Myocardial injury in systemic lupus erythematosus according to cardiac magnetic resonance tissue characterization: clinical and echocardiographic features

Abstract

<jats:sec><jats:title>Objectives</jats:title><jats:p> To determine the prevalence of myocardial injury (MInj) in systemic lupus erythematosus (SLE) according to cardiac magnetic resonance (CMR) criteria. To compare clinical and echocardiographic features of patients with and without MInj and identify predictors of myocardial tissue characteristics according to CMR. </jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p> SLE inpatients underwent CMR screening for MInj based on the Lake Louise Criteria (LLC). Tissue characteristics included inflammation (increased T2-weighted signal or early gadolinium enhancement ratio (EGEr)) and necrosis or fibrosis (late gadolinium enhancement (LGE)). Echocardiographic parameters included left (left ventricular ejection fraction (LVEF)) and right ventricular function (tricuspid annular plane systolic excursion (TAPSE)), global longitudinal strain (GLS), wall motion score (WMSi) and left ventricular internal diameter index (LVIDi). Variables were compared with regards to the presence/absence of CMR criteria. Logistic regression identified variables predictive of CMR tissue characteristics. </jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p> A hundred and six SLE patients were screened of whom 49 patients were included. Fifty-seven patients were excluded due to intolerance of or contraindication to CMR (27/57 due to renal impairment). Twenty-three patients had CMR evidence of MInj, of which 60.9% was subclinical. Inflammation occurred in 16/23 and necrosis/fibrosis in 12/23 patients. Patients with any evidence of MInj were more frequently anti-dsDNA positive ( p = 0.026) and patients fulfilling LLC for myocarditis had higher SLE disease activity ( p = 0.022). The LVIDi ( p = 0.005), LVEF ( p = 0.005) and TAPSE ( p = 0.011) were more abnormal in patients with an increased EGEr, whereas WMSi ( p = 0.002) and GLS (0.020) were more impaired in patients with LGE. On multivariable logistic regression analyses, TAPSE predicted inflammation (OR: 0.045, p = 0.006, CI: 0.005–0.415) and GLS predicted necrosis/fibrosis (OR: 1.329, p = 0.031, CI: 1.026–1.722). A model including lymphocyte count, TAPSE and LVIDi predicted an increased EGEr on CMR (receiver operating characteristic-curve analyses: area under the curve: 0.901, p &lt; 0.001, sensitivity: 88.9%, specificity: 76.3%). </jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p> CMR evidence of MInj frequently occurs in SLE and is often subclinical. The utility of CMR in SLE is limited by a high exclusion rate, mainly due to renal involvement. Models including echocardiographic parameters (TAPSE, LVIDi and GLS) are predictive of CMR myocardial injury. Echocardiography can be used as a cost-effective screening tool with a high negative predictive value, in particular when CMR is contraindicated or unavailable. </jats:p></jats:sec>

Characterization and clinical significance of biventricular mechanics in patients with systemic lupus erythematosus by 3T cardiovascular magnetic resonance tissue tracking

“…We also found that LGE positivity in the LV wall was associated with LV GLS and PDGLSR, and the latter had an independent correlation. du Toit et al (30) recently found that the LV GLS based on speckle-tracking echocardiography may be an independent predictor of the presence of LV LGE in SLE patients, which represents fibrosis/necrosis and potentially less reversible myocardial injury. The impaired LV GLS represents the longitudinal fibrous systolic dysfunction located predominantly in the sub-endocardium (10,31), confirming past reports of early SLE being prone to endocardial microvascular injury and diffuse myocarditis (32,33).…”

Outcome of clinical and subclinical myocardial injury in systemic lupus erythematosus – A prospective cohort study

“…Forty-nine patients were included in the original cohort. 16 Three patients were lost to follow-up while ten patients died during the follow-up period. Mortality was related to SLE in two patients (neuropsychiatric SLE [NPSLE] and lupus nephritis [LN]) while five patients died due to infection related complications.…”

“…Between August 2016 and May 2018, all hospitalised SLE patients fulfilling the 2012 Systemic Lupus International Collaborating Clinics Classification (SLICC) criteria were screened for inclusion. 15,16 Exclusion criteria included existing myocarditis, cardiomyopathy (CMO), coronary artery disease, valvular/congenital heart disease and contraindications to undergo CMR (magnetic factors; contra-indications to gadolinium contrast). 17,18 Inflammatory skeletal myopathy co-existing with myocarditis limits the application of the LLC, thereby excluding these patients from the study.…”

“…Clinical LM was defined as clinical features of myocardial dysfunction attributed to SLE and supported by echocardiography and biochemical markers in keeping with myocarditis, without consideration of the CMR findings. 16 Subclinical LM was defined as CMR evidence of myocardial tissue injury (as per Lake Louise criteria) without clinical features of LM. Patients were divided into three groups, based on clinical and CMR parameters at inclusion: A. absence of CMR evidence of myocardial injury; B. presence of CMR evidence of myocardial injury with clinical LM; C. presence of CMR evidence of myocardial injury without clinical LM (subclinical).…”

Impaired left ventricular systolic synchrony in patients with lupus Nephritis: A speckle tracking echocardiography study

“…28 Moreover, a cardiac magnetic resonance (CMR) study showed that subclinical myocardial injury often exists in patients with SLE. 29 Myocardial injury is mainly characterized by fibrosis of the LV middle wall myocardium, which is not associated with the duration or severity of SLE. Extensive late gadolinium enhancement was found in patients with SLE who underwent CMR, which was attributed to the effects of aging.…”