Ventricular-arterial coupling derived from proximal aortic stiffness and aerobic capacity across the heart failure spectrum

Ventricular-arterial coupling (VAC) describes the mechanical interaction between the left ventricle (LV) and the systemic arterial tree. It reflects the efficiency of cardiovascular energy transfer, that is, how effectively LV work is translated into forward flow under a given arterial load to sustain organ perfusion while minimizing myocardial energy expenditure. Traditionally, VAC is quantified as the ratio of arterial elastance (Ea) to end-systolic elastance (Ees), derived from invasive pressure-volume analysis or non-invasive surrogates, such as echocardiography. While this framework is physiologically robust, it has limited applicability in routine practice because it often requires invasive acquisition or technically demanding modelling. A pragmatic, non-invasive surrogate has therefore been proposed: the ratio between pulse wave velocity (PWV), a marker of arterial stiffness, and global longitudinal strain (GLS), a sensitive measure of LV systolic deformation.1,2 Carotid-femoral PWV (cf-PWV), usually assessed by applanation tonometry, is considered the reference standard for aortic stiffness. However, it requires sequential recordings and offline post-processing and is sensitive to waveform acquisition and path-length estimation (particularly in obesity). In addition, cf-PWV may under-represent proximal (arch) stiffness, which plays a central role in early vascular ageing and in determining the timing of wave reflections.1 Proximal aortic stiffness can be assessed by measuring aortic arch PWV (aa-PWV) with cardiovascular magnetic resonance, but its use is limited by costs and workflow constraints. Conversely, real-time estimation of aa-PWV can be obtained at the bedside using a Doppler-derived, single-beat technique from the suprasternal window, with dual-gate, simultaneous pulsed-wave Doppler sampling.1 Increased proximal stiffness raises early systolic load and shifts the return of reflected waves from diastole to systole, augmenting late-systolic afterload and potentially promoting subendocardial ischaemia and diastolic dysfunction.