Page 14 - ADD-ON ABLATION SURGERY IN PATIENTS WITH ATRIAL FIBRILLATION

Chapter 1
discharge typical of AF may result from an irregular atrial response to a rapidly discharging regularly firing driver resulting from either local ectopic firing or a single localized re-entry circuit. Alternatively, fibrillatory activity may be caused directly by multiple functional re-entry circuits varying in time and space. Several recent studies have focused on the underlying substrate in patients with LAF29. For instance, patients with LAF have an abnormal atrial substrate and these abnormalities are essential contributors to the “second factor” that promotes progression of AF. Studies employing electrophysiological and electro-anatomic mapping gave new insights into the nature of abnormalities within the atria of patients with LAF: a) Structural abnormalities characterized by atrial dilation and lower mean atrial voltage, suggesting the loss of atrial myocardium; b) Conduction abnormalities, characterized by prolongation of conduction times, longer P-wave duration and slower conduction; c) Impaired sinus node function; d) Increase in effective refractory period consistent with prior studies evaluating clinical substrates for AF but in contrast to the remodeling attributed to AF itself. Furthermore, it has been demonstrated that left ventricular diastolic dysfunction relates to left atrial dilatation and stretch as well as to the development of AF30. In addition, a recent echocardiographic case-control study demonstrated that in patients with paroxysmal LAF, LA area and volume were larger than in healthy volunteers, despite there being similar LV dimensions, ejection fraction, and diastolic function and regardless of the recurrence of the arrhythmia30. Thus, 2-dimensional echocardiography in the antero-posterior dimension underestimates the true LA size in patients with paroxysmal LAF31. Even in the presence of normal LV systolic and diastolic functions, LA diameter, and LA systolic activity, the LA diastolic performance may be compromised in patients with LAF, as evidenced by abnormalities of the systolic phase of pulmonary vein (PV) flow32. It would seem that LV diastolic and LA abnormalities are prevalent in apparently LAF but it is still unclear whether they represent a cause and/or consequence of the arrhythmia.
Genetic factors
Evidence of a genetic contribution in the development of AF was first provided in 1943 byWolff33 who documented transmission of LAF in a family with an autosomal dominant pattern of inheritance. Since that time, large epidemiological studies have documented evidence of heritability in AF, in particular in the context of LAF34-36. It is now evident that LAF may be caused by mutations of different genes
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