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J Thorac Cardiovasc Surg 2000;119:834-841
© 2000 The American Association for Thoracic Surgery

CARDIOPULMONARY SUPPORT AND PHYSIOLOGY

TEN WEEKS OF RAPID VENTRICULAR PACING CREATES A LONG-TERM MODEL OF LEFT VENTRICULAR DYSFUNCTION

From the Divisions of Cardiothoracic Surgery^a and Cardiology,^b University of Pennsylvania School of Medicine, Philadelphia, Pa.

Address for reprints: Michael A. Acker, MD, Associate Professor of Surgery, Division of Cardiothoracic Surgery, Hospital of the University of Pennsylvania, Silverstein 4, 3400 Spruce St, Philadelphia, PA 19104.

Objective: Rapid ventricular pacing produces a reliable model of heart failure. Cessation after 4 weeks of rapid ventricular pacing results in rapid normalization of left ventricular function, but the left ventricle remains persistently dilated. We present novel data that show that prolonged rapid ventricular pacing (10 weeks) creates a model of chronic left ventricular dysfunction.
Methods: In 9 dogs undergoing 10 weeks of rapid ventricular pacing, left ventricular function and volumes were serially assessed by using 2-dimensional echocardiography and pressure-volume analysis for 12 weeks after cessation of pacing.
Results: Increased end-diastolic volume and decreased systolic and diastolic function were seen at the end of pacing. By 2 weeks of recovery from rapid ventricular pacing, end-diastolic volume and ejection fraction were partially 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 diastolic dysfunction. In addition, left ventricular mass increased with pacing and remained elevated at 8 and 12 weeks of recovery. Four of these dogs studied at 6 months of recovery showed similar left ventricular abnormalities.
Conclusion: Ten weeks of rapid ventricular pacing creates a long-term model of left ventricular dysfunction.

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