Left Ventricular Mechanics and Myocardial Blood Flow: LV contractile dysfunction

This means that long-term asynchronous ventricular activation leads to LV contractile dysfunction that is, at least in part, reversible immediately after the restoration of a normal ventricular activation sequence. In a study by Nielsen et al, it was found that a change in pacing mode from DDD to AAI in patients receiving long-term pacing (ie, mean duration of pacing, 22 ± 8 months) caused an immediate and significant increase in LVEF. However, the latter is only a rough index of systolic function, being load-dependent, and so no sure conclusions can be drawn regarding changes in myocardial contractility following an alteration of pacing mode. In contrast to the systolic indexes, the diastolic indexes we evaluated, apart from dP/dtmin, showed no significant changes. More info
In fact, we cannot explain the increase in the magnitude of dP/dtmin while other, more objective indexes of LV relaxation (such as t) did not change significantly. Accordingly, it may be a potential statistical error, due to the small number of patients studied. On the other hand, it has been found that, following long-term asynchronous ventricular activation, the disturbances of diastolic function begin to regress 24 h after the restoration of a normal ventricular activation sequence. In the present study, we also found that the Ees/Ea ratio, which expresses ventriculoarterial coupling, increased significantly after the restoration of a normal ventricular activation sequence and that the predicted MVO2 remained unchanged.
Although MVO2 had no clear change, in contrast to the situation after the use of most positive inotropic agents, the improvement of contractility should be attributed to the more “economic” function of the heart and to the improved ventriculoarterial coupling after the restoration of a normal ventricular activation sequence.

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