Yoshifusa Aizawa1, Yukio Hosaka2, Hirotaka Oda2, Koichi Fuse3, Masaaki Okabe3, Yoshiaki Kaneko4, Naohiko Takahashi5, Hirofumi Zaizen6, Yoshiyasu Aizawa7, Keiichi Fukuda7. 1. Research and Development, Tachikawa Medical Center/Niigata University, Nagaoka/Niigata, Japan. Electronic address: aizaways@med.niigata-u.ac.jp. 2. Department of Cardiology, Niigata City Hospital, Niigata, Japan. 3. Department of Cardiology, Tachikawa General Hospital, Nagaoka, Japan. 4. Department of Medicine and Biological Science, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan. 5. Department of Internal Medicine, Oita University, Oita, Japan. 6. Department of Internal Medicine, Koseiren Ttsurumi Hospital, Oita, Japan. 7. Department of Cardiology, Keio University School of Medicine, Tokyo, Japan.
Abstract
BACKGROUND: J waves develop during hypothermia, but the dynamicity of hypothermia-induced J waves is poorly understood. OBJECTIVE: The purpose of this study was to investigate the mechanism of the rate-dependent change in the amplitude of hypothermia-induced J waves. METHODS: Nineteen patients with severe hypothermia were included (mean age 70 ± 12 years; 16 men [84.2%]). The rectal temperature at the time of admission was 27.8° ± 2.5°C. In addition to prolonged PR, QRS complex, and corrected QT intervals, the distribution of prominent J waves was widespread in all 19 patients. RESULTS: Nine patients showed changes in RR intervals. When the RR interval shortened from 1353 ± 472 to 740 ± 391 ms (P = .0002), the J-wave amplitude increased from 0.50 ± 0.29 to 0.61 ±0.27 mV (P = .0075). The J-wave amplitude increased in 7 patients (77.8%) and decreased in 2 patients (22.2%) after short RR intervals. The augmentation of J waves at short RR intervals was associated with a significant prolongation of ventricular activation time (35 ± 5 ms vs 46 ± 5 ms; P = .0020), suggesting accentuated conduction delay. Increased conduction delay at short RR intervals was suggested to accentuate the phase 1 notch of the action potential and J waves in hypothermia. None developed ventricular fibrillation, and in 2 of 9 patients with atrial fibrillation, atrial fibrillation persisted after rewarming to normothermia. CONCLUSION: J waves in severe hypothermia were augmented after short RR intervals in 7 patients as expected for depolarization abnormality, whereas 2 patients showed a bradycardia-dependent augmentation as expected for transient outward current-mediated J waves. Increased conduction delay at short RR intervals can be responsible for the accentuation of the transient outward current and J waves during severe hypothermia.
BACKGROUND: J waves develop during hypothermia, but the dynamicity of hypothermia-induced J waves is poorly understood. OBJECTIVE: The purpose of this study was to investigate the mechanism of the rate-dependent change in the amplitude of hypothermia-induced J waves. METHODS: Nineteen patients with severe hypothermia were included (mean age 70 ± 12 years; 16 men [84.2%]). The rectal temperature at the time of admission was 27.8° ± 2.5°C. In addition to prolonged PR, QRS complex, and corrected QT intervals, the distribution of prominent J waves was widespread in all 19 patients. RESULTS: Nine patients showed changes in RR intervals. When the RR interval shortened from 1353 ± 472 to 740 ± 391 ms (P = .0002), the J-wave amplitude increased from 0.50 ± 0.29 to 0.61 ±0.27 mV (P = .0075). The J-wave amplitude increased in 7 patients (77.8%) and decreased in 2 patients (22.2%) after short RR intervals. The augmentation of J waves at short RR intervals was associated with a significant prolongation of ventricular activation time (35 ± 5 ms vs 46 ± 5 ms; P = .0020), suggesting accentuated conduction delay. Increased conduction delay at short RR intervals was suggested to accentuate the phase 1 notch of the action potential and J waves in hypothermia. None developed ventricular fibrillation, and in 2 of 9 patients with atrial fibrillation, atrial fibrillation persisted after rewarming to normothermia. CONCLUSION: J waves in severe hypothermia were augmented after short RR intervals in 7 patients as expected for depolarization abnormality, whereas 2 patients showed a bradycardia-dependent augmentation as expected for transient outward current-mediated J waves. Increased conduction delay at short RR intervals can be responsible for the accentuation of the transient outward current and J waves during severe hypothermia.