nach oben

Die Innere Medizin

Erschienen in:

01.04.2009 | Schwerpunkt: Hypertonie

Hypertensive Folgeschäden am Herzen

verfasst von: M. Steinmetz, G. Nickenig

Erschienen in: Die Innere Medizin | Ausgabe 4/2009

Einloggen, um Zugang zu erhalten

Zusammenfassung

Die arterielle Hypertonie führt zu Umstrukturierung und Schädigung des Herzens. Diese „Hypertensive Herzkrankheit“ umfasst die linksventrikuläre Hypertrophie. Ihr werden zudem diastolische und systolische Dysfunktion, die vaskulären Manifestationen der Mikroangiopathie und im weiteren Sinn auch koronare Herzkrankheit, sowie Herzrhythmusstörungen und plötzlicher Herztod zugeschrieben. Die pathophysiologischen Mechanismen beruhen auf einer komplexen neurohumoralen Regulation und der daraus entstehenden Änderung der Struktur und Leistung des Herzens. Der initialen Kompensation des vermehrten kardialen Leistungsbedarfs folgt die dauerhafte Schädigung des Herzens und sukzessive Dekompensation. Erst hier werden typische Beschwerden von Herzinsuffizienz oder -ischämie evident. Eine Diagnosestellung ist besonders zu Beginn wichtig, da sich die Prognose hinsichtlich Morbidität und Mortalität mit Fortbestehen des Hypertonus und Entwicklung einer dauerhaften Schädigung des Herzens verschlechtert.

Abassi Z, Karram T, Ellaham S et al. (2004) Implications of the natriuretic peptide system in the pathogenesis of heart failure: diagnostic and therapeutic importance. Pharmacol Ther 102: 223–241PubMedCrossRef

Abraham WT, Hensen J, Schrier RW (1990) Elevated plasma noradrenaline concentrations in patients with low-output cardiac failure: dependence on increased noradrenaline secretion rates. Clin Sci (Lond) 79: 429–435

Akiyama-Uchida Y, Ashizawa N, Ohtsuru A et al. (2002) Norepinephrine enhances fibrosis mediated by TGF-beta in cardiac fibroblasts. Hypertension 40: 148–154PubMedCrossRef

Aurigemma GP, Gaasch WH (2004) Clinical practice. Diastolic heart failure. N Engl J Med 351: 1097–1105PubMedCrossRef

Baker CS, Dutka DP, Pagano D et al. (2002) Immunocytochemical evidence for inducible nitric oxide synthase and cyclooxygenase-2 expression with nitrotyrosine formation in human hibernating myocardium. Basic Res Cardiol 97: 409–415PubMedCrossRef

Barton M, Yanagisawa M (2008) Endothelin: 20 years from discovery to therapy. Can J Physiol Pharmacol 86: 485–498PubMedCrossRef

Bers Dm, Despa S, Bossuyt J (2006) Regulation of Ca2+ and Na+ in normal and failing cardiac myocytes. Ann N Y Acad Sci 1080: 165–177PubMedCrossRef

Bikkina M, Larson MG, Levy D (1993) Asymptomatic ventricular arrhythmias and mortality risk in subjects with left ventricular hypertrophy. J Am Coll Cardiol 22: 1111–1116PubMed

Boldt A, Wetzel U, Weigl J et al. (2003) Expression of angiotensin II receptors in human left and right atrial tissue in atrial fibrillation with and without underlying mitral valve disease. J Am Coll Cardiol 42: 1785–1792PubMedCrossRef

10.

Brilla CG, Weber KT (1992) Mineralocorticoid excess, dietary sodium, and myocardial fibrosis. J Lab Clin Med 120: 893–901PubMed

11.

Bristow MR (1998) Why does the myocardium fail? Insights from basic science. Lancet 352 (Suppl 1): SI8–S14PubMedCrossRef

12.

Bristow MR, Ginsburg R, Minobe W et al. (1982) Decreased catecholamine sensitivity and beta-adrenergic-receptor density in failing human hearts. N Engl J Med 307: 205–211PubMed

13.

