Mitral Regurgitation and Atrial Fibrillation: The Contribution of Impaired Left Atrial Appendage Function to Atrial Thrombogenesis

Assessment and management of a 1.77‐cm2 mitral leaflet perforation as a subclinical cause of mitral regurgitation

“…As a consequence of acute regurgitation, there is an increase in pulmonary pressure and volume, resulting in pulmonary edema and ensuing shortness of breath . Due to pulmonary overload, myocardial voltage around the pulmonary veins is disrupted, and the patient also becomes prone to developing arrhythmias …”

“…6 Due to pulmonary overload, myocardial voltage around the pulmonary veins is disrupted, and the patient also becomes prone to developing arrhythmias. 7 Moreover, left atrial enlargement contributes to the generation of atrial re-entry and AF, and progressive left atrial enlargement increases the risk of AF development. 7 A recent study found that the underlying pathology seen in patients with MV disease was found to have elevated Type 1 collagen levels within left atrial appendage tissue, ultimately causing atrial remodeling predisposing the patient to possible development of AF.…”

“…7 Moreover, left atrial enlargement contributes to the generation of atrial re-entry and AF, and progressive left atrial enlargement increases the risk of AF development. 7 A recent study found that the underlying pathology seen in patients with MV disease was found to have elevated Type 1 collagen levels within left atrial appendage tissue, ultimately causing atrial remodeling predisposing the patient to possible development of AF. 8 Identifying AF is essential in patients with mitral regurgitation because the heart already has a decreased ability to maintain cardiac output.…”

The current profile of the patient with atrial fibrillation

“…AF occurs in 29% of patients with isolated mitral stenosis, 11% in those with mitral regurgitation and only 1% in those with aortic valve disease. In patients with mitral stenosis, it has been shown that left atrium dilation, reduction in driving speed and prolongation of the effective refractory period contribute to the onset and persistence of AF [11,12].…”