![]() Over time, both sympathetic and parasympathetic reinnervation will occur, but the degree of reinnervation is incomplete, nonuniform, variable between patients, and heterogeneous within the same patient. 17, 18 Studies have correlated changes in the corrected QT interval to sympathetic reinnervation and have postulated that there may be a subset of patients with increased ventricular arrhythmia and mortality risk associated with heterogeneous reinnervation. 19, 20 Autonomic denervation may partially account for several unique electro‐physiological findings in HT patients, beginning with the low incidence of AF after HT. Denervation is also an intriguing possible factor in the lower incidence of ventricular fibrillation (VF) as the terminal rhythm among HT patients who have sudden cardiac death (SCD). 21 Finally, hypersensitivity to adenosine as a result of denervation is the likely mechanism for exaggerated sinus node and AV node suppression with adenosine after HT. Over time, the incidence of rejection has decreased to 20% to 30% in the first posttransplantation year but can occur at any time period after HT. 5 Many arrhythmias, especially AF and flutter, have been attributed to acute rejection. 24, 25 Although some studies observing high incidence of atrial arrhythmia reported no association with rejection, 26, 27, 28 other studies have shown an association of sustained AF and atrial flutter with rejection episodes. 15, 16, 25, 29 The occurrence of persistent or paroxysmal AF should prompt evaluation for rejection. 15 In HT patients, atrial flutter can occur in the setting of rejection 25, 28, 30 or can be a manifestation of remodeled and scarred atria that can be associated with cardiac allograft vasculopathy. 15, 16 Repeated rejection episodes may lead to cumulative damage as a mechanism of atrial flutter.
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