Role of interatrial block in modulating cryptogenic stroke risk in patients with patent foramen ovale: a

Ye Du1, Yanxing Zhang1, Yangbo Xing2

  • 1Department of Neurology, Shaoxing People's Hospital (Shaoxing Hospital, Zhejiang University School of Medicine), Shaoxing, 312000, China.

BMC Neurology
|September 13, 2024
PubMed

Insights

The interaction between interatrial block (IAB) and patent foramen ovale (PFO) is linked to cryptogenic stroke (CS). This study highlights that low-risk PFO significantly increases CS risk when co-occurring with IAB.

Area of Science:

  • Cardiology
  • Neurology
  • Genetics

Background:

  • Patent foramen ovale (PFO) and interatrial block (IAB) are recognized risk factors for cryptogenic stroke (CS).
  • The specific interplay between PFO and IAB in the pathogenesis of CS remains incompletely understood.

Purpose of the Study:

  • To investigate the interaction between PFO and IAB in patients experiencing cryptogenic stroke.
  • To determine if the combination of PFO and IAB poses a greater risk for CS than either condition alone.

Main Methods:

  • A case-control study involving 256 CS patients and 156 controls.
  • IAB defined by P wave duration > 120 ms; PFO assessed via transesophageal echocardiography (no-PFO, low-risk PFO, high-risk PFO).
  • Multiplicative and additive interaction analyses were employed to evaluate the combined effect of PFO and IAB on CS risk.

Main Results:

  • A significant multiplicative interaction was found between IAB and low-risk PFO in CS (OR=3.653, P=0.037).
  • Additive interaction analysis revealed that IAB accounted for 68.4% of the increased CS risk associated with low-risk PFO (P<0.001).
  • High-risk PFO was independently associated with CS regardless of IAB status, while low-risk PFO was only associated with CS in the presence of IAB.

Conclusions:

  • The interaction between IAB and PFO plays a significant role in cryptogenic stroke.
  • This interaction is particularly pronounced in patients with low-risk PFO, suggesting a specific synergistic mechanism contributing to stroke risk.
Abstract

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