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Related Concept Videos

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...
Cardiomyopathy II: Dilated Cardiomyopathy01:30

Cardiomyopathy II: Dilated Cardiomyopathy

Dilated cardiomyopathy, or DCM, is a progressive myocardial disorder characterized by ventricular chamber dilation and contractile dysfunction.EtiologyVarious factors can cause DCM, including hypertension and heavy alcohol intake, which contribute to the weakening and enlargement of the heart muscle. Viral infections, such as Coxsackievirus B, adenoviruses, and influenza, can lead to DCM by causing inflammation and damage to heart tissue. Certain chemotherapeutic agents, including daunorubicin,...
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
Cardiomyopathy IV: Restrictive Cardiomyopathy01:29

Cardiomyopathy IV: Restrictive Cardiomyopathy

Restrictive cardiomyopathy (RCM) is a rare heart muscle disease characterized by impaired ventricular filling due to stiffened ventricular walls, leading to significant diastolic dysfunction.EtiologyRestrictive cardiomyopathy can arise from both inherited and acquired diseases, many of which are systemic. It is categorized into four main types: infiltrative, storage, non-infiltrative, and endomyocardial diseases.Infiltrative diseases, such as amyloidosis, lead to RCM by depositing amyloid...
Cardiomyopathy V: Interprofessional Care01:29

Cardiomyopathy V: Interprofessional Care

Managing cardiomyopathy involves addressing underlying or precipitating causes, treating heart failure with medications, and implementing dietary changes and a balanced exercise and rest regimen.Lifestyle ModificationsCardiomyopathy patients should adopt a low-sodium diet to reduce fluid retention and manage heart failure. A personalized exercise and rest plan helps maintain physical fitness without overstraining the heart. Avoiding alcohol and tobacco is essential to prevent further damage to...

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A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
05:14

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo

Published on: May 16, 2020

New developments in anthracycline-induced cardiotoxicity.

A Mordente1, E Meucci, A Silvestrini

  • 1Institute of Biochemistry and Clinical Biochemistry, Catholic University School of Medicine, 00168 Roma, Italy. alvaro.mordente@rm.unicatt.it

Current Medicinal Chemistry
|May 16, 2009
PubMed
Summary
This summary is machine-generated.

Anthracyclines are potent anticancer drugs but cause dose-dependent heart damage. New research explores mechanisms and strategies to prevent this cardiotoxicity, focusing on metabolites and genetic factors.

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Chemotherapy-induced Vascular Toxicity - Real-time In vivo Imaging of Vessel Impairment
04:48

Chemotherapy-induced Vascular Toxicity - Real-time In vivo Imaging of Vessel Impairment

Published on: January 7, 2015

Area of Science:

  • Cardiology
  • Oncology
  • Pharmacology

Background:

  • Anthracyclines are effective anticancer agents.
  • Their use is limited by dose-dependent cardiotoxicity, leading to heart failure.
  • The exact mechanisms of anthracycline-induced cardiomyopathy are not fully understood.

Purpose of the Study:

  • To review the molecular mechanisms of anthracycline cardiotoxicity.
  • To discuss the role of drug metabolism in cardiotoxicity.
  • To explore strategies for preventing or limiting anthracycline-induced heart damage.

Main Methods:

  • Review of current literature on anthracycline cardiotoxicity.
  • Analysis of molecular pathways and metabolic processes.
  • Discussion of genetic influences and novel therapeutic strategies.

Main Results:

  • Anthracyclines can cause cardiotoxicity via reactive oxygen species (ROS) or C-13 alcohol metabolites.
  • ROS may explain acute cardiotoxicity, while alcohol metabolites might drive progressive cardiomyopathy.
  • Genetic polymorphisms can influence individual susceptibility to cardiotoxicity.

Conclusions:

  • Understanding anthracycline metabolism is crucial for addressing cardiotoxicity.
  • Novel approaches including targeted therapies and cardioprotective agents show promise.
  • Further research is needed to mitigate the cardiotoxic effects of these vital anticancer drugs.