We characterized the relationship between systolic ventricular function and left ventricular (LV) end-diastolic pressure (LVEDP) in patients with heart failure (HF) and baseline asynchrony during ventricular stimulation. The role of preload in the systolic performance improvement that can be obtained in HF patients with LV stimulation is uncertain.We measured the maximum rate of increase of LV pressure, LVEDP, aortic pulse pressure (PP) and the atrioventricular mechanical latency (AVL) between left atrial systole and LV pressure onset in 39 patients with HF. Two subgroups were identified: "responder" if PP improved, or "nonresponder."Maximum hemodynamic improvement occurred at an atrioventricular (AV) delay that did not decrease LVEDP. Left ventricular and biventricular (BV) stimulation increased systolic hemodynamics significantly, despite no significant increase in LVEDP. All parameters decreased when the LVEDP was decreased by shorter AV delay. Left ventricular and BV stimulation provided better hemodynamics than right ventricular (RV) stimulation. For the nonresponder subgroup, systolic hemodynamics only worsened during AV delay shortening. For the responder subgroup, optimum PP was achieved when AVL was near zero. Restoration of optimal left atrial-ventricular mechanical timing partly contributes to the hemodynamic improvements observed in this patient subgroup. However, preload alone cannot explain the differences seen between RV and BV stimulation and the contradictory PP decreases even at maximal preload in the nonresponder subgroup. These results may be explained by a site-dependent mechanism such as the degree of ventricular synchrony. Caution should be taken in these patients when optimizing AV delays using echocardiography techniques that focus on LV inflow.

We tested whether biventricular resynchronization explains contractile function changes with univentricular and biventricular pacing in heart failure patients with varying magnitudes of baseline biventricular asynchrony. Thirty patients (New York Hospital Association class > or = III, QRS duration > or =120 ms) were tested. Contractile function was measured by left ventricular maximum first derivative of pressure over time (dP/dtmax). Biventricular mechanical asynchrony was quantified by the normalized pressure-pressure (NPP) loop area formed by the cross-plot of right and left intraventricular pressure curves from each cardiac cycle. Any ventricular pacing increased dP/dtmax if it decreased baseline NPP loop area and almost always worsened dP/dtmax and asynchrony when baseline NPP loop area <0.3. The quantitative relationship between dP/dtmax and NPP loop area change depended on ventricular pacing site and timing relative to intrinsic activation. For similar NPP loop decreases, dP/dtmax increased 16% more with left and biventricular pacing compared with right ventricular pacing. In conclusion, right, left, or biventricular pacing can improve contractile function only in patients having sufficient baseline biventricular asynchrony. However, biventricular resynchronization is only one of the improvement mechanisms.

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The presence of a larger amount of LV area with late Endo-AT and preserved LV myocardium measured by electromechanical mapping could identify patients who have better acute improvement in systolic performance during LV stimulation.

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