Prevalence of Patent Foramen Ovale in Ischaemic Stroke in Italy: Results of SISIFO Study

Abstract

Background: Although several authors have studied the association between patent foramen ovale (PFO) and ischaemic stroke, the matter is still controversial; few have suggested an association between cryptogenetic stroke and PFO, while others have denied this association. The aim of this study was to evaluate PFO prevalence in the whole ischaemic stroke population, independently from age and stroke subtypes and to identify the characteristics associated with the presence of PFO. Methods: SISIFO study was a multicenter, prospective, single-wave, cross-sectional survey conducted on consecutive patients with acute ischemic stroke admitted to selected clinical centres. Data regarding vascular risk factors were registered for each patient; all patients underwent computed tomography scan and/or magnetic resonance imaging of the brain; an electrocardiogram and standard laboratory blood tests were performed. A Doppler ultrasound study of extra-cranial arteries was performed too. The cases were classified according to TOAST and OCSP criteria. Each patient underwent transcranial Doppler or transcranial color-coded duplex sonography with bubble test as diagnostic tool for right-to-left-shunt. Where right-to-left shunt was detected, PFO presence was confirmed by echocardiography. Findings: 1,130 consecutive patients were included. We found a PFO in 247 (21.9%; 95% CI, 19.5-24.3%) patients; PFO was present in 23.5% of patients with cryptogenic stroke and in 21.3% of patients with stroke of known causes; this difference was not statistically significant. At the univariate analysis, decreasing age, hypertension, diabetes mellitus, and atrial fibrillation, and stroke characteristics such as NIHSS, OCSP and TOAST were predictors of PFO presence. At the multivariate analysis, we found a significant interaction between age and OCSP syndrome. Being LACI the reference category, the prevalence of PFO in PACI and POCI decreased significantly along with age, whereas there was no change in TACI. Conclusion: If any relationship exists between stroke and PFO, this is more likely in PACI and POCI at a younger age. Our results are consistent with recent findings that underline PFO alone must not be considered a significant independent predictor for stroke; so the presence of PFO alone doesn't permit rushed causal correlations or ‘therapeutic aggressiveness'.

Patent Foramen Ovale and Cryptogenic Strokes in the Stroke in Young Fabry Patients Study

“…Although PFO screening in SIFAP study was not mandatory, we got data from nearly 80% of all patients. Finally, the rates of PFO in our cryptogenic stroke cohort are in accordance with those of several other studies, 21,35,36 making underreporting because of a lack of information or overestimation by PFO screening unblinded to the clinical situation 37 unlikely. In agreement with other studies, 22 even in SIFAP1 study, the PFO prevalence was generally higher in younger patients.…”

Clinical and infarction patterns of PFO‐related cryptogenic strokes and a prediction model

“…As described previously,8, 22 contrast agent was generated by agitating a mixture of 9 mL of isotonic saline solution and 1 mL of air between two 10 mL syringes connected by a three‐way stopcock. A drop of the patient's blood was allowed to mix with the contrast agent, which can slightly increase the detection sensitivity.…”

“…Epidemiological studies demonstrated that the prevalence of patent foramen ovale (PFO) in CS patients (40–56%) is much higher than that in normal healthy population (4–18%), suggesting a potential association between PFO and CS 4, 5, 6, 7. PFO may act as the pathway of thrombi from the venous circulation to cerebral circulation2 and could induce transient arrhythmia, both of which are recognized as potential underlying mechanisms for PFO‐induced CS 8. However, some researchers considered PFO as an anatomic variant,9 which could be just an incidental event for CS, rather than a cause 8, 10.…”

“…PFO may act as the pathway of thrombi from the venous circulation to cerebral circulation2 and could induce transient arrhythmia, both of which are recognized as potential underlying mechanisms for PFO‐induced CS 8. However, some researchers considered PFO as an anatomic variant,9 which could be just an incidental event for CS, rather than a cause 8, 10. A few randomized clinical trials even showed that closure of PFO does not significantly reduce cerebral ischemic events when compared with controls 7, 11.…”

Clinical Relevance of Patent Foramen Ovale and Atrial Septum Aneurysm in Stroke: Findings of a Single-Center Cross-Sectional Study

“…Nevertheless, it would be of great interest to reasonably integrate the role of PFO alone and PFO with ASA into concurring etiologies for ischemic stroke. A number of studies tried to address this question, unfortunately with major shortcomings, as they had either smaller study populations [2], or right-left-shunt analysis was done by neurological doppler/duplexsonography with a bubble test [11], whereby it is impossible to distinguish between shunts on cardiac or pulmonary level.…”