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Кардиопротективные эффекты эплеренона
Кардиопротективные эффекты эплеренона
Кириченко А.А. Кардиопротективные эффекты эплеренона. Consilium Medicum. 2018; 20 (1): 15–20. DOI: 10.26442/2075-1753_2018.1.15-20
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Аннотация
Негативная роль гиперальдостеронизма при хронической сердечной недостаточности (ХСН) связана не только с задержкой жидкости и электролитным дисбалансом. Альдостерон способен оказывать прямое воздействие на эндотелий и гладкомышечные клетки сосудов, кардиомиоциты, индуцируя фиброз и гипертрофию этих тканей, что способствует развитию диастолической дисфункции, возникновению нарушений ритма. Блокада минералокортикоидных рецепторов (МКР) сопровождается уменьшением массы миокарда левого желудочка, улучшением его сократительной функции, приводит к параллельному уменьшению уровня мозгового натрийуретического пептида. Исследования EPHESUS и EMPHASIS-HF доказали, что присоединение антагонистов МКР к стандартной терапии ингибиторами ангиотензинпревращающего фермента и b-адреноблокаторами дополнительно улучшает клиническое течение и прогноз больных с ХСН. Раннее назначение эплеренона больным с инфарктом миокарда с подъемом сегмента ST позволяет снизить частоту развития ХСН. Согласно современным рекомендациям по лечению ХСН начиная со II функционального класса рекомендуется применение именно тройной нейрогормональной блокады – комбинации блокатора ренин-ангиотензин-альдостероновой системы (ингибиторы ангиотензинпревращающего фермента или блокаторы рецепторов ангиотензина II) с b-адреноблокатором и антагонистом МКР. Такая схема ведения больного с ХСН (включая назначение по показаниям диуретиков и сердечных гликозидов) позволяет улучшить не только качество жизни тяжелых больных, но и прогноз. По терапевтической эффективности спиронолактон и эплеренон считаются эквивалентными. В клинической практике эплеренон предпочтительнее вследствие лучшей его переносимости из-за меньшего количества побочных эффектов.
Ключевые слова: альдостерон, антагонисты минералокортикоидных рецепторов, эплеренон.
Ключевые слова: альдостерон, антагонисты минералокортикоидных рецепторов, эплеренон.
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The negative impact of hyperaldosteronism in patients with congestive heart failure (CHF) is related not only to fluid retention but also to electrolyte imbalance. Aldosterone that can influence endothelium, vascular smooth muscle cells, and cardiomyocytes directly, induces fibrosis and hypertrophy that in turn promotes the diastolic dysfunction development and rhythm disturbance. Mineralocorticoid receptor (MCR) blockade is followed by left ventricular mass reduction that improves its contractile function and results in brain natriuretic peptide level reduction. EPHESUS and EMPHASIS-HF trials showed that adding MCR antagonists to ACE inhibitors and b-adrenoblockers additionally improves the clinical course and prognosis in patients with CHF. Early administration of eplerenone in patients with myocardial infarction with ST-segment elevation results in CHF development decrease. According to the latest guidelines on CHF treatment it is recommended to use threefold neurohormonal blockade – combination of renin-angiotensin-aldosterone system blockers (ACE inhibitors and angiotensin II receptor blockers) combined with b-adrenoblockers and MCR antagonists in patients with CHF after class II. This management regimen (including diuretics and cardiac glycoside prescription) improves not only patients’ quality of live but also disease prognosis. Spironolactone and eplerenone are considered equally effective. Though in clinical practice eplerenone an agent of choice because of its better tolerability and fewer side effects.
Key words: aldosterone, mineralocorticoid receptor antagonist, eplerenone.
Полный текст
Список литературы
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4. Epstein M. Aldosterone and the hypertensive kidney: its emerging role as a mediator of progressive renal dysfunction: a paradigm shift. J Hypertens 2001; 19: 829–42.
