-
Mashup Score: 5Partial Heart Transplantation: Early Experience With Pediatric Heart Valve Replacements That Grow | Circulation - 7 hour(s) ago
Heart valve replacement in children is fraught with long-term morbidity and mortality rates, largely because conventional implants lack the capacity to grow with the child. Partial heart transplantation presents a potential solution by transplanting only specific segments of a donor heart, thereby providing a living and growing heart valve implant. This approach harnesses the full spectrum of cardiac tissues, which, when freshly procured and supported by immunosuppression, can integrate as functional and potentially growth-capable tissue. This state-of-the-art review discusses the history and development of partial heart transplantation, its indications, recent clinical experiences, regulation, and future directions.
Source: www.ahajournals.orgCategories: General Medicine NewsTweet
-
Mashup Score: 2Leveraging Transcriptional Readouts as a Platform for Drug Repurposing in Cardiomyopathy | Circulation - 7 hour(s) ago
View all available purchase options and get full access to this article. Fatkin D, MacRae C, Sasaki T, Wolff MR, Porcu M, Frenneaux M, Atherton J, Vidaillet HJ, Spudich S, De Girolami U, et al. Missense mutations in the rod domain of the lamin A/C gene as causes of dilated cardiomyopathy and conduction-system disease. N Engl J Med. 1999;341:1715–1724. doi: 10.1056/NEJM199912023412302 Siu CW, Lee YK, Ho JC, Lai WH, Chan YC, Ng KM, Wong LY, Au KW, Lau YM, Zhang J, et al. Modeling of lamin A/C mutation
Source: www.ahajournals.orgCategories: General Medicine NewsTweet-
#Editorial on the potential of Olmesartan to restore LMNA function in haploinsufficient cardiomyocytes https://t.co/dbcp2NrLvK
-
-
Mashup Score: 0
View all available purchase options and get full access to this article. Piccini JP, Patel MR, Steffel J, Ferdinand K, Van Gelder IC, Russo AM, Ma C-S, Goodman SG, Oldgren J, Hammett C, et al; OCEANIC-AF Steering Committee and Investigators. Asundexian versus apixaban in patients with atrial fibrillation. N Engl J Med. 2025;392:23–32. doi: 10.1056/NEJMoa2407105 Ruff CT, Patel SM, Giugliano RP, Morrow DA, Hug B, Kuder JF, Goodrich EL, Chen S-A, Goodman SG, Joung B, et al; AZALEA-TIMI 71 Investigators.
Source: www.ahajournals.orgCategories: General Medicine NewsTweet-
Factor XI inhibition in atrial fibrillation: it remians to be seen whether FXI inhibitors will match the efficacy of DOACs or VKAs in prevention of thromboembolic events. https://t.co/0Zc6LKyRSw
-
-
Mashup Score: 3Genomic Editing of a Pathogenic Mutation in ACTA2 Rescues Multisystemic Smooth Muscle Dysfunction Syndrome in Mice | Circulation - 8 hour(s) ago
Background: Vascular smooth muscle cells (vSMCs), the predominant cell type in the aortic wall, play a crucial role in maintaining aortic integrity, blood pressure, and cardiovascular function. vSMC contractility and function depend on smooth muscle alpha-actin 2 (ACTA2). The pathogenic variant ACTA2 c.536G>A (p. R179H) causes multisystemic smooth muscle dysfunction syndrome (MSMDS), a severe disorder marked by widespread smooth muscle abnormalities, resulting in life-threatening aortic disease and high-risk early mortality from aneurysms or stroke. No effective treatments exist for MSMDS. Methods: To develop a comprehensive therapy for MSMDS, we utilized CRISPR-Cas9 adenine base editing to correct the ACTA2 R179H mutation. We generated isogenic human induced pluripotent stem cell (iPSC) lines and humanized mice carrying this pathogenic missense mutation. iPSC-SMCs were evaluated for key functional characteristics, including proliferation, migration, and contractility. The adenine base
Source: www.ahajournals.orgCategories: General Medicine NewsTweet-
