Diffuse fibrosis leads to a decrease in unipolar voltage: Validation in a swine model of premature ventricular contraction-induced cardiomyopathy

Yasuaki Tanaka, Dolkun Rahmutula, Srikant Duggirala, Babak Nazer, Qizhi Fang, Jeffrey Olgin, Richard Sievers, Edward P. Gerstenfeld

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Background 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. Objectives 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. Methods 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. Results 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 voltage <1.5 mV (pre 1.2% vs post 2.2%; P =.34) or % unipolar voltage <5.5 mV (pre 4.0% vs post 3.5%; P =.20). In the PVC group, there was a significant increase in % unipolar voltage <5.5 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). Conclusion 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.

Original languageEnglish (US)
Pages (from-to)547-554
Number of pages8
JournalHeart Rhythm
Volume13
Issue number2
DOIs
StatePublished - Feb 1 2016
Externally publishedYes

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Ventricular Premature Complexes
Cardiomyopathies
Fibrosis
Swine
Control Groups
Dilated Cardiomyopathy
Stroke Volume

Keywords

  • Cardiomyopathy
  • Electroanatomic mapping
  • Fibrosis
  • Premature ventricular contraction
  • Voltage mapping

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Diffuse fibrosis leads to a decrease in unipolar voltage : Validation in a swine model of premature ventricular contraction-induced cardiomyopathy. / Tanaka, Yasuaki; Rahmutula, Dolkun; Duggirala, Srikant; Nazer, Babak; Fang, Qizhi; Olgin, Jeffrey; Sievers, Richard; Gerstenfeld, Edward P.

In: Heart Rhythm, Vol. 13, No. 2, 01.02.2016, p. 547-554.

Research output: Contribution to journalArticle

Tanaka, Yasuaki ; Rahmutula, Dolkun ; Duggirala, Srikant ; Nazer, Babak ; Fang, Qizhi ; Olgin, Jeffrey ; Sievers, Richard ; Gerstenfeld, Edward P. / Diffuse fibrosis leads to a decrease in unipolar voltage : Validation in a swine model of premature ventricular contraction-induced cardiomyopathy. In: Heart Rhythm. 2016 ; Vol. 13, No. 2. pp. 547-554.
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abstract = "Background 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. Objectives 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. Methods 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. Results 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 voltage <1.5 mV (pre 1.2{\%} vs post 2.2{\%}; P =.34) or {\%} unipolar voltage <5.5 mV (pre 4.0{\%} vs post 3.5{\%}; P =.20). In the PVC group, there was a significant increase in {\%} unipolar voltage <5.5 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). Conclusion 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.",
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T1 - Diffuse fibrosis leads to a decrease in unipolar voltage

T2 - Validation in a swine model of premature ventricular contraction-induced cardiomyopathy

AU - Tanaka, Yasuaki

AU - Rahmutula, Dolkun

AU - Duggirala, Srikant

AU - Nazer, Babak

AU - Fang, Qizhi

AU - Olgin, Jeffrey

AU - Sievers, Richard

AU - Gerstenfeld, Edward P.

PY - 2016/2/1

Y1 - 2016/2/1

N2 - Background 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. Objectives 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. Methods 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. Results 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 voltage <1.5 mV (pre 1.2% vs post 2.2%; P =.34) or % unipolar voltage <5.5 mV (pre 4.0% vs post 3.5%; P =.20). In the PVC group, there was a significant increase in % unipolar voltage <5.5 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). Conclusion 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.

AB - Background 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. Objectives 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. Methods 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. Results 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 voltage <1.5 mV (pre 1.2% vs post 2.2%; P =.34) or % unipolar voltage <5.5 mV (pre 4.0% vs post 3.5%; P =.20). In the PVC group, there was a significant increase in % unipolar voltage <5.5 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). Conclusion 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.

KW - Cardiomyopathy

KW - Electroanatomic mapping

KW - Fibrosis

KW - Premature ventricular contraction

KW - Voltage mapping

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