Last word on point: Counterpoint: Left ventricular volume during diastasis is not the physiological in vivo equilibrium volume and is not related to diastolic suction.

The truth regarding ventricular equilibrium and diastolic suction has been elusive since Galen (26) observed blood moving into the ventricle with a force “vis a fronte.” The continued debate (29) justifies that we readdress the conceptual (i.e., kinematic) basis of ventricular equilibrium and diastolic suction. Equilibrium at diastasis. We propose a physiologically intuitive, functional equilibrium: diastasis. When ventricular filling commences, the chamber expands (recoils) faster than it can fill and aspirates blood from the atrium by rapidly decreasing chamber pressure with simultaneous volume expansion dP/dV 0 (10, 15). Wall recoil requires a net restoring force generated by the integrated action of loaded elastic elements seeking to return to their equilibrium dimension (2, 8, 12–14). As ventricular filling (Doppler E-wave) continues, the elastic elements approach their equilibrium dimension and elastic forces decrease. Once diastasis is reached, there is no wall motion, no atrioventricular pressure gradient, no flow, and no change in volume or pressure (19). Thus at diastasis, all forces and strains must be balanced (they are not zero), and there is no net force or wall motion. Hence, diastasis must be the in vivo equilibrium volume, and every ventricle approaches diastasis by suction initiated filling. Kinematics of equilibrium. Before the contributors to ventricular elastic properties, such as titin, collagen, and visceral pericardium (12–14, 23) were appreciated, Brecher et al.(3) defined ventricular elastic equilibrium volume intuitively as the volume where the ventricle’s “transmural pressure is zero ( P 0) and no stress is applied on its structural elements.” On the basis of this definition, Nikolic, Yellin, and others used elegant experimental techniques to show that the ventricle generates subatmospheric filling pressures only when the endsystolic volume (ESV) is below a certain value, Vo (21). This value was taken to be the Brecher defined [ P 0] equilibrium volume and reinforced the traditional view that suction only occurs when ventricular ESV Vo. In contrast, more recent work by Omens and Fung (22) and Balaban (14) shows that even when fully relaxed, the LV wall has residual stress. This presence of residual stresses negates Brecher’s implied connection between P 0 and a state where “no stress is applied” on ventricular elastic elements. Because the fully relaxed ventricle’s thick walls maintain residual stress (22), the requirement that transmural pressures vanish ( P 0), need not be invoked to achieve equilibrium. Toward equilibrium. Attainment of diastasis requires ventricular recoil, driven in part, by molecular elastic elements (5, 13, 14) releasing elastic strain stored during systole. If we assume Vo is equilibrium, a serious kinematic inconsistency arises if Vo ESV. In this setting the elastic elements would remain displaced above their equilibrium position and would be expected to exert force opposing chamber enlargement at the start of filling. However, as the mitral valve opens and filling commences, there is always a net expansive force responsible for recoil of the ventricular tissue. An atrial “push” cannot account for this force, because it would cause LV pressure to increase immediately on mitral-valve opening. Relaxation of the LV tissue by itself cannot account for this force either, because relaxation only relieves a compressive force, but does not generate motion. When elastic elements are displaced above equilibrium (Fig. 1), it is not clear what provides the expansive force opposing the early filling-related