This study describes how genomic editing of a pathogenic mutation in ACTA2 restores key aortic smooth muscle functions, and life-threatening aortic dilation and dissection are mitigated in humanized mice. @volkersmirko @vietloandaothi https://t.co/1afyocenQL https://t.co/i3dDfla8D1
-
-
Mashup Score: 0
BACKGROUND: Exercise improves functional outcomes in patients with diabetic cardiomyopathy (DiaCM). The molecular mechanism underlying cardiac benefits of exercise in DiaCM remains incompletely understood. N6-methyladenosine (m6A) is the most common form of messenger RNA modification in eukaryotes and has been implicated in cardiac development and disease. However, the role of m6A in DiaCM and in the mitigating effects of exercise on this disease are unclear. METHODS: Cardiomyocyte-specific N6-adenosine-methyltransferase-like 3 (METTL3, an m6A methyltransferase) knockout mice and their wild-type littermates were subjected to either chow diet or high-fat diet feeding and injection of streptozotocin to induce DiaCM, followed by an 8-week exercise training and assessment of cardiac function. Some of the mice were injected with adeno-associated viral vector encoding METTL3 to overexpress METTL3 in cardiomyocytes. Cardiac METTL3 expressions were assessed in patients with nonischemic primary
Source: www.ahajournals.orgCategories: General Medicine NewsTweet-
METTL3, an m6A methyltransferase for mRNA modification, mediates the exercise benefits in diabetic cardiomyopathy via a direct downstream effector, YBX1. @lihaobo https://t.co/eIHZyH7Xav https://t.co/UHEELRfOy3
-
-
Mashup Score: 5CD206+IL-4Rα+ Macrophages Are Drivers of Adverse Cardiac Remodeling in Ischemic Cardiomyopathy | Circulation - 8 hour(s) ago
BACKGROUND: The role of cardiac CD (cluster of differentiation) 206+ macrophages in chronic heart failure (HF) is unknown. We examined whether CD206+ macrophages expressing IL (interleukin)–4Rα are key drivers of adverse left ventricular (LV) remodeling in HF. METHODS: Adult C57BL/6 mice underwent nonreperfused myocardial infarction to induce HF. Macrophages in murine and human hearts were profiled using flow cytometry and immunostaining. In vivo myeloid-specific IL-4Rα deletion and intramyocardial macrophage adoptive transfer defined the functional effects of M[IL-4] macrophages. Antisense oligonucleotides were used for in vivo IL-4Rα gene silencing in mice. RESULTS: CD206+ macrophages steadily expanded in hearts after myocardial infarction, such that at 8 weeks after myocardial infarction, they comprised ≈85% of all macrophages. These macrophages were proliferative, predominantly CCR2– (C-C motif chemokine receptor) and MHC (major histocompatibility complex) IIhi, and correlated with
Source: www.ahajournals.orgCategories: General Medicine NewsTweet-
CD206⁺IL-4Rα⁺ macrophages proliferate and drive adverse LV remodeling via FIZZ1-mediated fibrosis. IL-4Rα deletion or silencing reverses remodeling and improves function. A novel therapeutic target in ischemic cardiomyopathy https://t.co/HOOVpOexvY https://t.co/wRLQ5IAyOj
-
-
Mashup Score: 2Dusp14-Mediated Dephosphorylation of MLKL Protects Against Cardiomyocyte Necroptosis in Hypothyroidism-Induced Heart Failure | Circulation - 8 hour(s) ago
BACKGROUND: Hypothyroidism leads to multiple organ dysfunction, with the heart the most affected. However, the pathologic mechanism of hypothyroidism-induced heart failure remains to be completely elucidated. Thyroid hormone replacement therapy enhances myocardium systolic function but increases the occurrence of arrythmias. There is an urgent need to explore these mechanisms in detail and to discover and develop drugs that can target and manage heart failure in patients with hypothyroidism. METHODS: In this study, a mouse model of hypothyroidism-induced heart failure was established through the administration of propylthiouracil. Dusp14 knockout mice were generated, and adeno-associated virus–mediated cardiomyocyte-specific overexpression of Dusp14 (dual specificity phosphatase 14) was used in combination with related cellular experiments to investigate the protective effects of Dusp14 on hypothyroidism-induced heart failure. Further analyses confirmed the crucial involvement of necro
