Prospective Study to Ascertain the Advantages of Adding Neprilysin Inhibitor to Standard Care Among Patients with Congestive Cardiac Failure

  • Dr.Vivekananda Chood O.M
  • Dr.Sriram.K
  • Dr.Thilagar
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Dr.Vivekananda Chood O.M, Dr.Sriram.K, and Dr.Thilagar, “Prospective Study to Ascertain the Advantages of Adding Neprilysin Inhibitor to Standard Care Among Patients with Congestive Cardiac Failure”, ijmhs, vol. 12, no. 05, pp. 1903–1909, May 2022.
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Abstract

Neprilysin, a neural endopeptidase, degrades several endogenous vasoactive peptides, including natriuretic peptides, bradykinin, and adrenomedullin. Inhibition of neprilysin increases the levels of these substances, countering the neurohormonal over activation that contributes to vasoconstriction, sodium retention, and maladaptive remodeling. Sacubitril-Valsartan, a angiotensin neprilysin inhibitor when added to standard care among congestive heart failure patients, reduces the risk of cardiovascular death, heart failure hospitalizations and also it incrementally improves symptoms and physical limitations due to heart failure. There are many studies in western countries which showed neprilysin inhibition added to standard care reduces mortality and morbidity in patients with heart failure with reduced ejection fraction. But in India studies were limited, to show these facts. In this study we will compare the angiotensin receptor neprilysin inhibitor (sacubitril- valsartan) with telmisartan in patients who had heart failure with a borderline reduced ejection fraction

Methods:

Patients with heart failure those who met the inclusion criteria for the study were randomly divided into two groups namely Group one, receiving Telmisartan(40mg od) and other Group receiving sacubitril – valsartan(100mg BD) therapy in addition to standard care of heart failure. Two groups were followed up for a period of 8months and the improvement in LVEF, rehospitalisation for heart failure, reduction in NT-ProBNP levels, improvement in NYHA class, adverse events and other key parameters were observed in both the groups.

Statistical Analysis:

The data was analysed by SPSS 20.0 with unpaired t test and chi square test.

Results:

We      found  that      the       sacubitril/valsartan      group   has significant improvement in EF, reduced hospitalization for HF, improved quality of life in patients of Heart failure with EF <40%, against Telmisartan group.. Sacubitril/valsartan group has total no of hospitalisation of 5 against 16 of Telmisartan group during study period, with p value of <0.05. Sacubitril/valsartan group has an average 10% improvements in EF against 5% in Telmisartan group, which is statistically significant with p value of <0.05. The average NT-proBNP level decreased from 1259 pg/mL to 343 pg/mL in sacubitril/valsartan group with p value of <0.05.

Conclusion:

The study showed that, there is significant improvement in EF, REDUCED  hospitalization     for    HF,    improved    quality    of     life,

improvement in NYHA class and a significant reduction in NT-ProBNP    levels among      patients with HF with reduced EF<40%

initiated on sacubitril-valsartan compared to telmisartan group. Results support the use of sacubitril/valsartan in Indian patients with chronic HF with reduced ejection fraction with acceptable safety profile and treatment benefits.

KEYWORDS:

