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Atrial Cardiopathy and Likely Pathogenic Patent Foramen Ovale in Embolic Stroke of Undetermined Source

Ioannis A Leventis1, Dimitrios Sagris1, Davide Strambo2

  • 1Department of Internal Medicine, Faculty of Medicine, School of Health Sciences, University of Thessaly, Larissa, Greece.

Thrombosis and Haemostasis
|September 3, 2020
PubMed

Insights

In patients with embolic stroke of undetermined source (ESUS), atrial cardiopathy and likely pathogenic patent foramen ovale (PFO) are inversely related. This suggests these conditions may not frequently coexist as causes of stroke.

Area of Science:

  • Cardiology
  • Neurology
  • Stroke Research

Background:

  • Atrial cardiopathy and patent foramen ovale (PFO) are potential causes of embolic stroke of undetermined source (ESUS).
  • The co-occurrence and relationship between these two embolic sources in ESUS patients are not well understood.

Purpose of the Study:

  • To investigate the relationship between atrial cardiopathy and likely pathogenic PFO in patients diagnosed with ESUS.

Main Methods:

  • Atrial cardiopathy was defined by electrocardiogram findings (left atrial enlargement, PR prolongation, supraventricular extrasystoles).
  • PFO presence was assessed using echocardiography; likely pathogenic PFO was determined by a Risk of Paradoxical Embolism score of 7-10.
  • The study analyzed 367 ESUS patients with data on both conditions.

Main Results:

  • Likely pathogenic PFO was found in 16.9% and atrial cardiopathy in 33.2% of ESUS patients.
  • Only 1.1% of patients had both conditions.
  • Atrial cardiopathy was less prevalent in patients with likely pathogenic PFO (6.5%) compared to those without (40.6%).
  • Likely pathogenic PFO was less prevalent in patients with atrial cardiopathy (3.3%) compared to those without (23.7%).

Conclusions:

  • The presence of atrial cardiopathy is inversely associated with the presence of likely pathogenic PFO in ESUS patients.
  • These findings suggest that atrial cardiopathy and pathogenic PFO may be alternative rather than concurrent embolic mechanisms in ESUS.
Abstract

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