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Echocardiographic Assessment Using Subxiphoid-Only Examination for Hypotensive Patients
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Echocardiographic Assessment Using Subxiphoid-Only Examination for Hypotensive Patients

Published on: April 18, 2025

Echocardiographic evaluation of patients with primary antiphospholipid syndrome

N Espínola-Zavaleta1, J Vargas-Barrón, T Colmenares-Galvis

  • 1Department of Echocardiography, Instituto Nacional de Cardiología "Ignacio Chávez.", Mexico City, Mexico.

American Heart Journal
|April 30, 1999
PubMed

Insights

Primary antiphospholipid syndrome frequently causes valve disease. Anticoagulant or antiplatelet therapy did not improve existing valve lesions in patients with antiphospholipid syndrome.

Area of Science:

  • Cardiology
  • Rheumatology
  • Internal Medicine

Background:

  • Primary antiphospholipid syndrome (APS) is associated with a high prevalence of cardiac involvement, particularly valvular disease.
  • Approximately 33-50% of patients with APS exhibit some form of valve compromise.

Purpose of the Study:

  • To analyze echocardiographic features of APS-related heart disease.
  • To evaluate the efficacy of anticoagulant and/or antiplatelet therapy in managing valvular lesions in APS patients over one year.

Main Methods:

  • Transesophageal echocardiography (TEE) was used to assess valvular lesions in 29 APS patients before and after one year of treatment.
  • Patients received anticoagulant and/or antiplatelet therapy (acetylsalicylic acid).

Main Results:

  • Valvular lesions were detected in 75.9% of patients at baseline.
  • After one year, TEE revealed no improvement in existing lesions in 46.2% of patients, while 53.8% developed new lesions.
  • Associated cardiac issues included myocardial infarction and atrial septal defect.

Conclusions:

  • Valvular disease is the primary cardiac manifestation of APS.
  • Current anticoagulant/antiplatelet therapies do not appear to resolve or prevent the progression of noninfective valvular lesions in APS.
  • APS can be linked to myocardial infarction even with normal coronary arteries.
Abstract

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