PATHOPHYSIOLOGICAL PRINCIPLES UNDERLYING THE EFFECT OF SACUBITRIL-VALSARTAN ON HYPERTENSION-INDUCED CARDIOVASCULAR REMODELING
DOI:
https://doi.org/10.52340/jecm.2022.06.23Ключевые слова:
sacubitril/valsartan, arterial hypertension, cardiac remodelingАннотация
Myocardial remodeling is a process executed by cardiomyocytes, other cells within the myocardium (i.e, endothelial cells, fibroblasts, pericytes, and immune cells), and cells recruited from the circulation (e.g, immune and inflammatory cells) in response to mechanical and non-mechanical stimuli. As a result, the composition, volume, and physiology of cardiomyocytes, the interstitial matrix, and the coronary vessels undergo interrelated changes. These changes detrimentally affect the clinical outcomes of patients with hypertensive heart disease (HHD), due to the risk of fibrillation and increased ventricular stiffness leading to systolic or diastolic dysfunction. Therefore, to reduce cardiovascular remodeling is the main aim for the overall clinical care of these patients.Several drugs, such as angiotensin-converting enzyme inhibitors, beta blockers, and aldosterone antagonists, have been consistently shown to decrease remodeling in animal models and in clinical trials, and are currently widely used to decrease myocardial remodeling. A combination of sacubitril, a neprilysin inhibitor, and valsartan, an angiotensin receptor antagonist, which has positive clinical outcomes in patients with heart failure with reduced ejection fraction, has recently gained public and scientific attention for patients with heart failure with preserved ejection fraction. By promoting the accumulation of natriuretic peptides, which have natriuretic and vascular smooth muscle relaxant properties and by reducing the effects of the renin-angiotensin-aldosterone system, the combination of these two drugs has cardioprotective and antihypertensive effects and reduces cardiovascular fibrosis. It is noteworthy, that sacubitril/valsartan showed a better effect on cardiac remodeling and reversal fraction compared with ACE inhibitor perindopril in rats. However, these are only preliminary data and more extensive studies should be conducted in both experimental and clinical settings in order to fully reveal the mechanisms of action of the drug in the management of various types of arterial hypertension.
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Altara R, Mallat Z, Booz GW, Zouein FA. The CXCL10/CXCR3 axis and cardiac inflammation: implications for immunotherapy to treat infectious and noninfectious diseases of the heart. J Immunol Res. 2016; 2016:4396368. doi: 10.1155/2016/4396368.
Behr TM, Willette RN, Coatney RW, Berova M, Angermann CE, Anderson K, Sackner-Bernstein JD, Barone FC. Eprosartan improves cardiac performance, reduces cardiac hypertrophy and mortality and downregulates myocardial monocyte chemoattractant protein-1 and inflammation in hypertensive heart disease. J Hypertens. 2004; 22:583–592.
Berk BC, Fujiwara K, Lehoux S. ECM remodeling in hypertensive heart disease. J Clin Invest. 2007; 117:568–575. doi: 10.1172/JCI31044.
Chen MA (2009). Heart failure with preserved ejection fraction in older adults. Am J Med122, 713–723.
Creemers EE & Pinto YM (2011). Molecular mechanisms that control interstitial fibrosis in the pressure‐overloaded heart. Cardiovasc Res 89, 265–272.
Deckx S, Heggermont W, Carai P, Rienks M, Dresselaers T, Himmelreich U, van Leeuwen R, Lommen W, van der Velden J, Gonzalez A, Diez J, Papageorgiou AP, Heymans S. Osteoglycin prevents the development of age-related diastolic dysfunction during pressure overload by reducing cardiac fibrosis and inflammation. Matrix Biol. 2018; 66:110–124. doi: 10.1016/j.matbio.2017.09.002.
Dickhout JG, Carlisle RE, Austin RC. Interrelationship between cardiac hypertrophy, heart failure, and chronic kidney disease: endoplasmic reticulum stress as a mediator of pathogenesis. Circ Res. 2011; 108:629–642. doi: 10.1161/CIRCRESAHA.110.226803.
