Among delivery hospitalizations complicated by peripartum cardiomyopathy; does co-presence of preeclampsia or eclampsia increase the odds of cardiogenic shock?

Introduction Peripartum cardiomyopathy (PPCM) is a potentially fatal pregnancy-associated cardiomyopathy with overlapping pathophysiology with preeclampsia and eclampsia, including shared angiogenic dysregulation, endothelial dysfunction, and systemic inflammation. Whether concurrent hypertensive disorders of pregnancy modify in-hospital outcomes in PPCM remains unknown. We examined the impact of concurrent preeclampsia/eclampsia on cardiogenic shock and other acute adverse outcomes in patients hospitalized with PPCM. Methods Using 2016-2022 National Inpatient Sample (NIS) databases we identified delivery hospitalizations complicated by PPCM with ICD-10-CM code 090.3.Concurrent preeclampsia/eclampsia was identified through co-documentation of codes 011.x, 014.x, or 015.x. Survey weighted logistic regression was performed adjusting for necessary comorbidities and confounders, taking into account the sampling style of NIS. The primary outcome of our study was cardiogenic shock, secondary outcomes included acute kidney injury (AKI), in-hospital mortality, cardiac arrest, acute respiratory failure, mechanical circulatory support (MCS), venous thromboembolism (VTE), and a composite adverse outcome. Results Among 1,293 unweighted PPCM delivery hospitalizations (≈5,114 nationally weighted), 553 (42.8%) had concurrent preeclampsia/eclampsia. Strikingly, concurrent preeclampsia/eclampsia was associated with significantly lower adjusted odds of cardiogenic shock (6.62% vs. 2.89%; aOR 0.35; 95% CI 0.18–0.67; p=0.002) and VTE (4.19% vs. 1.81%; aOR 0.43; 95% CI 0.20–0.93; p=0.033). Conversely, concurrent preeclampsia/eclampsia independently predicted higher odds of acute respiratory failure (28.92% vs. 40.33%; aOR 1.67; 95% CI 1.29–2.17; p<0.001) and a higher composite adverse outcome rate (38.24% vs. 49.37%; aOR 1.52; 95% CI 1.19–1.96; p=0.001). AKI was more prevalent in the concurrent group (9.73% vs. 14.47%) but the adjusted association was borderline (aOR 1.41; p=0.074). In-hospital mortality, cardiac arrest, and MCS use did not differ significantly. Conclusion In our nationally representative cohort of the United States, coexisting preeclampsia/eclampsia paradoxically conferred protection against cardiogenic shock in PPCM, the most catastrophic inhospital event, yet increased acute respiratory failure and composite morbidity. This challenges the presumption that preeclampsia worsens PPCM outcomes. The findings of our study signal for the potential adjustment of how we identify PPCM risk for hypertensive pregnancies. Our results also identify a need to develop hemodynamic monitoring and pulmonary edema prevention protocols informed by syndrome specific cardio-obstetric stratification.