5. Sato A, Funder JW. High glucose stimulates aldosterone-induced hypertrophy via type I mineralocorticoid receptors in neonatal rat cardiomyocytes. Endocrinol 1996; 137: 4145–53.
6. Weber KT, Brilla CG. Pathological hypertrophy and cardiac interstitium: fibrosis and renin-angiotensin-aldosterone system. Circulation 1991; 83: 1849–65.
7. Tsutamoto T, Wadw A, Maeda K et al. Effect of spironolactone on Plasma brain natriuretic peptide and left ventricular remodeling in patients with congestive heart failure. J Am Col Cardiol 2001; 37: 1228–33.
8. Mano A, Tatsumi T, Shiraishi J et al. Aldosterone directly induces myocyte apoptosis through calcineurin-dependent pathways. Circulation 2004; 110: 317–23.
9. Yu Q. Оsteopontin mediates cardiac fibrosis and diastolic dysfunction in mice. Am J Physiol Heart Circ Physiol 2009; 297 (1): 76–85.
10. Tanaka K, Zlochivier S, Vikstrom K et al. Spatial distribution of fibrosis governs fibrillation wave dynamics in the posterior left atrium during heart failure. Circ Res 2007; 101: 839–47.
11. Zeisberg E, Kalluri R. Origins of cardiac fibroblasts. Circ Res 2010; 107 (11): 1304–12.
12. B Julie He, Mei-ling A Joiner, Madhu V Singh et al. Oxidation of CaMKII determines the cardiotoxic effects of aldosterone. Nat Med 2011; 17 (12): 1610–8.
13. Brilla CG, Matsubara LS, Weber KT. Anti-aldosterone treatment and the prevention of myocardial fibrosis in primary and secondary hyperaldosteronism. J Mol Cell Cardiol 1993; 25 (5): 563–75.
14. De Jong S, van Veen TA, van Rijen HV, de Bakker JM. Fibrosis and cardiac arrhythmias. J Cardiovasc Pharmacol 2011; 57 (6): 630–8.
15. Dąbrowski R, Szwed H. Antiarrhythmic potential of aldosterone antagonists in atrial fibrillation. Cardiol J 2012; 19 (3): 223–9.
16. Zannad F, Alla F, Dousset B et al. Limitation of excessive extracellular matrix turnover may contribute to survival benefit of spironolactone therapy in patients with congestive heart failure: insights from the randomized aldactone evaluation study (RALES). Circulation 2000; 102: 2700–6.
17. McFaiden R, Barr C, Struthers A. Aldosterone blocade reduces vascular collagen turnover, improves heart rate variability and reduces early morning rise in heart rate in heart failure patients Cardiovasc Res 1997; 35: 30–4.
18. Swedberg K, Eneroth P, Kjekshus J, Wilhelmsen L; The CONSENSUS Trial Study Group. Hormones regulating cardiovascular function in patients with severe congestive heart failure and their relation to mortality. Circulation 1990; 82: 1730–6.
19. The CONSENSUS Trial Study Group. Effects of enalapril on mortality in severe congestive heart failure. N Engl J Med 1987; 316: 1429–35
20. Staessen J, Lijnen P, Fagard P et al. Rise in plasma concentration of aldosterone during long-term angiotensin II suppression. J Endocrinol 1981; 91: 457–65.
21. Borghi C, Boschi S, Ambrosioni E et al. Evidence of a partial escape of renin-angiotensine-aldosterone blocade in patients with acute myocardial infarction treated with ACE inhibitors. J Clin Pharmacol 1993; 33: 40–5.
22. Lee AFC, MacFadyen RJ, Struthers AD. Neurohormonal reactivation in heart failure patients on chronic ACE inhibitor therapy: a longitudinal study. Eur J Heart Fail 1999; 1: 401–6.
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28. Pitt B, Zannad F, Remme WJ et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators. N Engl J Med 1999; 341 (10): 709–17.
