When c-TTE and/or c-TCD were used, the rate of residual RLSs detected in patients who underwent PFO closure was 26.32%, which was significantly different than the rate detected using TEE (P < .05)c-TTE and c-TCD showed equivalent sensitivity in evaluating transcatheter closure of a PFO. c-TTE could be a more cost-effective and reliable method to detect the residual shunt after PFO closure.
Cutoff values of BNP, E/e', and left atrial appendage flow velocity capable of distinguishing CS without large PFO from noncardioembolic stroke were 65.0 pg/mL (sensitivity 55.3%; specificity 70.9%), 13.0 (45.5%; 68.0%), and 46.0 cm/s (37.1%; 87.5%), respectively.
We describe the case of one patient with pure sporadic hemiplegic migraine (SHM) with a novel ATP1A2 gene variant and a large patent foramen ovale (PFO) with atrial septal aneurysm.
Between January 2012 and August 2016, 151 patients (mean age 41 ± 11 years) who had suffered from a cryptogenic thromboembolic event underwent transcatheter PFO closure with the PFM Nit-Occlud PFO device.
Three different polymorphisms located in the prothrombin, F2 (20210G/A), and apolipoprotein-C3 (-641A/C and -455T/A) genes were significantly associated with ICVD and PFO.
We identified a male Polish patient with a very rare minor homozygous GG genotype of the tissue factor (TF) +5466A>G polymorphism, who within two months experienced a transient ischemic attack (TIA) and ischemic stroke of unknown origin associated with the presence of patent foramen ovale below 40 years of age.
Migraine, particularly with aura, is an independent risk factor for IS, and the patient's IS risk is probably affected by other individual risk factors (e.g., age, genetic predisposition to thrombosis, presence of patent foramen ovale or enhanced platelet aggregation) which seem to be over-represented in migraine patients.
Purported mechanisms for migraine-associated stroke include involvement of the vasculature (including vasospasm, arterial dissection and small vessel arteriopathy), hypercoagulability (elevated von Willebrand Factor, platelet activation) and elevated risk of cardioembolism (patent foramen ovale, atrial septal aneurysm).
We assessed the occurrence of several prothrombotic states (factor V Leiden, prothrombin G20210A, deficiencies in protein S, protein C and antithrombin, lupus anticoagulant, anticardiolipin antibodies, elevated factor VIII, resistance to activated protein C) and classical risk factors for venous thrombosis in 57 adult patients with cryptogenic stroke and patent foramen ovale and in 104 matched controls.
After finding that the thienopyridines clopidogrel and prasugrel reduced migraine headache (MHA) symptoms in some patients with patent foramen ovale (PFO), this small pilot study was undertaken to determine whether ticagrelor, a nonthienopyridine P2Y12 inhibitor, would have similar MHA effects and might be better suited for a future randomized trial.
Significantly more frequent prevalence of PFO in migraine patients with aura (with homozygous recessive genotype of MTHFR probably suggests their common genetic basis.
This study investigated if in uncomplicated hypertensive subjects (HTs) with isolated PFO and H-Hcys, a different MTHFR polymorphism pattern for C667→T gene mutation could influence PFO management and to reduce the CV risk.
Conscious sedation for transcatheter implantation of ASO is a feasible, safe, and efficient technique, allowing successful PFO and ASD closure in the majority of patients.
Twenty-one cases of infective endocarditis after atrial defect device closure have been reported in the literature (13 ostium secundum ASD and 8 patent foramen ovale).Seven pediatric cases were reported.
Three different polymorphisms located in the prothrombin, F2 (20210G/A), and apolipoprotein-C3 (-641A/C and -455T/A) genes were significantly associated with ICVD and PFO.
Across the population the presence of the FIIG20210A mutation (OR: 2.97;95% CI: 1.32-6.69), a history of DVT (OR: 1.04; 95% CI: 1.02-1.06), and oestrogen-containing contraceptive therapy (OR: 1.14; 95% CI: 1.09-1.18) were all associated with stroke of unknown cause after adjustment for other risk factors, This was not the case with PFO.
We comprehensively sought and identified studies of the association of both the factor V Leiden (FV(G1691A) mutation) and the prothrombin mutation (PT(G20210A) mutation) with PFO-related cerebral ischaemia and did meta-analyses to assess the evidence for such a relation.
We comprehensively sought and identified studies of the association of both the factor V Leiden (FV(G1691A) mutation) and the prothrombin mutation (PT(G20210A) mutation) with PFO-related cerebral ischaemia and did meta-analyses to assess the evidence for such a relation.