Brunner-La Rocca HP, Kaye DM, Woods RL et al. (2001) Effects of intravenous brain natriuretic peptide on regional sympathetic activity in patients with chronic heart failure as compared with healthy control subjects. J Am Coll Cardiol 37: 1221–1227CrossRef

14.

Brush JE, Cannon RO, Schenke WH et al. (1988) Angina due to coronary microvascular disease in hypertensive patients without left ventricular hypertrophy. N Engl J Med 319: 1302–1307PubMed

15.

Casale PN, Devereux RB, Milner M et al. (1986) Value of echocardiographic measurement of left ventricular mass in predicting cardiovascular morbid events in hypertensive men. Ann Intern Med 105: 173–178PubMed

16.

Casiglia E, Schiavon L, Tikhonoff V et al. (2008) Electrocardiographic criteria of left ventricular hypertrophy in general population. Eur J Epidemiol 23: 261–271PubMedCrossRef

17.

Cecil MP, Pilcher WC, Eisner RL et al. (1994) Absence of defects in SPECT thallium-201 myocardial images in patients with systemic hypertension and left ventricular hypertrophy. Am J Cardiol 74: 43–46PubMedCrossRef

18.

Choi DJ, Koch WI, Hunter JI et al. (1997) Mechanism of beta-adrenergic receptor desensitization in cardiac hypertrophy is increased beta-adrenergic receptor kinase. J Biol Chem 272: 17223–17229PubMedCrossRef

19.

Collins R, Armitage J, Parish S et al. (2003) MRC/BHF Heart Protection Study of cholesterol-lowering with simvastatin in 5963 people with diabetes: a randomised placebo-controlled trial. Lancet 361: 2005–2016PubMedCrossRef

20.

Colucci WS, Packer M, Bristow MR et al. (1996) Carvedilol inhibits clinical progression in patients with mild symptoms of heart failure. US Carvedilol Heart Failure Study Group. Circulation 94: 2800–2806PubMed

21.

Davis D, Baily R, Zelis R (1988) Abnormalities in systemic norepinephrine kinetics in human congestive heart failure. Am J Physiol 254: E760–E766PubMed

22.

Devereux RB, Lutas EM, Casale PN et al. (1984) Standardization of M-mode echocardiographic left ventricular anatomic measurements. J Am Coll Cardiol 4: 1222–1230PubMed

23.

Devereux RB, Reichek N (1977) Echocardiographic determination of left ventricular mass in man. Anatomic validation of the method. Circulation 55: 613–618PubMed

24.

Drazner MH, Rame JE, Marino EK et al. (2004) Increased left ventricular mass is a risk factor for the development of a depressed left ventricular ejection fraction within five years: the Cardiovascular Health Study. J Am Coll Cardiol 43: 2207–2215PubMedCrossRef

25.

Fearon WF, Lee DP, Froelicher VF (2000) The effect of resting ST segment depression on the diagnostic characteristics of the exercise treadmill test. J Am Coll Cardiol 35: 1206–1211PubMedCrossRef

26.

Forette F, Seux ML, Staessen JA et al. (1998) Prevention of dementia in randomised double-blind placebo-controlled Systolic Hypertension in Europe (Syst-Eur) trial. Lancet 352: 1347–1351PubMedCrossRef

27.

Francis GS, Mcdonald KM (1992) Left ventricular hypertrophy: an initial response to myocardial injury. Am J Cardiol 69: 3G–7GPubMedCrossRef

28.

Fu YC, Chi CS, Yin SC et al. (2004) Norepinephrine induces apoptosis in neonatal rat cardiomyocytes through a reactive oxygen species-TNF alpha-caspase signaling pathway. Cardiovasc Res 62: 558–567PubMedCrossRef

29.

Gianrossi R, Detrano R, Mulvihill D et al. (1989) Exercise-induced ST depression in the diagnosis of coronary artery disease. A meta-analysis. Circulation 80: 87–98PubMed

30.

Gibson CM, Cannon CP, Daley WL et al. (1996) TIMI frame count: a quantitative method of assessing coronary artery flow. Circulation 93: 879–888PubMed

31.

