Clinical Risk Predictors for Abnormal Left Ventricular and Atrial Function in Lupus Erythematosus

Abstract

Background

In systemic lupus erythematosus (SLE), ventricular dysfunction can occur from primary immune injury or secondarily from SLE-related comorbidities. The aim of this study was to determine clinical predictors of reduced left ventricular (LV) systolic and diastolic function in an effort to understand potentially mitigating strategies.

Methods

The authors retrospectively studied 76 patients with SLE who underwent comprehensive transthoracic echocardiography within 3 months of an appointment with a rheumatologist to correlate clinical, laboratory, and echocardiographic features. All key echocardiographic measurements were reviewed and remeasured, when appropriate, by an expert blinded to other study data. Abnormal LV systolic function was defined as a global longitudinal strain threshold of −18.0%. Hierarchical cluster analysis was used to define feature interaction.

Results

The mean age of the population was 49 ± 15 years, and 83% were women. Reduced GLS was found in 24% of the population, of whom 44% had LV ejection fractions <50%. Previously documented heart failure symptoms were more prevalent in the reduced GLS cohort (50% vs 12%, P = .002). Those with reduced GLS had clinical features indicating greater SLE severity over time, including reduced renal function and prior pericardial involvement. GLS was strongly associated with right ventricular free wall strain (r = 0.67, P < .01) and degree of LV diastolic dysfunction. Worsening grades of diastolic dysfunction, like GLS, were associated with renal disease and pericardial involvement. Patients with SLE with reduced GLS and diastolic function also had abnormal left atrial reservoir strain (LASr). Hierarchical cluster analysis segregated populations with reduced GLS, reduced LASr, pericardial and renal involvement, and an additional feature of C-reactive protein known to be associated with chronic disease activity.

Conclusions

Reduced GLS is common in patients with SLE and is associated with heart failure symptoms and markers of increased disease activity over time, particularly pericardial involvement, suggesting common immune mechanisms. The associations of GLS with right ventricular function, diastolic dysfunction, and impairment in LASr suggests a common mechanistic basis involving immune injury.