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Heart Failure Treatments Such As Angiotensin Receptor/Neprilysin Inhibitor Improve Heart Failure Status and Glucose Metabolism
A recent study suggested that angiotensin receptor/neprilysin inhibitor (ARNI; sacubitril/valsartan) can improve functional capacity and cardiac reverse remodeling in patients with heart failure with reduced ejection fraction (HFrEF). Another study suggested that ARNI reduced glycated hemoglobin (Hb...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Cureus
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8971101/ https://www.ncbi.nlm.nih.gov/pubmed/35371876 http://dx.doi.org/10.7759/cureus.22762 |
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author | Kashiwagi, Yusuke Nagoshi, Tomohisa Ogawa, Kazuo Kawai, Makoto Yoshimura, Michihiro |
author_facet | Kashiwagi, Yusuke Nagoshi, Tomohisa Ogawa, Kazuo Kawai, Makoto Yoshimura, Michihiro |
author_sort | Kashiwagi, Yusuke |
collection | PubMed |
description | A recent study suggested that angiotensin receptor/neprilysin inhibitor (ARNI; sacubitril/valsartan) can improve functional capacity and cardiac reverse remodeling in patients with heart failure with reduced ejection fraction (HFrEF). Another study suggested that ARNI reduced glycated hemoglobin (HbA1c) in patients with diabetes and HFrEF; however, the details of its efficacy are unknown. We herein report a case of HFrEF with abnormal glucose metabolism in which ARNI was initiated. On the 7(th) day of admission (before the initiation of ARNI), blood tests showed an abnormal glucose metabolism as follows: fasting blood glucose 134 mg/dL; and fasting blood insulin 11.4 µU/mL (homeostasis model assessment of insulin resistance (HOMA-IR) index 3.77; homeostasis model assessment of β-cell function (HOMA-β), 57.8%). On the 23(rd) day after the initiation of ARNI, even though the patient was not using hypoglycemic drugs, his fasting blood glucose markedly decreased to 70 mg/dL without hypoglycemic symptoms, and his fasting blood insulin decreased to 5.4 µU/mL (HOMA-IR decreased to 0.93, HOMA-β increased to 277.7%). These results imply that ARNI has the potential to improve insulin resistance and the islet beta-cell function in patients with heart failure, in addition to the original effect of improving the hemodynamics, although the effect of improving the glucose metabolism is also considered to have been influenced by the improvement of the heart failure status and other drugs that the patient was taking. |
format | Online Article Text |
id | pubmed-8971101 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Cureus |
record_format | MEDLINE/PubMed |
spelling | pubmed-89711012022-04-01 Heart Failure Treatments Such As Angiotensin Receptor/Neprilysin Inhibitor Improve Heart Failure Status and Glucose Metabolism Kashiwagi, Yusuke Nagoshi, Tomohisa Ogawa, Kazuo Kawai, Makoto Yoshimura, Michihiro Cureus Cardiology A recent study suggested that angiotensin receptor/neprilysin inhibitor (ARNI; sacubitril/valsartan) can improve functional capacity and cardiac reverse remodeling in patients with heart failure with reduced ejection fraction (HFrEF). Another study suggested that ARNI reduced glycated hemoglobin (HbA1c) in patients with diabetes and HFrEF; however, the details of its efficacy are unknown. We herein report a case of HFrEF with abnormal glucose metabolism in which ARNI was initiated. On the 7(th) day of admission (before the initiation of ARNI), blood tests showed an abnormal glucose metabolism as follows: fasting blood glucose 134 mg/dL; and fasting blood insulin 11.4 µU/mL (homeostasis model assessment of insulin resistance (HOMA-IR) index 3.77; homeostasis model assessment of β-cell function (HOMA-β), 57.8%). On the 23(rd) day after the initiation of ARNI, even though the patient was not using hypoglycemic drugs, his fasting blood glucose markedly decreased to 70 mg/dL without hypoglycemic symptoms, and his fasting blood insulin decreased to 5.4 µU/mL (HOMA-IR decreased to 0.93, HOMA-β increased to 277.7%). These results imply that ARNI has the potential to improve insulin resistance and the islet beta-cell function in patients with heart failure, in addition to the original effect of improving the hemodynamics, although the effect of improving the glucose metabolism is also considered to have been influenced by the improvement of the heart failure status and other drugs that the patient was taking. Cureus 2022-03-02 /pmc/articles/PMC8971101/ /pubmed/35371876 http://dx.doi.org/10.7759/cureus.22762 Text en Copyright © 2022, Kashiwagi et al. https://creativecommons.org/licenses/by/3.0/This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Cardiology Kashiwagi, Yusuke Nagoshi, Tomohisa Ogawa, Kazuo Kawai, Makoto Yoshimura, Michihiro Heart Failure Treatments Such As Angiotensin Receptor/Neprilysin Inhibitor Improve Heart Failure Status and Glucose Metabolism |
title | Heart Failure Treatments Such As Angiotensin Receptor/Neprilysin Inhibitor Improve Heart Failure Status and Glucose Metabolism |
title_full | Heart Failure Treatments Such As Angiotensin Receptor/Neprilysin Inhibitor Improve Heart Failure Status and Glucose Metabolism |
title_fullStr | Heart Failure Treatments Such As Angiotensin Receptor/Neprilysin Inhibitor Improve Heart Failure Status and Glucose Metabolism |
title_full_unstemmed | Heart Failure Treatments Such As Angiotensin Receptor/Neprilysin Inhibitor Improve Heart Failure Status and Glucose Metabolism |
title_short | Heart Failure Treatments Such As Angiotensin Receptor/Neprilysin Inhibitor Improve Heart Failure Status and Glucose Metabolism |
title_sort | heart failure treatments such as angiotensin receptor/neprilysin inhibitor improve heart failure status and glucose metabolism |
topic | Cardiology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8971101/ https://www.ncbi.nlm.nih.gov/pubmed/35371876 http://dx.doi.org/10.7759/cureus.22762 |
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