Cardiac Fibrosis and Atrial Fibrillation
- Dzeshka MS, Lip GY, Snezhitskiy V, Shantsila E.
- Cardiac Fibrosis in Patients With Atrial Fibrillation: Mechanisms and Clinical Implications. J Am Coll Cardiol 2015;66:943-959.
The following are key points to remember from this review of the significance of cardiac fibrosis in patients with atrial fibrillation (AF):
- Atrial fibrosis is the hallmark of structural remodeling in AF, and acts as a substrate for the perpetuation of AF.
- Overt and subclinical inflammatory states are associated with up-regulation of several inflammatory cytokines and chemokines that promote atrial fibrosis.
- Age-related cardiac fibrosis explains why the prevalence of AF increases with age.
- Cardiovascular conditions that result in atrial overload and stretch, such as hypertension, valvular heart disease, and heart failure, are associated with atrial fibrosis that predisposes to AF.
- Noncardiac factors that predispose to atrial fibrosis (and therefore AF) include obesity, metabolic syndrome, and obstructive sleep apnea.
- Diabetes is associated with cardiac fibrosis, and triples the risk of AF in obese individuals.
- The extent of atrial fibrosis can be evaluated by delayed-enhancement cardiac magnetic resonance (CMR), CMR-based T1 mapping, and echocardiography, and is predictive of AF recurrence after catheter or surgical ablation of AF and after cardiothoracic surgery.
- Ventricular fibrosis may be an independent predictor of AF, but this requires further study.
- Components of profibrotic pathways in the heart potentially could be therapeutic targets to prevent AF, but evidence of primary or secondary prevention of AF in humans with agents that block profibrotic pathways (e.g., angiotensin-receptor antagonists and angiotensin-converting enzyme inhibitors) has been inconclusive.
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