Regional evolution of mechanical dyssynchrony in a closed-chest porcine model of myocardial infarction as assessed by cardiac magnetic resonance

Introduction

Mechanical dyssynchrony in the setting of an acute myocardial infarction (MI) is associated with adverse left ventricular remodeling and increased mortality.

Purpose

We investigate the relationship between dyssynchrony and infarct location and their evolution over time in a closed-chest porcine model of MI.

Methods

In six pigs, cine, late gadolinium enhancement, and tagged cardiac magnetic resonance imaging were performed at baseline (before MI) and early (10 ± 2 days) and late (34 ± 10 days) after balloon induced occlusion-reperfusion myocardial injury. Infarct, peri-infarct, and remote normal regions were defined as previously described. Cardiac morphology, function, location and extent of MI, and regional mechanics (circumferential strain (εC)) were measured.

Results

Baseline ejection fraction (52 ± 5%) was significantly reduced both early (44 ± 7%) and late (45 ± 4%) post MI (p < 0.01). Delayed enhancement was ∼ 20% of LV mass and peak εC was significantly reduced in MI segments (before -26 ± 4, early -10 ± 7, late -9 ± 7%; p < 0.001) and peri-MI (before -24 ± 6, early -19 ± 6, late -17 ± 4%; p < 0.001). Dyssynchrony index increased from 29 ms at baseline to 65 ms at early (p = 0.007) and 98 ms (p = 0.002) at late post-MI. Inter-segmental mechanical delay between peri-MI and MI versus normal segments at early post-MI stage were 23 ± 36 ms and 118 ± 58 ms, respectively (p < 0.0001). Delays between peri-MI and MI segments versus normal segments in late post-MI stage were 9 ± 12 and 122 ± 14 ms, respectively.

Conclusion

Mechanical dyssynchrony occurs early after acute MI and does not worsen with time despite further reduction in regional function. Delayed mechanical activation is restricted to MI segments and does not persist in peri-MI segments.