Last update 01 Nov 2024

Edema, Cardiac

Last update 01 Nov 2024

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.

Otsuka Pharmaceutical 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

Acute decompensated heart failure [+14]

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 / RecruitingPhase 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

595

Literatures (Medical) associated with Edema, Cardiac

01 Dec 2024·Molecular Biology Reports

Inhibition of cytochrome P450 epoxygenase promotes endothelium-to-mesenchymal transition and exacerbates doxorubicin-induced cardiovascular toxicity

Article

Author: Maayah, Zaid H ; Therachiyil, Lubna ; Younis, Shahd M ; Yalcin, Huseyin C ; Dhulkifle, Hevna ; Sayed, Tahseen S ; Hasan, Maram H ; Korashy, Hesham M

AbstractBackgroundDoxorubicin (DOX) is a potent chemotherapy widely used in treating various neoplastic diseases. However, the clinical use of DOX is limited due to its potential toxic effect on the cardiovascular system. Thus, identifying the pathway involved in this toxicity may help minimize chemotherapy risk and improve cancer patients’ quality of life. Recent studies suggest that Endothelial-to-Mesenchymal transition (EndMT) and endothelial toxicity contribute to the pathogenesis of DOX-induced cardiovascular toxicity. However, the molecular mechanism is yet unknown. Given that arachidonic acid and associated cytochrome P450 (CYP) epoxygenase have been involved in endothelial and cardiovascular function, we aimed to examine the effect of suppressing CYP epoxygenases on DOX-induced EndMT and cardiovascular toxicity in vitro and in vivo.Methods and ResultsTo test this, human endothelial cells were treated with DOX, with or without CYP epoxygenase inhibitor, MSPPOH. We also investigated the effect of MSPPOH on the cardiovascular system in our zebrafish model of DOX-induced cardiotoxicity. Our results showed that MSPPOH exacerbated DOX-induced EndMT, inflammation, oxidative stress, and apoptosis in our endothelial cells. Furthermore, we also show that MSPPOH increased cardiac edema, lowered vascular blood flow velocity, and worsened the expression of EndMT and cardiac injury markers in our zebrafish model of DOX-induced cardiotoxicity.ConclusionOur data indicate that a selective CYP epoxygenase inhibitor, MSPPOH, induces EndMT and endothelial toxicity to contribute to DOX-induced cardiovascular toxicity.

01 Nov 2024·Aquatic Toxicology

Aryl phosphate ester-induced pericardial edema in zebrafish embryos is influenced by the ionic composition of exposure media

Article

Author: Mersman, Zoe ; Volz, David C ; Wiegand, Jenna ; Volz, David C. ; Jimenez, Nicholas ; Michalicek, Kevin ; Hoang, John

Pericardial edema - fluid accumulation within the pericardium - is a frequently observed malformation in zebrafish embryo-based chemical toxicity screens. We recently discovered that the severity of triphenyl phosphate (TPHP)-induced pericardial edema was dependent on the ionic strength of exposure media. TPHP is an aryl phosphate ester (APE) widely used as a plasticizer and flame retardant. APEs are characterized by having one or more aryl groups bound to a phosphate center, with TPHP containing only unsubstituted aryl groups. Therefore, the objective of this study was to begin investigating whether, similar to TPHP, pericardial edema induced by other structurally related APEs is dependent on the ionic composition of exposure media. We first mined the peer-reviewed literature to identify other APEs that 1) induced pericardial edema in zebrafish embryos within a minimum of three peer-reviewed publications, and 2) demonstrated a statistically significant induction of pericardial edema in at least 70 % of the studies evaluated. Based on this meta-analysis, we identified four other APEs that caused pericardial edema in zebrafish embryos: isopropylated triphenyl phosphate (IPTPP), cresyl diphenyl phosphate (CDP), tricresyl phosphate (TMPP), and 2-ethylhexyl diphenyl phosphate (EDHPHP). Using TPHP as a positive control and pericardial edema as a readout, we developed concentration-response curves for all four APEs based on static exposure from 24 to 72 h post-fertilization (hpf). We then conducted co-exposures with D-Mannitol (an osmotic diuretic) and exposures within reverse osmosis (RO) water determine whether the ionic composition of exposure media mitigated APE-induced pericardial edema at 72 hpf. Using pericardial edema as an endpoint, the approximate EC₅₀s for TPHP (positive control), IPTPP, CDP, TMPP, and EDHPHP were 6.25, 3.125, 3.125, 25, and 100 µM, respectively, based on exposure from 24 to 72 hpf. Interestingly, similar to our findings with TPHP, co-exposure with D-Mannitol and exposure within ion-deficient water significantly mitigated IPTPP- CDP-, TMPP-, and EDHPHP-induced pericardial edema in zebrafish embryos, suggesting that chemically-induced pericardial edema may be 1) dependent on the ionic composition of exposure media and 2) driven by a disruption in osmoregulation across the embryonic epidermis. Therefore, similar to other assay parameters, our findings underscore the need to standardize the osmolarity of exposure media in order to minimize the potential for false positive/negative hits in zebrafish embryo-based chemical toxicity screens conducted around the world.

01 Nov 2024·Cardiovascular Toxicology

Therapeutic Efficacy of Selenium Pre-treatment in Mitigating Cadmium-Induced Cardiotoxicity in Zebrafish (Danio rerio)

Article

Author: Noor, Md Imran ; Covington, Myles A ; Guevara, Gabriella A ; Heuer, Rachael M ; Heuer, Rachael M. ; Covington, Myles A. ; Shelton, Delia S ; Falagan-Lotsch, Priscila ; Umeh, Olaedo G. ; Guevara, Gabriella A. ; Deperalto, Madison ; Shelton, Delia S. ; Koop, Rebekka R. ; Koop, Rebekka R ; Okutsu, Jessica ; Umeh, Olaedo G

AbstractCardiovascular diseases are a rampant public health threat. Environmental contaminants, such as Cadmium (Cd), a toxic metal, are risk factors for cardiovascular diseases. Given that human exposure to Cd is increasing, there is a need for therapies to ameliorate Cd toxicity. Selenium (Se), an essential trace element, has been proposed to rescue the effects of Cd toxicity, with mixed effects. Se's narrow therapeutic window necessitates precise dosing to avoid toxicity. Here, we assessed the effects of various waterborne Cd and Se concentrations and sequences on cardiac function using zebrafish (Danio rerio). We showed that Cd induced pericardial edemas and modified heart rates in zebrafish larvae in a concentration-dependent manner. To identify the therapeutic range of Se for Cd-induced cardiotoxicity, zebrafish embryos were treated with 0, 10, 50, 100, 150, or 200 μg/L Se for 1–4 days prior to exposure to 2.5 and 5 μg/L Cd. We found that a 50 µg/L Se pre-treatment before 2.5 μg/L Cd, but not 5 μg/L Cd, reduced the prevalence of pericardial edemas and ameliorated Cd-induced bradycardia in zebrafish. Zebrafish exposed to 10 and 50 μg/L of Se for up to 4 days showed typical heart morphology, whereas other Se-exposed and control fish presented pericardial edemas. Longer Se pre-treatment durations led to fewer incidences of pericardial edemas. Overall, this study highlights the importance of optimizing Se concentrations and pre-treatment periods to harness its protective effects against Cd-induced cardiotoxicity. These findings provide insights into potential therapeutic strategies for reducing Cd-related cardiovascular damage in humans.Graphical Abstract

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