Drazner MH (2011). The progression of hypertensive heart disease. Circulation123, 327–334.
Egan Benova T, Szeiffova Bacova B, Viczenczova C, Diez E, Barancik M & Tribulova N (2016). Protection of cardiac cell‐to‐cell coupling attenuates myocardial remodeling and proarrhythmia induced by hypertension. Physiol Res 65 Suppl 1, S29–S42.
Goldberg LI, Bloodwell RD, Braunwald E & Morrow AG (1960). The direct effects of norepinephrine, epinephrine, and methoxamine on myocardial contractile force in man. Circulation 22, 1125–1132.
González A, Arantxa González From the Program of Cardiovascular Diseases, Ravassa S, et al. Myocardial remodeling in hypertension. Hypertension. https://www.ahajournals.org/doi/10.1161/HYPERTENSIONAHA.118.11125. Published July 23, 2018. Accessed April 13, 2022.
González A, López B, Querejeta R & Díez J (2002). Regulation of myocardial fibrillar collagen by angiotensin II. A role in hypertensive heart disease? J Mol Cell Cardiol 34, 1585–1593.
González A, Ravassa S, Loperena I, López B, Beaumont J, Querejeta R, Larman M, Díez J. Association of depressed cardiac gp130-mediated antiapoptotic pathways with stimulated cardiomyocyte apoptosis in hypertensive patients with heart failure. J Hypertens. 2007; 25:2148–2157. doi: 10.1097/HJH.0b013e32828626e2.
González GE, Rhaleb N‐E, D'Ambrosio MA, Nakagawa P, Liao T‐D, Peterson EL, Leung P, Dai X, Janic B, Liu Y‐H, Yang X‐P & Carretero OA (2016). Cardiac‐deleterious role of galectin‐3 in chronic angiotensin II‐induced hypertension. Am J Physiol Hear Circ Physiol 311, H1287–H1296.
González A, Schelbert EB, Díez J, Butler J. Myocardial interstitial fibrosis in heart failure: biological and translational perspectives. J Am Coll Cardiol. 2018; 71:1696–1706. doi: 10.1016/j.jacc.2018.02.021.
Knöll R, Iaccarino G, Tarone G, Hilfiker-Kleiner D, Bauersachs J, Leite-Moreira AF, Sugden PH, Balligand JL; European Society of Cardiology. Towards a re-definition of ‘cardiac hypertrophy’ through a rational characterization of left ventricular phenotypes: a position paper of the Working Group ‘Myocardial Function’ of the ESC. Eur J Heart Fail. 2011; 13:811–819. doi: 10.1093/eurjhf/hfr071.
Kvakan H, Luft FC, Muller DN. Role of the immune system in hypertensive target organ damage. Trends Cardiovasc Med. 2009; 19:242–246. doi: 10.1016/j.tcm.2010.02.004.
Kyuma M, Nakata T, Hashimoto A & Nagao K (2004). Incremental prognostic implications of brain natriuretic peptide, cardiac sympathetic nerve innervation, and noncardiac disorders in patients with heart failure. J Nucl Med 45, 155–164.
Leask A & Abraham DJ (2004). TGF‐β signaling and the fibrotic response. FASEB J 18, 816–827.
Levick SP, Murray DB, Janicki JS, Brower GL. Sympathetic nervous system modulation of inflammation and remodeling in the hypertensive heart. Hypertension. 2010; 55:270–276. doi: 10.1161/HYPERTENSIONAHA.109.142042.
McCormick RJ & Thomas DP (1998). Collagen crosslinking in the heart: relationship to development and function. Basic Appl Myol8, 143–150.
Ogata T, Miyauchi T, Sakai S, Takanashi M, Irukayama-Tomobe Y, Yamaguchi I. Myocardial fibrosis and diastolic dysfunction in deoxycorticosterone acetate-salt hypertensive rats is ameliorated by the peroxisome proliferator-activated receptor-alpha activator fenofibrate, partly by suppressing inflammatory responses associated with the nuclear factor-kappa-B pathway. J Am Coll Cardiol. 2004; 43:1481–1488. doi: 10.1016/j.jacc.2003.11.043.
