provides a complete overview of the potential role of galectin-3 in the pathophysiology of heart failure.PubMedCrossRef
47.
Zurück zum Zitat Dickstein K, Cohen-Solal A, Filippatos G, et al.: ESC guidelines for the diagnosis treatment of acute, chronic heart failure 2008. The task force for the diagnosis and treatment of acute and chronic heart failure 2008 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM). Eur J Heart Fail 2008, 10:933–989.PubMedCrossRef Dickstein K, Cohen-Solal A, Filippatos G, et al.: ESC guidelines for the diagnosis treatment of acute, chronic heart failure 2008. The task force for the diagnosis and treatment of acute and chronic heart failure 2008 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM). Eur J Heart Fail 2008, 10:933–989.PubMedCrossRef
Metadaten
Titel
Galectin-3 in Cardiac Remodeling and Heart Failure
verfasst von
Rudolf A. de Boer
Lili Yu
Dirk J. van Veldhuisen
Publikationsdatum
01.03.2010
Verlag
Springer-Verlag
Erschienen in
Current Heart Failure Reports / Ausgabe 1/2010
Print ISSN: 1546-9530
Elektronische ISSN: 1546-9549
DOI
https://doi.org/10.1007/s11897-010-0004-x

Weitere Artikel der Ausgabe 1/2010

Current Heart Failure Reports 1/2010 Zur Ausgabe

Ein Drittel der jungen Ärztinnen und Ärzte erwägt abzuwandern

07.05.2024 Medizinstudium Nachrichten

Extreme Arbeitsverdichtung und kaum Supervision: Dr. Andrea Martini, Sprecherin des Bündnisses Junge Ärztinnen und Ärzte (BJÄ) über den Frust des ärztlichen Nachwuchses und die Vorteile des Rucksack-Modells.

Vorhofflimmern bei Jüngeren gefährlicher als gedacht

06.05.2024 Vorhofflimmern Nachrichten

Immer mehr jüngere Menschen leiden unter Vorhofflimmern. Betroffene unter 65 Jahren haben viele Risikofaktoren und ein signifikant erhöhtes Sterberisiko verglichen mit Gleichaltrigen ohne die Erkrankung.

Chronisches Koronarsyndrom: Gefahr von Hospitalisierung wegen Herzinsuffizienz

06.05.2024 Herzinsuffizienz Nachrichten

Obwohl ein rezidivierender Herzinfarkt bei chronischem Koronarsyndrom wahrscheinlich die Hauptsorge sowohl der Patienten als auch der Ärzte ist, sind andere Ereignisse womöglich gefährlicher. Laut einer französischen Studie stellt eine Hospitalisation wegen Herzinsuffizienz eine größere Gefahr dar.

Das Risiko für Vorhofflimmern in der Bevölkerung steigt

02.05.2024 Vorhofflimmern Nachrichten

Das Risiko, im Lauf des Lebens an Vorhofflimmern zu erkranken, ist in den vergangenen 20 Jahren gestiegen: Laut dänischen Zahlen wird es drei von zehn Personen treffen. Das hat Folgen weit über die Schlaganfallgefährdung hinaus.

Update Kardiologie

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