The response of the left ventricle to pacing-induced changes in heart rate and the atrioventricular (A-V) relation was examined with equilibrium gated radionuclide ventriculography in 20 patients who had normal ventricular function after surgery for recurrent Supraventricular tachycardia. In 10 patients count-derived left ventricular ejection fraction, end-diastolic volume and stroke volume were measured during sinus rhythm and during atrial pacing at 120,140 and 160 beats/min. In the other 10 patients similar determinations were made during sequential A-V and simultaneous ventricular and atrial (V/A) pacing, both at rates of 100 and 160 beats/min. Left ventricular ejection fraction did not change significantly with atrial pacing (from 0.65 ± 0.02 [mean ± standard error of the mean]at a baseline sinus rale of 91 ± 3 beats/min to 0.62 ± 0.03 at 160 beats/min) despite a progressive decrease in end-diastolic volume. The percent reduction in end-diastolic volume (% ΔEDV) and stroke volume (% ΔSV) from the baseline values was linear and related to change in heart rate (ΔHR) as % ΔEDV = -0.60 ΔHR + 5.19 (r = 0.71; p < 0.01) and % ΔSV = -0.62 ΔHR + 5.03 (r = 0.76; p < 0.001). Left ventricular ejection fraction with baseline sequential A-V pacing at 100 beats/min was 0.67± 0.03 and not significantly altered by either sequential A-V or simultaneous V/A pacing at 160 beats/min. At 100 beats/min, loss of atrial transport with simultaneous V/A pacing resulted in a small reduction in end-diastolic volume from a baseline value of -9.0 ±1.9 percent (p <0.01) and a nonsignificant reduction in stroke volume of -3.7 ± 1.6 percent. During simultaneous V/A pacing at 160 beats/min, the reduction in end-diastolic and stroke volumes from the baseline value was -26.6 ± 3.8 percent and -28.8 ± 4.3 percent, respectively (both p <0.01), but was significantly smalfer (-16.1 ± 3.6 percent and -19.2 ± 4.1 percent, respectively [p <0.05]) when atrial transport was maintained during sequential A-V pacing at the same heart rate. During simultaneous V/A pacing at 160 beats/min, two thirds of the reduction in end-diastolic and stroke volumes from the baseline value was due to the increment in heart rate as assessed from sequential A-V pacing and the other third was due to loss of atrial transport. The data indicate that the hemodynamic consequences of Supraventricular tachyarrhythmias in patients with normal ventricular function are due primarily to decreases in ventricular volume as heart rate is increased and atrial contribution is lost rather than to any changes in left ventricular ejection fraction.