Left Ventricular Mechanics and Myocardial Blood Flow: Study Limitations

Besides, the fact that the observed functional abnormalities during ventricular pacing, like reduced regional myocardial work, reduced oxygen uptake, and free fatty metabolism, are found in regions supplied by the dominant artery further reinforces our results.
Previous studies have speculated that the impairment of LV systolic function is due to the reduction in coronary flow that is seen in patients receiving long-term pacing. However, the fact that systolic function improves following the restoration of a normal ventricular activation sequence, whereas CFR worsens, suggests that these changes are probably independent of the asynchronous ventricular activation induced by right ventricular apical pacing. there

Although the LV contractility in our patients improved significantly, we are unable to know whether it reached its prepacing levels, since prepacing measurements of Ees were not available to us. Furthermore, the evaluation of systolic and diastolic functional indexes was made only a few minutes after the restoration of a normal ventricular activation sequence. It would be interesting to investigate whether the improvement in systolic function would continue over the following hours or days, and whether an improvement would be seen in diastolic function, in which we observed no clear short-term change. Coronary flow and CFR also might exhibit different behavior if they were evaluated some time after the restoration of a normal ventricular activation sequence.
Clinical Implications
For a number of reasons, which vary from country to country and from one pacing center to another, right ventricular apical pacing under VVI or DDD pacing modes is common. The findings of this study demonstrate that patients who receive pacing in this way can expect to benefit from the restoration of a more normal ventricular activation sequence even after long-term ventricular asynchrony.
Conclusions
The restoration of a normal ventricular activation sequence after long-term ventricular asynchrony enhances the short-term contractile function without affecting MV02. These changes do not seem to relate to myocardial blood flow changes. Although more studies are needed to examine whether the improvement in LV contractility translates into a clinical benefit, it seems reasonable to restore a normal activation sequence where possible, even following long-term ventricular asynchrony.

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