Angiotensin receptor neprilysin inhibitor (ARNI) and cardiac arrhythmias

doi:10.3877/cma.j.issn.2095-6568.2023.01.008

Abstract

Na Li, Jun Li, Liping Guo, Haixiong Wang. Angiotensin receptor neprilysin inhibitor (ARNI) and cardiac arrhythmias[J]. Chinese Journal of Heart and Heart Rhythm(Electronic Edition), 2023, 11(01): 39-44.

/ / Recommend

Add to citation manager EndNote|Ris|BibTeX

URL: https://zhxzyxldzzz.cma-cmc.com.cn/EN/10.3877/cma.j.issn.2095-6568.2023.01.008

https://zhxzyxldzzz.cma-cmc.com.cn/EN/Y2023/V11/I01/39

Figures/Tables 3

References 33

[1]	Fountain JH, Lappin SL. Physiology, renin angiotensin system[M]. Treasure Island: StatPearls Publishing, 2022.
[2]	Rossi F, Mascolo A, Mollace V. The pathophysiological role of natriuretic peptide-RAAS cross talk in heart failure[J]. Int J Cardiol, 2017, 226:121-125.
[3]	李小荣, 郑旭辉, 李新立. 血管紧张素受体脑啡肽酶抑制剂在心力衰竭治疗中的研究进展及展望[J]. 中国循环杂志, 2018, 33(2):195-198.
[4]	Dorey TW, Mackasey M, Jansen HJ, et al. Natriuretic peptide receptor B maintains heart rate and sinoatrial node function via cyclic GMP-mediated signalling[J]. Cardiovasc Res, 2022, 118(8):1917-1931.
[5]	Gong B, Wu Z, Li Z. Efficacy and safety of nesiritide in patients with decompensated heart failure: a meta-analysis of randomised trials[J]. BMJ Open, 2016, 6(1):e008545.
[6]	Polina I, Spicer MJ, Domondon M, et al. Inhibition of neprilysin with sacubitril without RAS blockage aggravates renal disease in Dahl SS rats[J]. Ren Fail, 2021, 43(1):315-324.
[7]	Kostis JB, Packer M, Black HR, et al. Omapatrilat and enalapril in patients with hypertension: the omapatrilat cardiovascular treatment vs. enalapril (OCTAVE) trial[J]. Am J Hypertens, 2004, 17(2):103-111.
[8]	Bas M, Adams V, Suvorava T, et al. Nonallergic angioedema: role of bradykinin[J]. Allergy, 2007, 62(8):842-856.
[9]	Ksander GM, Ghai RD, deJesus R, et al. Dicarboxylic acid dipeptide neutral endopeptidase inhibitors[J]. J Med Chem, 1995, 38(10):1689-1700.
[10]	Vanneste Y, Michel A, Dimaline R, et al. Hydrolysis of alpha-human atrial natriuretic peptide in vitro by human kidney membranes and purified endopeptidase-24.11. Evidence for a novel cleavage site[J]. Biochem J, 1988, 254(2):531-537.
[11]	Chen CH. Critical questions about PARADIGM-HF and the Future[J]. Acta Cardiol Sin, 2016, 32(4):387-396.
[12]	Verhaert D, Brunner-La Rocca HP, van Veldhuisen DJ, et al. The bidirectional interaction between atrial fibrillation and heart failure: consequences for the management of both diseases[J]. Europace, 2021, 23(23 Suppl 2):ii40-ii45.
[13]	Sutanto H, Lyon A, Lumens J, et al. Cardiomyocyte calcium handling in health and disease: insights from in vitro and in silico studies[J]. Prog Biophys Mol Biol, 2020, 157:54-75.
[14]	Verma A, Kalman JM, Callans DJ. Treatment of patients with atrial fibrillation and heart failure with reduced ejection fraction[J]. Circulation, 2017, 135(16):1547-1563.
[15]	Rohde LE, Chatterjee NA, Vaduganathan M, et al. Sacubitril/valsartan and sudden cardiac death according to implantable cardioverter-defibrillator use and heart failure cause: a PARADIGM-HF analysis[J]. JACC Heart Fail, 2020, 8(10):844-855.
[16]	Russo V, Bottino R, Rago A, et al. The effect of sacubitril/valsartan on device detected arrhythmias and electrical parameters among dilated cardiomyopathy patients with reduced ejection fraction and implantable cardioverter defibrillator[J]. J Clin Med, 2020, 9(4):1111.
[17]	Guerra F, Pimpini L, Flori M, et al. Sacubitril/valsartan reduces atrial fibrillation and supraventricular arrhythmias in patients with HFrEF and remote monitoring: preliminary data from the SAVE THE RHYTHM[J]. European Heart Journal, 2020, 41(suppl2): ehaa946.0926.
[18]	De Vecchis R, Paccone A, Di Maio M. Favorable effects of sacubitril/valsartan on the peak atrial longitudinal strain in patients with chronic heart failure and a history of one or more episodes of atrial fibrillation: a retrospective cohort study[J]. J Clin Med Res, 2020, 12(2):100-107.
[19]	Martens P, Nuyens D, Rivero-Ayerza M, et al. Sacubitril/valsartan reduces ventricular arrhythmias in parallel with left ventricular reverse remodeling in heart failure with reduced ejection fraction[J]. Clin Res Cardiol, 2019, 108(10):1074-1082.
[20]	McMurray JJ, Packer M, Desai AS, et al. Angiotensin-neprilysin inhibition versus enalapril in heart failure[J]. N Engl J Med, 2014, 371(11):993-1004.
[21]	McMurray J, Jackson AM, Lam C, et al. Effects of sacubitril-valsartan versus valsartan in women compared with men with heart failure and preserved ejection fraction: insights from PARAGON-HF[J]. Circulation, 2020, 141(5):338-351.
[22]	Vicent L, Méndez-Zurita F, Viñolas X, et al. Clinical characteristics of patients with sustained ventricular arrhythmias after sacubitril/valsartan initiation[J]. Heart Vessels, 2020, 35(1):136-142.
[23]	Chang PC, Wo HT, Lee HL, et al. Sacubitril/valsartan therapy ameliorates ventricular tachyarrhythmia inducibility in a rabbit myocardial infarction model[J]. J Card Fail, 2020, 26(6):527-537.
[24]	Chang PC, Lin SF, Chu Y, et al. LCZ696 Therapy reduces ventricular tachyarrhythmia inducibility in a myocardial infarction-induced heart failure rat model[J]. Cardiovasc Ther, 2019, 2019:6032631.
[25]	Li LY, Lou Q, Liu GZ, et al. Sacubitril/valsartan attenuates atrial electrical and structural remodelling in a rabbit model of atrial fibrillation[J]. Eur J Pharmacol, 2020, 881:173120.
[26]	Cheng WH, Lugtu IC, Chang SL, et al. Effects of angiotensin receptor-neprilysin inhibitor in arrhythmogenicity following left atrial appendage closure in an animal model[J]. Cardiovasc Drugs Ther, 2021, 35(4):759-768.
[27]	Sung YL, Lin TT, Syu JY, et al. Reverse electromechanical modelling of diastolic dysfunction in spontaneous hypertensive rat after sacubitril/valsartan therapy[J]. ESC Heart Fail, 2020, 7(6):4040-4050.
[28]	Tsai YN, Cheng WH, Chang YT, et al. Mechanism of angiotensin receptor-neprilysin inhibitor in suppression of ventricular arrhythmia[J]. J Cardiol, 2021, 78(4):275-284.
[29]	Huo JY, Jiang WY, Chen C, et al. Effects of angiotensin receptor neprilysin inhibitors on inducibility of ventricular arrhythmias in rats with ischemic cardiomyopathy[J]. Int Heart J, 2019, 60(5):1168-1175.
[30]	Eiringhaus J, Wünsche CM, Tirilomis P, et al. Sacubitrilat reduces pro-arrhythmogenic sarcoplasmic reticulum Ca(2+) leak in human ventricular cardiomyocytes of patients with end-stage heart failure[J]. ESC Heart Fail, 2020, 7(5):2992-3002.
[31]	Palaniyandi SS, Sun L, Ferreira JC, et al. Protein kinase C in heart failure: a therapeutic target?[J]. Cardiovasc Res, 2009, 82(2):229-239.
[32]	Aguilar M, Rose RA, Takawale A, et al. New aspects of endocrine control of atrial fibrillation and possibilities for clinical translation[J]. Cardiovasc Res, 2021, 117(7):1645-1661.
[33]	van Heerebeek L, Paulus WJ. Understanding heart failure with preserved ejection fraction: where are we today?[J]. Neth Heart J, 2016, 24(4):227-236.