Ravassa S, González A, López B, Beaumont J, Querejeta R, Larman M, Díez J. Upregulation of myocardial Annexin A5 in hypertensive heart disease: association with systolic dysfunction. Eur Heart J. 2007; 28:2785–2791. doi: 10.1093/eurheartj/ehm370.
Ruwhof C & Laarse A Van Der (2000). Mechanical stress‐induced cardiac hypertrophy: mechanisms and signal transduction pathways. Cardiovasc Res47, 23–37.
Santulli G & Iaccarino G (2016). Adrenergic signaling in heart failure and cardiovascular aging. Maturitas93, 65–72.
Sun Y, Liu G, Song T, Liu F, Kang W, Zhang Y, Ge Z. Upregulation of GRP78 and caspase-12 in diastolic failing heart. Acta Biochim Pol. 2008; 55:511–516.
Swynghedauw B. Molecular mechanisms of myocardial remodeling. Physiol Rev. 1999; 79:215–262. DOI: 10.1152/physrev.1999.79.1.215.
Tomek J, Bub G. Hypertension-induced remodeling: on the interactions of cardiac risk factors. J Physiol. 2017;595(12):4027-4036. doi:10.1113/JP273043
Yoshida K, Kim-Mitsuyama S, Wake R, Izumiya Y, Izumi Y, Yukimura T, Ueda M, Yoshiyama M, Iwao H. Excess aldosterone under normal salt diet induces cardiac hypertrophy and infiltration via oxidative stress. Hypertens Res. 2005; 28:447–455. doi: 10.1291/hypres.28.447.
González A, Ravassa S, López B, Moreno MU, Beaumont J, San José G, Querejeta R, Bayés-Genís A, Díez J. Myocardial Remodeling in Hypertension. Hypertension. 2018 Sep;72(3):549-558.
Renna NF, de Las Heras N, Miatello RM. Pathophysiology of vascular remodeling in hypertension. Int J Hypertens. 2013;2013:808353. doi: 10.1155/2013/808353. Epub 2013 Jul 22. PMID: 23970958; PMCID: PMC3736482.
James PA, Oparil S, Carter BL, et al.: 2014 evidence-based guideline for the management of high blood pressure in adults: report from the panel members appointed to the Eighth Joint National Committee (JNC 8).JAMA. 2014; 311(5): 507–20.
Kostis JB, Packer M, Black HR, et al.: Omapatrilat and enalapril in patients with hypertension: the Omapatrilat Cardiovascular Treatment vs.Enalapril (OCTAVE) trial. Am J Hypertens. 2004; 17(2):103–11.
Oparil S, Schmieder RE: New approaches in the treatment of hypertension. Circ Res. 2015; 116(6): 1074–95.
Macdonald PS: Combined angiotensin receptor/neprilysin inhibitors: a review of the new paradigm in the management of chronic heart failure. Clin Ther. 2015; 37(10): 2199–205.
Hubers SA, Brown NJ: Combined Angiotensin Receptor Antagonism and Neprilysin Inhibition.Circulation. 2016; 133(11): 1115–24
Riddell E, Vader JM. Potential expanded indications for neprilysin inhibitors. Curr Heart Fail Rep. 2017; 14(2):134-145.
Renato De Vecchis, Silvia Soreca, Carmelina Ariano, Anti-Hypertensive Effect of Sacubitril/Valsartan: A MetaAnalysis of Randomized Controlled Trials, Cardiol Res. 2019; 10 (1), 24-33.
Andersen MB, Simonsen U, Wehland M, Pietsch J, Grimm D. LCZ696 (Valsartan/Sacubitril) - A possible new treatment for hypertension and heart failure. Basic Clin Pharmacol Toxicol. 2016; 118(1):14-22.
Guet al., 2010; Ruilope et al., 2010; McMurray et al., 2013;Vardeny et al., 2014.
