Fozinopril in the treatment of cardiorenal syndrome in chronic cardiac failure


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Abstract

Renal dysfunction is an independent risk factor of chronic cardiac failure (CCF) and death due to this disease. CCF patients are elderly patients with diabetes mellitus, arterial hypertension and long-term chronic cardiac insufficiency. CCF patients do not often have left ventricular systolic dysfunction, renal affection is not associated with low ejection syndrome. Renal affection in CCF is primarily caused by activation of the system rennin-angiotensin, inflammation, disturbed bioavailability of nitric oxide, hyperactivation of the sympathetic nervous system. ACE inhibitors correct pathophysiological disorders of renal flow in CCF. Fosinopril shows the highest efficacy and safety in management of cardiorenal syndrome in CCF patients. Fosinopril can alsoprevent renal dysfunction in CCF patients.

References

  1. Sarnak M. J., Levey A. S., Schoolwerth A. C. et al. Kidney disease as a risk factor for development of cardiovascular disease: a statement from the American Heart Association Councils on Kidney in Cardiovascular Disease. High Blood Pressure Research, Clinical Cardiology, and Epidemiology and Prevention. Circulation 2003; 108; 2154-2169.
  2. Al Suwaidi J., Reddan D. N., Williams K. et al. Prognostic implications of abnormalities in renal function in patients with acute coronary syndromes. Circulation 2002; 106: 974-980.
  3. Best P. J., Lennon R., Ting H. H. et al. The impact of renal insufficiency on clinical outcomes in patients undergoing percutaneous coronary interventions. J. Am. Coll. Cardiol. 2002; 39: 1113-1119.
  4. Rao V., Weisel R. D., Buth K. J. et al. Coronary artery bypass grafting in patients with non-dialysis-dependent renal insufficiency. Circulation 1997; 96(suppl.): II-38-II-43; discus. II-44-II-45.
  5. Gibson C. M., Pinto D. S., Murphy S. A. et al. Association of creatinine and creatinine clearance on presentation in acute myocardial infarction with subsequent mortality. J. Am. Coll. Cardiol. 2003; 42: 1535-1543.
  6. Dries D. L., Exner D. V., Domanski M. J. et al. The prognostic implications of renal insufficiency in asymptomatic and symptomatic patients with left ventricular systolic dysfunction. J. Am. Coll. Cardiol. 2000; 35: 681-689.
  7. Mahan N. G., Blackstone E. H., Francis G. S. et al. The prognostic value of estimated creatinine clearance alongside functional capacity in patients with chronic congestive heart failure. J. Am. Coll. Cardiol. 2002; 40: 1106-1113.
  8. Hillege H. L., Girbes A. R., de Kam P. J. et al. Renal function, neurohormonal activation, and survival in patients with chronic heart failure. Circulation 2000; 102: 203-210.
  9. Krumholz H. M., Chen Y. T., Vaccarino V. et al. Correlates and impact on outcomes of worsening renal function in patients < or > 65 years of age with heart failure. Am. J. Cardiol. 2000; 85: 1110-1113.
  10. Forman D. E., Butler J., Wang Y. et al. Incidence, predictors at admission, and impact of worsening renal function among patients hospitalized with heart failure. J. Am. Coll. Cardiol. 2004; 43: 61-67.
  11. Gottlieb S. S., Abraham W., Butler J. et al. The prognostic importance of different definitions of worsening renal function in congestive heart failure. J. Card. Fail. 2002; 8: 136-141.
  12. Smith G. L., Vaccarino V., Kosiborod M. et al. Worsening renal function: what is a clinically meaningful change in creatinine during hospitalization with heart failure? J. Card. Fail. 2003; 9: 13-25.
  13. Ruiz-Ortega M., Lorenzo O., Egido J. Angiotensin III increases MCP-l and activates NF-kappaB and AP-1 in cultured mesangial and mononuclear cells. Kidney Int. 2000; 57: 2285-2298.
  14. Pueyo M. E., Gonzalez W., Nicoletti A. et al. Angiotensin II stimulates endothelial vascular cell adhesion molecule-1 via nuclear factor kappa B activation induced by intracellular oxidative stress. Arterioscler. Thromb. Vasc. Biol. 2000; 20: 645-651.
