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Published on: January 27, 2023
Coagulation Profile in Neonates with Congenital Heart Disease: A Pilot Study
Paraskevi Papadogeorgou1, Serena Valsami2, Maria Boutsikou1
1Neonatal Department, Aretaieio Hospital, Medical School, National and Kapodistrian University of Athens, 115 28 Athens, Greece.
Congenital heart disease (CHD) in neonates shows moderate coagulation impairment, with prolonged prothrombin time and altered factor levels. Increased thrombogenicity is present early, highlighting the need for careful monitoring in these infants.
Area of Science:
- Neonatal Medicine
- Hematology
- Cardiology
Background:
- Congenital heart disease (CHD) is frequently associated with coagulation abnormalities, affecting patient morbidity and mortality.
- Previous studies have not established consistent hemostatic patterns in neonates with CHD due to population heterogeneity.
Purpose of the Study:
- To investigate the hemostatic profile in neonates with CHD.
- To assess the role of ADAMTS-13 (a disintegrin and metalloprotease with thrombospondin type-1 motives) in neonates with CHD.
- To compare these parameters with healthy, age-matched controls.
Main Methods:
- A cohort of 20 neonates with CHD and 18 healthy neonates were included.
- Hemostatic profiles, including prothrombin time, factor VII (FVII), factor VIII (FVIII), von Willebrand factor (VWF), ristocetin cofactor activity (Rcof), and ADAMTS-13 concentrations, were analyzed.
Main Results:
- Neonates with CHD exhibited significantly prolonged prothrombin time and decreased FVII levels compared to controls.
- Elevated FVIII, VWF, and Rcof levels were observed in the CHD group.
- ADAMTS-13 concentrations were lower in the CHD group, though not statistically significant.
Conclusions:
- The coagulation profile in neonates with CHD is moderately impaired early in the disease course.
- Despite impairments, increased thrombogenicity is evident and requires clinical attention.
- Developmental aspects of coagulation are apparent in this patient population, indicating a balanced yet variable hemostatic mechanism.
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