Bruce Tockman

Effect of Pacing Chamber and Atrioventricular Delay on Acute Systolic Function of Paced Patients With Congestive Heart Failure

BACKGROUNDnPrevious studies of pacing therapy for dilated congestive heart failure (CHF) have not established the relative importance of pacing site, AV delay, and patient heterogeneity on outcome. These variables were compared by a novel technique that evaluated immediate changes in hemodynamic function during brief periods of atrial-synchronous ventricular pacing.nnnMETHODS AND RESULTSnTwenty-seven CHF patients with severe left ventricular (LV) systolic dysfunction and LV conduction disorder were implanted with endocardial pacing leads in the right atrium and right ventricle (RV) and an epicardial lead on the LV and instrumented with micromanometer catheters in the LV, aorta, and RV. Patients in normal sinus rhythm were stimulated in the RV, LV, or both ventricles simultaneously (BV) at preselected AV delays in a repeating 5-paced/15-nonpaced beat sequence. Maximum LV pressure derivative (LV+dP/dt) and aortic pulse pressure (PP) changed immediately at pacing onset, increasing at a patient-specific optimal AV delay in 20 patients with wide surface QRS (180+/-22 ms) and decreasing at short AV delays in 5 patients with narrower QRS (128+/-12 ms) (P<0.0001). Overall, BV and LV pacing increased LV+dP/dt and PP more than RV pacing (P<0.01), whereas LV pacing increased LV+dP/dt more than BV pacing (P<0.01).nnnCONCLUSIONSnIn this population, CHF patients with sufficiently wide surface QRS benefit from atrial-synchronous ventricular pacing, LV stimulation is required for maximum acute benefit, and the maximum benefit at any site occurs with a patient-specific AV delay.

Experimental validation of pulse contour methods for estimating stroke volume at pacing onset

Stroke volume (SV) might be an important variable in assessing cardiac function of patients under pacing therapy. To assess the accuracy of estimating SV changes from aortic pressure during VDD pacing, we implanted electromagnetic flowmeters in the aortic root of five mongrel dogs. Three pacing sites, including right ventricle, left ventricle and both ventricles were selected and paced at 5 atrioventricular delays. Each pacing site/AV delay combination was repeated 5 times in a randomized order. The protocol alternated 5 paced beats and 15 intrinsic beats. Flow and aortic pressure data were recorded and analyzed. We evaluated five pulse contour equations relating pulse pressure (PP), ejection time (ET), diastolic time (DT) and aortic pressure area during systole over the end-diastolic pressure (Psa). A good correlation (r=0.84-0.89) was shown between percent change in SV and percent change in PP, PP*ET, Psa, Psa*ET and Psa*(1+ET/DT) over the preceding baseline. The average estimated percent change in SV also correlated with the average measured percent change in SV for each pacing site/AV delay combination. In conclusion, PP, PP*ET, Psa, Psa*ET and Psa*(1+ET/DT) may be clinically applicable for assessing SV at the start of VDD pacing and may effectively predict the effects of pacing sites and AV delays on SV.