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The WATCHMAN Left Atrial Appendage Closure Device for Atrial Fibrillation
23:33

The WATCHMAN Left Atrial Appendage Closure Device for Atrial Fibrillation

Published on: February 28, 2012

Left atrial appendage: structure, function, and role in thromboembolism

N M Al-Saady1, O A Obel, A J Camm

  • 1Cardiological Sciences, St George's Hospital Medical School, Cranmer Terrace, London SW17 0RE, UK. nalsaady@sghms.ac.uk

Heart (British Cardiac Society)
|October 20, 1999
PubMed

Insights

The left atrial appendage (LAA) functions as a decompression chamber due to its unique properties. However, interventions like LAA obliteration may reduce thromboembolism risk but can impact atrial compliance and ANF secretion.

Area of Science:

  • Cardiology
  • Embryology
  • Physiology

Background:

  • The left atrial appendage (LAA) originates from the primary atrium during embryonic development.
  • It possesses distinct developmental, ultrastructural, and physiological features compared to the main left atrium.
  • Its anatomical proximity to the left ventricle influences its function.

Purpose of the Study:

  • To elucidate the distinct physiological roles and anatomical relations of the LAA.
  • To understand the factors contributing to thrombus formation in the LAA.
  • To evaluate the consequences of LAA interventions on cardiac function.

Main Methods:

  • Review of developmental and anatomical data.
  • Analysis of physiological properties including distensibility and neuroanatomy.
  • Examination of factors contributing to thrombus formation.
  • Assessment of potential sequelae from LAA obliteration or amputation.

Main Results:

  • The LAA acts as a decompression chamber due to its position, distensibility, atrial natriuretic factor (ANF) content, and neuronal structure.
  • Thrombus formation in the LAA is common in conditions like atrial fibrillation and mitral valve disease, likely due to blood stasis.
  • LAA obliteration may reduce thromboembolic risk but can lead to reduced atrial compliance and ANF secretion.

Conclusions:

  • The LAA has specialized physiological functions, including acting as a decompression chamber and secreting ANF.
  • Blood stasis within the LAA's unique shape and trabeculations contributes to thrombus formation.
  • Interventions targeting the LAA require careful consideration of potential adverse physiological effects.

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