29. Kramer DG, Trikalinos TA, Kent DM et al. Quantitative evaluation of drug or device effects on ventricular remodeling as predictors of therapeutic effects on mortality in patients with heart failure and reduced ejection fraction: a meta-analytic approach. J Am Coll Cardiol 2010; 56 (5): 392–406.
30. Jeunemaitre X, Chatellier G, Kreft-Jais C et al. Efficacy and tolerance of spironolactone in essential hypertension. Am J Cardiol 1987; 60: 820–5.
31. Pitt B, Remme W, Zannad F et al.; Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study Investigators. Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med 2003; 348: 1309–21.
32. Pitt B, White H, Nicolau J et al. Eplerenone reduces mortality 30 days after randomization following acute myocardial infarction in patients with left ventricular systolic dysfunction and heart failure. J Am Coll Cardiol 2005; 46 (3): 425–31.
33. Pitt B, Gheorghiade M, Zannad F et al. Evaluation of eplerenone in the subgroup of EPHESUS patients with baseline left ventricular ejection fraction <or=30 %. Eur J Heart Fail 2006; 8 (3): 295–301.
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36. Adamopoulos Ch, Ahmed A, Fay R et al.; the EPHESUS Investigators. Timing of eplerenone initiation and outcomes in patients with heart failure after acute myocardial infarction complicated by left ventricular systolic dysfunction: insights from the EPHESUS trial. Eur J Heart Failure 2009; 11: 1099–105.
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38. Carillo S, Zhang Y, Fay R et al. Heart failure with systolic dysfunction complicating acute myocardial infarction – differential outcomes but similar eplerenone efficacy by ST-segment or non-ST-segment elevation: a post hoc substudy of the EPHESUS trial. Arch Cardiovasc Dis 2014; 107: 149–57.
39. Montalescot G, Pitt B, Lopez de Sa E et al. Early eplerenone treatment in patients with acute ST-elevation myocardial infarction without heart failure: the Randomized Double-Blind Reminder Study. Eur Heart J 2014; 35 (34): 2295–302.
40. Zannad F, McMurray JJ, Krum Н et al.; EMPHASIS-HF Study Group. Eplerenone in patients with systolic heart failure and mild symptoms. N Engl J Med 2011; 364: 11–21.
41. Phelan D, Thavendiranathan P, Collier P, Marwick TH. Aldosterone antagonists improve ejection fraction and functional capacity independently of functional class: a meta-analysis of randomised controlled trials. Heart 2012; 98 (23): 1693–700.
42. Udelson JE, Feldman AM, Greenberg B et al. Randomized, doubleblind, multicenter, placebo-controlledstudy evaluating the effect of aldosterone antagonism with eplerenone on ventricular remodeling in patients with mild-to-moderate heart failure and left ventricular systolic dysfunction. Circ Heart Fail 2010; 3 (3): 347–53.
43. Swedberg K, Zannad F, McMurray JJ et al. Eplerenone and atrial fibrillation in mild systolic heart failure: results from the EMPHASIS-HF (Eplerenone in Mild Patients Hospitalization And SurvIval Study in Heart Failure) study. J Am Coll Cardiol 2012; 59 (18): 1598–603.
44. Bapoje SR, Bahia A, Hokanson JE et al. Effects of mineralocorticoid receptor antagonists on the risk of sudden cardiac death in patients with left ventricular systolic dysfunction: a meta-analysis of randomized controlled trials. Circ Heart Fail 2013; 6 (2): 166–73.
45. Edelmann F, Wachter R, Schmidt AG et al.; Aldo-DHF Investigators. Effect of spironolactone on diastolic function and exercise capacity in patients with heart failure with preserved ejection fraction: the Aldo-DHF randomized controlled trial. JAMA 2013; 309: 781–91.
46. Pfeffer МА, McKinlay S, Pitt В et al.; ТОРСАТ Investigators. Treatment Of Preserved Cardiac Function Heart Failure with an Aldosterone anТagonist (ТОРСАТ). abstracts of the American Heart Association Scientific Sessions 2013; November 16–20, 2013.
