Journal of the American Heart Association · 2026
Pulsed Ultrahigh Frequency Spinal Cord Stimulation for Arrhythmia After Myocardial Infarction.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Lin Chin-Yu, Chiu Yung-Tsung, Chang Ting-Yung, Tsai Yung-Nan, Lin Yenn-Jiang, Chang Shih-Lin, Lo Li-Wei, Chung Fa-Po, Wang Pei-Yi, Huang Hsin-Lei, Lu Kuo-Hsiang, Phang Yuen Hoong, Chen Shih-Ann
Аннотация
BACKGROUND: Acute myocardial infarction (MI) increases sympathetic tone and increases the risk of life-threatening ventricular arrhythmias. We tested the hypothesis that spinal cord stimulation (SCS) using pulsed ultrahigh frequency (PUF) from T1 to T3 remodels the sympathetic activity and reduces ventricular arrhythmias.
METHODS: Twenty pigs were used in this study. Six were assigned to the control group, 7 received MI (MI Group), and 7 received MI plus PUF-SCS (MI+SCS Group). Seven pigs underwent a second surgery to implant the spinal stimulator. Echocardiography, 7-day Holter monitoring, and blood analyses were performed at baseline, 1 month after MI, and 1 month after PUF-SCS. All the pigs underwent an electrophysiological study and were euthanized. The left ventricular tissue was extracted for norepinephrine and adrenaline analyses. The sympathetic and stellate ganglia were analyzed.
RESULTS: Sympathetic tone and ventricular arrhythmia episodes from the Holter monitor increased after MI but were suppressed after PUF-SCS. The left ventricular ejection fraction decreased in the MI group and improved after PUF-SCS. The ventricular fibrillation induction rates were 17%, 100%, and 29% in the Control, MI, and MI+SCS groups respectively (P=0.0016). Pathological analysis of the sympathetic and stellate ganglia revealed no significant apoptosis.
CONCLUSIONS: PUF-SCS effectively suppressed sympathetic tone and reduced ventricular arrhythmia burden without causing permanent damage to the sympathetic ganglia. In the MI model, heart function and ventricular fibrillation vulnerability were reversed 1 month after PUF-SCS.
METHODS: Twenty pigs were used in this study. Six were assigned to the control group, 7 received MI (MI Group), and 7 received MI plus PUF-SCS (MI+SCS Group). Seven pigs underwent a second surgery to implant the spinal stimulator. Echocardiography, 7-day Holter monitoring, and blood analyses were performed at baseline, 1 month after MI, and 1 month after PUF-SCS. All the pigs underwent an electrophysiological study and were euthanized. The left ventricular tissue was extracted for norepinephrine and adrenaline analyses. The sympathetic and stellate ganglia were analyzed.
RESULTS: Sympathetic tone and ventricular arrhythmia episodes from the Holter monitor increased after MI but were suppressed after PUF-SCS. The left ventricular ejection fraction decreased in the MI group and improved after PUF-SCS. The ventricular fibrillation induction rates were 17%, 100%, and 29% in the Control, MI, and MI+SCS groups respectively (P=0.0016). Pathological analysis of the sympathetic and stellate ganglia revealed no significant apoptosis.
CONCLUSIONS: PUF-SCS effectively suppressed sympathetic tone and reduced ventricular arrhythmia burden without causing permanent damage to the sympathetic ganglia. In the MI model, heart function and ventricular fibrillation vulnerability were reversed 1 month after PUF-SCS.