临床试验	研究对象	试验组及对照组	心律失常相关研究指标	结论
SAVE THE RHYTHM研究^［17］	HFrEF+ CRT-D或ICD	60例患者接受ARNI治疗并随访12个月	每月平均持续AT或AF发作次数、AT/AF总负荷、平均每小时PVC次数和 CRT-D患者每日双心室起搏比例	抗心律失常（对于既往无AF或非永久性AF的患者，使用ARNI可降低AF的发生率和负荷）
De Vecchis等^［18］	心功能Ⅱ~III级（NYHA分级）慢性心衰；窦性心律伴非永久性AF；近6个月无心梗，无体循环或肺循环栓塞	80例患者（40例使用ARNI， 40例使用RAAS阻滞剂）	随访12个月AF复发的风险	抗心律失常（ARNI比RAAS阻滞剂降低AF复发的风险）
McMurray等^［20］	心功能Ⅱ~Ⅳ级（NYHA分级）的HFrEF，LVEF≤40%	8 442例（ARNI 4 187例，依那普利4 212例）	新发AF发生率	无影响（ARNI组新发AF84例，依那普利组83例，P=0.84）
PARAGON-HF研究^［21］	心功能Ⅱ~Ⅳ级（NYHA分级）的HFpEF，最近6个月内LVEF≥45%	4 796例（2 479例女性和2 317例男性被随机分配到ARNI组和缬沙坦组）	新发AF发生率	致心律失常（女性使用ARNI及缬沙坦后发生新发AF为84例和60例；男性使用ARNI及缬沙坦后发生新发AF为53例和65例）
Martens等^［19］	心功能Ⅱ~Ⅳ级（NYHA分级）的HFrEF，LVEF≤ 35%，植入ICD或CRT，先口服RSSA阻滞剂，后替换为ARNI	151例患者进行了12个月的随访	仪器记录到的心律失常事件（VT/VF，非持续性VT，每小时PVC负荷；AF负荷）	抗心律失常（启动ARNI治疗前后VT/VF发作≥1次的患者例数为19对10，P＜0.001；总VT/VF 发作次数51对14，P＜0.001；ARNI干预对AF负荷无影响）
PARADIGM-HF研究^［15］	心功能Ⅱ~Ⅳ级（NYHA分级）的HFrEF，LVEF≤35%	8 399例（其中1 243例植入 ICD）	SCD和全因死亡率	抗心律失常（降低SCD风险，与ICD状态无关）
Vicent等^［22］	接受ARNI治疗	218例	持续性VT	致心律失常（19例患者应用SV后出现持续性室性心律失常；6例患者在停用SV后出现新的心律失常事件）
Chang等^［23］	心梗后心衰的兔模型	21例（安慰剂组、缬沙坦组、 ARNI组各7例）	VT的诱导率	抗心律失常（降低了VT的诱导率）
Chang等^［24］	心梗后心衰的鼠模型	19例（9例依那普利，10例AR NI）	VT的诱导率	抗心律失常（降低了VT的诱导率）