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1. Belenkov Iu.N., Mareev V.Iu. Printsipy ratsional'nogo lecheniia serdechnoi nedostatochnosti. M.: Media Medika, 2000. [in Russian]
2. Duprez D, De Buyzere M, Rietzchel ER, Clement DL. Aldosterone and vascular damage. Curr Hypertens Rep 2000; 2: 327–34. 3. Williams GH. Cardiovascular benefits of aldosterone receptor antagonists: what about potassium? Hypertension 2005; 46: 265–6.
4. Epstein M. Aldosterone and the hypertensive kidney: its emerging role as a mediator of progressive renal dysfunction: a paradigm shift. J Hypertens 2001; 19: 829–42.
5. Sato A, Funder JW. High glucose stimulates aldosterone-induced hypertrophy via type I mineralocorticoid receptors in neonatal rat cardiomyocytes. Endocrinol 1996; 137: 4145–53.
6. Weber KT, Brilla CG. Pathological hypertrophy and cardiac interstitium: fibrosis and renin-angiotensin-aldosterone system. Circulation 1991; 83: 1849–65.
7. Tsutamoto T, Wadw A, Maeda K et al. Effect of spironolactone on Plasma brain natriuretic peptide and left ventricular remodeling in patients with congestive heart failure. J Am Col Cardiol 2001; 37: 1228–33.
8. Mano A, Tatsumi T, Shiraishi J et al. Aldosterone directly induces myocyte apoptosis through calcineurin-dependent pathways. Circulation 2004; 110: 317–23.
9. Yu Q. Оsteopontin mediates cardiac fibrosis and diastolic dysfunction in mice. Am J Physiol Heart Circ Physiol 2009; 297 (1): 76–85.
10. Tanaka K, Zlochivier S, Vikstrom K et al. Spatial distribution of fibrosis governs fibrillation wave dynamics in the posterior left atrium during heart failure. Circ Res 2007; 101: 839–47.
11. Zeisberg E, Kalluri R. Origins of cardiac fibroblasts. Circ Res 2010; 107 (11): 1304–12.
12. B Julie He, Mei-ling A Joiner, Madhu V Singh et al. Oxidation of CaMKII determines the cardiotoxic effects of aldosterone. Nat Med 2011; 17 (12): 1610–8.
13. Brilla CG, Matsubara LS, Weber KT. Anti-aldosterone treatment and the prevention of myocardial fibrosis in primary and secondary hyperaldosteronism. J Mol Cell Cardiol 1993; 25 (5): 563–75.
14. De Jong S, van Veen TA, van Rijen HV, de Bakker JM. Fibrosis and cardiac arrhythmias. J Cardiovasc Pharmacol 2011; 57 (6): 630–8.
15. Dąbrowski R, Szwed H. Antiarrhythmic potential of aldosterone antagonists in atrial fibrillation. Cardiol J 2012; 19 (3): 223–9.16. Zannad F, Alla F, Dousset B et al. Limitation of excessive extracellular matrix turnover may contribute to survival benefit of spironolactone therapy in patients with congestive heart failure: insights from the randomized aldactone evaluation study (RALES). Circulation 2000; 102: 2700–6.
17. McFaiden R, Barr C, Struthers A. Aldosterone blocade reduces vascular collagen turnover, improves heart rate variability and reduces early morning rise in heart rate in heart failure patients Cardiovasc Res 1997; 35: 30–4.
18. Swedberg K, Eneroth P, Kjekshus J, Wilhelmsen L; The CONSENSUS Trial Study Group. Hormones regulating cardiovascular function in patients with severe congestive heart failure and their relation to mortality. Circulation 1990; 82: 1730–6.
19. The CONSENSUS Trial Study Group. Effects of enalapril on mortality in severe congestive heart failure. N Engl J Med 1987; 316: 1429–35
20. Staessen J, Lijnen P, Fagard P et al. Rise in plasma concentration of aldosterone during long-term angiotensin II suppression. J Endocrinol 1981; 91: 457–65.
