• Acute stretch changes ion-channel behavior. Stretch activates mechanically sensitive ion channels in atrial myocytes. This can cause abnormal depolarizations, including premature atrial beats, which may trigger AF.
• The enlarged atrium has a longer electrical pathway. Re-entry is easier when the electrical impulse has more tissue over which to travel. Instead of one coordinated wave from the sinus node, multiple circulating wavelets can persist within the enlarged atrium.
• Chronic stretch causes structural remodeling. Persistent pressure or volume overload promotes inflammation, myocyte injury, and especially interstitial fibrosis. Fibrosis separates muscle bundles and disrupts cell-to-cell coupling, so conduction becomes slow and patchy.
• Slow, uneven conduction promotes re-entry. Different parts of the atrium conduct at different speeds and recover excitability at different times. An impulse can then encounter a one-way block, travel around it, and re-enter tissue that has recovered, creating a circulating electrical loop.
• Electrical remodeling then reinforces AF. Once AF occurs repeatedly or persists, it alters calcium handling and ion-channel expression, generally shortening atrial refractoriness. That makes sustained AF still easier. This is the idea that “AF begets AF.”

Atrial stretch can trigger abnormal impulses; chronic dilation and fibrosis create the substrate for chaotic re-entry.