临床试验	研究对象	试验组及对照组	心律失常相关研究指标	结论
SAVE THE RHYTHM研究^［17］	HFrEF+ CRT-D或ICD	60例患者接受ARNI治疗并随访12个月	每月平均持续AT或AF发作次数、AT/AF总负荷、平均每小时PVC次数和 CRT-D患者每日双心室起搏比例	抗心律失常（对于既往无AF或非永久性AF的患者，使用ARNI可降低AF的发生率和负荷）
De Vecchis等^［18］	心功能Ⅱ~III级（NYHA分级）慢性心衰；窦性心律伴非永久性AF；近6个月无心梗，无体循环或肺循环栓塞	80例患者（40例使用ARNI， 40例使用RAAS阻滞剂）	随访12个月AF复发的风险	抗心律失常（ARNI比RAAS阻滞剂降低AF复发的风险）
McMurray等^［20］	心功能Ⅱ~Ⅳ级（NYHA分级）的HFrEF，LVEF≤40%	8 442例（ARNI 4 187例，依那普利4 212例）	新发AF发生率	无影响（ARNI组新发AF84例，依那普利组83例，P=0.84）
PARAGON-HF研究^［21］	心功能Ⅱ~Ⅳ级（NYHA分级）的HFpEF，最近6个月内LVEF≥45%	4 796例（2 479例女性和2 317例男性被随机分配到ARNI组和缬沙坦组）	新发AF发生率	致心律失常（女性使用ARNI及缬沙坦后发生新发AF为84例和60例；男性使用ARNI及缬沙坦后发生新发AF为53例和65例）
Martens等^［19］	心功能Ⅱ~Ⅳ级（NYHA分级）的HFrEF，LVEF≤ 35%，植入ICD或CRT，先口服RSSA阻滞剂，后替换为ARNI	151例患者进行了12个月的随访	仪器记录到的心律失常事件（VT/VF，非持续性VT，每小时PVC负荷；AF负荷）	抗心律失常（启动ARNI治疗前后VT/VF发作≥1次的患者例数为19对10，P＜0.001；总VT/VF 发作次数51对14，P＜0.001；ARNI干预对AF负荷无影响）
PARADIGM-HF研究^［15］	心功能Ⅱ~Ⅳ级（NYHA分级）的HFrEF，LVEF≤35%	8 399例（其中1 243例植入 ICD）	SCD和全因死亡率	抗心律失常（降低SCD风险，与ICD状态无关）
Vicent等^［22］	接受ARNI治疗	218例	持续性VT	致心律失常（19例患者应用SV后出现持续性室性心律失常；6例患者在停用SV后出现新的心律失常事件）
Chang等^［23］	心梗后心衰的兔模型	21例（安慰剂组、缬沙坦组、 ARNI组各7例）	VT的诱导率	抗心律失常（降低了VT的诱导率）
Chang等^［24］	心梗后心衰的鼠模型	19例（9例依那普利，10例AR NI）	VT的诱导率	抗心律失常（降低了VT的诱导率）

Please choose a citation manager

Content to export

Angiotensin receptor neprilysin inhibitor (ARNI) and cardiac arrhythmias

RichHTML

Knowledge

Cited

Abstract

Cite this article

share this article

Figures/Tables 3

References 33

Related Articles 0

Recommended Articles

Metrics

Comments

模态框（Modal）标题

Please choose a citation manager

Content to export

Angiotensin receptor neprilysin inhibitor (ARNI) and cardiac arrhythmias

RichHTML

Knowledge

Cited

Abstract

Cite this article

share this article

Figures/Tables 3

References 33

Related Articles 0

Recommended Articles

Metrics

Comments