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

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.

Figure 1

Representative voltage and activation maps from 1 animal using the CARTO system (CARTO XP, Biosense-Webster Inc.). The infarcted region was characterized by low voltage (< 0.5 mV) and delayed activation.

Figure 2

A. Representative isochrone map (corresponding to voltage/activation maps in Figure 1) from 1 animal using the CARTO system (CARTO XP, Biosense-Webster Inc.) reveals crowding of isochrones indicative of greatly reduced conduction velocity in the infarct. B. Summary of conduction of velocities in the infarct, border-zone and remote myocardium derived from all pigs (n = 6), using the CARTO system. Conduction velocity was very low in the infarct and intermediate in the infarct border-zone region, when compared to remote myocardium.

Figure 3

Representative left ventricular short-axis CMR images illustrating absence of LGE pre-infarct. (A) with normal color-coded strain display (B) and strain tracings showing synchronized mechanical activity with all segments peaking near simultaneously (C); Early post-MI images show LGE in the septum (D, arrow) with low strain in the septum (E) and strain traces showing mechanical dyssynchrony from early stretching (dyskinesis) and late hypokinesis of the infarcted segment (F). Late post- MI images show persistent LGE in the septum (G, arrow) with low strain in the septum (H) and strain traces showing mechanical dyssynchrony from early stretching (dyskinesis) and late hypokinesis of the infarcted segment (I). Representative 3-dimensional reconstruction of the area of delayed enhancement illustrating the extent of infarction (J).

Figure 4

Scatter plots illustrating peak strain (eC) and time to peak strain (TTP) at baseline, early and late post-MI time-points for normal, peri-MI and MI segments. MI segments demonstrate low strain and delayed mechanical activation at early and late post-MI time-points. Peri-MI segments demonstrate reduction in eC with no significant delay in TTP at both time-points.