Native myocardial T1 mapping by cardiovascular magnetic resonance imaging in subclinical cardiomyopathy in patients with systemic lupus erythematosus

Abstract

Background: Increased systemic inflammation has been linked to myocardial dysfunction and heart failure in patients with systemic lupus erythematosus (SLE). Accurate detection of early myocardial changes may be able to guide preventive intervention. We investigated whether multiparametric imaging by cardiovascular magnetic resonance can detect differences between controls and asymptomatic SLE patients.

Methods and results: A total of 33 SLE predominantly female patients (mean age, 40±9 years) underwent cardiovascular magnetic resonance for routine assessment of myocardial perfusion, function, and late gadolinium enhancement. T1 mapping was performed in single short-axis slice before and after 15 minutes of gadolinium administration. Twenty-one subjects with a low pretest probability and normal cardiovascular magnetic resonance served as a control group. Both groups had similar left ventricular volumes and mass and normal global systolic function. SLE patients had significantly reduced longitudinal strain (controls versus SLE, -20±2% versus -17±3%; P<0.01) and showed intramyocardial and pericardial late gadolinium enhancement. SLE patients had significantly increased native myocardial T1 (1056±27 versus 1152±46 milliseconds; P<0.001) and extracellular volume fraction (26±5% versus 30±6%; P=0.007) and reduced postcontrast myocardial T1 (454±53 versus 411±62 milliseconds; P=0.01). T1-derived indices were associated with longitudinal strain (r=0.37-0.47) but not with the presence of late gadolinium enhancement. Native myocardial T1 values showed the greatest concordance with the presence of clinical diagnosis of SLE.

Conclusions: In patients with SLE and free of cardiac symptoms, there is evidence of subclinical perimyocardial impairment. We further demonstrate that T1 mapping may have potential to detect subclinical myocardial involvement in patients with SLE.