Archive for the ‘Aortic Pressures’ Category


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. (more…)

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  • Differences of Postextrasystolic Behavior of Left Ventricular and Aortic Pressures: DiscussionWhen 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. (more…)

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  • Individual hemodynamic data in both baseline and post-PVC conditions are listed in Table 1 for OCM, in Tables 2 and 3 for the whole group of WAS, and in Table 3 for the subgroup of nonsevere WAS. Collective data of OCM and VAS series of patients are shown in Table 4. Comparisons are made between OCM and the whole group of WAS (ie, severe + nonsevere WAS) and between OCM and the subgroup of nonsevere WAS, which have a similar basal gradient. Left ventricular ejection fraction (EF) was significantly higher for OCM than for WAS (OCM, 83.2 ± 6.4, range 71 to 92 percent vs WAS, 65.9 ± 16.1, range 32 to 82 percent; p<0.01). (more…)

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  • Differences of Postextrasystolic Behavior of Left Ventricular and Aortic PressuresThe recognition of muscular LVOT obstruction associated with fixed stenosis has therapeutic implications. Since a catheter within the left ventricular chamber can easily induce PVCs during left heart catheterization, the induction of this arrhythmia has been considered as the standard hemodynamic intervention for evaluation of LVOT gradients. In fact, post-PVC LVOT gradient increments (dynamic obstruction) were usually considered to be indicative of hypertrophic OCM. However, fixed stenosis in the LVOT, as in WAS, might also show a post-PVC gradient potentiation, even in the documented absence of OCM. Although post-PVC decrement of arterial pulse pressure (PP) and peak systolic aortic pressure are suggestive of OCM, some cases of \AS might also show such behavior. In view of these observations we prospectively evaluated the hemodynamic behavior of the post-PVC beat in patients with OCM and with WAS free of OCM. http://www.medicines-for-diabetes.com/ (more…)

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