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.
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http://dx.doi.org/10.1016/j.amjmed.2017.12.017 | DOI Listing |
Front Neurol
December 2024
Department of Neurosurgery, Ajou University Hospital, Ajou University School of Medicine, Suwon, Republic of Korea.
Objective: The optimal timing of bypass surgery for patients with moyamoya disease (MMD) or moyamoya syndrome (MMS) following an acute stroke episode remains unclear, mainly owing to the risk of postoperative complications. In this study, we aim to validate the safety and efficacy of early intervention using multiple burr hole (MBH) and erythropoietin (EPO) therapy, thereby refining the management strategy for patients with acute stroke episode of MMD or MMS.
Methods: We retrospectively analyzed data from 70 patients with MMD or MMS who underwent MBH and EPO therapy.
Front Transplant
December 2024
Laboratory of Respiratory Diseases and Thoracic Surgery (BREATHE), Department of CHROMETA, KU Leuven, Leuven, Belgium.
Long-term survival after lung transplantation is limited due to chronic lung allograft dysfunction (CLAD), which encompasses two main phenotypes: bronchiolitis obliterans syndrome (BOS) and restrictive allograft syndrome (RAS). Donor-derived cell-free DNA (dd-cfDNA) is a biomarker for (sub)clinical allograft injury and could be a tool for monitoring of lung allograft health across the (pre)clinical spectrum of CLAD. In this proof-of-concept study, we therefore assessed post-transplant plasma dd-cfDNA levels in 20 CLAD patients (11 BOS and 9 RAS) at three consecutive time points free from concurrent infection or acute rejection, during stable condition, preclinical CLAD, and established CLAD ( = 3 × 20 samples).
View Article and Find Full Text PDFIt is well known that activation of NMDA receptors can trigger long-term synaptic depression (LTD) and that a morphological correlate of this functional plasticity is spine retraction and elimination. Recent studies have led to the surprising conclusion that NMDA-induced spine shrinkage proceeds independently of ion flux and requires the initiation of protein synthesis, highlighting an unappreciated contribution of mRNA translation to non-ionotropic NMDAR signaling. Here we used NMDA-induced spine shrinkage in slices of mouse hippocampus as a readout to investigate this novel modality of synaptic transmission.
View Article and Find Full Text PDFBackground: Long QT Syndrome Type-2 (LQT2) is due to loss-of-function variants. encodes K 11.1 that forms a delayed-rectifier potassium channel in the brain and heart.
View Article and Find Full Text PDFClin Appl Thromb Hemost
January 2025
Hemostasis and Thrombosis Research Laboratories, Loyola University Medical Center, Maywood, Illinois, USA.
Introduction: Persistent elevation of biomarkers associated with endothelial dysfunction in convalescent COVID-19 patients has been linked to an increased risk of long-term cardiovascular complications, including long COVID syndrome. Sulodexide, known for its vascular endothelial affinity, has demonstrated pleiotropic protective properties. This study aims to evaluate the impact of sulodexide on serum levels of endothelial dysfunction biomarkers in patients during the convalescent phase of COVID-19.
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