Source: www.ahajournals.orgCategories: General Medicine NewsTweet-
Hypothyroidism triggers cardiomyocyte necroptosis in heart failure, which can be reversed by Dusp14-mediated MLKL dephosphorylation https://t.co/uPGpbjTsDj https://t.co/ONPoPv5l9U
-
-
Mashup Score: 4
Can’t sign in? Forgot your password? If the address matches an existing account you will receive an email with instructions to reset your password. Can’t sign in? Forgot your username? The mission of the Annals of Internal Medicine: Clinical Cases (AIMCC) is to promote excellence in critical thinking around prevention, diagnosis, and management of challenging clinical situations and awareness of new or unique clinical entities by disseminating rigorously peer-reviewed reports of real clinical cases
Source: www.acpjournals.orgCategories: General Medicine News, Cardiac SurgeryTweet-
Co-published by @ACPinternists and @AHAScience #AHAJournals, @AnnalsofIMCC is a peer-reviewed, open access journal that publishes #casereports, case series, and image/video cases across the spectrum of medicine. Learn more and submit to AIMCC today at https://t.co/IzoNqdQ2Qo https://t.co/JeRhlpgiXj
-
-
Mashup Score: 22
BACKGROUND: The activation and polarization of T cells play a crucial role in atherosclerosis and dictate athero-inflammation. The epigenetic enzyme EZH2 (enhancer of zeste homolog 2) mediates the H3K27me3 (trimethylation of histone H3 lysine 27) and is pivotal in controlling T cell responses. METHODS: To detail the role of T cell EZH2 in atherosclerosis, we used human carotid endarterectomy specimens to reveal plaque expression and geography of EZH2. Atherosclerosis-prone Apoe (apolipoprotein E)–deficient mice with CD (cluster of differentiation) 4+ or CD8+ T cell–specific Ezh2 deletion (Ezh2cd4-knockout [KO], Ezh2cd8-KO) were analyzed to unravel the role of T cell Ezh2 in atherosclerosis and T cell–associated immune status. RESULTS: EZH2 expression is elevated in advanced human atherosclerotic plaques and primarily expressed in the T cell nucleus, suggesting the importance of canonical EZH2 function in atherosclerosis. Ezh2cd4-KO, but not Ezh2cd8-KO, mice showed reduced atheroscleros
Source: www.ahajournals.orgCategories: General Medicine NewsTweet-
Ezh2 in T cells regulates atherosclerosis @LarsMaeg @5antus @FlorianaFarina @AtzlerLab https://t.co/ksuhpqbuN1 https://t.co/K5sGeknAaN
-
-
Mashup Score: 6
View all available purchase options and get full access to this article. Kosiborod MN, Abildstrøm SZ, Borlaug BA, Butler J, Rasmussen S, Davies M, Hovingh GK, Kitzman DW, Lindegaard ML, Møller DV, et al; STEP-HFpEF Trial Committees and Investigators. Semaglutide in people with heart failure with preserved ejection fraction and obesity. N Engl J Med. 2023;389:1069–1084. doi: 10.1056/NEJMoa2306963 Kosiborod MN, Petrie MC, Borlaug BA, Butler J, Davies MJ, Hovingh GK, Kitzman DW, Møller DV, Treppendahl MB,
Source: www.ahajournals.orgCategories: General Medicine NewsTweet-
When adjusted for baseline NT-proBNP, a greater reduction in NT-proBNP was observed with tirzepatide compared with insulin glargine in persons with elevated baseline NTproBNP in a post hoc analyses of the SURPASS 4 trial @_HeartFailure_ @matthewmylee https://t.co/BUHH7Y9dUh https://t.co/HWLimIhJxW
-
Partial Heart Transplantation: a comprehensive review of partial heart transplantation, including current status, clinical adaptation, and future directions.@Neel_Prabhu @TurekPedHearts @justlikemike45 https://t.co/EFMJgMKest https://t.co/z5H0om6zo3