Key result
Neonatal hypoxic-ischemic encephalopathy is linked to ~3-fold higher cardiac troponin I levels.
Why the study?
Hypoxic-ischemic encephalopathy often affects myocardial function in newborns, but the relationship between cardiac biomarkers, myocardial function, and NOS3 gene polymorphism is not well defined.
Do elevated cTnI levels and NOS3 rs1808593 polymorphism correlate with impaired myocardial function and severity in newborns with hypoxic-ischemic encephalopathy?
Case-Control (n=50)
No
Do elevated cTnI levels and NOS3 rs1808593 polymorphism correlate with impaired myocardial function and severity in newborns with hypoxic-ischemic encephalopathy?
Elevated cTnI levels and impaired myocardial function on echocardiography are strongly associated with the severity of hypoxic-ischemic encephalopathy in newborns.
May indicate myocardial injury in HIE; leaves open whether cTnI aids prognosis or management.
Introduction: Hypoxic-ischemic encephalopathy (HIE) is a neonatal neurological disorder caused by reduced cerebral blood flow and oxygen supply, often affecting myocardial function. Objective: To evaluate cardiac troponin, I (cTnI) levels in newborns with HIE, correlate them with myocardial function, and analyze HIE association with nitric oxide synthase (NOS3) gene polymorphism. Methods: This study included 30 newborns with perinatal asphyxia and 20 healthy controls matched for gestational age and birth weight. All underwent history taking, clinical assessment, and cardiac evaluation. Serum cTnI was measured as a biomarker for myocardial injury. NOS3 (rs1808593) polymorphism was detected using real-time PCR (RT-qPCR). Echocardiography assessed systolic function via Shortening Fraction (SF%), Ejection Fraction (EF%), Mitral Annular Plane Systolic Excursion (MAPSE), and Tricuspid Annular Plane Systolic Excursion (TAPSE) using M-mode. Pulsed-wave Doppler of mitral valve inflow was performed to evaluate diastolic function (E/A ratio, Deceleration Time). Results: Serum cTnI was significantly higher in HIE cases (2.97 ± 1.74 ng/ml) than controls (1.01 ± 0.57 ng/ml, P<0.05). Levels were significantly elevated in Sarnat stage III (3.96 ± 1.95 ng/ml) compared to stage II (2.11 ± 0.91 ng/ml, P<0.05). The TT genotype of NOS3 rs1808593 occurred in 66.7% of HIE cases, showing a significant correlation with cTnI (P=0.024). Both systolic and diastolic functions were significantly impaired in HIE compared to controls (P<0.001). Stage III HIE showed significant cardiac impairment in SF%, EF%, TAPSE, MAPSE, and mitral valve deceleration time versus stage II (P<0.001, <0.001, 0.007, 0.003, respectively). Conclusion: Elevated cTnI levels, NOS3 rs1808593 polymorphism, and impaired myocardial function are strongly associated with HIE severity. Combined biomarker and echocardiographic assessment may provide valuable diagnostic and prognostic information for affected newborns.
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Marwa Yahia Qwema, Iman A.Ehsan Abdel Meguid, Abdelrahman Ahmed abdelrazek, Olfat G. Shaker, Samia Bekheet (2025) conducted a case-control in Hypoxic-Ischemic Encephalopathy (HIE) (n=50). Hypoxic-Ischemic Encephalopathy vs. Healthy newborns was evaluated on Serum cardiac troponin I (cTnI) levels (ng/ml) (p=<0.001). Newborns with hypoxic-ischemic encephalopathy had significantly higher serum cardiac troponin I levels compared to healthy controls (2.97 vs 1.01 ng/ml, p<0.001), which correlated with disease severity.
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