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Kardiovaskuläre Endorganschäden des Hochdrucks

Hypertension-specific cardiovascular organ manifestations

  • Schwerpunkt: Hypertonie
  • Published:
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Zusammenfassung

Die arterielle Hypertonie ist die häufigste Form der Druckbelastung des linken Ventrikels. Bei länger bestehender arterieller Hypertonie entwickeln sich kardiovaskuläre Endorganschäden, die unter dem Begriff „Hochdruckherz“ zusammengefasst werden. Dieser Begriff umfasst die stenosierende Makroangiopathie, koronare Mikroangiopathie, ischämische Kardiomyopathie, linksventrikuläre Hypertrophie, Störungen der Endothelfunktion, Fibrose des perivaskulären und interstitiellen Gewebes, einen erhöhten Sympathikotonus und degenerative Veränderungen der Aortenklappe. Als Frühveränderungen können eine diastolische Funktionsstörung und eine Einschränkung der Koronarreserve dokumentiert werden. Das klinische Bild des Patienten mit Hochdruckherz wird durch die Koronarinsuffizienz mit typischer Angina pectoris, aber auch Herzinsuffizienz (systolische und diastolische Dysfunktion) und Herzrhythmusstörungen bestimmt. Für die Erstdiagnostik und Verlaufskontrolle kommen unterschiedliche diagnostische Verfahren zum Einsatz. Primäres Therapieziel ist neben der effektiven Blutdrucknormalisierung die Rückführung der hypertensiv bedingten kardialen Veränderungen durch die Einleitung spezifischer Therapiemaßnahmen.

Abstract

Arterial hypertension is the most frequent cause of pressure overload on the left ventricle. Longer lasting arterial hypertension leads to hypertension-specific organ manifestations summarized as “hypertensive heart disease”. Hypertensive heart disease comprise the manifestation of stenosis in epicardial arteries, hypertensive microvascular disease, ischemic cardiomyopathy, left ventricular hypertrophy, endothelial dysfunction, increased sympathetic drive and degeneration of aortic valve. Diastolic dysfunction and reduced coronary flow reserve can be evaluated as early markers of hypertensive heart disease. These alterations lead to the major clinical manifestations of hypertensive heart disease that are symptoms of reduced coronary insufficiency with typical angina pectoris, but also of symptoms of heart failure (systolic and diastolic dysfunction) and arrhythmia. Different non-invasive and invasive procedures are available for screening and follow-up of patients with hypertensive heart disease. Primary therapeutic target is, apart from lowering blood pressure, to reverse cardiac manifestations of arterial hypertension using specific therapeutic algorithms.

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Literatur

  1. Antony J, Lerebours G, Nitenberg A (1996) Angiotensin-converting enzyme inhibition restores flow-dependent and cold pressor test-induced dilatations in coronary arteries of hypertensive patients. Circulation 94: 3115–3122

    Google Scholar 

  2. Cameron JS, Myerburg RJ, Wong SS et al. (1983) Electrophysiologic consequences of chronic experimentally induced left ventricular pressure overload. J Am Coll Cardiol 2: 481–487

    Google Scholar 

  3. Casale PN, Devereux RB, Alonso DR, Campo E, Kligfield P (1987) Improved sex-specific criteria of left-ventricular hypertrophy for clinical and computer interpretation of electrocardiograms — validation with autopsy findings. Circulation 75: 565–572

    Google Scholar 

  4. Dahlof B, Devereux RB, Kjeldsen SE et al. (2002) Cardiovascular morbidity and mortality in the Losartan Intervention For Endpoint reduction in hypertension study (LIFE): a randomised trial against atenolol. Lancet 359: 995–1003

    Article  CAS  PubMed  Google Scholar 

  5. Dernellis J, Stefanadis C, Toutouzas PK (2000) From science to bedside: the clinical role of atrial function. Eur Heart J 2 [Suppl K]: K48-K57

    Google Scholar 

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

    Google Scholar 

  7. Gottdiener JS, Reda DJ, Williams DW, Materson BJ, Cushman W, Anderson WJ, for the VA Cooperative Group on Antihypertensive Agents (1998) Effect of single-drug therapy on reduction of left atrial size in mild to moderate hypertension. Circulation 98: 140–148

    Google Scholar 

  8. Heidland UE, Strauer BE (2001) Left ventricular muscle mass and elevated heart rate are associated with coronary plaque disruption. Circulation 104: 1477–1482

    Google Scholar 

  9. Heller LI, Cates C, Popma J et al. (1997) Intracoronary doppler assessement of moderate coronary artery disease. Comparison with 201TI imaging and coronary angiography. Circulation 96: 484–490

