Related Experiment Video

Updated: Jul 8, 2026

Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing
12:45

Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing

Published on: December 11, 2017

Reversing advanced heart failure by targeting Ca2+ cycling

David M Kaye1, Masahiko Hoshijima, Kenneth R Chien

  • 1Heart Failure Research Group, Baker Heart Research Institute, Melbourne, Victoria 8008, Australia. david.kaye@baker.edu.au

Annual Review of Medicine
|January 12, 2008
PubMed

Insights

Heart failure remains a significant cardiovascular disease with limited treatment options for severe cases. Targeting the cardiomyocyte calcium-handling pathway shows promise for developing new heart failure therapies.

Area of Science:

  • Cardiovascular Medicine
  • Molecular Biology
  • Genetics

Background:

  • Heart failure (HF) is a leading cause of cardiovascular morbidity and mortality.
  • Current pharmacotherapy for HF has limitations, especially for end-stage patients.
  • Recent research has identified molecular targets for progressive heart failure.

Purpose of the Study:

  • To investigate the role of cardiomyocyte calcium-handling pathway defects in heart failure.
  • To evaluate the therapeutic potential of targeting these defects.

Main Methods:

  • Analysis of molecular basis of progressive heart failure.
  • Examination of cardiomyocyte calcium-handling pathway alterations in heart failure models.
  • Studies in genetically engineered mouse models of heart failure.
  • Myocardial gene transfer techniques in experimental models.

Main Results:

  • Characteristic changes in the cardiomyocyte calcium-handling pathway are observed in heart failure.
  • Restoration of these calcium-handling defects in experimental models shows therapeutic promise.
  • Evidence strongly supports the calcium-handling pathway as a viable clinical intervention target.

Conclusions:

  • The cardiomyocyte calcium-handling pathway is a critical area for therapeutic development in heart failure.
  • Targeting molecular defects, particularly in calcium handling, offers a promising strategy for future heart failure treatments.

More Related Videos

Optical Mapping of Intra-Sarcoplasmic Reticulum Ca2+ and Transmembrane Potential in the Langendorff-perfused Rabbit Heart09:26

Optical Mapping of Intra-Sarcoplasmic Reticulum Ca2+ and Transmembrane Potential in the Langendorff-perfused Rabbit Heart

Published on: September 10, 2015

Related Concept Videos

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...
Heart Failure V: Medical Management01:30

Heart Failure V: Medical Management

Medical Management of Acute Decompensated Heart Failure (ADHF)The primary goals of therapy for patients hospitalized with acute decompensated heart failure (ADHF) include:Relieving symptomsOptimizing volume statusSupporting oxygenation and ventilationMaintaining cardiac output (CO) and end-organ perfusionIdentifying and addressing the cause of ADHFPreventing complicationsProviding patient education on factors precipitating HF exacerbationPlanning for dischargeOngoing monitoring and assessment...
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 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...
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,...
Heart Failure VI: Adjunct Therapies01:22

Heart Failure VI: Adjunct Therapies

Additional therapies for treating patients with heart failure (HF) may include procedural interventions, supplemental oxygen, the management of sleep disorders, and nutritional therapy.Procedural InterventionsImplantable Cardioverter-Defibrillator: For patients at risk of life-threatening arrhythmias due to severe left ventricular dysfunction, an Implantable Cardioverter-Defibrillator (ICD) can detect and terminate these arrhythmias, preventing sudden cardiac death and improving survival rates.