Goette A, Arndt M, Rocken C et al. (2000) Regulation of angiotensin II receptor subtypes during atrial fibrillation in humans. Circulation 101: 2678–2681PubMed

32.

Goette A, Staack T, Rocken C et al. (2000) Increased expression of extracellular signal-regulated kinase and angiotensin-converting enzyme in human atria during atrial fibrillation. J Am Coll Cardiol 35: 1669–1677PubMedCrossRef

33.

Goldstein RA, Haynie M (1990) Limited myocardial perfusion reserve in patients with left ventricular hypertrophy. J Nucl Med 31: 255–258PubMed

34.

Gottdiener JS, Mcclelland RL, Marshall R et al. (2002) Outcome of congestive heart failure in elderly persons: influence of left ventricular systolic function. The Cardiovascular Health Study. Ann Intern Med 137: 631–639PubMed

35.

Graham I, Atar D, Borch-Johnsen K et al. (2007) European guidelines on cardiovascular disease prevention in clinical practice: full text. Fourth Joint Task Force of the European Society of Cardiology and other societies on cardiovascular disease prevention in clinical practice (constituted by representatives of nine societies and by invited experts). Eur J Cardiovasc Prev Rehabil 14 (Suppl 2): S1–S113PubMedCrossRef

36.

Granger BB, Swedberg K, Ekman I et al. (2005) Adherence to candesartan and placebo and outcomes in chronic heart failure in the CHARM programme: double-blind, randomised, controlled clinical trial. Lancet 366: 2005–2011PubMedCrossRef

37.

Gustafsson AB, Gottlieb RA (2008) Heart mitochondria: gates of life and death. Cardiovasc Res 77: 334–343PubMedCrossRef

38.

Hasegawa K, Iwai-Kanai E, Sasayama S (2001) Neurohormonal regulation of myocardial cell apoptosis during the development of heart failure. J Cell Physiol 186: 11–18PubMedCrossRef

39.

Hasking GJ, Esler MD, Jennings GL et al. (1986) Norepinephrine spillover to plasma in patients with congestive heart failure: evidence of increased overall and cardiorenal sympathetic nervous activity. Circulation 73: 615–621PubMed

40.

Hennekens CH, Dyken ML, Fuster V (1997) Aspirin as a therapeutic agent in cardiovascular disease: a statement for healthcare professionals from the American Heart Association. Circulation 96: 2751–2753PubMed

41.

Hjalmarson A, Goldstein S, Fagerberg B et al. (2000) Effects of controlled-release metoprolol on total mortality, hospitalizations, and well-being in patients with heart failure: the Metoprolol CR/XL Randomized Intervention Trial in congestive heart failure (MERIT-HF). MERIT-HF Study Group. JAMA 283: 1295–1302PubMedCrossRef

42.

Hoffman JI (1984) Maximal coronary flow and the concept of coronary vascular reserve. Circulation 70: 153–159PubMed

43.

Jackson R, Lawes CM, Bennett DA et al. (2005) Treatment with drugs to lower blood pressure and blood cholesterol based on an individual’s absolute cardiovascular risk. Lancet 365: 434–441PubMed

44.

Jessup M, Brozena S (2003) Heart failure. N Engl J Med 348: 2007–2018PubMedCrossRef

45.

Kai H, Kuwahara F, Tokuda K et al. (2005) Diastolic dysfunction in hypertensive hearts: roles of perivascular inflammation and reactive myocardial fibrosis. Hypertens Res 28: 483–490PubMedCrossRef

46.

Kannel WB, Dannenberg AL, Levy D (1987) Population implications of electrocardiographic left ventricular hypertrophy. Am J Cardiol 60: 85I–93IPubMedCrossRef

47.

Kannel WB, Wolf PA, Benjamin EJ et al. (1998) Prevalence, incidence, prognosis, and predisposing conditions for atrial fibrillation: population-based estimates. Am J Cardiol 82: 2N–9NPubMedCrossRef

48.

Kaplan NM, Opie LH (2006) Controversies in hypertension. Lancet 367: 168–176PubMedCrossRef

49.

