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Mechanisms of left ventricular dyssynchrony: A multinational SPECT study of patients with bundle branch block

  • Saara Sillanmäki
  • Alessia Gimelli
  • Shahzad Ahmad
  • Saba Samir
  • Tomi Laitinen
  • Prem SomanEmail author
ORIGINAL ARTICLE

Abstract

Background

To better understand the mechanisms of left ventricular (LV) mechanical dyssynchrony (LVMD), we explored the relative contributions of QRS duration (QRSd), LV ejection fraction (EF), volumes and scar to LVMD measured by gated single-photon emission tomography in a population of consecutive patients with left bundle branch block (LBBB) and right bundle branch block (RBBB) compared to controls.

Methods

Myocardial perfusion imaging studies of 275 LBBB and 83 RBBB patients from three centers were analyzed. LVMD was defined as an abnormal phase bandwidth or phase standard deviation. Hospital and gender-specific normal values were obtained from 172 controls.

Results

The prevalence of LVMD was 85 and 40% in LBBB and RBBB, respectively. Ejection fraction, scar severity, and LBBB morphology independently explained 70% of variance seen in PhaseBW. Ejection fraction had the highest area under the curve (AUC 0.918) in the receiver operating characteristics analysis of LVMD with an optimal cut-off of 47% (sensitivity 73% and specificity 98%). Notably, QRSd was not predictive.

Conclusion

LV mechanical dysfunction plays a greater role than conduction abnormality in the genesis of LVMD, a finding that is intriguing in the context of contemporary literature which suggests that QRSd is the parameter that is most predictive of CRT response.

Keywords

Physiology of LV/RV function heart failure SPECT dyssynchrony 

Abbreviations

LVMD

Left ventricular mechanical dyssynchrony

PhaseBW

Phase analysis bandwidth

phaseSD

Phase analysis standard deviation

BBB

Bundle branch block

LBBB

Left bundle branch block

RBBB

Right bundle branch block

EF

Ejection fraction

QRSd

QRS duration

Notes

Acknowledgments

We thank Jonathan Dietz for his technical assistance with the study.

Disclosures

The research was supported by Finnish Foundation for Cardiovascular Research, Finnish Society of Nuclear Medicine, Finnish Society of Clinical Physiology, Finnish Society of Cardiology, Onni and Hilja Tuovinen Foundation, Paavo Nurmi Foundation and Scandinavian Society of Clinical Physiology. The first author (Dr. Saara Sillanmäki) has a research collaboration with AstraZeneca and has had educational support and lecture fee from GE Healthcare. Dr. Prem Soman has had a research funds from Astellas Pharma (not related to this project). Other co-authors have nothing to declare.

Supplementary material

12350_2020_2054_MOESM1_ESM.pptx (555 kb)
Supplementary material 1 (PPTX 554 kb)
12350_2020_2054_MOESM2_ESM.docx (12 kb)
Supplementary material 2 (DOCX 12 kb)

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Copyright information

© American Society of Nuclear Cardiology 2020

Authors and Affiliations

  • Saara Sillanmäki
    • 1
    • 2
  • Alessia Gimelli
    • 3
  • Shahzad Ahmad
    • 4
  • Saba Samir
    • 4
  • Tomi Laitinen
    • 1
    • 2
  • Prem Soman
    • 4
    • 5
    Email author
  1. 1.Institute of Clinical MedicineUniversity of Eastern FinlandJoensuuFinland
  2. 2.Department of Nuclear Medicine and Clinical PhysiologyKuopio University HospitalKuopioFinland
  3. 3.Fondazione Toscana/CNR Gabriele MonasterioPisaItaly
  4. 4.Division of Cardiology and The Heart and Vascular InstituteUniversity of Pittsburgh Medical CenterPittsburghUSA
  5. 5.University of Pittsburgh Medical CenterPittsburghUSA

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