Related Experiment Video

Updated: Aug 7, 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

Enalapril effects on atrial remodeling and atrial fibrillation in experimental congestive heart failure

Yanfen Shi1, Danshi Li, Jean-Claude Tardif

  • 1Montreal Heart Institute, Research Center and Department of Medicine, 5000 Belanger Street East, Montreal HlT 1C8 Quebec, Canada.

Cardiovascular Research
|June 14, 2002
PubMed

Insights

Angiotensin-converting enzyme (ACE) inhibitors like enalapril can reduce atrial remodeling and fibrosis in experimental congestive heart failure (CHF). This treatment also significantly decreases the duration of atrial fibrillation (AF) in canine models.

Area of Science:

  • Cardiology
  • Cardiac Electrophysiology
  • Pharmacology

Background:

  • Atrial remodeling is a key factor in maintaining atrial fibrillation (AF) in various cardiac conditions.
  • Angiotensin-converting enzyme (ACE) inhibitors have shown promise in reducing AF prevalence in patients with congestive heart failure (CHF).
  • The specific impact of ACE inhibitors on atrial dimensions, function, and AF vulnerability in experimental CHF remains understudied.

Purpose of the Study:

  • To investigate the effects of enalapril (EN), an ACE inhibitor, on atrial remodeling and AF vulnerability in a canine model of experimental CHF.
  • To assess how EN therapy influences atrial dimensions, emptying function, and fibrosis in the context of CHF.
  • To determine the correlation between atrial structural/functional changes and AF duration.

Main Methods:

  • Congestive heart failure (CHF) was induced in 20 dogs via rapid right ventricular pacing over 5 weeks.
  • Dogs were randomized to receive either enalapril (EN) therapy (2 mg/kg/day) or a control treatment.
  • Echocardiography was used for weekly assessments of atrial dimensions and fractional area shortening (FAS).
  • At 5 weeks, AF was induced by burst pacing to measure AF duration.

Main Results:

  • CHF led to significant increases in atrial areas and decreased left atrial (LA) and right atrial (RA) fractional area shortening (FAS).
  • Enalapril treatment significantly attenuated the decrease in LA and RA FAS compared to controls.
  • Atrial fibrosis, strongly correlated with reduced LA FAS, was significantly reduced by enalapril therapy.
  • AF duration was substantially shorter in the enalapril group compared to controls.
  • Atrial dimensions and FAS at 5 weeks, as well as the decrease in FAS, were significantly correlated with AF duration.

Conclusions:

  • Experimental CHF induces structural and functional atrial abnormalities that correlate with AF duration.
  • ACE inhibition effectively mitigates CHF-induced atrial fibrosis and remodeling, thereby reducing AF promotion.
  • These findings highlight the role of the renin-angiotensin system in promoting arrhythmogenic atrial remodeling during CHF.
Abstract

More Related Videos

Isolation of Atrial Cardiomyocytes from a Rat Model of Metabolic Syndrome-related Heart Failure with Preserved Ejection Fraction08:31

Isolation of Atrial Cardiomyocytes from a Rat Model of Metabolic Syndrome-related Heart Failure with Preserved Ejection Fraction

Published on: July 26, 2018

Transesophageal Atrial Burst Pacing for Atrial Fibrillation Induction in Rats05:12

Transesophageal Atrial Burst Pacing for Atrial Fibrillation Induction in Rats

Published on: February 14, 2022

Related Concept Videos

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...
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 Drugs: β-Blockers01:22

Heart Failure Drugs: β-Blockers

β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation, vasodilation, and...
Aortic Regurgitation III: Medical Management01:25

Aortic Regurgitation III: Medical Management

Aortic regurgitation (AR) is when the aortic valve does not close or seal properly, leading to backward blood circulation from the aorta into the left ventricle during diastole. Common causes of AR include rheumatic heart disease, congenital valve defects, and aortic root dilation. Managing AR requires a multifaceted approach to alleviate symptoms, preserve left ventricular function, and address the underlying cause of the regurgitation. Patients with symptomatic AR or significant left...
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
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...