Changes in left ventricular electromechanical relations during targeted hypothermia

Abstract

Background Targeted hypothermia, as used after cardiac arrest, increases electrical and mechanical systolic duration. Differences in duration of electrical and mechanical systole are correlated to ventricular arrhythmias. The electromechanical window (EMW) becomes negative when the electrical systole outlasts the mechanical systole. Prolonged electrical systole corresponds to prolonged QT interval, and is associated with increased dispersion of repolarization and mechanical dispersion. These three factors predispose for arrhythmias. The electromechanical relations during targeted hypothermia are unknown. We wanted to explore the electromechanical relations during hypothermia at 33 °C. We hypothesized that targeted hypothermia would increase electrical and mechanical systolic duration without more profound EMW negativity, nor an increase in dispersion of repolarization and mechanical dispersion. Methods In a porcine model (n = 14), we registered electrocardiogram (ECG) and echocardiographic recordings during 38 °C and 33 °C, at spontaneous and atrial paced heart rate 100 beats/min. EMW was calculated by subtracting electrical systole; QT interval, from the corresponding mechanical systole; QRS onset to aortic valve closure. Dispersion of repolarization was measured as time from peak to end of the ECG T wave. Mechanical dispersion was calculated by strain echocardiography as standard deviation of time to peak strain. Results Electrical systole increased during hypothermia at spontaneous heart rate (p < 0.001) and heart rate 100 beats/min (p = 0.005). Mechanical systolic duration was prolonged and outlasted electrical systole independently of heart rate (p < 0.001). EMW changed from negative to positive value (− 20 ± 19 to 27 ± 34 ms, p = 0.001). The positivity was even more pronounced at heart rate 100 beats/min (− 25 ± 26 to 41 ± 18 ms, p < 0.001). Dispersion of repolarization decreased (p = 0.027 and p = 0.003), while mechanical dispersion did not differ (p = 0.078 and p = 0.297). Conclusion Targeted hypothermia increased electrical and mechanical systolic duration, the electromechanical window became positive, dispersion of repolarization was slightly reduced and mechanical dispersion was unchanged. These alterations may have clinical importance. Further clinical studies are required to clarify whether corresponding electromechanical alterations are accommodating in humans.

Myocardial electrophysiological and mechanical changes caused by moderate hypothermia—A clinical study

“…Arrhythmogenic gradients in repolarization may occur in the heart without changes in ECG‐measured TpTe (Cluitmans et al, 2021 ). However, our findings are consistent with previous experimental (Hsieh et al, 2014 ; Wisløff‐Aase et al, 2020 ) and clinical findings (Kim et al, 2014 ; Thomsen et al, 2021 ) at moderate hypothermia. Experimental in vitro models have demonstrated a profound increase in dispersions of repolarization at temperatures <30°C, but a remarkable shift at temperatures ≥32°C with reduced dispersion compared to lower temperatures, and an arrhythmogenicity similar to 36°C (Hsieh et al, 2014 ; Piktel et al, 2011 ).…”

“…Interestingly, the mechanical systolic prolongation exceeded this QT prolongation with a corresponding increase in electromechanical window positivity at 32°C, at spontaneous and comparable paced HR. These findings are consistent with earlier experimental results describing increased electromechanical window at temperatures <36°C (Guns et al, 2012 ; Wisløff‐Aase et al, 2020 ). The electromechanical window is experimentally shown to have better predictive power for ventricular arrhythmias than the QT duration, in ischemic heart disease (Limprasutr et al, 2018 ) and in patients with long QT syndrome (ter Bekke et al, 2015 ).…”

“…The duration of electromechanical window positivity increased, and dispersion of repolarization decreased. Mechanical dispersion remained unchanged (Wisløff‐Aase et al, 2020 ). Whether corresponding temperature‐related changes occur in humans, has not previously been explored.…”

“…The aim of the present clinical study was to assess the isolated effects of moderate hypothermia on electrophysiological and mechanical relationships in human hearts without cardiac dysfunction and previous cardiac arrest, during standardized clinical conditions. The study had a unique design analogous to the experimental model applied in our previous animal study (Wisløff‐Aase et al, 2020 ). Based on the experimental results, we hypothesized that during moderate hypothermia at 32°C, left ventricle electrophysiological and mechanical conditions would lead to increased electromechanical window, but without any increase in electrical and mechanical dispersion.…”