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| Main Authors: | , , |
|---|---|
| Format: | Recurso digital |
| Language: | English |
| Published: |
Zenodo
2025
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| Online Access: | https://doi.org/10.5281/zenodo.16662863 |
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Table of Contents:
- <p><strong>Postprandial ventricular extrasystoles represent a complex interplay of hemodynamic, metabolic,</strong></p> <p><strong>and autonomic mechanisms that create a predictable window of heightened arrhythmogenic</strong></p> <p><strong>vulnerability 30–60 minutes after meals. In patients with chronic insomnia and catecholamine</strong></p> <p><strong>dysregulation, these physiological responses become pathologically exaggerated and prolonged,</strong></p> <p><strong>significantly increasing the risk of clinically relevant arrhythmias. This paper explores the underlying</strong></p> <p><strong>mechanisms — including hemodynamic stress, macronutrient-specific metabolic pathways, gastro-</strong></p> <p><strong>cardiac reflexes, and glucose-catecholamine interactions — as well as the impact of sleep deprivation</strong></p> <p><strong>on sustained sympathetic dominance. Clinically, the distinction between benign VES in structurally</strong></p> <p><strong>normal hearts and pathological patterns requiring further evaluation is critical. Therapeutic strategies</strong></p> <p><strong>should adopt a multidimensional approach, combining sleep restoration, nutritional modifications, and</strong></p> <p><strong>autonomic function monitoring. Understanding the temporal patterns and pathophysiological drivers of</strong></p> <p><strong>postprandial arrhythmias provides actionable insights for managing complex patients presenting with</strong></p> <p><strong>postprandial cardiac symptoms.</strong></p>