The Complex Interplay Between Aging, Cardiac Remodeling, And Atrial Fibrillation
As we age, our hearts undergo various changes that can increase the risk of developing a common heart rhythm disorder called atrial fibrillation. This condition, often referred to as AFib, is characterized by an irregular and often rapid heart rate that can lead to symptoms like palpitations, fatigue, and shortness of breath, and significantly raises the risk of stroke and heart failure.
Recent research highlights that the aging process contributes to AFib through several interconnected biological mechanisms. For instance, “fibrosis” – the excessive accumulation of fibrous connective tissue – stiffens the heart muscle, impairing its normal function. Additionally, cellular processes like “DNA damage” and “chromatin remodeling” (changes in how DNA is packaged) can alter gene expression, affecting heart cell health. The buildup of abnormal proteins, known as “amyloid deposition,” can also interfere with the heart’s structure and electrical signals.
Furthermore, “mitochondrial dysfunction,” where the energy-producing parts of cells don’t work properly, and “inflammation” – the body’s immune response – both play crucial roles in the deterioration of heart tissue. These changes collectively lead to what is known as “cardiac remodeling,” which refers to structural and functional alterations in the heart muscle. This remodeling creates an environment in the atria (the upper chambers of the heart) that makes them more susceptible to developing and sustaining irregular electrical activity, ultimately leading to atrial fibrillation. Understanding these intricate connections is vital for developing better strategies to prevent and treat AFib in an aging population.
Source: link to paper