Don't Wait- Ablate! Catheter Ablation in Patients with Advanced Heart Failure and Atrial Fibrillation

Figures

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  Fig. 1. Atrial fibrillation and heart failure – a bidirectional relationship. Bidirectional pathophysiological interaction between atrial fibrillation (AF) and heart failure (HF). AF contributes to HF progression through loss of atrial contraction, impaired diastolic filling, and irregular ventricular activation, resulting in reduced cardiac efficiency and hemodynamic deterioration. Conversely, HF promotes the development and maintenance of AF through increased atrial and ventricular filling pressures, myocardial inflammation and fibrosis, and progressive atrial remodeling and enlargement. Both disease entities share common mechanistic pathways, including neurohormonal activation, chronic inflammation, and structural atrial remodeling, thereby creating a self-perpetuating vicious cycle that accelerates disease progression and worsens clinical outcomes

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  Fig. 2. Evolution in atrial fibrillation therapy: from rate to rhythm control. Evolution of evidence supporting the transition from rate control to rhythm control strategies in atrial fibrillation (AF). The y-axis represents publication year, whereas the x-axis illustrates the conceptual shift from predominantly ratecontrol approaches toward rhythm control and catheter ablation-based strategies. Early landmark trials, including RACE Trial, AFFIRM Trial, and AF-CHF Trial, demonstrated no significant survival advantage of pharmacological rhythm control over rate control. Subsequent catheter ablation studies, including PABA-CHF Trial, AATAC Trial, CAMERA-MRI Trial, and CASTLE-AF Trial, established the prognostic and functional benefits of catheter ablation, particularly in patients with heart failure. More recent studies, including CABANA Trial, and CASTLE-HTx Trial, further supported earlier rhythm control strategies and extended the concept of AF ablation as a disease-modifying therapy across the spectrum of heart failure severity

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  Fig. 3. Mechanistic insights of atrial fibrillation in advanced heart failure. The detrimental remodeling of atrial fibrillation (AF) on the left ventricle. AF causes excessive reactive oxygen species (ROS) formation that actives Ca2 + –calmodulin-dependent protein kinase II (CaMKII) thereby causing diastolic sarcoplasmic Ca2 + loss and depressed Ca2 + transients. Experimental data indicate, that remodeling of ventricular remodeling cardiomyocytes occurs between an AF burden of 30–60% [34], [38]