FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2945250770> ?p ?o ?g. }

• W2945250770 endingPage "1519" @default.
• W2945250770 startingPage "1519" @default.
• W2945250770 abstract "HomeCirculation ResearchVol. 124, No. 11The Medical and Device-Related Treatment of Heart Failure Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBThe Medical and Device-Related Treatment of Heart Failure James T. Willerson James T. WillersonJames T. Willerson Correspondence to James T. Willerson, MD, University of Texas Health Sciences Center at Houston, Texas Heart Institute, 6770 Bertner Ave, MC 3-116, Houston, TX 77030. Email E-mail Address: [email protected] From the President Emeritus of the Texas Heart Institute, Houston. Search for more papers by this author Originally published23 May 2019https://doi.org/10.1161/CIRCRESAHA.119.315268Circulation Research. 2019;124:1519Heart failure is the main cardiovascular problem in the world today, affecting large numbers of men, women, and children without regard to age, sex, or ethnicity. We have made some progress treating it with medications, diet, interventions, devices, and heart transplants, but large numbers of people are still short of breath, cannot lead an active life, and die sooner than they should because of heart failure.In this compendium, contemporary physicians and scientists have summarized current knowledge and progress in the medical, interventional, and surgical treatment of heart failure.1–10However, the contributors to this compendium, as well as many of its readers, realize that the future will bring new and far more powerful methods of preventing and treating heart failure. We predict that the following new approaches may be adopted in the near future:Treatment of heart failure will be targeted to the individual patient, based on a detailed understanding of each patient’s genes that promote heart failure and the elucidation of the subcellular pathways that regulate the development of heart failure.Gene editing to prevent heart failure may be possible, at least in some—and probably many—patients.Interventions may become available that disrupt intracellular signaling pathways that prevent cardiogenesis and blood vessel renewal, thereby promoting the regeneration of myocytes in the heart and the development of new blood vessels anywhere in the body.Increasingly sensitive noninvasive imaging methodology and specific inhibitors of tissue injury might be available that allow one to detect and treat tissue inflammation and dangerous vascular lesions before they can cause heart attacks, strokes, or life-threatening cardiac arrhythmias.Drug development will be focused on interrupting intracellular signaling pathways that are injurious to cardiovascular tissue and on stimulating signaling pathways that protect cardiovascular tissues.New inhibitors of transplant rejection are likely to be developed so that transplanting nonhuman hearts will be possible, and smaller and relatively easy-to-place cardiac and brain support devices/interventions will be available.New devices could be developed to prevent or ablate cardiac arrhythmias more successfully than is possible today and that pace and defibrillate the heart without external leads or connections.Functional cardiovascular stem cells might be developed and identified that serve as robust paracrine delivery factors and replicate themselves in vivo.Encouraging progress toward most of these advances is already well underway, but we can enjoy—and we must contribute to—these developments as best we can as physicians, scientists, and all those who care for patients with cardiovascular disease.DisclosuresNone.FootnotesThe opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.Correspondence to James T. Willerson, MD, University of Texas Health Sciences Center at Houston, Texas Heart Institute, 6770 Bertner Ave, MC 3-116, Houston, TX 77030. Email james.t.