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      The role of recombinant human brain natriuretic peptide on the cardiac output of patients with acute decompensated heart failure using Guyton venous return curve : A STROBE-compliant retrospective study

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          Abstract

          rbBNP has positive cardiac effects in patients with acute decompensated heart failure, but its effects on the systemic venous circulation are not known.

          A single-center retrospective, self-controlled study was conducted on 14 patients undergone recombinant human brain natriuretic peptide (rhBNP) treatment between January 1, 2015 to December 31, 2018.

          The cardiac output (CO) significantly increased from 3.75 ± 1.14 L min-1 to 4.24 ± 0.97 L min-1 30 minutes after rbBNP infusion, and to 4.20 ± 1.19 L min-1 3 hours later. The systemic vascular resistance significantly decreased from 18.85 ± 7.66 mm Hg min L-1 to 14.62 ± 6.13 mm Hg min L-1 30 minutes. The resistance to venous return (VR) significantly decreased from 5.93 ± 4.97 mm Hg min L-1 to 4.46 ± 1.53 mmHg min L-1 3 hours later. The mean systemic filling pressure significantly decreased from 32.71 ± 20.00 mm Hg to 28.254 ± 6.09 mm Hg 3 hours later.

          The role of rhBNP on CO was to reduce the peripheral circulation resistance at 30 minutes after rhBNP infusion and to reduce the resistance to VR at 3 hours later.

          This trial is registered at ChiCTR: ID ChiCTR1900024562.

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          The war against heart failure: the Lancet lecture.

          Eugene Braunwald (2015)
          Heart failure is a global problem with an estimated prevalence of 38 million patients worldwide, a number that is increasing with the ageing of the population. It is the most common diagnosis in patients aged 65 years or older admitted to hospital and in high-income nations. Despite some progress, the prognosis of heart failure is worse than that of most cancers. Because of the seriousness of the condition, a declaration of war on five fronts has been proposed for heart failure. Efforts are underway to treat heart failure by enhancing myofilament sensitivity to Ca(2+); transfer of the gene for SERCA2a, the protein that pumps calcium into the sarcoplasmic reticulum of the cardiomyocyte, seems promising in a phase 2 trial. Several other abnormal calcium-handling proteins in the failing heart are candidates for gene therapy; many short, non-coding RNAs--ie, microRNAs (miRNAs)--block gene expression and protein translation. These molecules are crucial to calcium cycling and ventricular hypertrophy. The actions of miRNAs can be blocked by a new class of drugs, antagomirs, some of which have been shown to improve cardiac function in animal models of heart failure; cell therapy, with autologous bone marrow derived mononuclear cells, or autogenous mesenchymal cells, which can be administered as cryopreserved off the shelf products, seem to be promising in both preclinical and early clinical heart failure trials; and long-term ventricular assistance devices are now used increasingly as a destination therapy in patients with advanced heart failure. In selected patients, left ventricular assistance can lead to myocardial recovery and explantation of the device. The approaches to the treatment of heart failure described, when used alone or in combination, could become important weapons in the war against heart failure.
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            Heart failure.

            John R. Teerlink, Marco Metra (2017)
            Heart failure is common in adults, accounting for substantial morbidity and mortality worldwide. Its prevalence is increasing because of ageing of the population and improved treatment of acute cardiovascular events, despite the efficacy of many therapies for patients with heart failure with reduced ejection fraction, such as angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), β blockers, and mineralocorticoid receptor antagonists, and advanced device therapies. Combined angiotensin receptor blocker neprilysin inhibitors (ARNIs) have been associated with improvements in hospital admissions and mortality from heart failure compared with enalapril, and guidelines now recommend substitution of ACE inhibitors or ARBs with ARNIs in appropriate patients. Improved safety of left ventricular assist devices means that these are becoming more commonly used in patients with severe symptoms. Antidiabetic therapies might further improve outcomes in patients with heart failure. New drugs with novel mechanisms of action, such as cardiac myosin activators, are under investigation for patients with heart failure with reduced left ventricular ejection fraction. Heart failure with preserved ejection fraction is a heterogeneous disorder that remains incompletely understood and will continue to increase in prevalence with the ageing population. Although some data suggest that spironolactone might improve outcomes in these patients, no therapy has conclusively shown a significant effect. Hopefully, future studies will address these unmet needs for patients with heart failure. Admissions for acute heart failure continue to increase but, to date, no new therapies have improved clinical outcomes.
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              Guanylyl cyclases and signaling by cyclic GMP.

              K A Lucas, G M Pitari, S Kazerounian … (2000)
              Guanylyl cyclases are a family of enzymes that catalyze the conversion of GTP to cGMP. The family comprises both membrane-bound and soluble isoforms that are expressed in nearly all cell types. They are regulated by diverse extracellular agonists that include peptide hormones, bacterial toxins, and free radicals, as well as intracellular molecules, such as calcium and adenine nucleotides. Stimulation of guanylyl cyclases and the resultant accumulation of cGMP regulates complex signaling cascades through immediate downstream effectors, including cGMP-dependent protein kinases, cGMP-regulated phosphodiesterases, and cyclic nucleotide-gated ion channels. Guanylyl cyclases and cGMP-mediated signaling cascades play a central role in the regulation of diverse (patho)physiological processes, including vascular smooth muscle motility, intestinal fluid and electrolyte homeostasis, and retinal phototransduction. Topics addressed in this review include the structure and chromosomal localization of the genes for guanylyl cyclases, structure and function of the members of the guanylyl cyclase family, molecular mechanisms regulating enzymatic activity, and molecular sequences coupling ligand binding to catalytic activity. A brief overview is presented of the downstream events controlled by guanylyl cyclases, including the effectors that are regulated by cGMP and the role that guanylyl cyclases play in cell physiology and pathophysiology.
              Article 0 comments Cited 127 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Medicine (Baltimore)
                Journal ID (iso-abbrev): Medicine (Baltimore)
                Journal ID (publisher-id): MEDI
                Title: Medicine
                Publisher: Lippincott Williams & Wilkins (Hagerstown, MD )
                ISSN (Print): 0025-7974
                ISSN (Electronic): 1536-5964
                Publication date Collection: 30 April 2021
                Publication date (Electronic): 30 April 2021
                Volume: 100
                Issue: 17
                Electronic Location Identifier: e25492
                Affiliations
                [a ]Department of Intensive Care Unit, Qingyuan People's Hospital,Qingyuan,China
                [b ]Department of Intensive Care Unit, The Sixth Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
                Author notes
                [∗ ]Correspondence: Qiu ye Kou, Department of Intensive Care Unit, The Sixth Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510655, China (e-mail: kouqiuye@ 123456126.com ).
                Article
                Publisher ID: MD-D-20-11053 Accession ID: 25492
                DOI: 10.1097/MD.0000000000025492
                PMC ID: 8084054
                PubMed ID: 33907098
                SO-VID: d2fd460a-81e8-4f72-b236-22efc270221e
                Copyright © Copyright © 2021 the Author(s). Published by Wolters Kluwer Health, Inc.
                License:

                This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. http://creativecommons.org/licenses/by/4.0

                History
                Date received : 22 November 2020
                Date revision received : 17 March 2021
                Date accepted : 20 March 2021
                Categories
                Subject: 3400
                Subject: Research Article
                Subject: Observational Study
                Custom metadata
                OPEN-ACCESS TRUE

                Keywords: acute decompensated heart failure,cardiac output,recombinant human brain natriuretic peptide,venous return curve
                Data availability:
                Keywords: acute decompensated heart failure, cardiac output, recombinant human brain natriuretic peptide, venous return curve

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