Objective To investigate serum cardiac troponin I, a sensitive marker of cardiac rnyocyte damage, in normal pregnancy and pregnancies complicated by hypertension with and without significant proteinuria.Design Prospective cross sectional study.Setting University hospital delivery suite.Sample Serum samples obtained from women in normal pregnancy and in pregnancies complicated by hypertension with and without significant proteinuria.Method Women with hypertension in pregnancy (at least two readings of systolic blood pressure > 140 mmHg and diastolic blood pressure > 90 mmHg) (n = 26) and norrnotensive women (n = 43) were included in the study. Serum cardiac troponin I was measured using Beckman Access immunoassay.Main outcome measure Serum cardiac troponin I level in the pregnancies complicated by hypertension (with and without significant proteinuria) compared with the levels measured in normotensive women.Results The median serum cardiac troponin I level in pregnancies complicated by hypertension was 0.11 8 ng/mL (n = 26) which was significantly greater than that measured in samples obtained from normotensive women in pregnancy (0.03 ng/n&; n = 43) (P < O@OOl). There were higher median serum cardiac troponin I levels in hypertensive women with sigdicant proteinuria (0.155 ng/mL; n = 6), compared with those without proteinuria (0.089 ng/nL; n = 20; P = 0.03).Conclusion Serum cardiac troponin I is elevated in women with hypertensive disorders of pregnancy indicating some degree of cardiac myofibrillary damage in these disorders.

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The objective of this study was to measure fetal cardiac troponin I in umbilical artery blood in relation to intrapartum events and umbilical artery pH. Umbilical artery blood samples were obtained after delivery from 110 infants and cardiac troponin I was measured. The onset of labor, mode of delivery, presence of meconium, and umbilical artery pH were examined in relation to cardiac troponin I. The median cardiac troponin I level was 0.03 ng/mL (range, 0.03 to 0.881 ng/mL). Neonates with a cardiac troponin I level above the normal range had a lower umbilical artery pH when compared with those neonates with a normal cardiac troponin I level (p = 0.005). No relationship between the following parameters and cardiac troponin I was observed: gestational age, parity, presence of labor, meconium staining, mode of delivery, birth weight, and Apgar scores. Fetal cardiac troponin I shows little variation at birth. Increased levels of cardiac troponin I are associated with a lower umbilical artery pH.

The use of continuous fetal heart rate (FHR) recordings to monitor fetal well-being during labor is standard clinical practice in developed countries. Little is known about the relationship, if any, that exists between these FHR abnormalities and the fetal cardiac musculature and function. The aim of this study was to investigate umbilical artery serum levels of cardiac troponin I, a sensitive and specific marker of myocardial necrosis, and N-terminal pro-brain natriuretic peptide (pro-BNP), a sensitive marker of left ventricular dysfunction, in relation to FHR abnormalities. Umbilical artery blood samples were taken from 27 cases immediately after delivery of the infant. There was evidence of significant FHR abnormalities in 11 of these cases (group 2) and the FHR recording was normal in 16 cases (group 1). The mean N-terminal pro-BNP level in umbilical artery serum in group 2 was 413 fmol/L (SEM = 85) and in group 1 was 223 fmol/L (SEM = 28)(p = 0.022). There was no significant difference observed in cardiac troponin I levels between the two groups. Umbilical artery serum N-terminal pro-BNP is elevated in association with fetal heart rate abnormality in the late stage of labor. This finding suggests that some degree of cardiac compromise accompanies FHR abnormality.

We performed a meta-analysis of published trials to determine the predictive value of cardiac troponin I (cTnI) and T (cTnT) levels for adverse events (death and myocardial infarction) in acute coronary syndrome without ST elevation (ACS). The accumulated odds ratio (OR) for adverse events (30 days) in ACS with elevated cTnI (n = 5,759) and cTnT (n = 5,483) was 4.9 (95% confidence interval, CI, 3.9–6.2) and 4.6 (95% CI 3.8–5.5), respectively. Trials that mandated timed serum sampling (6 or more hours after symptom onset) had an improved predictive value for elevated cTnI (n = 2,807, OR 8.8; 95% CI 5.9–13.2) and cTnT (n = 1,990, OR 8.5; 95% CI 5.9–12.5). In conclusion, cTnI and cTnT provide similar information in ACS. The risk of adverse events is 4-fold higher in patients with suspected ACS and elevated serum cTn. For patients with an elevated timed (6-hour) sample the risk is over 8-fold higher.