Systemic lupus erythematosus predicts increased left ventricular mass

Janice Pieretti1, Mary J Roman, Richard B Devereux

  • 1Division of Cardiology, Weill Medical College of Cornell University and the Hospital for Special Surgery, New York, NY 10021, USA.

Circulation
|July 11, 2007
PubMed

Insights

Systemic lupus erythematosus (SLE) is linked to increased left ventricular (LV) mass and hypertrophy, even without other heart conditions. This suggests inflammation-related arterial stiffening may impact cardiac health in SLE patients.

Area of Science:

  • Cardiology
  • Rheumatology
  • Vascular Biology

Background:

  • Systemic lupus erythematosus (SLE) is known to accelerate atherosclerosis and vascular stiffening.
  • The impact of SLE on left ventricular (LV) structure and function, independent of valvular or coronary artery disease, remains unclear.

Purpose of the Study:

  • To investigate whether SLE alters LV structure and function in patients without overt cardiovascular disease.
  • To explore the relationship between SLE, arterial stiffness, and LV remodeling.

Main Methods:

  • Age and gender-matched comparison of SLE patients (n=173) and a reference group (n=173).
  • Echocardiography for LV structure and function assessment.
  • Carotid ultrasonography for atherosclerosis detection and radial applanation tonometry for arterial stiffness measurement.

Main Results:

  • SLE patients exhibited significantly higher LV mass (P<0.001) and a greater prevalence of LV hypertrophy (17.9% vs. 6.4%, P<0.001) compared to controls.
  • LV mass in SLE patients was independently associated with SLE itself (P<0.001) and arterial stiffness (P<0.001).
  • Hypertension exacerbated LV mass increase in SLE patients.

Conclusions:

  • Systemic lupus erythematosus is a predictor of increased LV mass, potentially mediated by inflammation-induced arterial stiffening.
  • Elevated LV hypertrophy in SLE may contribute to the observed increase in cardiac morbidity and mortality.
Abstract

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