TY - JOUR
T1 - The Blinding Period Following Ablation Therapy for Atrial Fibrillation: Proarrhythmic and Antiarrhythmic Pathophysiological Mechanisms
AU - Gottlieb, Lisa A.
AU - Dekker, Lukas R. C.
AU - Coronel, Ruben
N1 - Funding Information: This work was supported by the Leducq Foundation (RHYTHM [16CVD02]) to Dr. Coronel; a Medtronic unrestricted research grant to Dr. Dekker; and a Catharina Hospital research grant to Dr. Dekker. The authors have reported that they have no relationships relevant to the contents of this paper to disclose. Publisher Copyright: © 2021 The Authors
PY - 2021/3/1
Y1 - 2021/3/1
N2 - Atrial fibrillation (AF) causes heart failure, ischemic strokes, and poor quality of life. The number of patients with AF is estimated to increase to 18 million in Europe in 2050. Pharmacological therapy does not cure AF in all patients. Ablative pulmonary vein isolation is recommended for patients with drug-resistant symptomatic paroxysmal AF but is successful in only about 60%. In patients in whom ablative therapy is successful on the long term, recurrence of AF may occur in the first weeks to months after pulmonary vein ablation. The early recurrence (or delayed cure) of AF is not understood but forms the basis for the generally accepted 3-month blinding (or blanking) period after ablation therapy, which is not included in the evaluation of the eventual success rate of the procedures. The underlying pathophysiological processes responsible for early recurrence and the delayed cure are unknown. The implicit assumption of the blinding period is that the AF mechanism in this period is different from the ablation-targeted AF mechanism (ectopy from the pulmonary veins). In this review, we evaluate the temporary and long-lasting pro- and antiarrhythmic effects of each of the pathophysiological processes and interventions (necrosis, ischemia, oxidative stress, edema, inflammation, autonomic nervous activity, tissue repair, mechanical remodeling, and use of antiarrhythmic drugs) occurring in the blinding period that can modulate AF mechanisms. We propose that stretch-reducing ablation scar is a permanent antiarrhythmic mechanism that develops during the blinding period and is the reason for delayed cure.
AB - Atrial fibrillation (AF) causes heart failure, ischemic strokes, and poor quality of life. The number of patients with AF is estimated to increase to 18 million in Europe in 2050. Pharmacological therapy does not cure AF in all patients. Ablative pulmonary vein isolation is recommended for patients with drug-resistant symptomatic paroxysmal AF but is successful in only about 60%. In patients in whom ablative therapy is successful on the long term, recurrence of AF may occur in the first weeks to months after pulmonary vein ablation. The early recurrence (or delayed cure) of AF is not understood but forms the basis for the generally accepted 3-month blinding (or blanking) period after ablation therapy, which is not included in the evaluation of the eventual success rate of the procedures. The underlying pathophysiological processes responsible for early recurrence and the delayed cure are unknown. The implicit assumption of the blinding period is that the AF mechanism in this period is different from the ablation-targeted AF mechanism (ectopy from the pulmonary veins). In this review, we evaluate the temporary and long-lasting pro- and antiarrhythmic effects of each of the pathophysiological processes and interventions (necrosis, ischemia, oxidative stress, edema, inflammation, autonomic nervous activity, tissue repair, mechanical remodeling, and use of antiarrhythmic drugs) occurring in the blinding period that can modulate AF mechanisms. We propose that stretch-reducing ablation scar is a permanent antiarrhythmic mechanism that develops during the blinding period and is the reason for delayed cure.
KW - ablation therapy
KW - atrial fibrillation
KW - blinding period
KW - myocardial stretch
KW - pulmonary veins isolation
UR - http://www.scopus.com/inward/record.url?scp=85102135181&partnerID=8YFLogxK
U2 - https://doi.org/10.1016/j.jacep.2021.01.011
DO - https://doi.org/10.1016/j.jacep.2021.01.011
M3 - Review article
C2 - 33736761
SN - 2405-500X
VL - 7
SP - 416
EP - 430
JO - JACC: Clinical Electrophysiology
JF - JACC: Clinical Electrophysiology
IS - 3
ER -