[email protected]tmc.eduReferences1. Elgendy IY, Mahtta D, Pepine CJ. Medical therapy for heart failure caused by ischemic heart disease.Circ Res. 2019; 124:1520–1535. doi: 10.1161/CIRCRESAHA.118.313568LinkGoogle Scholar2. Repetti GG, Toepfer CN, Seidman JG, Seidman CE. Novel therapies for prevention and early treatment of cardiomyopathies: now and in the future.Circ Res. 2019; 124:1536–1550. doi: 10.1161/CIRCRESAHA.119.313569LinkGoogle Scholar3. Zelt JGE, Chaudhary KR, Cadete VJ, Mielniczuk LM, Stewart DJ. Medical therapy for heart failure associated with pulmonary hypertension.Circ Res. 2019; 124:1551–1567. doi: 10.1161/CIRCRESAHA.118.313650LinkGoogle Scholar4. Tschöpe C, Cooper LT, Toree-Amione G, Van Linthout S. Management of myocarditis-related cardiomyopathy in adults.Circ Res. 2019; 124:1568–1583. doi: 10.1161/CIRCRESAHA.118.313578LinkGoogle Scholar5. Hussein AA, Wilkoff BL. Cardiac implantable device therapy in heart failure.Circ Res. 2019; 124:1584–1597. doi: 10.1161/CIRCRESAHA.118.313571LinkGoogle Scholar6. Pfeffer MA, Shah AM, Borlaug BA. Heart failure with preserved ejection fraction: in perspective.Circ Res. 2019; 124:1598–1617. doi: 10.1161/CIRCRESAHA.119.313572LinkGoogle Scholar7. Pinilla-Vera M, Hahan VS, Kass DA. Leveraging signaling pathways to treat heart failure with reduced ejection fraction: past, present, and future.Circ Res. 2019; 124:1618–1632. doi: 10.1161/CIRCRESAHA.119.313682LinkGoogle Scholar8. Cowgill JA, Francis SA, Sawyer DB. Anthracycline and peripartum cardiomyopathies: predictably unpredictable.Circ Res. 2019; 124:1633–1646. doi: 10.1161/CIRCRESAHA.119.313577LinkGoogle Scholar9. Heallen TR, Kadow ZA, Kim JH, Wang J, Martin JM. Stimulating cardiogenesis as a treatment for heart failure.Circ Res. 2019; 124:1647–1657. doi: 10.1161/CIRCRESAHA.118.313573LinkGoogle Scholar10. Miller L, Birks E, Guglin M, Lamba H, Frazier OH. Use of ventricular assist devices and heart transplantation for advanced heart failure.Circ Res. 2019; 124:1658–1678. doi: 10.1161/CIRCRESAHA.119.313574LinkGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Liu Q, Ji G, Chu Y, Hao T, Qian M and Zhao Q (2022) Enzyme-responsive hybrid prodrug of nitric oxide and hydrogen sulfide for heart failure therapy, Chemical Communications, 10.1039/D2CC02267B, 58:53, (7396-7399) Zhang H, Xue Y, Pan T, Zhu X, Chong H, Xu C, Fan F, Cao H, Zhang B, Pan J, Zhou Q, Yang G, Wang J and Wang D (2022) Epicardial injection of allogeneic human-induced-pluripotent stem cell-derived cardiomyocytes in patients with advanced heart failure: protocol for a phase I/IIa dose-escalation clinical trial, BMJ Open, 10.1136/bmjopen-2021-056264, 12:5, (e056264), Online publication date: 1-May-2022. Li Y, Li X, Chen X, Sun X, Liu X, Wang G, Liu Y, Cui L, Liu T, Wang W, Wang Y and Li C (2022) Qishen Granule (QSG) Inhibits Monocytes Released From the Spleen and Protect Myocardial Function via the TLR4-MyD88-NF-κB p65 Pathway in Heart Failure Mice, Frontiers in Pharmacology, 10.3389/fphar.2022.850187, 13 Borow K, Yaroshinsky A, Greenberg B and Perin E (2019) Phase 3 DREAM-HF Trial of Mesenchymal Precursor Cells in Chronic Heart Failure, Circulation Research, 125:3, (265-281), Online publication date: 19-Jul-2019. May 24, 2019Vol 124, Issue 11 Advertisement Article InformationMetrics © 2019 American Heart Association, Inc.https://doi.org/10.1161/CIRCRESAHA.119.315268PMID: 31120816 Originally publishedMay 23, 2019 Keywordsheart failuretherapeuticsEditorialsPDF download Advertisement SubjectsHeart FailureTreatment" @default.
• W2945250770 created "2019-05-29" @default.
• W2945250770 creator A5045515686 @default.
• W2945250770 date "2019-05-24" @default.
