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Diffuse fibrosis leads to a decrease in unipolar voltage: Validation in a swine model of premature ventricular
Yasuaki Tanaka1, Dolkun Rahmutula1, Srikant Duggirala1
1Section of Cardiac Electrophysiology, Department of Medicine, University of California, San Francisco, San Francisco, California.
Heart Rhythm
|September 30, 2015
Summary
Frequent premature ventricular contractions (PVCs) can cause cardiomyopathy. This study shows that in a swine model, PVCs increase fibrosis and alter voltage distribution, mirroring human conditions.
Area of Science:
- Cardiology
- Electrophysiology
- Cardiac Pathology
Background:
- Frequent premature ventricular contractions (PVCs) are linked to dilated cardiomyopathy.
- A leftward shift in unipolar voltage distribution in cardiomyopathy is attributed to increased fibrosis.
Purpose of the Study:
- Establish a swine model of PVC-induced cardiomyopathy.
- Assess if increased left ventricular fibrosis occurs due to PVCs.
- Determine if fibrosis leads to a leftward shift in unipolar voltage distribution.
Main Methods:
- Ten swine received ventricular pacemakers; 6 had a 50% PVC burden, 4 served as controls.
- Voltage maps were acquired at baseline and after 14 weeks of ventricular bigeminy.
- Histological analysis quantified fibrosis.
Main Results:
- PVCs significantly decreased left ventricular ejection fraction (67% to 44%) compared to controls.
- A significant increase in unipolar voltage <5.5 mV (5.4% to 12.6%) and a leftward shift were observed in the PVC group.
- Histology confirmed increased fibrosis in the PVC group (1.8% to 3.4%) versus controls.
Conclusions:
- PVC-induced cardiomyopathy in swine increases interstitial fibrosis.
- This fibrosis correlates with a leftward shift in unipolar voltage distribution.
- Findings align with observations in human PVC-induced cardiomyopathy.
