Abnahme der arteriellen Compliance: Beurteilung und Behandlung

  • M. E. Safar
  • J. L. Cuche
  • B. M. Pannier
Conference paper

Zusammenfassung

Die Hypertonie gilt seit vielen Jahren als Gefäßerkrankung, die sich haupsächlich auf das Kaliber kleiner Arterien auswirkt, woraus eine Zunahme des Gefäß Widerstands und sekundäre schädliche Folgen für das Herz resultieren. Die Tatsache, daß die Hypertonie alle Komponenten des kardiovaskulären Systems beeinflußt, wozu auch eine Abnahme der arteriellen und venösen Compliance gehört, blieb zum Teil unbeachtet [1]. Veränderungen der Compliance, v. a. im Bereich des arteriellen Systems, müssen jedoch für ein besseres Verständnis der kardiovaskulären Morbidität und Mortalität bei Patienten, die wegen einer Hypertonie behandelt werden, unbedingt in Betracht gezogen werden. Tatsächlich stehen kardiovaskuläre Ereignisse bei antihypertensiv behandelten Patienten hauptsächlich mit einer Durchblutungsstörung größerer Arterien in Zusammenhang [2].

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Literatur

  1. 1.
    Safar ME, London GM (1987) Arterial and venous compliance in sustained essential hypertension. Hypertension 10: 133–139PubMedGoogle Scholar
  2. 2.
    Kannel WB, Stokes III (1985) Hypertension as a cardiovascular risk factor. In: Blupitt CJ (ed) Epidemiology of hypertension. Elsevier, Amsterdam (Handbook of hypertension, vol 6, pp 15–34 )Google Scholar
  3. 3.
    O’Rourke MF (1982) Arterial function in health and disease. Churchill Livingstone, Edinburgh London Melbourne New York, pp 3–32, 53–93, 170–224Google Scholar
  4. 4.
    Westerhof N, Huisman RM (1987) Arterial haemodynamics of hypertension. Clin Sei 72: 391–398Google Scholar
  5. 5.
    Safar ME (1985) Focus on the large arteries in hypertension. J Cardiovasc Pharmacol [Suppl 2] 7: S1 - S4CrossRefGoogle Scholar
  6. 6.
    Milnor WR (1982) Hemodynamics. Williams & Wilkins, Baltimore London, pp 11–48, 56–96, 192–239Google Scholar
  7. 7.
    Safar ME & Simon (1986) Hemodynamics in systolic hypertension. In: Zanchetti A, Tarazi RC (eds) Pathophisiology of hypertension, cardiovascular aspect. Elsevier, Amsterdam (Handbook of hypertension, vol 7, pp 225–241 )Google Scholar
  8. 8.
    Safar M, Peronneau J, Levenson J, Simon A (1981) Pulsed Doppler: diameter, velocity and flow of brachial artery in sustained essential hypertension. Circulation 63 /2: 393–400PubMedCrossRefGoogle Scholar
  9. 9.
    Laurent S, Lacolley P, London G, Safar M (1988) Hemodynamics of the carotid artery after vasodilatation in essential hypertension. Hypertension 11: 134–1490PubMedGoogle Scholar
  10. 10.
    Isnard RN, Pannier BM, Laurent S, London GM, Diebold B, Safar ME (1989) Pulsatile diameter and elastic modulus of the aortic arch in essential hypertension: a noninvasive study. J Am Coli Cardiol 13: 399–405CrossRefGoogle Scholar
  11. 11.
    Safar ME, Laurent S, Pannier BM, London GM (1987) Structural and functional modifications of peripheral large arteries in hypertensive patients. J Clin Hypertens 3: 360–367PubMedGoogle Scholar
  12. 12.
    Levy BI, Michel JB, Salzmann JL, Azizi M, Poitevin P, Safar M, Camilleri JP (1988) Effects of chronic inhibition of Converting enzyme on mechanical and structural properties of arteries in rat renovascular hypertension. Circ Res 63: 227–229PubMedGoogle Scholar
  13. 13.
    Cox RH (1979) Comparison of arterial wall mechanics in normotensive and spontaneously hypertensive rats. Am J Physiol 237 /2: H159 - H167PubMedGoogle Scholar
  14. 14.
    Safar ME, Simon A, Levenson JA, Cazor JL (1983) Hemodynamic effects of diltiazem in hypertension. Circ Res [Suppl 1] 52: 169–173Google Scholar
  15. 15.
    Safar ME, Laurent S, Bouthier JA, London GM (1986) Comparative effects of Captopril and isorbide dinitrate on the arterial wall of hypertensive human brachial arteries. J Cardiovasc Pharmacol 8: 1257–1261PubMedCrossRefGoogle Scholar
  16. 16.
    Safar ME, Toto–Moukouo JJ, Bouthier JA, Asmar RE, Levenson JA, Simon AC, London GM (1987) Arterial dynamics, cardiac hypertrophy, and antihypertensive treatment. Circulation [Suppl 1] 75: 1–156–1–165Google Scholar
  17. 17.
    Safar ME (1988) Therapeutic trials and large arteries in hypertension. Am Heart J 115: 702–710PubMedCrossRefGoogle Scholar
  18. 18.
    Safar ME, London GM, Asmar RG, Hugues CJ, Laurent S (1986) An indirect approach for the study of the elastic modulus of the brachial artery in patients with essential hypertension. Cardiovasc Res 20: 563–567PubMedCrossRefGoogle Scholar
  19. 19.
    Levy BI, Michel JB, Salumann JL, Azizi M, Poitevin P, Camilleri JP, Safar ME (1988) Arterial effects of angiotensin Converting enzyme inhibition in renovascular and spontaneously hypertensive rats. J Hypertens [Suppl 3] 6: S23 - S25CrossRefGoogle Scholar
  20. 20.
    Asmar RG, Pannier B, Santoni JP, Laurent S, London GM, Levy BI, Safar ME (1988) Reversion of cardiac hypertrophy and reduced arterial compliance after Converting enzyme inhibition in essential hypertension. Circulation 789: 941–950CrossRefGoogle Scholar
  21. 21.
    Asmar RG, Journo HJ, Lacolley PJ, Santoni JP, Billaud E, Levy BI, Safar ME (1988) Treatment for one year with perindopril: effect on cardiac mass and arterial compliance in essential hypertension. J Hypertens [Suppl 3] 6: S23 - S25CrossRefGoogle Scholar
  22. 22.
    Kannel WB, Gordon T, Schwartz MJ (1971) Systolic versus diastolic blood pressure and risk of coronary heart disease: The Framingham Study. Am J Cardiol 27: 335–346PubMedCrossRefGoogle Scholar
  23. 23.
    Darne B, Girerd X, Safar M, Cambien F, Guize L (1989) Pulsatile versus steady component of blood pressure: A cross-sectional analysis and a prospective analysis on cardiovascular mortality. Hypertension 13: 392–400PubMedGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1991

Authors and Affiliations

  • M. E. Safar
  • J. L. Cuche
  • B. M. Pannier

There are no affiliations available

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