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04.09.2015 | Original Article | Ausgabe 4/2016

Journal of Nuclear Cardiology 4/2016

Determinants of left ventricular mechanical dyssynchrony in patients submitted to myocardial perfusion imaging: A cardiac CZT study

Journal of Nuclear Cardiology > Ausgabe 4/2016
MD Alessia Gimelli, MD Riccardo Liga, MD Assuero Giorgetti, RT Brunella Favilli, MD Emilio Maria Pasanisi, MD Paolo Marzullo
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1007/​s12350-015-0247-8) contains supplementary material, which is available to authorized users.
See related editorial, doi:10.​1007/​s12350-015-0276-3.
Alessia Gimelli and Riccardo Liga have contributed equally to this study.



An interaction between coronary anatomy, myocardial perfusion, and left ventricular (LV) functional parameters in the development of mechanical LV dyssynchrony (LVD) has been suggested. This study examined the correlates of LVD in a large sample size of patients with known or suspected coronary artery disease (CAD) using cadmium-zinc-telluride camera.


Six-hundred and fifty-seven consecutive patients who underwent myocardial perfusion imaging (MPI) and coronary angiography were included. Coronary stenosis >70% was considered significant. LV perfusion and functional parameters were computed from MPI images. The presence of significant LVD was evaluated by phase standard deviation and histogram bandwidth.


415/657 (63%) patients had significant CAD. LVD was present in 247 (38%) patients and was associated with the presence of a higher CAD burden (P < .001), more impaired measures of LV perfusion (P < .001), contractile function (P < .001), and larger LV volumes (P < .001). By multivariate analysis, the LV end-systolic volume index (P < .001) and ischemic burden (P < .001) were the strongest predictors of LVD independent of CAD extent and LV systolic dysfunction.


LVD is frequent in patients undergoing MPI for suspected or known CAD. Its presence is independent of CAD burden and LV systolic dysfunction, but is dependent on the presence of myocardial perfusion abnormalities and LV end-systolic volume.

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Supplementary material 1 (DOC 35 kb)
Supplementary material 2 (DOC 35 kb)
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