Title:Ignored Role of Paroxysmal Atrial Fibrillation in the Pathophysiology of
Cryptogenic Stroke in Patients with Patent Foramen Ovale and Atrial
Septal Aneurysm
Volume: 20
Issue: 2
Author(s): Ertan Yetkin*, Hasan Atmaca, Bilal Çuğlan and Kenan Yalta
Affiliation:
- Division of Cardiology, Türkiye Hospital, Istanbul, Turkey
Keywords:
Stroke, cryptogenic stroke, atrial septal aneurysm, patent foramen ovale, atrial fibrillation, pathophysiology.
Abstract:
The association between cryptogenic stroke (CS) and patent foramen ovale (PFO)
with or without atrial septal aneurysm (ASA) has been a debate for decades in terms of pathophysiologic
processes and clinical courses. This issue has become more interesting and complex,
because of the concerns associating the CS with so-called normal variant pathologies of interatrial
septum, namely ASA and PFO. While there is an anatomical pathology in the interatrial septum,
namely PFO and ASA, the embolic source of stroke is not clearly defined. Moreover, in patients
with PFO and CS, the risk of recurrent stroke has also been associated with other PFOunrelated
factors, such as hyperlipidemia, body mass index, diabetes mellitus, and hypertension,
leading to the difficulty in understanding the pathophysiologic mechanism of CS in patients with
PFO and/or ASA. Theoretically, the embolic source of cryptogenic stroke in which PFO and/or
ASA has been involved can be categorized into three different anatomical locations, namely PFO
tissue and/or ASA tissue itself, right or left atrial chambers, and venous vascular territory distal
to the right atrium, i.e., inferior vena cava and lower extremity venous system. However, the
possible role of paroxysmal atrial fibrillation associated with PFO and/or ASA as a source of
cryptogenic stroke has never been mentioned clearly in the literature. This review aims to explain
the association of cryptogenic stroke with PFO and/or ASA in a comprehensive manner,
including anatomical, clinical, and mechanistic aspects.
The potential role of paroxysmal atrial fibrillation and its contribution to clinical course have
been also discussed in a hypothetical manner to elucidate the pathophysiology of CS and support
further treatment modalities.
