Time course of left ventricular volumes in severe congestive heart failure patients treated by optimized AV sequential left ventricular pacing alone--a 3-dimensional echocardiographic study.

BACKGROUND: This study evaluates the acute and chronic resynchronizing effects of AV sequential left ventricular (LV) pacing on LV function in patients with impaired cardiac function and conduction disorders by 3-dimensional transesophageal echocardiography. METHODS AND RESULTS: Twenty-nine patients with congestive heart failure, with LV ejection fraction (LVEF) < or = 30%, QRS duration > or = 120 milliseconds, and New York Heart Association Class II to IV, were implanted with a cardiac resynchronization device using an LV lead only, according to the invasively determined hemodynamic optimal pacing site and AV delay. Patients underwent 3-dimensional transesophageal echocardiography before randomization to treatment (baseline) and at 12-month follow-up (resynchronization--12 months). Three-dimensional volumes were acquired on resynchronization and during intermittent switch-off at intrinsic depolarization. The values of stroke volume were 43.2 +/- 13.3 (intrinsic-baseline), 51.7 +/- 17.4 (intrinsic--12 months), 57.2 +/- 15.6 (resynchronization-baseline), and 64.6 +/- 18.9 (resynchronization--12 months). Analysis of variance demonstrated a significant effect of resynchronization at different periods (P < .001) and a significant time effect (P < .05) for stroke volume. Similar results were observed with ejection fraction (LVEF). No effect was observed with LV end-diastolic volume, whereas a therapy effect with no time effect was observed with LV end-systolic volume. CONCLUSIONS: A significant acute increase of LV stroke volume and LVEF was found by resynchronization by LV pacing alone. A continuous improvement of LV stroke volume and LVEF occurred with time of follow-up (reverse remodeling). The initial therapeutic effect persisted during 12-month follow-up independently of time of follow-up and QRS width. No significant decrease of LV end-diastolic size during chronic resynchronization was detected in contrast to previous studies with resynchronization by biventricular pacing.

Area of left ventricular regional conduction delay and preserved myocardium predict responses to cardiac resynchronization therapy.

UNLABELLED: Cardiac resynchronization therapy. BACKGROUND: A significant proportion of patients with dilated cardiomyopathy and left bundle branch block (LBBB) do not respond to cardiac resynchronization therapy (CRT). The purpose of this study was to investigate whether the electromechanical properties of the myocardium would predict acute hemodynamic improvement during left ventricular (LV) pacing. METHODS AND RESULTS: We studied 10 patients with idiopathic dilated cardiomyopathy and LBBB (ejection fraction (EF): 27%+/-7%; QRS duration: 166+/-16 msec) using three-dimensional electromechanical endocardial mapping technique to assess endocardial activation time (Endo-AT), unipolar voltage, and local linear shortening during sinus rhythm. LV stimulation was performed in VDD mode at five different sites and three atrioventricular delays within the coronary sinus. LV+dP/dtmax changes from baseline were measured during LV stimulation at each site (%DeltadP/dtmax). There was no significant relationship between maximum %DeltadP/dtmax during LV stimulation at the best coronary sinus site and LV EF, baseline LV+dP/dtmax, total LV Endo-AT, baseline QRS duration nor changes in QRS duration during LV pacing. However, the maximum %DeltadP/dtmax was significantly positively correlated with percentage area of late Endo-AT (r=0.97, P<0.001) and preserved LV myocardium (r=0.81, P=0.005), respectively. Patients with >20% of LV area with late Endo-AT and >30% of preserved LV myocardium had five times better acute hemodynamic response with LV stimulation. Multivariate analysis showed that only percentage area of late Endo-AT was independently correlated with %DeltadP/dtmax (P<0.05). CONCLUSION: 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.

Biventricular mechanical asynchrony predicts hemodynamic effect of uni- and biventricular pacing.

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.

Cardiac resynchronization therapy restores optimal atrioventricular mechanical timing in heart failure patients with ventricular conduction delay.

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.