by Hande Oktay Tureli
As physicians, we probably all have an almost innate fear of making matters worse while trying to help our patients. The maxim of “first, do no harm” is invoked when considering an intervention that carries a risk of harm but a less certain chance of benefit. For a sizeable part of the medical community, transcatheter closure of atrial septal defect (ASD) and patent foramen ovale (PFO) are such risky interventions.
One of the main arguments against closure is that the intervention carries procedural and long-term risks. Clinically apparent or silent peri-interventional cerebral embolism is one such risk and in this study we investigated its incidence with diffusion-weighted magnetic resonance imaging (DW-MRI) and plasma neuron specific enolase (NSE) levels.
All our PFO patients were under medical therapy with aspirin at the time of recurrent cryptogenic stroke or transient ischemic attack; percutaneous device closure procedures were in accordance with the guidelines (Class IIb; level of evidence, C), but one still fears inducing cerebral emboli while trying to fix the cause of stroke.
We did not detect clinically apparent cerebral emboli in any patient; however, silent embolic events may also cause deficits having more subtle manifestations not assessable by simple neurological examinations. With DW-MRI, one new microembolic lesion was found in only 1 of 30 patients; this incidence was much lower than we initially expected.
Given the rather small number of patients; only one brand of closure devices was used in order to increase the statistical power of the study. We used the newest commercially available nitinol meshwire occluder devices at the time of the study. I think any device’s safety must be addressed with many studies and DW-MRI appears to be the most reliable tool for detecting cerebral embolic complications in follow-up of patients undergoing potentially high-risk angiographic procedures. On the other hand, NSE levels after the procedure were found to be not correlated with presence of DW-MRI lesion and intervention times.
This study is not a superiority trial of medical therapy versus device closure; there are multiple ongoing and published trials comparing treatment alternatives. Long-term observations are needed to determine if the mentioned silent ischemic events culminate in any form of clinically apparent cerebral dysfunction.
Oktay Tureli H, Ungan I, Tureli D, Demir B, Pirhan O, Bayrak HI, Caglar IM, Karakaya O, Inci E. Risk of Cerebral Embolism After Interventional Closure of Symptomatic Patent Foramen Ovale or Atrial Septal Defect: A Diffusion-Weighted MRI and Neuron-Specific Enolase-Based Study. J Invasive Cardiol. 2013;25(10):519-524.
Selected Related Articles:
- Lertsapcharoen P, Srimahachota S, Charoonrut P. Transcatheter Ventricular Septal Defect Closure With a New Nanoplatinum-Coated Nitinol Device in a Swine Model. J Invasive Cardiol. 2013 Oct;25(10):525-528.
- Prashanth P, Mukhaini MK. Primary antiphospholipid syndrome with recurrent coronary thrombosis, acute pulmonary thromboembolism and intracerebral hematoma. J Invasive Cardiol. 2009 Dec;21(12):E254-8.
- Musto C, Cifarelli A, Fiorilli R, De Felice F, Parma A, Pandolfi C, Confessore P, Bernardi L, Violini R. Gore Helex septal occluder for percutaneous closure of patent foramen ovale associated with atrial septal aneurysm: short- and mid-term clinical and echocardiographic outcomes. J Invasive Cardiol. 2012 Oct;24(10):510-4.
- Krasniqi N, Roth J, Siegrist PT, Toggweiler S, Gruner C, Greutmann M, Tanner FC, Lüscher TF, Corti R. Percutaneous closure of patent foramen ovale and valvular function — effect of the amplatzer occluder. J Invasive Cardiol. 2012 Jun;24(6):274-7.