Katz AM (1990) Interplay between inotropic and lusitropic effects of cyclic adenosine monophosphate on the myocardial cell. Circulation 82: I7–11PubMed

50.

Kearney PM, Whelton M, Reynolds K et al. (2004) Worldwide prevalence of hypertension: a systematic review. J Hypertens 22: 11–19PubMedCrossRef

51.

Kelm M (2001) Interaction of the coronary macro- and microcirculation. Z Kardiol 90: 946–952PubMedCrossRef

52.

Kimura E, Tabata T, Tanaka H et al. (2005) Left ventricular geometry and myocardial contractility in patients with essential hypertension evaluated by myocardial velocity profile. J Am Soc Echocardiogr 18: 1222–1229PubMedCrossRef

53.

Klingbeil AU, Schneider M, Martus P et al. (2003) A meta-analysis of the effects of treatment on left ventricular mass in essential hypertension. Am J Med 115: 41–46PubMedCrossRef

54.

Kobayashi N, Mori Y, Nakano S et al. (2001) TCV-116 stimulates eNOS and caveolin-1 expression and improves coronary microvascular remodeling in normotensive and angiotensin II-induced hypertensive rats. Atherosclerosis 158: 359–368PubMedCrossRef

55.

Kober L, Torp-Pedersen C, Carlsen JE et al. (1995) A clinical trial of the angiotensin-converting-enzyme inhibitor trandolapril in patients with left ventricular dysfunction after myocardial infarction. Trandolapril Cardiac Evaluation (TRACE) Study Group. N Engl J Med 333: 1670–1676PubMedCrossRef

56.

Krum H, Carson P, Farsang C et al. (2004) Effect of valsartan added to background ACE inhibitor therapy in patients with heart failure: results from Val-HeFT. Eur J Heart Fail 6: 937–945PubMedCrossRef

57.

Kumar R, Singh VP, Baker KM (2008) The intracellular renin-angiotensin system: implications in cardiovascular remodeling. Curr Opin Nephrol Hypertens 17: 168–173PubMedCrossRef

58.

Lamba S, Abraham WT (2000) Alterations in adrenergic receptor signaling in heart failure. Heart Fail Rev 5: 7–16PubMedCrossRef

59.

Landmesser U, Drexler H (2007) Endothelial function and hypertension. Curr Opin Cardiol 22: 316–320PubMedCrossRef

60.

Laurent GJ (1987) Dynamic state of collagen: pathways of collagen degradation in vivo and their possible role in regulation of collagen mass. Am J Physiol 252: C1–C9PubMed

61.

Law MR, Wald NJ (2002) Risk factor thresholds: their existence under scrutiny. BMJ 324: 1570–1576PubMedCrossRef

62.

Levine TB, Francis GS, Goldsmith SR et al. (1982) Activity of the sympathetic nervous system and renin-angiotensin system assessed by plasma hormone levels and their relation to hemodynamic abnormalities in congestive heart failure. Am J Cardiol 49: 1659–1666PubMedCrossRef

63.

Levy D, Anderson KM, Savage DD et al. (1987) Risk of ventricular arrhythmias in left ventricular hypertrophy: the Framingham Heart Study. Am J Cardiol 60: 560–565PubMedCrossRef

64.

Levy D, Anderson KM, Savage DD et al. (1988) Echocardiographically detected left ventricular hypertrophy: prevalence and risk factors. The Framingham Heart Study. Ann Intern Med 108: 7–13PubMed

65.

Levy D, Garrison RJ, Savage DD et al. (1990) Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study. N Engl J Med 322: 1561–1566PubMed

66.

Levy D, Kenchaiah S, Larson MG et al. (2002) Long-term trends in the incidence of and survival with heart failure. N Engl J Med 347: 1397–1402PubMedCrossRef

67.

Lin M, Sumimoto T, Hiwada K (1995) Left ventricular geometry and cardiac function in mild to moderate essential hypertension. Hypertens Res 18: 151–157PubMedCrossRef

68.

Lip GY, Felmeden DC, Li-Saw-Hee FL et al. (2000) Hypertensive heart disease. A complex syndrome or a hypertensive ‚cardiomyopathy’? Eur Heart J 21: 1653–1665PubMedCrossRef

69.

