Richard D Lane1, Harry T Reis2, Chiu-Hsieh Hsu3, Karl B Kern4, Jean Philippe Couderc5, Arthur J Moss6, Wojciech Zareba6. 1. Department of Psychiatry, University of Arizona, Tucson. Electronic address: lane@email.arizona.edu. 2. Department of Clinical and Social Sciences in Psychology, University of Rochester, Rochester, NY. 3. Department of Epidemiology and Biostatistics, University of Arizona, Tucson. 4. Division of Cardiology, Department of Medicine, University of Arizona, Tucson. 5. Department of Electrical and Computer Engineering, University of Rochester, Rochester, NY. 6. Division of Cardiology, Department of Medicine, University of Rochester, Rochester, NY.
Abstract
BACKGROUND: Rare, high-arousal negative emotions are known triggers of sudden death in individuals with preexisting heart disease. Whether everyday fluctuations in emotional arousal influence arrhythmia risk is unknown. METHODS: We studied 160 patients with the congenital long QT syndrome, 199 patients with coronary artery disease, and 2 groups of matched healthy volunteers (n = 52 and 50, respectively). Three-day home visits including a 12-hour Holter recording each day were completed. Subjects engaged in typical daily activities and were paged 10 times per day. On each occasion, subjects rated the intensity of 16 different emotions during the 5 minutes preceding the page. Holter data over those 5-minute epochs were analyzed for heart rate and QT interval corrected for heart rate (QTc). Analyses focused on within-subject covariation of momentary emotion and QTc. RESULTS: In patients with long QT syndrome, activated positive affect and activated negative affect were associated with QTc shortening, whereas low arousal positive affect (calm and relaxed) was associated with QTc lengthening, which at times exceeded 500 msec. Findings were not affected by beta-blocker status or observed in younger healthy subjects. Findings were 3 to 8 times stronger in the LQT2 genotype, known to be prone to emotion-induced events, relative to the LQT1 genotype. Findings in patients with long QT syndrome for activated positive affect and low arousal positive affect were replicated in patients with coronary artery disease relative to older healthy subjects. CONCLUSION: These findings suggest that even subtle changes in emotional arousal may alter repolarization reserve and contribute to sudden death risk in vulnerable individuals.
BACKGROUND: Rare, high-arousal negative emotions are known triggers of sudden death in individuals with preexisting heart disease. Whether everyday fluctuations in emotional arousal influence arrhythmia risk is unknown. METHODS: We studied 160 patients with the congenital long QT syndrome, 199 patients with coronary artery disease, and 2 groups of matched healthy volunteers (n = 52 and 50, respectively). Three-day home visits including a 12-hour Holter recording each day were completed. Subjects engaged in typical daily activities and were paged 10 times per day. On each occasion, subjects rated the intensity of 16 different emotions during the 5 minutes preceding the page. Holter data over those 5-minute epochs were analyzed for heart rate and QT interval corrected for heart rate (QTc). Analyses focused on within-subject covariation of momentary emotion and QTc. RESULTS: In patients with long QT syndrome, activated positive affect and activated negative affect were associated with QTc shortening, whereas low arousal positive affect (calm and relaxed) was associated with QTc lengthening, which at times exceeded 500 msec. Findings were not affected by beta-blocker status or observed in younger healthy subjects. Findings were 3 to 8 times stronger in the LQT2 genotype, known to be prone to emotion-induced events, relative to the LQT1 genotype. Findings in patients with long QT syndrome for activated positive affect and low arousal positive affect were replicated in patients with coronary artery disease relative to older healthy subjects. CONCLUSION: These findings suggest that even subtle changes in emotional arousal may alter repolarization reserve and contribute to sudden death risk in vulnerable individuals.
Authors: Marie L De Bruin; Pim N J Langendijk; Richard P Koopmans; Arthur A M Wilde; Hubert G M Leufkens; Arno W Hoes Journal: Br J Clin Pharmacol Date: 2006-07-21 Impact factor: 4.335
Authors: Carmen Anna Maria Spaccarotella; Serena Migliarino; Annalisa Mongiardo; Jolanda Sabatino; Giuseppe Santarpia; Salvatore De Rosa; Antonio Curcio; Ciro Indolfi Journal: Sci Rep Date: 2021-05-24 Impact factor: 4.379