IntroductionAbnormalities on CT imaging may contribute to the diagnosis of tuberculous meningitis (TBM). Recently, an expert consensus case definition (CCD) and set of imaging criteria for diagnosing basal meningeal enhancement (BME) have been proposed. This study aimed to evaluate the sensitivity, specificity and reliability of these in a prospective cohort of adult meningitis patients.MethodsInitial diagnoses were based on the CCD, classifying patients into: ‘Definite TBM’ (microbiological confirmation), ‘Probable TBM’ (diagnostic score ≥10), ‘Possible TBM’ (diagnostic score 6–9), ‘Not TBM’ (confirmation of an alternative diagnosis) or ‘Uncertain’ (diagnostic score of <6). CT images were evaluated independently on two occasions by four experienced reviewers. Intra-rater and inter-rater agreement were calculated using the kappa statistic. Sensitivities and specificities were calculated using both ‘Definite TBM’ and either ‘Definite TBM’ or ‘Probable TBM’ as gold standards.ResultsCT scan criteria for BME had good intra-rater agreement (κ range 0.35–0.78) and fair to moderate inter-rater agreement (κ range 0.20–0.52). Intra- and inter-rater agreement on the CCD components were good to fair (κ  =  ranges 0.47–0.81 and 0.21–0.63). Using ‘Definite TBM’ as a gold standard, the criteria for BME were very specific (61.5%–100%), but insensitive (5.9%–29.4%). Similarly, the imaging components of the CCD were highly specific (69.2–100%) but lacked sensitivity (0–56.7%). Similar values were found when using ‘Definite TBM’ or ‘Probable TBM’ as a gold standard.DiscussionThe fair to moderate inter-rater agreement and poor sensitivities of the criteria for BME suggest that little reliance should be placed in these features in isolation. While the presence of the CCD criteria of acute infarction or tuberculoma(s) appears useful as rule-in criteria, their absence is of little help in excluding TBM. The CCD and criteria for BME, as well as any new criteria, need to be standardized and validated in prospective cohort studies.

Objectives 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. Methods 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. Results 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 < 0.001, sensitivity: 88.9%, specificity: 76.3%). Conclusions 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.

Objectives To determine the outcome of subclinical lupus myocarditis (LM) over twelve months with regards to: mortality; incidence of clinical LM and change in imaging parameters (echocardiography and cardiac magnetic resonance [CMR]). To evaluate the impact of immunosuppression on CMR evidence of myocardial tissue injury. Methods SLE patients with and without CMR evidence of myocardial injury (as per 2009 Lake Louise criteria [LLC]) were included. Analysis at baseline and follow-up included: clinical evaluation, laboratory and imaging analyses (echocardiography and CMR). Clinical LM was defined as clinical features of LM supported by echocardiographic and/or biochemical evidence of myocardial dysfunction. Subclinical LM was defined as CMR myocardial injury without clinical LM. Results Forty-nine SLE patients were included with follow-up analyses (after 12 months) available in 36 patients. Twenty-five patients (51%) received intensified immunosuppressive therapy during follow-up for indications related to SLE. Disease activity (SLEDAI-2K) improved (p < 0.001) from 13 (median;IQR:9–20) to 7 (3–11). One patient without initial CMR evidence of myocardial injury developed clinical LM. Mortality (n = 10) and SLE clinical features were similar between patients with and without initial CMR myocardial injury. Echocardiographic left ventricular ejection fraction (LVEF) (p = 0.014), right ventricular function (p = 0.001) and wall motion abnormalities (p = 0.056) improved significantly but not strain analyses nor the left LV internal diameter index. CMR mass index (p = 0.011) and LVEF (p < 0.001) improved with follow-up but not parameters identifying myocardial tissue injury (LLC). A trend towards a reduction in the presence of CMR criteria was counterbalanced by persistence (n = 7) /development of new criteria (n = 11) in patients. Change in CMR mass index correlated with change in T2-weighted signal (myocardial oedema) (r = 386;p = 0.024). Intensified immunosuppressive therapy had no significant effect on CMR parameters. Conclusion CMR evidence of subclinical LM persisted despite improved SLEDAI-2K, serological markers, cardiac function and CMR mass index. Subclinical LM did not progress to clinical LM and had no significant prognostic implications over 12 months. Immunosuppressive therapy did not have any significant effect on the presence of CMR evidence of myocardial tissue injury. Improvement in CMR mass index correlated with reduction in myocardial oedema and may be used to monitor SLE myocardial injury.