Huber Roman, Grittner Ulrike, Weidemann Frank, Thijs Vincent, Tanislav Christian, Enzinger Christian, Fazekas Franz, Wolf Markus, Hennerici Michael G, McCabe Dominick J H, Putaala Jukaa, Tatlisumak Turgut, Kessler Christoph, von Sarnowski Bettina, Martus Peter, Kolodny Edwin, Norrving Bo, Rolfs Arndt
From the Department of Neurology, Medical Campus Lake Constance, Klinikum Friedrichshafen, Germany (R.H.); Department of Neurology, University of Ulm, Ulm, Germany (R.H.); Department for Biostatistics and Clinical Epidemiology (U.G.) and Center for Stroke Research (U.G.), Charité-Universitätsmedizin Berlin, Germany; Department of Internal Medicine II, Katharinen Hospital, Unna, Germany (F.W.); Department of Neurology, Austin Health and Florey Institute of Neuroscience and Mental Health, Heidelberg, Victoria, Australia (V.T.); Department of Neurology, Justus Liebig University Giessen, Germany (C.T.); Department of Neurology (C.E., F.F.) and Clinical Division of Neuroradiology, Vascular and Interventional Radiology, Department of Radiology (C.E.), Medical University of Graz, Austria; Department of Neurology, University of Mannheim, Germany (M.W., M.G.H.); Department of Neurology and Stroke Service, The Adelaide and Meath Hospital, incorporating the National Children's Hospital, Dublin, Ireland (D.J.H.M.); Department of Clinical Neurosciences, Royal Free Campus, UCL Institute of Neurology, London, United Kingdom (D.J.H.M.); Academic Unit of Neurology, School of Medicine, Trinity College Dublin, Ireland (D.J.H.M.); Department of Neurology, Helsinki University Central Hospital, Finland (J.P., T.T.); Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, Sweden (T.T.); Department of Neurology, Sahlgrenska University Hospital, Gothenburg, Sweden (T.T.); Department of Neurology, University Medicine Greifswald, Ernst Moritz Arndt University of Greifswald, Germany (C.K., B.v.S.); Department of Epidemiology and Biometrics, University of Tübingen, Germany (P.M.); Department of Neurology, New York University School of Medicine (E.K.); Department of Clinical Sciences, Section of Neurology, Lund University, Sweden (B.N.); and Albrecht-Kossel-Institute for Neuroregeneration, University of Rostock, Germany (A.R.).
Stroke. 2017 Jan;48(1):30-35. doi: 10.1161/STROKEAHA.116.013620. Epub 2016 Nov 29.
A patent foramen ovale (PFO) is disproportionately prevalent in patients with cryptogenic stroke. Without alternative explanations, it is frequently considered to be causative. A detailed stratification of these patients may improve the identification of incidental PFO.
We investigated the PFO prevalence in 3497 transient ischemic attack and ischemic stroke patients aged 18 to 55 years in the prospective multicenter SIFAP1 study (Stroke in Young Fabry Patients 1) using the ASCO classification. Patients without an obvious cause for transient ischemic attack/stroke (ASCO 0) were divided into subgroups with and without vascular risk factors (ASCO 0+ and 0-). In addition, we looked for PFO-related magnetic resonance imaging lesion patterns.
PFO was identified in 25% of patients. Twenty percent of patients with a definite or probable cause of transient ischemic attack/stroke (≥1 grade 1 or 2 ASCO criterion; n=1769) had a PFO compared with 29% of cryptogenic stroke patients (ASCO 0 and 3; n=1728; P<0,001); subdivision of cryptogenic strokes revealed a PFO in 24% of 978 ASCO 3 patients (n.s. versus ASCO 1 and 2) and a higher prevalence of 36% in 750 ASCO 0 cases (P<0.001 versus ASCO 3 and versus ASCO 1 and 2). PFO was more commonly observed in ASCO 0- (n=271) than in ASCO 0+ patients (n=479; 48 versus 29%; P<0.001). There was no PFO-associated magnetic resonance imaging lesion pattern.
Cryptogenic stroke patients demonstrate a heterogeneous PFO prevalence. Even in case of less conclusive diseases like nonstenotic arteriosclerosis, patients should preferentially be considered to have a non-PFO-mediated stroke.
URL: http://www.clinicaltrials.gov. Unique identifier: NCT00414583.
卵圆孔未闭（PFO）在不明原因卒中患者中极为常见。若无可替代的解释，通常认为其具有病因学意义。对这些患者进行详细分层可能有助于识别偶然发现的PFO。
我们在前瞻性多中心SIFAP1研究（年轻法布里病患者卒中1）中，采用ASCO分类法，调查了3497例年龄在18至55岁的短暂性脑缺血发作和缺血性卒中患者的PFO患病率。无明显短暂性脑缺血发作/卒中病因的患者（ASCO 0）被分为有和无血管危险因素的亚组（ASCO 0+和0-）。此外，我们还寻找了与PFO相关的磁共振成像病变模式。
25%的患者发现有PFO。1769例有明确或可能的短暂性脑缺血发作/卒中病因的患者（≥1个1级或2级ASCO标准）中，20%有PFO，而不明原因卒中患者中这一比例为29%（ASCO 0和3；n = 1728；P<0.001）；对不明原因卒中进行细分后发现，978例ASCO 3患者中有24%有PFO（与ASCO 1和2相比无显著差异），750例ASCO 0患者中PFO患病率更高，为36%（与ASCO 3相比以及与ASCO 1和2相比，P<0.001）。ASCO 0-患者（n = 271）中PFO的观察频率高于ASCO 0+患者（n = 479；48%对29%；P<0.001）。不存在与PFO相关的磁共振成像病变模式。
不明原因卒中患者的PFO患病率存在异质性。即使在诸如非狭窄性动脉硬化等不太明确的疾病中，患者也应优先被考虑为非PFO介导的卒中。
