Aging increases the risk of atrial fibrillation (AF) primarily through progressive changes in the structure and function of the heart’s atria, combined with longer exposure to cardiovascular stressors and diseases. As people grow older, their atrial tissue undergoes remodeling that makes it more susceptible to abnormal electrical activity, which is the hallmark of AF.
One of the key factors is **atrial fibrosis**, which means the development of excess fibrous connective tissue in the atria. This fibrosis disrupts the normal electrical pathways, causing irregular and rapid heartbeats. Aging promotes fibrosis through cellular senescence, a process where heart cells lose their ability to function properly and start secreting substances that encourage scarring and inflammation. This fibrotic remodeling stiffens the atrial walls and creates a substrate that favors the initiation and maintenance of AF.
In addition to fibrosis, aging affects the **electrophysiology** of the atria. The electrical signals that coordinate heartbeats become slower and more erratic due to changes in ion channel function and altered calcium handling within heart cells. These changes increase the likelihood of abnormal impulses and reentrant circuits, which trigger AF episodes.
Another important aspect is the **increased prevalence of cardiovascular diseases** with age, such as hypertension, coronary artery disease, and heart failure. These conditions cause structural and functional stress on the atria, further promoting remodeling and electrical instability. The longer a person lives with these conditions, the more the atria are exposed to damaging influences, increasing AF risk.
Inflammation also plays a significant role. Aging is associated with a chronic low-grade inflammatory state that contributes to atrial remodeling. Inflammatory mediators can alter the atrial tissue matrix and electrical properties, facilitating the development of AF. For example, inflammatory pathways activate fibroblasts that produce collagen, leading to fibrosis, and affect connexins, proteins critical for electrical conduction between heart cells.
Hormonal changes with aging, such as reduced estrogen levels after menopause in women, may also influence AF risk by promoting inflammation and fibrosis in the atria. This hormonal decline can exacerbate the structural and electrical changes that predispose to AF.
Furthermore, aging is linked to **cellular senescence** in the heart, where aged cells secrete factors that accelerate myocardial fibrosis and cardiovascular aging. This senescence-induced environment fosters the development of AF by creating a heart tissue landscape prone to arrhythmias.
The combination of these factors—fibrosis, electrical remodeling, inflammation, hormonal changes, and comorbid cardiovascular diseases—creates a progressively vulnerable atrial substrate. This substrate is more likely to develop the chaotic electrical activity characteristic of atrial fibrillation as people age.
In summary, aging increases AF risk by causing structural changes like fibrosis, altering electrical conduction, promoting inflammation, and increasing exposure to cardiovascular diseases. These changes collectively disrupt the normal rhythm of the heart’s atria, making atrial fibrillation more common in the elderly.