Diffuse fibrosis leads to a decrease in unipolar voltage: Validation in a swine model of premature ventricular contraction–induced cardiomyopathy
Autor: | Dolkun Rahmutula, Edward P. Gerstenfeld, Babak Nazer, Richard E. Sievers, Jeffrey E. Olgin, Qizhi Fang, Yasuaki Tanaka, Srikant Duggirala |
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Rok vydání: | 2016 |
Předmět: |
Cardiomyopathy
Dilated medicine.medical_specialty Swine Cardiomyopathy 030204 cardiovascular system & hematology Severity of Illness Index Ventricular Dysfunction Left 03 medical and health sciences 0302 clinical medicine Fibrosis Physiology (medical) Internal medicine medicine Animals Humans 030212 general & internal medicine Lead (electronics) Ejection fraction business.industry Models Cardiovascular Stroke Volume Dilated cardiomyopathy Stroke volume medicine.disease Ventricular Premature Complexes Electrophysiological Phenomena Disease Models Animal Bigeminy Diffuse fibrosis cardiovascular system Cardiology Electrophysiologic Techniques Cardiac Cardiology and Cardiovascular Medicine business |
Zdroj: | Heart Rhythm. 13:547-554 |
ISSN: | 1547-5271 |
DOI: | 10.1016/j.hrthm.2015.09.025 |
Popis: | Frequent premature ventricular contractions (PVCs) may lead to dilated cardiomyopathy. A leftward shift in the unipolar voltage distribution in patients with cardiomyopathy has also been described and attributed to increased fibrosis.We established a swine model of PVC-induced cardiomyopathy and assessed (1) whether an increase in left ventricular fibrosis occurs and (2) whether increased fibrosis leads to a leftward shift in the unipolar voltage distribution.Ten swine underwent implantation of ventricular pacemakers; 6 programmed to deliver a 50% PVC burden and 4 controls without pacing. Voltage maps were acquired at baseline and after 14 weeks of ventricular bigeminy.In the PVC group, left ventricular ejection fraction decreased from 67% ± 7% to 44% ± 15% (P.05) with no change in controls (71% ± 6% to 73% ± 4%; P = .56). The fifth percentile of the bipolar and unipolar voltage distribution at baseline was 1.63 and 5.36 mV, respectively. In the control group, after 14 weeks of pacing there was no significant change in % bipolar voltage1.5 mV (pre 1.2% vs post 2.2%; P = .34) or % unipolar voltage5.5 mV (pre 4.0% vs post 3.5%; P = .20). In the PVC group, there was a significant increase in % unipolar voltage5.5 mV (5.4% vs 12.6%; P.01), with a leftward shift in the unipolar voltage distribution. Histologically, % fibrosis was increased in the PVC group (control 1.8% ± 1.3% vs PVC 3.4% ± 2.6%; P.01).PVC-induced cardiomyopathy in swine leads to an increase in interstitial fibrosis and a leftward shift in the unipolar voltage distribution. These findings are consistent with findings in humans with PVC-induced cardiomyopathy. |
Databáze: | OpenAIRE |
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