Congestion as an electrophysiological state in heart failure: from mechano-electric coupling to dynamic arrhythmic risk.

Heart failure (HF) is traditionally characterized by hemodynamic impairment and neurohormonal activation, with congestion representing a central clinical feature. However, the electrophysiological consequences of congestion remain underexplored. Emerging evidence suggests that volume overload and elevated filling pressures actively modulate cardiac electrophysiology through mechano-electric coupling, myocardial stretch, and interstitial edema. Mechanical stretch activates stretch-sensitive ion channels, alters calcium handling, and increases cellular automaticity, thereby promoting triggered activity. Concurrently, atrial and ventricular dilation, combined with edema-induced conduction heterogeneity, create a dynamic substrate that facilitates re-entry and increases susceptibility to both atrial and ventricular arrhythmias. Clinically, episodes of congestion are frequently associated with the onset or worsening of atrial fibrillation and may contribute to ventricular arrhythmia burden, particularly in advanced HF. Importantly, congestion is a dynamic and potentially reversible condition, suggesting that arrhythmic risk in HF is not static but fluctuates over time. This concept challenges current approaches to risk stratification, which largely rely on fixed structural parameters. Decongestive therapies, including diuretics and device-based strategies, may exert antiarrhythmic effects beyond hemodynamic improvement, although this remains insufficiently characterized. In this narrative review, we integrate mechanistic, experimental, and clinical evidence to define the electrophysiological impact of congestion in HF. We propose a conceptual framework in which congestion acts as a transient but powerful arrhythmic modulator and discuss its implications for timing of interventions, risk stratification, and future monitoring strategies. Recognizing congestion as an active driver of arrhythmogenesis may open new avenues for personalized management in heart failure.