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Ten weeks of rapid ventricular pacing creates a long-term model of left ventricular dysfunction
H J Patel1, J J Pilla, D J Polidori
1Divisions of Cardiothoracic Surgery and Cardiology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
Insights
Prolonged rapid ventricular pacing (10 weeks) in dogs creates a chronic heart failure model. Left ventricular dysfunction persists long-term, unlike shorter pacing durations, offering a new model for chronic heart failure research.
Area of Science:
- Cardiology
- Physiology
- Heart Failure Research
Background:
- Rapid ventricular pacing is a common model for studying heart failure.
- Short-term pacing (4 weeks) leads to reversible left ventricular dysfunction.
- Persistent left ventricular dilation occurs even after function normalizes.
Purpose of the Study:
- To investigate if prolonged rapid ventricular pacing (10 weeks) induces chronic left ventricular dysfunction.
- To establish a long-term animal model for chronic heart failure.
Main Methods:
- Utilized 9 dogs for a 10-week rapid ventricular pacing protocol.
- Assessed left ventricular function and volumes using 2D echocardiography and pressure-volume analysis.
- Monitored recovery for 12 weeks post-pacing cessation, with some dogs studied up to 6 months.
Main Results:
- Pacing increased left ventricular end-diastolic volume and decreased systolic/diastolic function.
- Partial recovery of function and ejection fraction was observed within 2 weeks, but no further improvement.
- Persistent systolic and diastolic dysfunction, along with increased left ventricular mass, were confirmed at 8 and 12 weeks and 6 months post-pacing.
Conclusions:
- Ten weeks of rapid ventricular pacing establishes a reliable, long-term model of chronic left ventricular dysfunction.
- This model demonstrates persistent cardiac abnormalities beyond the pacing period.
- The findings suggest prolonged pacing is necessary to induce chronic, non-reversible heart failure changes.
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.