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 co-morbidities. 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: We retrospectively studied 76 patients with SLE who had 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 by 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 female. A reduced GLS was found in 24% of the population, of whom 44% had LVEF <50%. Previously documented heart failure symptoms was more prevalent in the reduced GLS cohort (50% vs 12%, p=0.002). 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 RV free wall strain (r = 0.67, p<0.01) and degree of LV diastolic dysfunction. Worsening grades of diastolic dysfunction, like GLS, were associated with renal disease and pericardial involvement. SLE patients 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.

Conclusion: 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 RV function, diastolic dysfunction, and impairment in LASr suggests a common mechanistic basis involving immune injury.