In this issue of the Journal, Nemes et al 1 consider alterations in aortic stiffness during a 1-year follow-up after aortic valve replacement (AVR). Twelve patients with severe aortic stenosis (AS) who underwent AVR were prospectively investigated. As expected, stenosis severity and left ventricular (LV) mass decreased significantly after AVR. Moreover, aortic luminal diameter changes (systolic minus diastolic dimensions) progressively increased and aortic stiffness decreased to levels comparable to those of age-, gender-, and risk factormatched controls at 1 year.Some readers might find it counterintuitive that the pulse pressure in uncorrected severe AS tended to be greater than at 12 months after AVR. Rethinking the apparently simple but actually complex is central to understanding the interacting hemodynamic changes beneath this seemingly paradoxical finding. We start with an integrative overview of ventricular loading.The ventricular systolic ejection load represents pressure against which the walls contract and is to be distinguished from myocardial loading or wall stress, to which it is related by complex cardiomorphometric and histoarchitectonic factors. The total ventricular systolic load, or afterload, determines the manner by which the mechanical energy generated by the actin-myosin interactions in the ventricular walls is converted to the work that pumps blood through the circulation. Under any given contractile state, increased afterload reduces ejection rate and stroke volume. Conversely, when afterload decreases, a larger volume is ejected at higher ejection velocities. 2-5 These changes result from the inverse force-velocity relation of the working myocardium. 3,4
Extrinsic component of the total ventricular systolic loadIt is the interaction of the ejection flow patterns generated by the left (right) ventricle at the aortic (pulmonic) root with the systemic (pulmonary) input impedance 6,7 that gives rise to the extrinsic component of the total ventricular systolic load. This view differs from the widely quoted formulation, by Milnor, 8 of the arterial impedance as the complete representation of the ventricular afterload. First, Milnor's formulation neglects entirely the intrinsic component of systolic ventricular loading (ie, the intraventricular flow-associated