Mechanism of hemodynamic improvement by dual-chamber pacing for severe left ventricular dysfunction: an acute Doppler and catheterization hemodynamic study

Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic, Rochester, Minnesota 55905.

OBJECTIVES. This study was undertaken to determine the mechanism by which improvement in hemodynamic variables may occur with dual-chamber pacing in patients with severe left ventricular dysfunction. BACKGROUND. Dual-chamber pacing has recently been proposed as a therapeutic alternative for the relief of symptoms in patients with dilated cardiomyopathy. METHODS. Fifteen patients with severe left ventricular systolic dysfunction were studied acutely during atrioventricular (AV) sequential pacing at various AV intervals (60, 100, 120, 140, 180 and 240 ms) with use of combined Doppler velocity curves and pressures obtained by high fidelity manometer-tipped catheters and thermodilution cardiac output. RESULTS. Neither cardiac output nor mean left atrial pressure was significantly different when hemodynamic variables in the baseline state were compared with those during AV sequential pacing at the various AV intervals in all patients. The patients were classified into two groups. In group I (eight patients with PR intervals > 200 ms on the rest 12-lead electrocardiogram), cardiac output was significantly increased when AV sequential pacing at the optimal AV interval to output was compared with that at the baseline state (3.0 +/- 1.0 vs. 3.9 +/- 0.43 liters/min, p = 0.005) because timing of mechanical atrial and ventricular synchrony was optimized. In addition, left ventricular end-diastolic pressure and duration of diastolic filling were increased, and diastolic mitral regurgitation was abolished. In group II (seven patients who had normal AV conduction at rest), cardiac output during AV pacing decreased from the baseline value without change in the diastolic filling period. CONCLUSIONS. Dual-chamber pacing may improve acute hemodynamic variables in selected patients with dilated cardiomyopathy, mainly by optimization of the timing of mechanical atrial and ventricular synchrony. Reestablishment of the optimal diastolic filling period and abolition of diastolic mitral regurgitation may also contribute to hemodynamic improvement.

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