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Last update 23 Jan 2025

Edema, Cardiac

Last update 23 Jan 2025

Basic Info

Synonyms

Cardiac Edema, Cardiac Edemas, Cardiac edema

+ [33]

Introduction

Abnormal fluid retention by the body due to impaired cardiac function or heart failure. It is usually characterized by increase in venous and capillary pressure, and swollen legs when standing. It is different from the generalized edema caused by renal dysfunction (NEPHROTIC SYNDROME).

Drugs associated with Edema, Cardiac

Tolvaptan Sodium Phosphate

Target

AVPR2

Mechanism

AVPR2 antagonists

Active Org.

Fuji Yakuhin Co., Ltd. [+1]

Originator Org.

Otsuka Pharmaceutical Co., Ltd.

Active Indication

Body fluid retention [+2]

Inactive Indication-

Drug Highest PhaseApproved

First Approval Ctry. / Loc.

First Approval Date28 Mar 2022

Etelcalcetide

Target

CaSR

Mechanism

CaSR agonists

Active Org.

Amgen Europe BV [+3]

Originator Org.

Amgen, Inc.

Active Indication

Chronic Kidney Diseases [+1]

Inactive Indication

Chronic Kidney Disease-Mineral and Bone Disorder [+2]

Drug Highest PhaseApproved

First Approval Ctry. / Loc.

EU [+3]

First Approval Date11 Nov 2016

Tolvaptan

Target

AVPR2

Mechanism

AVPR2 antagonists

Active Org.

Otsuka Pharmaceutical Co., Ltd. [+5]

Originator Org.

Otsuka Holdings Co., Ltd.

Active Indication

Ascites [+7]

Inactive Indication

Bipolar Disorder [+13]

Drug Highest PhaseApproved

First Approval Ctry. / Loc.

First Approval Date19 May 2009

Clinical Trials associated with Edema, Cardiac

NCT06021860

/ Not yet recruitingPhase 4

A Phase IV, Two-part, Open-label Study Assessing the Pharmacokinetics, Safety and Pharmacodynamics of Single and Multiple Doses of Spironolactone Oral Suspension in Pediatric Patients With Edema Due to Heart Failure or Cirrhosis

This is a 2-part, 2 periods per part, open-label study with spironolactone oral suspension in pediatric patients with edema due to HF or hepatic cirrhosis. Both study parts will evaluate the safety, PK and PD of multiple doses of spironolactone in patients aged from birth to ≤17 years of age.

Start Date01 Jun 2024

Sponsor / Collaborator

CMP Development LLC

JPRN-jRCT2071220069

/ RecruitingPhase 2IIT

A Multicenter, Randomized, Double-blind, Placebo-controlled, Parallel-group, Doseranging Trial of OPC-131461 in Cardiac Edema (Congestive Heart Failure [CHF])

Start Date10 Jan 2023

Sponsor / Collaborator-

NCT05615363

/ CompletedPhase 2

A Multicenter, Randomized, Double-blind, Placebo-controlled, Parallel-group, Doseranging Trial of OPC-131461 in Cardiac Edema (Congestive Heart Failure [CHF])

To investigate the dose response in respect of weight decrease following repeated oral administration of OPC-131461 at 1, 2, 5, and 10 mg or placebo in patients with CHF with volume overload despite having received diuretics other than vasopressin antagonists

Start Date10 Jan 2023

Sponsor / Collaborator

Otsuka Pharmaceutical Co., Ltd.

100 Clinical Results associated with Edema, Cardiac

100 Translational Medicine associated with Edema, Cardiac

0 Patents (Medical) associated with Edema, Cardiac

606

Literatures (Medical) associated with Edema, Cardiac

01 Mar 2025·Reproductive Toxicology

Embryotoxicity of statins and other prescribed drugs with reported off-target effects on cholesterol biosynthesis

Article

Author: Howe, Emily ; Mansion, Aliyah ; Hartley, Taryn ; Abdulsalam, Zeenat ; White, Kaylei ; Tadjuidje, Emmanuel ; Ramirez, Daniel ; Abdelmagid, Hagir

