Ten weeks of rapid ventricular pacing creates a long-term model of left ventricular dysfunction

Objective: Rapid ventricular pacing produces a reliable model of heart fail ure. Cessation after 4 weeks of rapid ventricular pacing results in rapid n ormalization of left ventricular function, but the left ventricle remains p ersistently dilated. We present novel data that show that prolonged rapid v entricular pacing (10 weeks) creates a model of chronic left ventricular dy sfunction. Methods: In 9 dogs undergoing 10 weeks of rapid ventricular pacing, left ve ntricular function and volumes were serially assessed by using 2-dimensiona l echocardiography and pressure-volume analysis for 12 weeks after cessatio n of pacing, Results: increased end-diastolic volume and decreased systolic and diastoli c function were seen at the end of pacing. By 2 weeks or recovery from rapi d ventricular pacing, end-diastolic volume and ejection fraction were parti ally recovered but did not improve further thereafter Load-independent and load-sensitive indices of function obtained by pressure-volume analysis at 8 and 12 weeks of recovery confirmed a persistence of both systolic and dia stolic dysfunction. In addition, left ventricular mass increased with pacin g and remained elevated at 8 and 12 weeks of recovery. Four of these dogs s tudied at 6 months of recovery showed similar left ventricular abnormalitie s. Conclusion: Ten weeks of rapid ventricular pacing creates a long-term model of left ventricular dysfunction.