Prevention of heart failure progression: current approaches
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Updated: Jun 23, 2026

Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in Göttingen Minipigs and Landrace Pigs
Published on: April 17, 2021
1Pharmacology Department, Pitié-Salpétrière Hospital, Paris, France.
Insights
Heart failure stems from myocardial damage. Therapies aim to reduce cardiac load and block detrimental neurohormonal effects, with ongoing trials seeking optimal prevention strategies for heart failure progression.
Area of Science:
- Cardiology
- Pathophysiology
- Pharmacology
Background:
- Heart failure arises from myocardial damage and stress, regardless of the cause.
- Compensatory mechanisms, including the sympathetic nervous system and renin-angiotensin-aldosterone system, initially manage cardiac overload but can lead to myocyte dysfunction and fibrosis.
- Progressive cell death and fibrous tissue replacement characterize advanced heart failure.
Purpose of the Study:
- To outline the pathophysiology of heart failure.
- To discuss current therapeutic strategies for managing heart failure.
- To highlight the potential of complete neurohormonal blockade as a future therapeutic goal.
Main Methods:
- Review of existing literature on heart failure mechanisms and treatments.
- Analysis of the roles of neurohormonal systems in cardiac remodeling.
- Discussion of pharmacological interventions, including diuretics, vasodilators, and adrenergic blockade.
Main Results:
- Compensatory mechanisms in heart failure can paradoxically promote disease progression.
- Current therapies focus on reducing cardiac workload and mitigating adverse neurohormonal effects.
- Complete blockade of detrimental neurohormonal pathways is a promising therapeutic objective.
Conclusions:
- Effective heart failure management requires reducing cardiac loading and avoiding therapies that exacerbate the condition.
- Targeting neurohormonal pathways involved in adverse cardiac remodeling is crucial for improving prognosis.
- Ongoing clinical trials are essential to establish definitive treatment protocols for preventing heart failure progression.
Abstract:
Heart failure results from damage and stress to the myocardium whatever the aetiology. An increase in stress by cardiac overload is initially overcome by compensatory mechanisms that maintain blood pressure through a combination of the sympathetic nervous system and the renin-angiotensin-aldosterone system. These mechanisms may also alter myocyte function and induce progressive cell death and replacement by fibrous tissue. Disease therapy must reduce cardiac loading and avoid blood pressure control by mechanisms that have deleterious effects. Therapy includes diuretics, vasodilators and alpha- and beta-adrenergic blockade. Complete blockade of all receptors involved in the adverse effects of neurohormonal stimulation might represent an ultimate therapy objective, and improve subsequent prognosis. Large clinical trials are in progress to determine the therapy of choice in the prevention of progression of heart failure.
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