Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Pulmonary Edema II: Pathophysiology01:18

Pulmonary Edema II: Pathophysiology

Pulmonary edema is the accumulation of fluid in the interstitial and alveolar spaces of the lungs, impairing gas exchange and oxygen delivery. It may be cardiogenic or noncardiogenic, but both reduce oxygenation and lung compliance.Cardiogenic Pulmonary EdemaCardiogenic edema results from increased hydrostatic pressure in pulmonary capillaries, usually due to left ventricular dysfunction from myocardial infarction, heart failure, or valvular disease. Ineffective cardiac pumping causes blood to...
Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
Heart Failure Drugs: Diuretics01:22

Heart Failure Drugs: Diuretics

Heart failure and kidney perfusion are interconnected in a complex way. Reduced renal perfusion and venous congestion are two significant factors that contribute to renal dysfunction in heart failure. The kidneys, primarily responsible for fluid balance in the body, are adversely affected due to compromised cardiac output and increased venous pressure. In response to reduced renal perfusion, the kidneys activate neurohumoral mechanisms to restore balance. However, these mechanisms can be...
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...
Heart Failure III: Clinical Manifestations01:26

Heart Failure III: Clinical Manifestations

Heart failure (HF) manifests primarily as dyspnea, fatigue, and fluid retention, resulting in peripheral and pulmonary edema. Symptoms may vary depending on which ventricle is more affected, left or right.Left-Sided Heart FailureAlso known as left ventricular failure, this condition results from the left ventricle's inability to fill or eject sufficient blood into the systemic circulation. It leads to pulmonary congestion, which occurs when the left ventricle fails to eject blood effectively...
Imbalances in Cardiac Output01:26

Imbalances in Cardiac Output

The heart's primary function is to pump blood throughout the body, maintaining a balance between blood sent out (cardiac output) and blood returning (venous return). If this balance is disrupted, it can result in congestive heart failure (CHF), a severe condition where the heart becomes an inefficient pump, leading to inadequate blood circulation.
CHF can occur due to the failure of either side of the heart. Left-side failure leads to pulmonary congestion—the right side continues to send blood...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Pulmonary vascular resistance is associated with two-year clinical outcomes in non-hypoxemic COPD with mild pulmonary hemodynamic abnormalities.

Respiratory investigation·2026
Same author

Anatomically Normal Aortic Valve Area in Relation to Age, Sex, Body Size, and Aortic Root Dimensions: A TEE Study.

The American journal of cardiology·2026
Same author

Prognostic impact of thyroid transcription factor-1 expression and the efficacy of carboplatin plus (nab-) paclitaxel in non-squamous non-small cell lung cancer complicated with idiopathic interstitial pneumonias.

Translational lung cancer research·2026
Same author

β-Nicotinamide mononucleotide preserves muscle strength in septic male mice.

Scientific reports·2026
Same author

Association between fundus sex index and hypertension, diabetes mellitus, and smoking in the Kumejima study.

Japanese journal of ophthalmology·2026
Same author

Utility of MostGraph in asthma management: Comparative study with cough-variant asthma.

Respiratory medicine·2026

Related Experiment Videos

[Cardiac toxicity and edema].

Susumu Takeuchi1, Hiroshi Sakai

  • 1Department of Respiratory Disease, Saitama Cancer Center, Saitama, Japan.

Gan to Kagaku Ryoho. Cancer & Chemotherapy
|October 22, 2008
PubMed
Summary
This summary is machine-generated.

Cancer therapies, including anthracyclines and molecular targeted agents, can cause cardiac toxicity and edema. Early monitoring and intervention are key, but new treatment strategies are needed.

Related Experiment Videos

Area of Science:

  • Cardiology
  • Oncology
  • Pharmacology

Context:

  • Cancer therapies, including anthracyclines (e.g., doxorubicin) and molecular targeted agents (e.g., trastuzumab, imatinib), have been associated with significant cardiac toxicity since the 1970s.
  • The incidence of drug-induced cardiac toxicity has risen due to advancements in multidisciplinary cancer care, high-dose chemotherapy, and targeted therapies.
  • Cardiac dysfunction and edema are recognized adverse events, with mechanisms often undefined, necessitating careful patient management.

Purpose:

  • To review the current understanding of anticancer drug-induced cardiac toxicity and edema.
  • To highlight the importance of cardiac function monitoring during cancer treatment.
  • To emphasize the need for further research into the mechanisms and treatment of these adverse events.

Summary:

  • Anticancer drugs, particularly anthracyclines and molecular targeted agents, can cause cardiac toxicity, potentially leading to irreversible dysfunction.
  • Molecular targeted agents like imatinib can also induce edema, a relatively new adverse event requiring prompt diagnosis and management.
  • Current management strategies focus on pre-treatment cardiac evaluation and on-treatment monitoring, with only symptomatic treatments available for edema.

Impact:

  • Early detection and monitoring of cardiac function are crucial for managing chemotherapy-induced cardiotoxicity.
  • Understanding the mechanisms of cardiotoxicity and edema is essential for developing effective preventative and therapeutic strategies.
  • Further research into novel treatments for anticancer drug-induced cardiac complications is warranted to improve patient outcomes and quality of life.