When OCM was first described, its hemodynamic diagnosis depended on the postextrasystolic behavior of LVOT gradient and systemic arterial pulse pressure. Since then, the two most reliable and accepted hemodynamic criteria for OCM diagnosis have been the increased post-PVC LVOT gradient and the decrement or the failure to increase of post-PVC systemic arterial pulse pressure. However, post-PVC LVOT gradient increments might also be detected in fixed LVOT stenosis. Additionally, severe isolated \AS, echocardiographi-cally free of OCM, might show a post-PVC decreased arterial pulse pressure. Therefore, the qualitative analysis of the directional changes of post-PVC LVOT gradient and arterial PP may not be as reliable and diagnostic as was once thought, and a quantitative approach to these post-PVC changes seems reasonable and necessary for the hemodynamic diagnosis of OCM, even if OCM is usually an echocardiographic diagnosis.
Our results support the fact that a qualitative analysis is not accurate enough, since 33 of the 36 isolated VAS did show a post-PVC LVOT gradient potentiation and since 17 of these 36 VAS failed to show a post-PVC increased arterial PP. The behavior of post-PVC LVOT gradient and PP in our series of OCM is in accordance to the criteria already validated in the literature: a post-PVC increased LVOT gradient and a decrement or failure to increase arterial PP. In our series of OCM, the post-PVC LVOT gradient increased more than 75 percent of the basal gradient in all cases, and a post-PVC PP decrement >5 mm Hg occurred in 12 of 14 cases. Only one patient with VAS (number 20 in Table 2) fulfills these two criteria.
When the subgroup of patients with nonsevere VAS with a basal gradient similar to that of OCM is analyzed, none of the patients fulfilled these hemodynamic criteria (Table 4).
The higher relative increment of post-PVC LVOT gradient in OCM is probably an expression of the increased contractility, as expected in post-PVC potentiation phenomenon, and a reduction in the orifice size or enhanced cavity obliteration.1(M3 Since in these patients the LVOT gradient is produced by the contraction of the hypertrophied muscle, its severity is a function of the strength of contraction. In fixed VAS, although the primary change in the hemodynamic factors associated with post-PVC potentiation and post-PVC compensatory pause are also present and quantitatively similar (similar increment in post-PVC RR), the obstructive orifice has a fixed size. Therefore, its changes in size must not influence the LVOT gradient There was a slight, although not statistically significant, difference between the post-PVC RR increment in the OCM and WAS groups. Figure 2 illustrates that the notably larger post-PVC LVOT gradient relative increment in OCM vs WAS (and even vs the subgroup of nonsevere VAS) is not at all related to the degree of PVC prematurity, since the different quantitative behavior in post-PVC LVOT gradient between both types of diseases is similar at all levels of the RR increment. The relative increment of post-PVC LVOT gradient is always higher for OCM than for \AS at all levels of RR increment.