Impaired atrioventricular time interaction contributes to tachycardia-induced hemodynamic deterioration: In vivo and in silico hybrid approach

Volume 449, 15 April 2026, 134192

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Atrioventricular time interaction critically determines the heart rate-induced hemodynamic deterioration

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Hybrid animal experiments and simulations systematically evaluate heart rate effects on hemodynamics

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Impaired atrioventricular time interaction fuses E-A waves, widening the gap between atrial and ventricular filling pressure

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Prolonged relaxation and atrioventricular delay markedly worsen atrioventricular time interaction

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Heart rate optimization requires individualized strategies based on underlying pathophysiology

AbstractBackground

Heart rate (HR) is a major determinant of cardiac output (CO). During tachycardia, adequate left ventricular (LV) filling becomes important; however, excessive tachycardia reduces CO by shortening filling time. The impact of HR on hemodynamics differs according to the underlying cardiac pathological conditions, making HR management challenging. The atrioventricular (AV) time interaction, which represents the temporal coordination between atrial and ventricular functions for optimal LV filling, is key to effective HR management during tachycardia. This study aimed to elucidate tachycardia-induced hemodynamic deterioration by focusing on AV time interaction.

Methods

A hybrid approach combining animal experiments and computer simulations was employed. In animal experiments, hemodynamics and mitral valve (MV) flow at HR of 90–180 bpm were recorded in eight beagles. The relationship among LV end-diastolic pressure (LVEDP), left atrial pressure (LAP), and changes in MV E–A waves were evaluated. In simulation experiments, hemodynamics at HR of 50–150 bpm were analyzed using a cardiovascular mathematical model across five pathological conditions.

Results

In animal experiments, CO peaked at HR of 130–140 bpm, coinciding with MV E–A wave fusion and a decreased LVEDP/LAP ratio. Simulation studies showed effective tachycardic compensation in systolic and diastolic dysfunction. However, prolonged relaxation time and prolonged AV delay led to decreased CO at high HR.

Conclusions

AV time interaction manifests as E–A wave fusion and decreased LVEDP/LAP ratio. Simulation studies suggest that conditions directly affecting filling time significantly impair AV time interaction and lead to circulatory deterioration during tachycardia. These findings highlight the importance of individualized HR management.

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