21. Borghi C, Boschi S, Ambrosioni E et al. Evidence of a partial escape of renin-angiotensine-aldosterone blocade in patients with acute myocardial infarction treated with ACE inhibitors. J Clin Pharmacol 1993; 33: 40–5.
22. Lee AFC, MacFadyen RJ, Struthers AD. Neurohormonal reactivation in heart failure patients on chronic ACE inhibitor therapy: a longitudinal study. Eur J Heart Fail 1999; 1: 401–6.
23. Mareev V.Iu., Skvortsov A.A., Chelmakina S.M. i dr. Sposobny li ingibitory APF effektivno kontrolirovat' aktivnost' renin-angiotenzin-al'dosteronovoi sistemy pri dlitel'nom lechenii khronicheskoi serdechnoi nedostatochnosti? Kardiologiia. 1999; 2: 27–34. [in Russian]
24. MacFadyen RJ, Lee AF, Morton JJ et al. How often are angiotensin II and aldosterone concentrations raised during chronic ACE inhibitor treatment in cardiac failure? Heart 1999; 82: 57–61.
25. Urata H, Healy BH, Stewart R et al. Angiotensin II forming pathways in normal and failing human hearts. Circ Res 1990; 66: 883–90.
26. Müller J. Regulation of aldosterone biosythesis: physiological and clinical aspects. Monographs on Endocrinology. 2nd ed. New York, Springer-Verlag. 1988; p. 29. 27.
27. Skvortsov A.A., Mareev V.Iu., Nasonova S.N. i dr. Neobkhodima li troinaia kombinatsiia razlichnykh grupp neirogormonal'nykh moduliatorov dlia lecheniia bol'nykh so stabil'noi umerennoi khronicheskoi serdechnoi nedostatochnost'iu? (Po rezul'tatam issledovaniia SADKO-KhSN). Terapevt. arkh. 2006; 78 (9): 61–71. [in Russian]
28. Pitt B, Zannad F, Remme WJ et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators. N Engl J Med 1999; 341 (10): 709–17.
29. Kramer DG, Trikalinos TA, Kent DM et al. Quantitative evaluation of drug or device effects on ventricular remodeling as predictors of therapeutic effects on mortality in patients with heart failure and reduced ejection fraction: a meta-analytic approach. J Am Coll Cardiol 2010; 56 (5): 392–406.
30. Jeunemaitre X, Chatellier G, Kreft-Jais C et al. Efficacy and tolerance of spironolactone in essential hypertension. Am J Cardiol 1987; 60: 820–5.
31. Pitt B, Remme W, Zannad F et al.; Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study Investigators. Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med 2003; 348: 1309–21.
32. Pitt B, White H, Nicolau J et al. Eplerenone reduces mortality 30 days after randomization following acute myocardial infarction in patients with left ventricular systolic dysfunction and heart failure. J Am Coll Cardiol 2005; 46 (3): 425–31.
33. Pitt B, Gheorghiade M, Zannad F et al. Evaluation of eplerenone in the subgroup of EPHESUS patients with baseline left ventricular ejection fraction <or=30 %. Eur J Heart Fail 2006; 8 (3): 295–301.
34. Sytnik N.V., Kokorin V.A., Liusov V.A. i dr. Aktivnost' RAAS i SAS u bol'nykh v otdalennye sroki posle pervichnogo infarkta miokarda. Ros. kardiol. zhurn. 2009; 4: 17–22. [in Russian]
35. Palmer BR, Pilbrow AP, Frampton CM et al. Plasma aldosterone levels during hospitalization are predictive of survival post-myocardial infarction. Eur Heart J 2008; 29: 2489–96.
36. Adamopoulos Ch, Ahmed A, Fay R et al.; the EPHESUS Investigators. Timing of eplerenone initiation and outcomes in patients with heart failure after acute myocardial infarction complicated by left ventricular systolic dysfunction: insights from the EPHESUS trial. Eur J Heart Failure 2009; 11: 1099–105.