Lombes M, Oblin ME, Gasc JM et al. (1992) Immunohistochemical and biochemical evidence for a cardiovascular mineralocorticoid receptor. Circ Res 71: 503–510PubMed

70.

Lopez Salazar B, Ravassa Albeniz S, Arias Guedon T et al. (2006) Altered fibrillar collagen metabolism in hypertensive heart failure. Current understanding and future prospects. Rev Esp Cardiol 59: 1047–1057CrossRef

71.

Massie BM, Carson PE, Mcmurray JJ et al. (2008) Irbesartan in patients with heart failure and preserved ejection fraction. N Engl J Med 359: 2456–2467PubMedCrossRef

72.

Mclenachan JM, Henderson E, Morris KI et al. (1987) Ventricular arrhythmias in patients with hypertensive left ventricular hypertrophy. N Engl J Med 317: 787–792PubMed

73.

Messerli FH, Ventura HO, Elizardi DJ et al. (1984) Hypertension and sudden death. Increased ventricular ectopic activity in left ventricular hypertrophy. Am J Med 77: 18–22PubMedCrossRef

74.

Miller JM, Rochitte CE, Dewey M et al. (2008) Diagnostic performance of coronary angiography by 64-row CT. N Engl J Med 359: 2324–2336PubMedCrossRef

75.

Miura K, Daviglus ML, Dyer AR et al. (2001) Relationship of blood pressure to 25-year mortality due to coronary heart disease, cardiovascular diseases and all causes in young adult men: the Chicago heart association detection project in industry. Arch Intern Med 161: 1501–1508PubMedCrossRef

76.

Moncrieff J, Lindsay MM, Dunn FG (2004) Hypertensive heart disease and fibrosis. Curr Opin Cardiol 19: 326–331PubMedCrossRef

77.

Murphy ML, Thenabadu PN, De Soyza N et al. (1985) Sensitivity of electrocardiographic criteria for left ventricular hypertrophy according to type of cardiac disease. Am J Cardiol 55: 545–549PubMedCrossRef

78.

Naga Prasad SV, Barak LS, Rapacciuolo A et al. (2001) Agonist-dependent recruitment of phosphoinositide 3-kinase to the membrane by beta-adrenergic receptor kinase 1. A role in receptor sequestration. J Biol Chem 276: 18953–18959CrossRef

79.

Naga Prasad SV, Laporte SA, Chamberlain D et al. (2002) Phosphoinositide 3-kinase regulates beta2-adrenergic receptor endocytosis by AP-2 recruitment to the receptor/beta-arrestin complex. J Cell Biol 158: 563–575CrossRef

80.

Olivetti G, Melissari M, Balbi T et al. (1994) Myocyte nuclear and possible cellular hyperplasia contribute to ventricular remodeling in the hypertrophic senescent heart in humans. J Am Coll Cardiol 24: 140–149PubMedCrossRef

81.

Owan TE, Hodge DO, Herges RM et al. (2006) Trends in prevalence and outcome of heart failure with preserved ejection fraction. N Engl J Med 355: 251–259PubMedCrossRef

82.

Pardo Mindan FJ, Panizo A (1993) Alterations in the extracellular matrix of the myocardium in essential hypertension. Eur Heart J 14(Suppl J): 12–14

83.

Paulus WJ, Tschope C, Sanderson JE et al. (2007) How to diagnose diastolic heart failure: a consensus statement on the diagnosis of heart failure with normal left ventricular ejection fraction by the Heart Failure and Echocardiography Associations of the European Society of Cardiology. Eur Heart J 28: 2539–2550PubMedCrossRef

84.

Pfeffer MA, Braunwald E, Moye LA et al. (1992) Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. Results of the survival and ventricular enlargement trial. The SAVE Investigators. N Engl J Med 327: 669–677PubMed

85.

Poole-Wilson PA, Swedberg K, Cleland JG et al. (2003) Comparison of carvedilol and metoprolol on clinical outcomes in patients with chronic heart failure in the Carvedilol Or Metoprolol European Trial (COMET): randomised controlled trial. Lancet 362: 7–13PubMedCrossRef

86.

