MECHANISM OF HEMODYNAMIC IMPROVEMENT BY DUAL-CHAMBER PACING FOR SEVERE LEFT-VENTRICULAR DYSFUNCTION - AN ACUTE DOPPLER AND CATHETERIZATION HEMODYNAMIC-STUDY

Objectives. This study was undertaken to determine the mechanism by wh ich improvement in hemodynamic variables may occur with dual-chamber p acing in patients with severe left ventricular dysfunction. Background . Dual-chamber pacing has recently been proposed as a therapeutic alte rnative for the relief of symptoms in patients with dilated cardiomyop athy. Methods. Fifteen patients with severe left ventricular systolic dysfunction were studied acutely during atrioventricular (AV) sequenti al 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 o utput. Results. Neither cardiac output nor mean left atrial pressure w as significantly different when hemodynamic variables in the baseline state were compared with those during AV sequential pacing at the vari ous AV intervals in all patients. The patients were classified into tw o groups. In group I (eight patients with PR intervals >200 ms on the rest 12-lead electrocardiogram), cardiac output was significantly incr eased when AV sequential pacing at the optimal AV interval to output w as compared with that at the baseline state (3.0 +/- 1.0 vs. 3.9 +/- 0 .0 liters/min, p = 0.005) because timing of mechanical atrial and vent ricular synchrony was optimized. In addition, left ventricular end dia stolic pressure and duration of diastolic filling were increased, and diastolic mitral regurgitation was abolished. In group II (seven patie nts mba had normal AV conduction at rest), cardiac output during AV pa cing decreased from the baseline value without change in the diastolic filling period. Conclusions. Dual chamber pacing may improve acute he mo dynamic variables in selected patients with dilated cardiomyopathy, mainly by optimization of tbe timing of mechanical atrial and ventric ular synchrony. Reestablishment of the optimal diastolic filling perio d and abolition of diastolic mitral regurgitation may also contribute to hemodynamic improvement.