The quantitative different behavior of post-PVC systemic arterial PP is mainly due to a different behavior of post-PVC systolic arterial pressure, since the post-PVC change in aortic diastolic pressure, a consequence of diastolic arterial peripheral runoff, is similar in both VAS and OCM groups owing to a similar post-PVC RR increment (Table 4). In OCM post-PVC ASP showed a statistically significantly larger decrement. This larger post-PVC decrement of ASP may be an expression of a post-PVC decreased forward stroke volume. It is an already accepted paradox that the Frank-Starling mechanism, which usually serves to increase stroke volume, might increase cavity obliteration or mitral regurgitation and actually reduce the forward stroke volume in patients with OCM. The lack of increment in forward stroke volume, coupled with a decreased post-PVC aortic impedance, might explain the post-PVC decrement of AS? since the main determinant factors of ASP are stroke volume and aortic impedance.
When a fixed outflow obstruction is present, most of the impedance to ejection resides in the area of stenosis, which does not vary during the compensatory pause. Therefore, the effect of the increased post-PVC LV systolic pressure may not be significantly transmitted to the circulation beyond the stenotic aortic valve, thus not causing an increment high enough in forward stroke volume to compensate for the decreased post-PVC peripheral aortic impedance. This may explain why most VAS show a post-PVC decrement in ASP. Since the reduction in aortic impedance might be similar in both groups of patients with VAS and OCM (owing to a similar post-PVC variation in arterial diastolic runoff time), the larger post-PVC ASP decrement in OCM must be related to a smaller increment, or even a decrement, of post-PVC forward stroke volume, a hypothesis already suggested by some authors in OCM and probably related to an enhanced post-PVC mitral dysfunction or to an increased outflow obstruction.
Post-PVC LVOT gradient potentiation occurs in patients with fixed as well as in patients with dynamic obstruction. However, increments of post-PVC LVOT gradient exceeding 75 percent of basal gradient strongly suggest OCM. Patients with fixed obstruction can show mild decrements of post-PVC arterial pulse pressure, especially in severe aortic stenosis. However, decrements of post-PVC arterial pulse pressure larger than 5 mm Hg suggest the existence of OCM. Therefore, we believe that the simultaneous fulfillment of these two post-PVC hemodynamic criteria is a reliable and useful method for the hemodynamic differentiation between OCM and fixed VAS.