 Special Issue

References

1. Eric J. Velazquez, M.D., David A. Morrow, M.D., M.P.H., Adam D. DeVore, M.D.,M.H.S., et al. Angiotensin–Neprilysin Inhibition in Acute Decompensated Heart Failure . N Engl J Med 2019; 380:539-548, DOI: 10.1056/NEJMoa1812851. 2. Ponikowski P, Voors AA, Anker SD, Bueno H, Cleland J, Coats A,et al. 2016 ESC Guidelines for the diagnosis and treatment ofacute and chronic heart failure: The task force for the diagnosisand treatment of acute and chronic heart failure of the European Society of Cardiology (ESC) developed with the special contribution of the Heart Failure Association (HFA) of the ESC.Eur Heart J 2016;37:2129‑200. doi: 10.1093/eurheartj/ehw128. 3. McMurray JJ, Petrie MC, Murdoch DR, Davie AP. Clinical epidemiology of heartfailure: public and private health burden. Eur Heart J. 1998; 19(suppl P):Mann D L, Chakinala M. Heart failure:pathophysiology and diagnosis.In:Harrison‘s principles of internal medicine 19th ed, McGraw-Hill; Longo DL,Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J eds. Vol 2, Chap 279:2112 4. Butler J, Braunwald E, Gheorghiade M. Recognizing worsening chronic heart failure as anentity and an end point in clinical trials. JAMA. 2014;312:789–790 5. Cleland JG. How to assess new treatments for the management of heart failure: composite scoring systems to assess the patients’ clinical journey. ur J Heart Fail. 2002;4:243–247. with reduced left ventricular ejection fractions and congestive heart failure. The SOLVD Investigators. N Engl J Med 1991;325:293–302. 6. Mann D L. Pathophysiology of heart failure. In: Braunwald's heart disease: A textbook of cardiovascular medicine. 9th ed. Elsevier; Chap 25:487-503 7. Mann DL: Mechanisms and models in HF: A combinatorial approach.Circulation 100:99, 1999; and Kaye DM, Krum H: Drug discovery for heart failure: A new era or the end of the pipeline? Nat Rev Drug Discov 6:127,2007. 8. Robb D. Kociol. Heart Failure Editors' Picks: Most Important Papers in Pathophysiology and genetics. Circ Heart Fail. 2012;5:e32-e49 9. Mann DL, Bristow MR: Mechanisms and models in heart failure: The biomechanical model and beyond. Circulation 111:2837, 2005 10. Dell‘Italia L, Sabri A: Activation of the renin-angiotensin system in hypertrophy and heart failure. In Mann DL (ed): Heart Failure: A Companion to Braunwald‘s Heart Disease. Philadelphia, Saunders, 2004, pp 129-143

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References

  1. Eric J. Velazquez, M.D., David A. Morrow, M.D., M.P.H., Adam D. DeVore, M.D.,M.H.S., et al. Angiotensin–Neprilysin Inhibition in Acute Decompensated Heart Failure . N Engl J Med 2019; 380:539-548, DOI: 10.1056/NEJMoa1812851.
  2. Ponikowski P, Voors AA, Anker SD, Bueno H, Cleland J, Coats A,et al. 2016 ESC Guidelines for the diagnosis and treatment ofacute and chronic heart failure: The task force for the diagnosisand treatment of acute and chronic heart failure of the European Society of Cardiology (ESC) developed with the special contribution of the Heart Failure Association (HFA) of the ESC.Eur Heart J 2016;37:2129?200. doi: 10.1093/eurheartj/ehw128.
  3. McMurray JJ, Petrie MC, Murdoch DR, Davie AP. Clinical epidemiology of heartfailure: public and private health burden. Eur Heart J. 1998; 19(suppl P):Mann D L, Chakinala M. Heart failure:pathophysiology and diagnosis.In:Harrison‘s principles of internal medicine 19th ed, McGraw-Hill; Longo DL,Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J eds. Vol 2, Chap 279:2112
  4. Butler J, Braunwald E, Gheorghiade M. Recognizing worsening chronic heart failure as anentity and an end point in clinical trials. JAMA. 2014;312:789–790
  5. Cleland JG. How to assess new treatments for the management of heart failure: composite scoring systems to assess the patients’ clinical journey. ur J Heart Fail. 2002;4:243–247. with reduced left ventricular ejection fractions and congestive heart failure. The SOLVD Investigators. N Engl J Med 1991;325:293–302.
  6. Mann D L. Pathophysiology of heart failure. In: Braunwald's heart disease: A textbook of cardiovascular medicine. 9th ed. Elsevier; Chap 25:487-503
  7. Mann DL: Mechanisms and models in HF: A combinatorial approach.Circulation 100:99, 1999; and Kaye DM, Krum H: Drug discovery for heart failure: A new era or the end of the pipeline? Nat Rev Drug Discov 6:127,2007.
  8. Robb D. Kociol. Heart Failure Editors' Picks: Most Important Papers in Pathophysiology and genetics. Circ Heart Fail. 2012;5:e32-e49
  9. Mann DL, Bristow MR: Mechanisms and models in heart failure: The biomechanical model and beyond. Circulation 111:2837, 2005
  10. Dell‘Italia L, Sabri A: Activation of the renin-angiotensin system in hypertrophy and heart failure. In Mann DL (ed): Heart Failure: A Companion to Braunwald‘s Heart Disease. Philadelphia, Saunders, 2004, pp 129-143

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