Abstract
<h3>Introduction</h3> Electric defibrillations and cardioversion are standard interventions to terminate arrhythmia. Recent evidence hints to acute post shock myocardial injury. However, that injury may follow unique pathways in every individual. Common functional measures such as ejection fraction are limited in that they represent only global ventricular function. Cardiovascular magnetic resonance feature tracking (CMR-FT) is a technique that can quantify myocardial contraction and relaxation on a regional level. The purpose of this analysis was to investigate the impact of acute myocardial injury after serial transthoracic shocks on regional systolic and diastolic myocardial deformation in a healthy animal model. <h3>Methods</h3> Ten healthy anaesthetized swine were scanned in a 3 Tesla MRI with a standard short axis cine and a clinical T1 mapping sequence in three short axis slices to detect myocardial edema. Five transthoracic shocks with 200 Joules each were applied within five minutes. Five hours post-shock the same images were re-acquired. Six control animals underwent the same protocol without shocks. Changes in regional peak strain as a measure of systolic function, and early diastolic strain rate as a measure of diastolic function were evaluated using CMR-FT analysis in circumferential orientation for both the left (LV) and right ventricle (RV). T1 maps of the LV were analyzed and reported per myocardial AHA segment as a measure of myocardial edema. For the RV, a region of interest (ROI) was contoured in each of the 3 short-axis slices. The regional changes in strain in comparison to the development of myocardial injury (ΔT1 mapping) over the course of 5h were statistically assessed using a mixed effects model accounting for the electrical intervention and multiple measurements per individual. <h3>Results</h3> Global circumferential peak strain worsened in both ventricles (LV: -15.6±3.3% to -13.0±3.6%, p<0.01; RV: -16.1±2.3% to -12.8±4.8%, p=0.03). Additionally, LV early diastolic strain rate slowed from baseline to the 5h timepoint (1.19±0.35 to 0.95±0.37/s, p = 0.02) in shocked animals. Whereas no change was observed for any global strain parameters in the control group. There was no linear association with regional LV peak strain with T1 changes (p=0.97). However, an increase in T1 was colocalized to a reduction in early diastolic strain rate (p = 0.03), where early diastolic strain rate slowed by -0.25/s every 100ms increase in T1. On the other hand, both RV systolic and diastolic function worsened in the presence of increased regional RV T1 with a change in peak strain of 2.7% and a deceleration of diastolic strain rate (–0.42/s) per 100ms increase in RV T1 (p<0.05). <h3>Conclusions</h3> Serial transthoracic shock in a healthy swine model attenuate biventricular systolic function, but it is the development of regional diastolic dysfunction that is associated with the onset of colocalized myocardial edema. Future studies are warranted to assess these effects of electrical interventions in clinical settings.
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