• W2945250770 modified "2023-10-02" @default.
• W2945250770 title "The Medical and Device-Related Treatment of Heart Failure" @default.
• W2945250770 cites W2945043974 @default.
• W2945250770 cites W2945334580 @default.
• W2945250770 cites W2945360683 @default.
• W2945250770 cites W2945710519 @default.
• W2945250770 cites W2945960024 @default.
• W2945250770 cites W2945960888 @default.
• W2945250770 cites W2946012845 @default.
• W2945250770 cites W2947352113 @default.
• W2945250770 cites W2947454282 @default.
• W2945250770 cites W2949088328 @default.
• W2945250770 doi "https://doi.org/10.1161/circresaha.119.315268" @default.
• W2945250770 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31120816" @default.
• W2945250770 hasPublicationYear "2019" @default.
• W2945250770 type Work @default.
• W2945250770 sameAs 2945250770 @default.
• W2945250770 citedByCount "8" @default.
• W2945250770 countsByYear W29452507702019 @default.
• W2945250770 countsByYear W29452507702022 @default.
• W2945250770 countsByYear W29452507702023 @default.
• W2945250770 crossrefType "journal-article" @default.
• W2945250770 hasAuthorship W2945250770A5045515686 @default.
• W2945250770 hasBestOaLocation W29452507701 @default.
• W2945250770 hasConcept C159110408 @default.
• W2945250770 hasConcept C164705383 @default.
• W2945250770 hasConcept C166957645 @default.
• W2945250770 hasConcept C177713679 @default.
• W2945250770 hasConcept C27415008 @default.
• W2945250770 hasConcept C2778198053 @default.
• W2945250770 hasConcept C2778473407 @default.
• W2945250770 hasConcept C2778849806 @default.
• W2945250770 hasConcept C2910855829 @default.
• W2945250770 hasConcept C71924100 @default.
• W2945250770 hasConcept C74909509 @default.
• W2945250770 hasConcept C95457728 @default.
• W2945250770 hasConceptScore W2945250770C159110408 @default.
• W2945250770 hasConceptScore W2945250770C164705383 @default.
• W2945250770 hasConceptScore W2945250770C166957645 @default.
• W2945250770 hasConceptScore W2945250770C177713679 @default.
• W2945250770 hasConceptScore W2945250770C27415008 @default.
• W2945250770 hasConceptScore W2945250770C2778198053 @default.
• W2945250770 hasConceptScore W2945250770C2778473407 @default.
• W2945250770 hasConceptScore W2945250770C2778849806 @default.
• W2945250770 hasConceptScore W2945250770C2910855829 @default.
• W2945250770 hasConceptScore W2945250770C71924100 @default.
• W2945250770 hasConceptScore W2945250770C74909509 @default.
• W2945250770 hasConceptScore W2945250770C95457728 @default.
• W2945250770 hasIssue "11" @default.
• W2945250770 hasLocation W29452507701 @default.
• W2945250770 hasLocation W29452507702 @default.
• W2945250770 hasOpenAccess W2945250770 @default.
• W2945250770 hasPrimaryLocation W29452507701 @default.
• W2945250770 hasRelatedWork W1559507832 @default.
• W2945250770 hasRelatedWork W1833663152 @default.
• W2945250770 hasRelatedWork W1970295087 @default.
• W2945250770 hasRelatedWork W1981983872 @default.
• W2945250770 hasRelatedWork W2401771602 @default.
• W2945250770 hasRelatedWork W2407717929 @default.
• W2945250770 hasRelatedWork W2546438271 @default.
• W2945250770 hasRelatedWork W2889317017 @default.
• W2945250770 hasRelatedWork W2963031479 @default.
• W2945250770 hasRelatedWork W4247718175 @default.
• W2945250770 hasVolume "124" @default.
• W2945250770 isParatext "false" @default.
• W2945250770 isRetracted "false" @default.
• W2945250770 magId "2945250770" @default.
• W2945250770 workType "article" @default.