  15. Braam B. Renal endothelial and macula densa NOS: integrated response to changes in extracellular fluid volume. Am. J. Physiol. 1999; 276 (1, pt 2): R1551-R1561.
  16. Zou A. P., Li N., Cowley A. W. Jr. Production and actions of superoxide in the renal medulla. Hypertension 2001; 37: 547-553.
  17. Vallance P., Leone A., Calver A. et al. Accumulation of an endogenous inhibitor of nitric oxide synthesis in chronic renal failure. Lancet 1992; 339: 572-575.
  18. Kielstein J. T., Bode-Boger S. M., Klein G. et al. Endogenous nitric oxide synthase inhibitors and renal perfusion in patients with heart failure. Eur. J. Clin. Invest. 2003; 33: 370-375.
  19. Witko-Sarsat V., Friedlander M., Capeillere-Blandin C. et al. Advanced oxidation protein products as a novel marker of oxidative stress in uremia. Kidney Int. 1996; 49: 1304-1313.
  20. Nguyen-Khoa T., Massy Z. A., Witko-Sarsat V. et al. Oxidized low-density lipoprotein induces macrophage respiratory burst via its protein moiety: A novel pathway in atherogenesis? Biochem. Biophys. Res. Commun. 1999; 263: 804--809.
  21. Katoh M., Egashira K., Usui M. et al. Cardiac angiotensin II receptors are upregulated by long-term inhibition of nitric oxide synthesis in rats. Circ. Res. 1998; 83: 743-751.
  22. Zebrack J. S., Anderson J. L., Beddhu S. et al. Do associations with C-reactive protein and extent of coronary artery disease account for the increased cardiovascular risk of renal insufficiency? J. Am. Coll. Cardiol. 2003; 42: 57-63.
  23. Converse R. L. Jr, Jacobsen T. N., Toto R. D. et al. Sympathetic overactivity in patients with chronic renal failure. N. Engl. J. Med. 1992; 327: 1912-1918.
  24. Leinewelder K., Heinroth-Hoffmann I., Ponicke K. et al. Cardiac betaadrenoceptor desensitization due to increased beta-adrenoceptor kinase activity in chronic uremia. J. Am. Soc. Nephrol. 2002; 13: 117-124.
  25. Bristow M. R., Ginsburg R., Minobe W. et al. Decreased catecholamine sensitivity and beta-adrenergic-receptor density in failing human hearts. N. Engl. J. Med. 1982; 307: 205-211.
  26. Erami C., Zhang H., Ho J. G. et al. Alpha(l)-adrenoceptor stimulation directly induces growth of vascular wall in vivo. Am. J. Physiol. Heart Circ. Physiol. 2002; 283: H1577-H1587.
  27. Bleeke T., Zhang H., Madamanchi N. et al. Catecholamine-induced vascular wall growth is dependent on generation of reactive oxygen species. Circ. Res. 2004; 94: 37-45.
  28. Ратова Л. Г., Чазова И. Е. Нефропротективный эффект антигипертензивной терапии: исследование ИРИС. Consilium Medicum 2004; 2, прил. 3-7.
  29. Фофанова Т. В., Агеев Ф. Т. Ингибиторы АПФ плюс низкие дозы тиазидных диуретиков: идеальная комбинация для лечения артериальной гипертонии. Сердце 2004; 3: 99-103.
  30. MacMahon S. Blood pressure lowering treatment trialist collaboration - second cycle of analyses. In: Abstracts of the l3th Meeting of hypertension. June 13-17. 2003; Milan, Italy.
  31. Беленков Ю. Н., Мареев В. Ю. Принципы рационального лечения сердечной недостаточности. М.: Медиа Медика; 2000.
  32. Тюилле К., Мур Н. Регионарный кровоток при застойной сердечной недостаточности. 1995. Медикография. Париж: 25-31.
  33. Bauer J., Reams G. The angiotensin type I receptor antagonists. Arch. Intern. Med. 1995; 155: 1361-1368.
  34. Арутюнов Г. П., Чернявская Т. К., Лукичева Т. И. и др. Микроальбуминурия: клиническое значение и пути медикаментозной коррекции. Клин. фармакол. и тер. 1999; 9(3): 23-29.
  35. Тареева И. Е., Кутырина И. М. Пути торможения прогрессирования хронической почечной недостаточности. Клин. фармакол. и тер. 1999; 8(5): 71-74.
  36. Стуров Н. В. Ингибиторы АПФ: опыт наиболее значимых клинических исследований для клинической практики. Трудный пациент 2006; 4(4): 48-54.

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