Key result
Targeted hypothermia increases electrical and mechanical systolic duration, shifting the electromechanical window to 27 ms.
Why the study?
Targeted hypothermia alters electrical and mechanical systolic duration predisposing to arrhythmias, but electromechanical relations during hypothermia were unknown.
Does targeted hypothermia at 33 °C alter the electromechanical window, dispersion of repolarization, and mechanical dispersion in a porcine model?
Does targeted hypothermia at 33 °C alter the electromechanical window, dispersion of repolarization, and mechanical dispersion in a porcine model?
In a healthy porcine model, targeted hypothermia at 33 °C prolonged mechanical systole more than electrical systole, resulting in a positive electromechanical window and potentially decreased arrhythmia susceptibility.
Answers are grounded in this paper and cite their sources.
Does not guide clinical hypothermia use; leaves open mechanistic role in arrhythmia susceptibility pending human data.
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.
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Wisløff‐Aase et al. (2020) studied Healthy (porcine model) (n=14). Targeted hypothermia vs. Normothermia (38 °C) was evaluated on Electromechanical window (EMW) at spontaneous heart rate (p=0.001). Targeted hypothermia at 33 °C increased electrical and mechanical systolic duration, changing the electromechanical window from -20 ms to 27 ms.
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