Pringle SD, Dunn FG, Lorimer AR et al. (1994) The role of nuclear cardiology in hypertension. Nucl Med Commun 15: 4–8PubMedCrossRef

87.

Querejeta R, Varo N, Lopez B et al. (2000) Serum carboxy-terminal propeptide of procollagen type I is a marker of myocardial fibrosis in hypertensive heart disease. Circulation 101: 1729–1735PubMed

88.

Redfield MM, Jacobsen SJ, Burnett JC Jr et al. (2003) Burden of systolic and diastolic ventricular dysfunction in the community: appreciating the scope of the heart failure epidemic. JAMA 289: 194–202PubMedCrossRef

89.

Remondino A, Kwon SH, Communal C et al. (2003) Beta-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 92: 136–138PubMedCrossRef

90.

Rocha R, Martin-Berger CL, Yang P et al. (2002) Selective aldosterone blockade prevents angiotensin II/salt-induced vascular inflammation in the rat heart. Endocrinology 143: 4828–4836PubMedCrossRef

91.

Rubattu S, Sciarretta S, Valenti V et al. (2008) Natriuretic peptides: an update on bioactivity, potential therapeutic use, and implication in cardiovascular diseases. Am J Hypertens 21: 733–741PubMedCrossRef

92.

Schafer A, Fraccarollo D, Tas P et al. (2004) Endothelial dysfunction in congestive heart failure: ACE inhibition vs. angiotensin II antagonism. Eur J Heart Fail 6: 151–159PubMedCrossRef

93.

Schirpenbach C, Reincke M (2008) Epidemiology and etiology of therapy-resistant hypertension. Internist (Berl)

94.

Serneri GG, Boddi M, Cecioni I et al. (2001) Cardiac angiotensin II formation in the clinical course of heart failure and its relationship with left ventricular function. Circ Res 88: 961–968PubMedCrossRef

95.

Shigematsu Y, Hamada M, Ohtsuka T et al. (1998) Left ventricular geometry as an independent predictor for extracardiac target organ damage in essential hypertension. Am J Hypertens 11: 1171–1177PubMedCrossRef

96.

Singh K, Xiao L, Remondino A et al. (2001) Adrenergic regulation of cardiac myocyte apoptosis. J Cell Physiol 189: 257–265PubMedCrossRef

97.

Teerlink JR (2002) Reversal of left ventricular remodeling: role of the endothelin pathway. J Card Fail 8: S494–S499PubMedCrossRef

98.

Thomas JA, Marks BH (1978) Plasma norepinephrine in congestive heart failure. Am J Cardiol 41: 233–243PubMedCrossRef

99.

Turner NA, Xia F, Azhar G et al. (1998) Oxidative stress induces DNA fragmentation and caspase activation via the c-Jun NH2-terminal kinase pathway in H9c2 cardiac muscle cells. J Mol Cell Cardiol 30: 1789–1801PubMedCrossRef

100.

Valgimigli M, Merli E, Malagutti P et al. (2004) Hydroxyl radical generation, levels of tumor necrosis factor-alpha and progression to heart failure after acute myocardial infarction. J Am Coll Cardiol 43: 2000–2008PubMedCrossRef

101.

Vasan RS, Larson MG, Benjamin EJ et al. (1999) Congestive heart failure in subjects with normal versus reduced left ventricular ejection fraction: prevalence and mortality in a population-based cohort. J Am Coll Cardiol 33: 1948–1955PubMedCrossRef

102.

Verdecchia P, Angeli F, Achilli P et al. (2007) Echocardiographic left ventricular hypertrophy in hypertension: marker for future events or mediator of events? Curr Opin Cardiol 22: 329–334PubMedCrossRef

103.

Von Harsdorf R, Li PF, Dietz R (1999) Signaling pathways in reactive oxygen species-induced cardiomyocyte apoptosis. Circulation 99: 2934–2941

104.

Walsh RA (1990) Sympathetic control of diastolic function in congestive heart failure. Circulation 82: I52–158PubMed

105.

