Key result
Peripartum cardiomyopathy is linked to elevated myocardial inflammation and early interstitial fibrosis vs. healthy controls.
Why the study?
Peripartum cardiomyopathy pathogenesis involves multiple putative mechanisms including inflammation, but the acute inflammatory processes required exploration using advanced imaging and inflammasome profiling.
Case-Control (n=20)
No
Acute peripartum cardiomyopathy is characterized by marked systemic immune dysregulation, myocardial inflammation, and early interstitial fibrosis, distinguishing it from normal postpartum physiological changes.
Supports inflammatory-fibrotic mechanisms in peripartum cardiomyopathy; hypothesis-generating and should not yet change practice.
Aims Peripartum cardiomyopathy (PPCM) is an idiopathic cardiomyopathy occurring in women in the late stages of pregnancy or in the postpartum period and is associated with significant morbidity, mortality, and persistent left ventricular dysfunction. PPCM pathogenesis involves multiple putative mechanisms including inflammation. We aimed to explore the acute inflammatory processes in PPCM using 18F-fluorodeoxyglucose positron emission tomography-computed tomography (18FDG-PET-CT), cardiovascular magnetic resonance (CMR), and inflammasome profiling. Methods and results Women with a new diagnosis of PPCM (n = 10, all within 3 months postpartum), five healthy postpartum controls (HPC), and five healthy non-postpartum controls (HNPC), underwent 18FDG-PET-CT, CMR, and serum inflammatory proteomic profiling. PPCM patients had a median age of 34 years (interquartile range [IQR] 30.3–38.5, similar in control groups), and a median parity of 3 (IQR 1–4). PPCM patients presented with severe, symptomatic heart failure (all New York Heart Association functional class III/IV), reduced median left ventricular ejection fraction of 35.5% (IQR 18.1–37.9). PPCM and HPC groups showed higher myocardial and splenic 18FDG uptake compared to HNPC. On CMR, myocardial interstitial fibrosis (elevated T1 time, extracellular volume, and late gadolinium enhancement mass) was solely present in PPCM. Inflammatory profiling showed pro-inflammatory cytokine dysregulation in PPCM (elevated neutrophil-to-lymphocyte ratio, C-reactive protein, interleukin-6, tumour necrosis factor-α, chemokine (C-C motif) ligand 3, hepatocyte growth factor, chemokine (C-X-C motif) ligand 10 and colony-stimulating factor-1) compared to controls. Conclusions Patients with PPCM exhibited a dysregulated immune response, associated with early myocardial interstitial fibrosis and adverse cardiac remodelling. This highlights the importance of rapid initiation of guideline-directed medical therapy especially with drugs documented to have anti-fibrotic effects.
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Hoevelmann et al. (2025) conducted a case-control in Peripartum cardiomyopathy (n=20). Peripartum cardiomyopathy vs. Healthy postpartum and non-postpartum controls was evaluated on Myocardial interstitial fibrosis, 18FDG uptake, and inflammatory proteomic profiling. Patients with peripartum cardiomyopathy exhibited dysregulated pro-inflammatory immune responses, early myocardial interstitial fibrosis, and higher myocardial 18FDG uptake compared to healthy controls.
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