There was no www.selleckchem.com/products/pexidartinib-plx3397.html significant difference in the duration of the PSN between the measurement levels (Table 2). Table 2 The velocity and duration characteristics of the PSN The onset and the peak velocities The

onset velocities of the PSN were significantly more negative (p < 0.001) and the peak velocities significantly higher (p < 0.001) at the Inhibitors,research,lifescience,medical AA than at all other measurement levels (Table 2). The onset of the PSN had a negative velocity in all the subjects at all measurement levels. The peak of the PSN showed a positive value in 90.6% of the subjects at the level of the AA. At the other studied levels it reached the positive values less frequently (AW 68.8%, MAS 56.3%, MA 59.4%). Additional findings In 10 of 32 (31%) studied subjects, the second PSN spike was identifiable at the AA level (Fig. 5). Of these, 9 (28%) exhibited a second PSN spike Inhibitors,research,lifescience,medical at the AW, 3 (9%) at the MAS and no one at the MA. Fig. 5 The second post-systolic velocity notch (PSN) spike at the level of the anterior aortic annulus. The arrow indicates the onset of the second PSN spike. Discussion A distinct PSN pattern could be distinguished in the TDI derived curves of all studied subjects. It was demonstrated that the PSN is the earliest and the largest at

the level of the AA when compared Inhibitors,research,lifescience,medical to other sites along the apical longitudinal axis. We suggest that the sudden cessation of the closing motion Inhibitors,research,lifescience,medical of the aortic valve at the onset of the PSN is associated with release of kinetic energy responsible for the abrupt change of direction of the myocardial acceleration, leading to an upstroke of the

velocity curve. Our findings form a circumstantial though significant plea to allocate the moment of the aortic valve closure to the PSN onset at the level of the AA. According to Inhibitors,research,lifescience,medical our hypothesis the resulting PSN wave propagates as well in proximal (compression wave) as in distal (rarefaction wave) direction. The decrease of the amplitude of the PSN at the remote segments relative to the AA fits this hypothesis. The significantly longer delay of the PSN onset at the MA as compared with the AW is, probably, explained by the longer distance for the PSN wave to travel from its origin and different velocities of the PSN wave while travelling through myocardium versus AW. Our findings seem to further develop the hypothesis of Remme et al.4) strongly suggesting that the impact of the closing aortic valve and not merely mafosfamide the interruption of the protodiastolic myocardial lengthening at the instant of the cessation of its closing motion accounts for the upstroke of the PSN. The existence of the pulsatile wave propagating from the base of interventricular septum to the apex was previously shown by a phased tracking method.5) The wave starts with a steep pulse near the base of interventricular septum just at the instant of the closure of the aortic valve and propagates with a speed about 5-6 m/s.