Diagnostic value of cardiovascular magnetic resonance in acute peripartum cardiomyopathy (PPCM)
Authors: Hoevelmann J , Viljoen C A , Jermy S , Cirota J , Kraus S , Sliwa K , Ntusi N A B 
Published: October 2022

Introduction

Peripartum cardiomyopathy (PPCM) is characterised by left ventricular (LV) dilatation and systolic dysfunction developing towards the end of pregnancy or in the first five months postpartum. Cardiovascular magnetic resonance (CMR) allows for comprehensive evaluation of myocardial structure, function, and tissue characteristics. There is a dearth of studies investigating utility of CMR in PPCM.

Purpose

To evaluate diagnostic benefit of multiparametric assessment of myocardial oedema, fibrotic burden, and strain impairment in PPCM using CMR.

Methods

Eighteen consenting women with newly diagnosed PPCM and 20 female, age-matched healthy controls (HCs) underwent CMR imaging on a 3T MR scanner. A comprehensive, contrast-enhanced CMR protocol was used including cines, native T1 and T2 mapping, myocardial strain analysis, and extracellular volume (ECV). Images were evaluated qualitatively and semi-quantitively for the presence of late gadolinium enhancement (LGE)

Results

Patients with PPCM (median age of 34.5 years [IQR 25–38]) presented with severely impaired LV ejection fraction (LVEF) of 31.4% (IQR 19.6–37.9) and reduced right ventricular (RV) ejection fraction (RVEF) of 37.2% (IQR 21.6–51.7). Global longitudinal strain (GLS) was significantly reduced in PPCM patients (−8.9% [IQR −10.8 to −5.6] vs. −19.7 [−21.9 to −16.3], p&lt;0.001) compared to HCs. LGE was present in 13 (81.2%) PPCM patients and included linear or circumferential mid-wall, patchy and diffuse patterns (LGE mass 19.1g [IQR 15.0–26.5] vs. 11.4g [8.8–13.2] in HCs, p&lt;0.001). Patients with PPCM had significantly higher T1 times (1369.3ms [IQR 1343.7–1409.7 vs. 1207.8ms [IQR 1194.8–1241.3], p&lt;0.001) and ECV (36.5% [32.7–37.0] vs. 27.5 [26.3–28.5], p&lt;0.001) compared to HCs. ECV, native T1 and T2 times did not differ between PPCM patients presenting with LVEF ≤35% and &gt;35%. RV dysfunction (present in 61.1% of PPCM cohort) was associated with significantly higher ECV (37.0% [IQR 36.5–38.4] vs 33.4% [IQR 28.5–37.0], p=0.05 and higher T1 (1409.0ms [IQR 1349.0–1443.0] vs. 1311.3ms [IQR 1299.3–1369.3], p=0.015) compared to those with preserved RV function. LV fibrosis was not significantly different between PPCM patients with and without RV dysfunction. LGE mass correlated negatively with LVEF and RVEF (r=−0.540, p=0.001; r=−0.568, p&lt;0.001), respectively. There was a strong positive correlation between LGE mass and native T1 (r=0.619, p&lt;0.001), LGE mass and GLS (r=0.638, p&lt;0.001) and moderate correlation with ECV (r=0.528, p=0.001) (Figure 1). Small, sub-centimetre pericardial effusions were noted in 83.3% of PPCM patients vs. 10% in HCs (p&lt;0.001).

Conclusion

For the first time, we report a high prevalence of myocardial fibrosis in well-phenotyped patients with newly diagnosed PPCM. Increased LGE mass was associated with severe impairments in LV strain, LVEF and RVEF. RV dysfunction was associated with significantly higher ECV and native T1 times.

Funding Acknowledgement

Type of funding sources: None.