Wang Y, Huang S, Sah VP et al. (1998) Cardiac muscle cell hypertrophy and apoptosis induced by distinct members of the p38 mitogen-activated protein kinase family. J Biol Chem 273: 2161–2168PubMedCrossRef

106.

Willenheimer R, Van Veldhuisen DJ, Silke B et al. (2005) Effect on survival and hospitalization of initiating treatment for chronic heart failure with bisoprolol followed by enalapril, as compared with the opposite sequence: results of the randomized Cardiac Insufficiency Bisoprolol Study (CIBIS) III. Circulation 112: 2426–2435PubMedCrossRef

107.

Yano M, Kim S, Izumi Y et al. (1998) Differential activation of cardiac c-jun amino-terminal kinase and extracellular signal-regulated kinase in angiotensin II-mediated hypertension. Circ Res 83: 752–760PubMed

108.

Yusuf S, Hawken S, Ounpuu S et al. (2004) Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study. Lancet 364: 937–952PubMedCrossRef

Titel: Hypertensive Folgeschäden am Herzen
verfasst von: M. Steinmetz
G. Nickenig
Publikationsdatum: 01.04.2009
Verlag: Springer-Verlag
Erschienen in: Die Innere Medizin / Ausgabe 4/2009
Print ISSN: 2731-7080
Elektronische ISSN: 2731-7099
DOI: https://doi.org/10.1007/s00108-008-2289-3

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

^{Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag}

Kostenlos registrieren

Neu im Fachgebiet Innere Medizin

NSCLC: Progressionsfreies Überleben unter Osimertinib fast versiebenfacht

06.06.2024 ASCO 2024 Kongressbericht

Erste Ergebnisse der Phase-III-Studie LAURA etablieren Osimertinib als neuen Therapiestandard für Menschen mit nicht-resezierbarem, EGFR-mutiertem, nicht-kleinzelligem Lungenkarzinom im Stadium III, die nach definitiver Radiochemotherapie progressionsfrei sind. Auf der ASCO-Tagung wurden diese beeindruckenden Ergebnisse besprochen.

Hodgkin Lymphom: BrECADD-Regime übertrifft die Erwartungen

05.06.2024 ASCO 2024 Kongressbericht

Das Kombinationsregime BrECADD mit Brentuximab vedotin ermöglichte in der Studie HD21 beim fortgeschrittenen klassischen Hodgkin-Lymphom eine unerwartet hohe progressionsfreie Überlebensrate von 94,3% nach vier Jahren. Gleichzeitig war das Regime besser tolerabel als der bisherige Standard eBEACOPP.

Antikörper-Drug-Konjugat verdoppelt PFS bei Multiplem Myelom

05.06.2024 ASCO 2024 Nachrichten

Zwei Phase-3-Studien deuten auf erhebliche Vorteile des Antikörper-Wirkstoff-Konjugats Belantamab-Mafodotin bei vorbehandelten Personen mit Multiplem Myelom: Im Vergleich mit einer Standard-Tripeltherapie wurde das progressionsfreie Überleben teilweise mehr als verdoppelt.

Neuer TKI gegen CML: Höhere Wirksamkeit, seltener Nebenwirkungen

05.06.2024 Chronische myeloische Leukämie Nachrichten

Der Tyrosinkinasehemmer (TKI) Asciminib ist älteren Vertretern dieser Gruppe bei CML offenbar überlegen: Personen mit frisch diagnostizierter CML entwickelten damit in einer Phase-3-Studie häufiger eine gute molekulare Response, aber seltener ernste Nebenwirkungen.

Update Innere Medizin

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

Newsletter bestellen

Adipositas in der Primärversorgung – Herausforderungen und Chancen einer ganzheitlichen Betreuung

Springer Medizin

Zusammenfassung

Bitte loggen Sie sich ein, um Zugang zu diesem Inhalt zu erhalten

Weitere Artikel der Ausgabe 4/2009

Mitteilungen des BDI

Rosuvastatin bei Patienten mit chronischer Herzinsuffizienz

Leitliniengerechte Therapie des Asthma bronchiale

Schlaganfall und Hypertonie

Niere und Hypertonie