Lauren B. Arendse, A. H. Jan Danser, Marko Poglitsch, Rhian M. Touyz, John C. Burnett, Jr., Catherine Llorens-Cortes, Mario R. Ehlers, and Edward D. Sturrock, Novel Therapeutic Approaches Targeting the Renin-Angiotensin System and Associated Peptides in Hypertension and Heart Failure, Pharmacol Rev, 2019; 71:539–570
Pandey KN (2005) Biology of natriuretic peptides and their receptors. Peptides 26:901–932.
Soualmia H, Barthelemy C, Masson F, Maistre G, Eurin J, and Carayon A (1997) Angiotensin II-induced phosphoinositide production and atrial natriuretic peptide release in rat atrial tissue. J Cardiovasc Pharmacol 29:605–611.
Abassi Z, Karram T, Ellaham S, Winaver J, and Hoffman A (2004) Implications of the natriuretic peptide system in the pathogenesis of heart failure: diagnostic and therapeutic importance. Pharmacol Ther 102:223–241.
Villar IC, Panayiotou CM, Sheraz A, Madhani M, Scotland RS, Nobles M, KempHarper B, Ahluwalia A, and Hobbs AJ (2007) Definitive role for natriuretic peptide receptor-C in mediating the vasorelaxant activity of C-type natriuretic peptide and endothelium-derived hyperpolarising factor. Cardiovasc Res 74:515–525.
O’Connor CM, Starling RC, Hernandez AF, Armstrong PW, Dickstein K, Hasselblad V, Heizer GM, Komajda M, Massie BM, McMurray JJ, et al. (2011) Effect ofnesiritide in patients with acute decompensated heart failure [published correctionappears in N Engl J Med (2011) 365:773]. N Engl J Med 365:32–43.
Campbell DJ and Habener JF (1986) Angiotensinogen gene is expressed and differentially regulated in multiple tissues of the rat. J Clin Invest 78:31–39.
Cleland JG and Swedberg K; The International Ecadotril Multi-centre Dose-ranging Study Investigators (1998) Lack of efficacy of neutral endopeptidase inhibitor ecadotril in heart failure. Lancet 351:1657–58.
Roksnoer LC, van Veghel R, de Vries R, Garrelds IM, Bhaggoe UM, Friesema EC, Leijten FP, Poglitsch M, Domenig O, Clahsen-van Groningen MC, et al. (2015) OptimumAT1 receptor-neprilysin inhibition has superior cardioprotective effects comparedwith AT1 receptor blockade alone in hypertensive rats. Kidney Int 88:109–120.
HFrEF (McMurray JJ, Packer M, Desai AS, Gong J, Lefkowitz MP, Rizkala AR, Rouleau JL, Shi VC, Solomon SD, Swedberg K, et al.; PARADIGM-HF Investigators and Committees (2014) Angiotensin-neprilysin inhibition versus enalapril in heart failure. N Engl J Med 371:993–1004.
Mogensen UM, Gong J, Jhund PS, Shen L, Kober L, Desai AS, Lefkowitz MP, Packer M, Rouleau JL, Solomon SD, et al. (2018) Effect of sacubitril/valsartan on recurrentevents in the Prospective.
Jarcho J (2019) PIONEERing the in-hospital initiation of sacubitril-valsartan. N Engl J Med 380:590–91.
Kompa AR, Lu J, Weller TJ, Kelly DJ, Krum H, von Lueder TG, and Wang BH (2018) Angiotensin receptor neprilysin inhibition provides superior cardioprotection compared to angiotensin converting enzyme inhibition after experimental myocardial infarction. Int J Cardiol 258:192–198.
Kougias P, Weakley SM, Yao Q, Lin PH, Chen C. Arterial baroreceptors in the management of systemic hypertension. Med Sci Monit. 2010; 16(1): RA1-RA8.
Head GA. Baroreflexes and cardiovascular regulation in hypertension. J Cardiovasc Pharmacol. 1995; 26 Suppl 2: S7-16. PMID: 8642810.