Assessment of distribution and evolution of mechanical dyssynchrony in a porcine model of myocardial infarction by cardiovascular magnetic resonance.
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.
Biomedical and Metabolic Imaging Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD, USA.
Khaled Z
KZ
Abd-Elmoniem
Miguel Santaularia
MS
Tomas
Tetsuo
T
Sasano
Sahar
S
Soleimanifard
Evert-Jan P
EJ
Vonken
Amr
A
Youssef
Harsh
H
Agarwal
Veronica L
VL
Dimaano
Hugh
H
Calkins
Matthias
M
Stuber
Jerry L
JL
Prince
Theodore P
TP
Abraham
M Roselle
MR
Abraham
D000818:Animals; D001696:Biomechanical Phenomena; D003287:Contrast Media; D004195:Disease Models, Animal; D019028:Magnetic Resonance Imaging, Cine; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology; D013552:Swine; D013997:Time Factors; D018487:Ventricular Dysfunction, Left / Q000175:diagnosis* / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D016277:Ventricular Function, Left; D020257:Ventricular Remodeling; D056969:Voltage-Sensitive Dye Imaging
D003287:Contrast Media