Impaired endothelial function in patients with cryptogenic stroke and patent foramen ovale is not affected by closure
Corresponding Author
Maria Lantz MD
Department of Clinical Neuroscience Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden
Correspondence
Maria Lantz, MD, Department of Neurology, R54, Karolinska University Hospital Huddinge, S-141 86 Huddinge, Sweden.
Email: [email protected]
Search for more papers by this authorKonstantinos Kostulas MD, PhD
Department of Clinical Neuroscience Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden
Search for more papers by this authorMagnus Settergren MD, PhD
Department of Medicine Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden
Search for more papers by this authorChristina Sjöstrand MD, PhD
Department of Clinical Neuroscience Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden
Search for more papers by this authorCorresponding Author
Maria Lantz MD
Department of Clinical Neuroscience Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden
Correspondence
Maria Lantz, MD, Department of Neurology, R54, Karolinska University Hospital Huddinge, S-141 86 Huddinge, Sweden.
Email: [email protected]
Search for more papers by this authorKonstantinos Kostulas MD, PhD
Department of Clinical Neuroscience Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden
Search for more papers by this authorMagnus Settergren MD, PhD
Department of Medicine Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden
Search for more papers by this authorChristina Sjöstrand MD, PhD
Department of Clinical Neuroscience Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden
Search for more papers by this authorAbstract
Introduction
Patent foramen ovale (PFO) is associated with cryptogenic stroke (CS) and migraine with aura (MA). Endothelial dysfunction (ED) is a risk factor for development of cardiovascular disease, but might also be involved in migraine pathophysiology. Short-term worsening of migraine has been described after closure of PFO. We evaluated endothelial function in patients with CS and PFO, before and after closure of PFO, and in patients with migraine, whether changes in endothelial function was related to a change in migraine frequency.
Material and Methods
Patients with CS and PFO were included; 20 with planned closure of PFO and seven controls on medical treatment only. Endothelial function was assessed by peripheral arterial tonometry (EndoPatR) and biomarkers of endothelial activation. Patients were followed longitudinally at baseline, day 1, 1 month, and 6 months. A headache diary was used to assess migraine frequency.
Result
Mean age of the cohort was 45.4 years, and migraine prevalence was 50% whereof 84.6% had MA. Median EndoPatR index (RHI) at baseline was 1.60 (IQR 1.41-2.00). There was no change in RHI over time, either in closure patients (P = 0.66), nor in controls (P = 0.31), and there was no change in biomarkers of endothelial activation. Three migraine patients experienced worsening of migraine frequency directly after closure.
Discussion
Endothelial function did not change after closure of PFO. Although patients were lacking cardiovascular risk factors, a high proportion had impaired endothelial function. Whether ED can have predictive value, identifying PFO at higher risk for recurrent stroke warrants further investigations.
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