Cardiac magnetic resonance imaging in preeclampsia complicated by pulmonary edema shows myocardial edema with normal left ventricular systolic function.

BACKGROUND: Preeclampsia complicates approximately 5% of all pregnancies. When pulmonary edema occurs, it accounts for 50% of preeclampsia-related mortality. Currently, there is no consensus on the degree to which left ventricular systolic dysfunction contributes to the development of pulmonary edema. OBJECTIVE: This study aimed to use cardiac magnetic resonance imaging to detect subtle changes in left ventricular systolic function and evidence of acute left ventricular dysfunction (through tissue characterization) in women with preeclampsia complicated by pulmonary edema compared with both preeclamptic and normotensive controls. STUDY DESIGN: Cases were postpartum women aged ≥18 years presenting with preeclampsia complicated by pulmonary edema. Of note, 2 control groups were recruited: women with preeclampsia without pulmonary edema and women with normotensive pregnancies. All women underwent echocardiography and 1.5T cardiac magnetic resonance imaging with native T1 and T2 mapping. Gadolinium contrast was administered to cases only. Because of small sample sizes, a nonparametric test (Kruskal-Wallis) with pairwise posthoc analysis using Bonferroni correction was used to compare the differences between the groups. Cardiac magnetic resonance images were interpreted by 2 independent reporters. The intraclass correlation coefficient was calculated to assess interobserver reliability. RESULTS: Here, 20 women with preeclampsia complicated by pulmonary edema, 13 women with preeclampsia (5 with severe features and 8 without severe features), and 6 normotensive controls were recruited. There was no difference in the baseline characteristics between groups apart from the expected differences in blood pressure. Left atrial sizes were similar across all groups. Women with preeclampsia complicated by pulmonary edema had increased left ventricular mass (P=.01) but had normal systolic function compared with the normotensive controls. Furthermore, they had elevated native T1 values (P=.025) and a trend toward elevated T2 values (P=.07) in the absence of late gadolinium enhancement consistent with myocardial edema. Moreover, myocardial edema was present in all women with eclampsia or hemolysis, elevated liver enzymes, and low platelet count. Women with preeclampsia without severe features had similar findings to the normotensive controls. All cardiac magnetic resonance imaging measurements showed a very high level of interobserver correlation. CONCLUSION: This study focused on cardiac magnetic resonance imaging in women with preeclampsia complicated by pulmonary edema, eclampsia, and hemolysis, elevated liver enzymes, and low platelet count. We have demonstrated normal systolic function with myocardial edema in women with preeclampsia with these severe features. These findings implicate an acute myocardial process as part of this clinical syndrome. The pathogenesis of myocardial edema and its relationship to pulmonary edema require further elucidation. With normal left atrial sizes, any hemodynamic component must be acute.

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

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.