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Open Access Research

Assessment of distribution and evolution of Mechanical dyssynchrony in a porcine model of myocardial infarction by cardiovascular magnetic resonance

Khaled Z Abd-Elmoniem1, Miguel Santaularia Tomas23, Tetsuo Sasano2, Sahar Soleimanifard4, Evert-Jan P Vonken2, Amr Youssef2, Harsh Agarwal4, Veronica L Dimaano2, Hugh Calkins2, Matthias Stuber5, Jerry L Prince4, Theodore P Abraham2 and M Roselle Abraham2*

Author Affiliations

1 Biomedical and Metabolic Imaging Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD, USA

2 Department of Medicine, Division of Cardiology, Johns Hopkins University, Baltimore, MD, USA

3 Department of Medicine, Division of Cardiology, Hospital Español de Mexico, Distrito Federal, Mexico

4 Department of Electrical and Computer Engineering, Johns Hopkins University, Baltimore, MD, USA

5 Department of Radiology, Division of Magnetic Resonance Research, Johns Hopkins University, Baltimore, MD, USA

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Journal of Cardiovascular Magnetic Resonance 2012, 14:1  doi:10.1186/1532-429X-14-1

Published: 6 January 2012

Abstract

Background

We sought to investigate the relationship between infarct and dyssynchrony post- myocardial infarct (MI), in a porcine model. Mechanical dyssynchrony post-MI is associated with left ventricular (LV) remodeling and increased mortality.

Methods

Cine, gadolinium-contrast, and tagged cardiovascular magnetic resonance (CMR) were performed pre-MI, 9 ± 2 days (early post-MI), and 33 ± 10 days (late post-MI) post-MI in 6 pigs to characterize cardiac morphology, location and extent of MI, and regional mechanics. LV mechanics were assessed by circumferential strain (eC). Electro-anatomic mapping (EAM) was performed within 24 hrs of CMR and prior to sacrifice.

Results

Mean infarct size was 21 ± 4% of LV volume with evidence of post-MI remodeling. Global eC significantly decreased post MI (-27 ± 1.6% vs. -18 ± 2.5% (early) and -17 ± 2.7% (late), p < 0.0001) with no significant change in peri-MI and MI segments between early and late time-points. Time to peak strain (TTP) was significantly longer in MI, compared to normal and peri-MI segments, both early (440 ± 40 ms vs. 329 ± 40 ms and 332 ± 36 ms, respectively; p = 0.0002) and late post-MI (442 ± 63 ms vs. 321 ± 40 ms and 355 ± 61 ms, respectively; p = 0.012). The standard deviation of TTP in 16 segments (SD16) significantly increased post-MI: 28 ± 7 ms to 50 ± 10 ms (early, p = 0.012) to 54 ± 19 ms (late, p = 0.004), with no change between early and late post-MI time-points (p = 0.56). TTP was not related to reduction of segmental contractility. EAM revealed late electrical activation and greatly diminished conduction velocity in the infarct (5.7 ± 2.4 cm/s), when compared to peri-infarct (18.7 ± 10.3 cm/s) and remote myocardium (39 ± 20.5 cm/s).

Conclusions

Mechanical dyssynchrony occurs early after MI and is the result of delayed electrical and mechanical activation in the infarct.