    Google Scholar 

  10. Hennersdorf MG, Schannwell CM, Schwartzkopff B, Strauer BE (2003) Hypertrophieregression als Therapieprinzip des Hochdruckherzens. Herz 28: 764–778

    Google Scholar 

  11. Hennersdorf MG, Strauer BE (2001) Arterial hypertension and cardiac arrhythmias. J Hypertens 19: 167–177

    Google Scholar 

  12. Houston MC (1992) New insights and approaches to reduce end-organ damage in the treatment of hypertension: subsets of hypertension approach. Am Heart J 123: 1337–1367

    Google Scholar 

  13. Johnson PC (1986) Autoregulation of blood flow. Circ Res 59: 483–495

    Google Scholar 

  14. Kelm M, Rath J, Pölitz B et al. (1998) Relevanz und Methoden zur Bestimmung der koronaren Flußreserve. Z Kardiol 87 [Suppl 2]: 74–79

    Google Scholar 

  15. Kelm M, Strauer BE (2003) Hochdruckherz und hypertensive Mikroangiopathie. Internist 44: 793–805

    Google Scholar 

  16. Kelm M (2001) Interaktion von koronarer Makro- und Mikrostrombahn. Z Kardiol 90: 946–952

    Google Scholar 

  17. Kjeldsen SE, Dahlof B, Devereux RB et al. (2002) Effects of losartan on cardiovascular morbidity and mortality in patients with isolated systolic hypertension and left ventricular hypertrophy: a Losartan Intervention For Endpoint reduction (LIFE) substudy. JAMA 288: 1491–1498

    Google Scholar 

  18. Koren MJ, Devereux RB, Casale PN et al. (1991) Relation of left ventricular mass and geometry to morbidity and mortality in uncomplicated essential hypertension. Ann Intern Med 114: 345–352

    Google Scholar 

  19. Kroon AA, Stalenhoef AFH, Buikema H, Demacker PNM, de Wilde PCM, Leijten PA, van Gilst WH (1993) The effect of cholesterol reduction on the endothelial function and progression of atherosclerosis in WHHL rabbits. Atherosclerosis 103: 221–230

    Google Scholar 

  20. Levington S, Clarke R, Qizilbash N, Peto R, Collins R (2002) Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies. Lancet 360: 1903–1913

    Google Scholar 

  21. Levy D, Savage DD, Garrison RJ et al. (1987) Echocardiographic criteria for left ventricular hypertrophy: The Framingham heart study. Am J Cardiol 59: 956–960

    Article  CAS  PubMed  Google Scholar 

  22. Mehta A, Jain AC, Mehta MC, Billie M (2000) Usefulness of left atrial abnormality for predicting left ventricular hypertrophy in the presence of left bundle branch block. Am J Cardiol 85: 354–359

    Google Scholar 

  23. Motz W (2004) Hochdruck und koronare Herzerkrankheit. Gibt es neue Therapieoptionen? Herz 29: 255–265

    Google Scholar 

  24. Muiesan ML, Rizzoni D, Salvetti M et al. (2002) Structural changes in small resistance arteries and left ventricular geometry in patients with primary and secondary hypertension. J Hypertens 20: 1439–1444

    Google Scholar 

  25. Nishikimi T, Yoshihara F, Morimoto A et al. (1996) Relationship between left ventricular geometry and natriuretic peptide levels in essential hypertension. Hypertension 28: 22–30

    CAS  PubMed  Google Scholar 

  26. Otterstad JE, Davies M, Ball S et al. (1993) Left ventricular hypertrophy and myocardial ischemia in hypertension. The THAMES Study. Eur Heart J 14: 1622–1628

    Google Scholar 

  27. Preik M, Kelm M, Strauer BE (2003) Management of the hypertensive patient with coronary insufficiency but without atherosclerosis. Curr Opin Cardiol 18: 255–259

    Google Scholar 

  28. Roman MJ, Pickering TG, Pini R et al. (1995) Prevalence and determinants of cardiac and vascular hypertrophy in hypertension. Hypertension 26: 369–373

    Google Scholar 

  29. Schäfer S, Kelm M, Mingers S et al. (2002) Left ventricular remodeling impairs coronary flow reserve in hypertensive patients. J Hypertens 1431–1437

  30. Schannwell CM, Marx R, Plehn G, Perings Ch, Leschke M, Strauer BE (2001) Kann eine pathologische linksventrikuläre Hypertrophie bei arterieller Hypertonie von einer physiologischen linksventrikulären Hypertrophie bei Sportlern unterschieden werden? Dtsch Med Wochenschr 126: 263–267

