Key result
Parasympathetic blockade with atropine reversed positive QT-RR hysteresis across all subject groups (P < 0.01), demonstrating it is predominantly mediated by differential autonomic states.
Why the study?
Does parasympathetic blockade with atropine alter QT-RR hysteresis during exercise and recovery?
Does parasympathetic blockade with atropine alter QT-RR hysteresis during exercise and recovery?
p-value: p=<0.01
QT-RR hysteresis is predominantly mediated by differential autonomic nervous system effects during exercise versus recovery, rather than a lagging QT response.
Supports parasympathetic mediation of QT-RR hysteresis; leaves open translation to clinical arrhythmia risk assessment.
QT-RR hysteresis is characterized by longer QT intervals at a given RR interval while heart rates are increasing during exercise and shorter QT intervals at the same RR interval while heart rates are decreasing during recovery. It has been attributed to a lagging QT response to different directional changes in RR interval during exercise and recovery. Twenty control subjects (8 males, age 51 ± 6 yr), 16 subjects with type 2 diabetes (12 males, age 56 ± 8 yr), 71 subjects with coronary artery disease (CAD) and preserved left ventricular ejection fraction (LVEF) (≥50%) (51 males, age 59 ± 12 yr), and 17 CAD subjects with depressed LVEF (<50%) (13 males, age 57 ± 10 yr) underwent two 16-min exercise tests followed by recovery. In session 2, parasympathetic blockade with atropine (0.04 mg/kg) was achieved at end exercise. QT-RR hysteresis was quantified as: 1) the area bounded by the QT-RR relationships for exercise and recovery in the range of the minimum RR interval at peak exercise to the minimum RR interval + 100 ms and 2) the difference in QT interval duration between exercise and recovery at the minimum RR interval achieved during peak exercise plus 50 ms (ΔQT). The effect of parasympathetic blockade was assessed by substituting the QT-RR relationship after parasympathetic blockade. QT-RR hysteresis was positive in all groups at baseline and reversed by parasympathetic blockade (P < 0.01). We conclude that QT-RR hysteresis is not caused by different directional changes in RR interval during exercise and recovery. Instead, it is predominantly mediated by differential autonomic nervous system effects as the heart rate increases during exercise vs. as it decreases during recovery.
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Pelchovitz et al. (2012) studied Coronary artery disease, type 2 diabetes, and healthy controls (n=124). Parasympathetic blockade with atropine vs. Baseline (without blockade) was evaluated on QT-RR hysteresis (p=<0.01). Parasympathetic blockade with atropine reversed positive QT-RR hysteresis across all subject groups (P < 0.01), demonstrating it is predominantly mediated by differential autonomic states.
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