![]() 8 Seferovic JP, Claggett B, Seidelmann SB, Seely EW, Packer M, Zile MR, Rouleau JL, Swedberg K, Lefkowitz M, Shi VC, Desai AS, McMurray JJV, Solomon SD.The role of sacubitril/valsartan in the treatment of chronic heart failure with reduced ejection fraction in hypertensive patients with comorbidities: from clinical trials to real-world settings. 7 Mazza A, Townsend DM, Torin G, Schiavon L, Camerotto A, Rigatelli G, Cuppini S, Minuz P, Rubello D.Sacubitril/valsartan reduces ventricular arrhythmias in parallel with left ventricular reverse remodeling in heart failure with reduced ejection fraction. 6 Martens P, Nuyens D, Rivero-Ayerza M, Van Herendael H, Vercammen J, Ceyssens W, Luwel E, Dupont M, Mullens W.Association of Change in N-terminal pro-B-type natriuretic peptide following initiation of Sacubitril-valsartan treatment with cardiac structure and function in patients with heart failure with reduced ejection fraction. 5 Januzzi JL Jr, Prescott MF, Butler J, Felker GM, Maisel AS, McCague K, Camacho A, Piña IL, Rocha RA, Shah AM, Williamson KM, Solomon SD.Heart failure drug treatment: the fantastic four. Angiotensin-neprilysin inhibition versus enalapril in heart failure. 3 McMurray JJ, Packer M, Desai AS, Gong J, Lefkowitz MP, Rizkala AR, Rouleau JL, Shi VC, Solomon SD, Swedberg K, Zile MR.Effect of losartan compared with captopril on mortality in patients with symptomatic heart failure: randomised trial-the losartan heart failure survival study ELITE II. 2 Pitt B, Poole-Wilson PA, Segal R, Martinez FA, Dickstein K, Camm AJ, Konstam MA, Riegger G, Klinger GH, Neaton J, Sharma D, Thiyagarajan B.Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure. 1 Yusuf S, Pitt B, Davis CE, Hood WB, Cohn JN.Although the ARNI group already had high insulin resistance at baseline, an additional SEM analysis revealed that the decreased insulin resistance was truly due to the effect of ARNI. In conclusion, even in a short period of only 3 months, the administration of ARNI improved insulin resistance and consequently reduced the serum uric acid levels in patients with stable chronic heart failure. Similarly, the initiation of ARNI resulted in a significant reduction in serum uric acid levels (6.28 ± 0.35 to 5.80 ± 0.30 mg/dL, P = 0.008). An additional SEM analysis demonstrated that the initiation of ARNI had caused a reduction in the fasting blood insulin and the HOMA-IR levels at 3 months independently of the baseline fasting blood insulin and HOMA-IR levels, respectively. Three months later, the fasting blood insulin and the HOMA-IR levels were both found to have decreased in comparison with the baseline values. The baseline insulin resistance in the ARNI group was already significantly higher in comparison with the control group. ResultsĪt baseline, although the ARNI group included fewer patients with heart failure with preserved ejection fraction in comparison with the control group ( P = 0.004), patients with heart failure with mildly reduced ejection fraction, and heart failure with reduced ejection fraction were mostly biased towards the ARNI group (although not statistically significant). Seventeen patients switched from ACE inhibitors or ARBs to an ARNI (ARNI group), and the other 17 patients continued treatment with ACE inhibitors or ARBs (control group). We analysed 34 patients who regularly visited to the outpatient department of our institute with heart failure from October 2021 and July 2022 and who were taking angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs). We retrospectively investigated the effect of ARNI on abnormal glucose metabolism in patients with stable chronic heart failure using an additional structural equation model (SEM) analysis. Although the haemodynamic effects of angiotensin receptor-neprilysin inhibitor (ARNI) on patients with heart failure have been demonstrated, the effect on glucose metabolism has not been fully elucidated.
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