    Google Scholar 

  31. Schannwell CM, Schoebel FC, Badiian M et al. (1998) Diastolic function parameters and atrial arrhythmias in patients with arterial hypertension. Dtsch Med Wochenschr 123: 957–964

    Google Scholar 

  32. Schannwell CM, Steiner St, Strauer BE (2005) Hypertensive mikrovaskuläre Erkrankung. Herz 30: 26–36

    Google Scholar 

  33. Scheler S, Motz W, Strauer BE (1994) Mechanisms of angina pectoris in patients with systemic hypertension and normal epicardial coronary arteries by arteriogramm. Am J Cardiol 73: 478–482

    Article  CAS  PubMed  Google Scholar 

  34. Schmieder RE, Martus P, Klingbeil A (1996) Reversal of left ventricular hypertrophy in essential hypertension. A meta-analysis of randomized double-blind studies. JAMA 275: 1507–1513

    Google Scholar 

  35. Schwartzkopff B, Brehm M, Mundhenke M et al. (2000) Repair of coronary arterioles after treatment with perindopril in hypertensive heart disease. Hypertension 36: 220–225

    Google Scholar 

  36. Schwartzkopff B, Motz W, Frenzel H et al. (1993) Structural and functional alterations of the intramyocardial coronary arterioles in patients with arterial hypertension. Circulation 88: 993–1003

    CAS  PubMed  Google Scholar 

  37. Schwartzkopff B, Motz W, Vogt M et al. (1993) Heart failure on the basis of hypertension. Circulation 87: IV66–IV72

    Google Scholar 

  38. Shigematsu Y, Hamada M, Mukai M et al. (1995) Clinical evidence for an association between left ventricular geometric adaption and extracardiac target-organ damage in essential hypertension. J Hypertens 13: 155–160

    Google Scholar 

  39. Strauer BE, Schwartzkopff B, Kelm M (1998) Assessing the coronary circulation in hypertension. J Hypertension 16: 1221–1233

    Google Scholar 

  40. Strauer BE (1991) Das Hochdruckherz. Springer, Berlin Heidelberg New York

  41. Strauer BE (1984) Functional dynamics of the left ventricle in hypertensive hypertrophy and failure. Hypertension [Suppl III]: 4–12

  42. Strauer BE (1981) Hypertonie und Herzfunktion. Triangel 20: 107–120

    Google Scholar 

  43. Strauer BE (1979) Myocardial oxygen consumption in chronic heart disease: role of wall stress, hypertrophy and coronary reserve. Am J Cardiol 44: 730–740

    Google Scholar 

  44. Strauer BE (1990) The significance of coronary reserve in clinical heart disease. J Am Coll Cardiol 15: 775–783

    CAS  PubMed  Google Scholar 

  45. Strauer BE (1979) Ventricular function and coronary hemodynamics in hypertensive heart disease. Am J Cardiol 44: 999–1006

    Article  CAS  PubMed  Google Scholar 

  46. Terpstra WF, May JF, Smit AJ et al. (2001) Silent ST depression and cardiovascular end-organ damage in newly found, older hypertensives. Hypertension 37: 1083–1088

    Google Scholar 

  47. Wachtell K, Dahlof B, Rokkedal J et al. (2002) Change of left ventricular geometric pattern after 1 year of antihypertensive treatment: the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. Am Heart J 144: 1057–1064

    Article  CAS  PubMed  Google Scholar 

  48. Weber KT, Brilla CG (1991) Pathologic hypertrophy and interstitium fibrosis and renin-angiotensin-aldosterone system. Circulation 83: 1849–1865

    CAS  PubMed  Google Scholar 

  49. Weber KT, Janicki JS, Pick R et al. (1987) Collagen in the hypertrophied pressure-overloaded myocardium. Circulation 75: 140–147

    Google Scholar 

  50. Zehender M, Meinertz T, Hohnloser S, Geibel A, Gerisch I, Olschewski M, Just H (1992) Prevalence of circadian variations and spontaneous variability of cardiac disorders and ECG changes suggestive of myocardial ischemis in systemic arterial hypertension. Circulation 85: 1808–1815

    Google Scholar 

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Schannwell, C.M., Steiner, S., Hennersdorf, M.G. et al. Kardiovaskuläre Endorganschäden des Hochdrucks. Internist 46, 496–508 (2005). https://doi.org/10.1007/s00108-005-1394-9

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  • DOI: https://doi.org/10.1007/s00108-005-1394-9

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