Tongprasert Fuanglada, Srisupundit Kasemsri, Luewan Suchaya, Tongsong Theera
Maternal Fetal Medicine Unit, Department of Obstetrics and Gynecology, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
Prenat Diagn. 2014 Sep;34(9):864-9. doi: 10.1002/pd.4384. Epub 2014 Apr 30.
The objective of this study was to compare the levels of fetal serum cardiac troponin T (cTnT), representing cardiac injury, and N-terminal pro-B-type natriuretic peptide (nt-proBNP), representing cardiac volume overload, between fetuses affected and not affected by hemoglobin (Hb) Bart's disease, as well as between anemic and nonanemic fetuses.
One hundred fourteen pregnancies at risk for fetal Hb Bart's disease scheduled for cordocentesis at 18 to 22 weeks were recruited into the study. Fetal blood was collected to test for cTnT, nt-proBNP and Hb levels as well as Hb typing.
Serum nt-proBNP was significantly higher in Hb Bart's fetuses (24 cases) than in unaffected fetuses (63 cases), whereas cTnT was significantly lower in the affected group than in the unaffected group. The serum nt-proBNP levels significantly increased with the degree of fetal anemia; cTnT levels decreased in fetuses with high degree of anemia.
At mid-pregnancy, nt-proBNP was significantly higher in fetuses with Hb Bart's disease than in nonanemic fetuses; cTnT was significantly lower in anemic than in normal fetuses. This study suggests that cardiomegaly from fetal anemia in early gestation is not associated with fetal cardiac injury or myocardial dysfunction but presents as cardiac volume overload from a compensatory process to maintain adequate tissue oxygenation.
本研究的目的是比较受血红蛋白（Hb）Bart病影响和未受影响的胎儿之间，以及贫血和非贫血胎儿之间，代表心脏损伤的胎儿血清心肌肌钙蛋白T（cTnT）水平和代表心脏容量超负荷的N末端B型利钠肽原（nt-proBNP）水平。
招募了114例计划在18至22周进行脐带穿刺术的有胎儿Hb Bart病风险的孕妇进入研究。采集胎儿血液以检测cTnT、nt-proBNP和Hb水平以及Hb分型。
Hb Bart病胎儿（24例）的血清nt-proBNP显著高于未受影响的胎儿（63例），而受影响组的cTnT显著低于未受影响组。血清nt-proBNP水平随胎儿贫血程度显著升高；高度贫血胎儿的cTnT水平降低。
在妊娠中期，患有Hb Bart病的胎儿的nt-proBNP显著高于非贫血胎儿；贫血胎儿的cTnT显著低于正常胎儿。本研究表明，妊娠早期胎儿贫血引起的心脏肥大与胎儿心脏损伤或心肌功能障碍无关，而是表现为一种代偿过程导致的心脏容量超负荷，以维持足够的组织氧合。
