["The Journal of Physiology, Volume 604, Issue 13, Page 5458-5492, 1 July 2026. ", "\nAbstract figure legend A sudden decrease in total peripheral resistance (TPR), as observed during vasovagal syncope, leads to a reduction in aortic systolic pressure (AO pressure) and afterload. In healthy individuals, the consequent decrease in left ventricular systolic pressure (LV pressure) lowers stroke work and myocardial energy expenditure. By contrast, in aortic stenosis, the persistent pressure gradient across the stenotic valve maintains elevated LV pressure and energy expenditure. The fall in AO pressure also diminishes coronary blood flow (CBF), thereby reducing myocardial energy supply. In healthy individuals, this reduction in energy delivery is counterbalanced by decreased energy expenditure and adequate compensatory mechanisms, preserving an energetically stable state. However, in aortic stenosis, the insufficient energy delivery, even with compensatory mechanisms, fails to meet the energy requirements of the heart, potentially leading to sudden cardiac death (SCD). VED, end‐diastolic volume; Rcor, coronary vascular resistance; Emax, maximal end‐systolic elastance; HR, heart rate.\n\n\n\n\n\n\n\n\n\nAbstract\nSevere aortic stenosis (AS) is a recognized risk factor for sudden cardiac death (SCD). Although ventricular tachyarrhythmias are the most common immediate cause of SCD, the majority of cases of SCD in patients with severe AS exhibited bradyarrhythmia as the primary rhythm. Enhanced activation of left ventricular baroreceptors (Bezold–Jarisch reflex) has been implicated in the pathogenesis of syncope in patients with AS. However, the precise mechanism by which an otherwise benign circulatory syncope can progress to cardiac arrest in severe AS remains unclear. This study proposes a haemodynamic‐energetic mechanism to explain this progression, and demonstrates its plausibility using a mathematical model of cardiac haemodynamics and energetics. The model identifies states of cardiac energy imbalance, in which the energy expenditure of the heart exceeds the energy delivered to it. In individuals with a normal aortic valve, compensatory mechanisms can restore energy balance following syncope. By contrast, in severe AS, all conditions involving low peripheral vascular resistance are energetically unstable, regardless of compensatory response. Because energy imbalance is incompatible with sustained cardiac function, such states inevitably result in cardiac arrest. Importantly, the proposed mechanism does not require an exaggerated Bezold–Jarisch reflex, although the reflex probably acts as a trigger of syncope by initiating peripheral vasodilatation. Additionally, the limited coronary vasodilatory reserve commonly observed in severe AS significantly contributes to the development of myocardial energy imbalance.\n\n\n\n\n\n\n\n\n\nKey points\n\nThe precise mechanism of sudden cardiac death in patients with severe aortic stenosis remains uncertain.\nIn the present study, we propose a novel haemodynamic‐energetic mechanism of sudden cardiac death explaining how otherwise benign circulatory syncope can progress to cardiac arrest in patients with severe aortic stenosis. The plausibility of the mechanism is verified using a mathematical model.\nThe model identifies states of cardiac energy imbalance in patients with severe aortic stenosis, where the energy expenditure of the heart exceeds the energy delivered to it, which inevitably leads to cardiac arrest.\nMathematical simulation of a circulatory syncope reveals significant differences in the effects of compensatory response in patients with and without severe aortic stenosis.\nThe results provide a comprehensive understanding of the mechanism of sudden cardiac death in patients with severe aortic stenosis.\n\n\n"]