Can Pediatric Heart Failure Therapy Be Improved? Yes It Can, But…

Area of Science:

• Pediatric Cardiology
• Regenerative Medicine
• Pharmacology

Background:

• Pediatric heart failure (pHF) has a heterogeneous etiology, complicating evidence-based treatment strategies.
• Current treatment paradigms for adult heart failure (HF) may not be suitable for children with potential for recovery.
• Age- and disease-related differences in myocardial physiology necessitate individualized precision medicine approaches.

Purpose of the Study:

• To advocate for a paradigm shift in pediatric heart failure (pHF) treatment towards individualized, regenerative strategies.
• To question the first-line use of diuretics in pediatric patients with potential for cardiac recovery.
• To highlight the role of highly selective beta-1 blockers in promoting myocardial regeneration and improving pHF management.

Main Methods:

• Review of existing literature and institutional experience regarding pediatric heart failure (pHF) treatment.
• Analysis of the physiological differences in pediatric versus adult cardiovascular systems.
• Evaluation of the safety and efficacy profile of selective beta-1 blockers, specifically bisoprolol.

Main Results:

• Inadequate diuretic use can worsen pHF by stimulating the neurohumoral axis and causing volume depletion.
• Highly selective beta-1 blockers (e.g., bisoprolol) protect against myocyte apoptosis while allowing for $\beta$2-receptor-mediated regeneration.
• Bisoprolol demonstrates a favorable safety-efficacy profile in infants, with heart rate reduction as a key efficacy indicator.

Conclusions:

• Individualized therapy is crucial for improving pediatric heart failure (pHF) symptoms and promoting functional cardiac regeneration.
• Selective beta-1 blockers like bisoprolol are recommended as a first-line treatment in infants with conditions such as dilated cardiomyopathy and post-stage-1 hypoplastic left heart syndrome.
• The use of beta-1 selective blockers should be considered for ventricular septal defects with significant left-to-right shunting to optimize cardiac function and recovery.