37. Iqbal J, Fay R, Adlam D et al. Effect of eplerenone in percutaneous coronary intervention- treated post-myocardial infarction patients with left ventricular systolic dysfunction: a subanalysis of the EPHESUS trial. Eur J Heart Fail 2014; 16: 685–91.
38. Carillo S, Zhang Y, Fay R et al. Heart failure with systolic dysfunction complicating acute myocardial infarction – differential outcomes but similar eplerenone efficacy by ST-segment or non-ST-segment elevation: a post hoc substudy of the EPHESUS trial. Arch Cardiovasc Dis 2014; 107: 149–57.
39. Montalescot G, Pitt B, Lopez de Sa E et al. Early eplerenone treatment in patients with acute ST-elevation myocardial infarction without heart failure: the Randomized Double-Blind Reminder Study. Eur Heart J 2014; 35 (34): 2295–302.
40. Zannad F, McMurray JJ, Krum Н et al.; EMPHASIS-HF Study Group. Eplerenone in patients with systolic heart failure and mild symptoms. N Engl J Med 2011; 364: 11–21.
41. Phelan D, Thavendiranathan P, Collier P, Marwick TH. Aldosterone antagonists improve ejection fraction and functional capacity independently of functional class: a meta-analysis of randomised controlled trials. Heart 2012; 98 (23): 1693–700.
42. Udelson JE, Feldman AM, Greenberg B et al. Randomized, doubleblind, multicenter, placebo-controlledstudy evaluating the effect of aldosterone antagonism with eplerenone on ventricular remodeling in patients with mild-to-moderate heart failure and left ventricular systolic dysfunction. Circ Heart Fail 2010; 3 (3): 347–53.
43. Swedberg K, Zannad F, McMurray JJ et al. Eplerenone and atrial fibrillation in mild systolic heart failure: results from the EMPHASIS-HF (Eplerenone in Mild Patients Hospitalization And SurvIval Study in Heart Failure) study. J Am Coll Cardiol 2012; 59 (18): 1598–603.
44. Bapoje SR, Bahia A, Hokanson JE et al. Effects of mineralocorticoid receptor antagonists on the risk of sudden cardiac death in patients with left ventricular systolic dysfunction: a meta-analysis of randomized controlled trials. Circ Heart Fail 2013; 6 (2): 166–73.
45. Edelmann F, Wachter R, Schmidt AG et al.; Aldo-DHF Investigators. Effect of spironolactone on diastolic function and exercise capacity in patients with heart failure with preserved ejection fraction: the Aldo-DHF randomized controlled trial. JAMA 2013; 309: 781–91.
46. Pfeffer МА, McKinlay S, Pitt В et al.; ТОРСАТ Investigators. Treatment Of Preserved Cardiac Function Heart Failure with an Aldosterone anТagonist (ТОРСАТ). abstracts of the American Heart Association Scientific Sessions 2013; November 16–20, 2013.
Авторы
А.А.Кириченко*
ФГБОУ ДПО «Российская медицинская академия непрерывного профессионального образования» Минздрава России. 125993, Россия, Москва, ул. Баррикадная, д. 2/1
*andrey.apollonovich@yandex.ru
ФГБОУ ДПО «Российская медицинская академия непрерывного профессионального образования» Минздрава России. 125993, Россия, Москва, ул. Баррикадная, д. 2/1
*andrey.apollonovich@yandex.ru
________________________________________________
A.A.Kirichenko*
Russian Medical Academy of Continuous Professional Education of the Ministry of Health of the Russian Federation. 125993, Russian Federation, Moscow, ul. Barrikadnaia, d. 2/1
*andrey.apollonovich@yandex.ru
Russian Medical Academy of Continuous Professional Education of the Ministry of Health of the Russian Federation. 125993, Russian Federation, Moscow, ul. Barrikadnaia, d. 2/1
*andrey.apollonovich@yandex.ru
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