Key result
Maternal myocardial strain impairment and glycemic variability in diabetic pregnancy linked to fetal cardiac remodeling.
Systematic Review
This systematic review supports reframing pregnancy with diabetes as an integrated maternal-placental-fetal cardiovascular syndrome, showing that maternal subclinical myocardial strain and CGM glycemic variability align with placental maladaptation and early fetal cardiac remodeling.
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Subtle maternal strain impairment signals fetal risk in diabetes; supports reframing as maternal-placental-fetal syndrome and integrated prospective studies.
Maternal diabetes has traditionally been approached as a metabolic disorder of pregnancy, yet its cardiovascular dimensions particularly on the maternal side remain insufficiently integrated into fetal risk assessment. Over the past decade, advances in myocardial deformation imaging, continuous glucose monitoring (CGM), and placental Doppler interrogation have expanded the capacity to interrogate maternal–fetal physiology, although these domains have largely progressed in parallel rather than in synthesis. In this systematic review, conducted in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 guidance, we identified and integrated evidence from 32 studies examining subclinical maternal myocardial dysfunction, CGM-derived glycemic exposure, placental–fetoplacental perfusion, and fetal cardiac structure and function in pregnancy with diabetes. Across heterogeneous populations and methodologies, a recurrent pattern emerged. Even in the absence of overt cardiomyopathy or reduced ejection fraction, subtle impairment in maternal myocardial strain, often accompanied by increased glycemic variability despite acceptable glycated hemoglobin (HbA1c) was consistently associated with altered placental perfusion and early fetal cardiac remodeling. Placental maladaptation appeared not merely secondary, but functionally intermediary, linking maternal cardiometabolic stress to fetal hemodynamic changes and myocardial adaptation. Notably, CGM-derived metrics, particularly glycemic variability and time outside target range, appeared more closely aligned with cardiovascular alterations than HbA1c alone. Fetal cardiac changes were frequently detectable before clinical compromise, suggesting that current surveillance strategies may underestimate early risk. While causality cannot be established, the convergence of findings across domains supports a more integrated interpretation. These observations support reframing pregnancy with diabetes as a maternal–placental–fetal cardiovascular syndrome rather than a purely metabolic disorder. This perspective may inform future risk stratification and underscores the need for longitudinal and mechanistically integrated studies.
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Suryawan et al. (2026) conducted a systematic review in Pregnancy with diabetes. Maternal diabetes and CGM-derived glycemic exposure (glycemic variability and time outside target range) was evaluated on Subclinical maternal myocardial dysfunction, altered placental–fetoplacental perfusion, and early fetal cardiac remodeling. Across 32 studies, subtle maternal myocardial strain impairment and CGM-derived glycemic variability in diabetic pregnancy were consistently associated with altered placental perfusion and early fetal cardiac remodeling.
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