Cholesterol plays pivotal cellular functions ranging from maintaining membrane fluidity to regulating cell-cell signaling. High cholesterol causes cardiovascular diseases, low cholesterol is linked to neuropsychiatric disorders, and inborn errors of cholesterol synthesis cause multisystem malformation syndromes. Statins lower cholesterol levels by inhibiting the first, rate-limiting reaction of the cholesterol biosynthesis pathway catalyzed by hydroxymethyl-glutaryl-Coenzyme A reductase (HMGCR). However, they have also been shown to interfere with cellular pathways that are unrelated to cholesterol synthesis. One of the last enzymes of cholesterol biosynthesis, 7-dehydrocholesterol reductase (DHCR7), is often mutated in the Smith-Lemli-Opitz syndrome (SLOS), a multisystem malformation syndrome. Strikingly, recent studies have shown that some prescribed psychotropic pharmaceuticals inhibit its activity. In this study, we used Xenopus laevis as a model organism to test the effects of 8 FDA-approved statins and selected prescribed psychotropic drugs on the developing vertebrate embryo. Drugs were tested at concentrations ranging from 0.1 µM to 50 µM. Embryos were exposed to the drugs from the blastula stage through the swimming tadpole stage with daily medium change. Our data show that statins are heterogenous with respect to their ability to cause embryonic lethality, with simvastatin, pitavastatin, lovastatin, cerivastatin, and fluvastatin being the most toxic ones. Observed phenotypes included delayed development, shortened body axis and pericardiac edema. On the other hand, psychotropic drugs were less embryonic lethal than statins but caused similar phenotypes as well as microcephaly and holoprosencephaly. Our findings suggest that the proximal and distal inhibition of cholesterol biosynthesis have different but overlapping effects on embryonic development.

01 Jan 2025·Toxicology Letters

Oxymatrine antagonises oxidative stress and apoptosis in Nemopilema nomurai toxin-induced cardiotoxicity by inhibiting mitogen-activated protein kinase

Article

Author: Wang, Yongfang ; Chen, Wei ; Zhang, Jinyu ; Wang, Xinming ; Geng, Xiaoyu ; Yang, Jishun ; Xiao, Liang ; Liu, Tianwen ; Wang, Zengfa ; Dong, Weibing

Jellyfish stings can trigger abrupt heart failure via toxins, leading acute mortality rise. Proposed mechanisms involve oxidative stress and apoptosis, but evidence for effective treatments is lacking. To explore the concrete molecular mechanisms of jellyfish toxin-induced cardiotoxicity and to explore effective therapeutic approaches, we established tentacle extract (TE) of jellyfish Nemopilema nomurai induced cardiotoxicity models in vivo and in vitro based Intelligent Character Recognition (ICR) mice and H9C2 cells, respectively,.We assessed toxin-induced cardiac injury and screened antagonists from natural compounds to evaluate their antagonistic effects and explore their mechanisms of action. In vitro experiments showed that TE reduced the viability of H9C2 cells and induced a large number of cells apoptotic, accompanied by the elevation of reactive oxygen species (ROS), malondialdehyde (MDA) and the decrease of total superoxide dismutase (T-SOD), activated the phosphorylation level of mitogen-activated protein kinase (MAPK) nuclear transcription factors p38, extracellular regulated protein kinases (ERK) and c-Jun N-terminal kinase (JNK), and increased the transcription level of upstream cytokines interleukin-1β (IL-1β) and tumour necrosis factor-α (TNF-α), and OMT can significantly antagonize the above changes caused by TE; in vivo experiments demonstrated that TE could lead to the death of mice, as well as induce cardiac edema and rupture of myocardial fibers. In contrast, Oxymatrine (OMT) effectively counteracts the lethal effects of TE and reduces both cardiac edema and myocardial fiber rupture. In summary, OMT can antagonise TE-induced cardiac injury and lethal effects by inhibiting the activation of the MAPK pathway and reducing oxidative stress and apoptosis. As a natural compound, OMT offers a potential therapeutic strategy for jellyfish stings.

01 Dec 2024·Development

Testosterone acts through the membrane protein GPRC6A to cause cardiac edema in zebrafish embryos

Article

Author: Shahriar, Shayan ; Gorelick, Daniel A. ; Zadmajid, Vahid

ABSTRACTAndrogens are classically thought to act through intracellular androgen receptors (AR/NR3C4), but they can also trigger non-genomic effects via membrane proteins. Although several membrane androgen receptors have been characterized in vitro, their functions in vivo remain unclear. Using a chemical-genetic screen in zebrafish, we found that GPRC6A, a G-protein-coupled receptor, mediates non-genomic androgen actions during embryonic development. Exposure to androgens (androstanedione, DHT and testosterone) caused cardiac edema or tail curvature in wild-type embryos, as well as in ar mutants, suggesting AR-independent pathways. We then mutated putative membrane androgen receptors [gprc6a, hcar1-4 and zip9 (slc39a9)] and found that only gprc6a mutants exhibited a significant reduction in cardiac edema after testosterone exposure. Additionally, co-treatment of wild-type embryos with testosterone and GPRC6A antagonists significantly suppressed the cardiac edema phenotype. Using RNA-seq and RNA rescue approaches, we found that testosterone and GPRC6A cause cardiac phenotypes by reducing Pak1 signaling. Our results indicate that testosterone induces cardiac edema in zebrafish embryos through GPRC6A, independent of nuclear androgen receptors, highlighting a previously unappreciated non-genomic androgen signaling pathway in embryonic development.

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