Cerebral microembolism during transcatheter closure of patent foramen ovale

Abstract

Silent cerebral embolism frequently occurs during transcatheter PFO and ASD closure. The peak of HITS at the time of crossing the septum with the guide wire may support the hypothesis that cerebral emboli in patients with PFO may originate from the septum itself. This may represent an alternative mechanism to the generally assumed paradoxical embolism.

Silent cerebral emboli following percutaneous closure of atrial septal defect in pediatric patients: a diffusion-weighted MRI study

“…Although transcatheter closure of ASD/ PFO has been applied to many patients to prevent those recurrent thromboembolic events, few studies focusing on adult patient groups revealed that transcatheter ASD/PFO closure itself is associated with periprocedural cerebral microembolic lesions. The incidence of cerebral lesions associated with ASD/PFO closure has been reported to be 0%-8.6% in adult patients (7,(10)(11)(12). In the current study, as the first DWI study investigating the incidence of cerebral microembolic lesions that appear following ASD closure in pediatric patients, no association was identified between the procedure and the cerebral lesions.…”

Early Experience with a Simplified Technique for Transcatheter Closure of the Patent Foramen Ovale

“…It is known that even a gentle push of the wire or catheter during transcatheter closure can easily perforate friable structures such as the left atrial appendage [9]. Various other complications such as spontaneous thrombus formation during balloon sizing [14] and silent cerebral embolism [15] resulting from catheter and wire manipulation have been reported.…”

Entrapment of right atrial pacemaker lead by patent foramen ovale closure device: Successful percutaneous salvage

“…With more widespread use of these procedures, novel complications and issues are increasingly encountered. Some of the known complications during atrial septal occlusion procedures include device embolization to the right or left cardiac chambers with reports of successful endovascular or surgical retrieval [5, 6, 9]; metal arm fracture from flexion forces exerted by the beating heart (observed less frequently secondary to better metal alloys and improved device engineering [4]); nickel toxicity, which is usually transient in nature with systemic nickel levels peaking at 1 month or until the device has endothelialized [10]; cerebral microembolization, which is often clinically silent and minimized by proper endovascular technique and deairing [11]; and erosion or perforation into adjacent cardiac structures directly related to device oversizing and closure of larger defects [12]. Atrial septal closure devices may also entrap a redundant Eustachian valve or interfere with atrioventricular valve function, especially when used in defects with deficient rims.…”