Balloon dilation and surgical valvotomy comparison in non-critical congenital aortic valve stenosis.

Percutaneous balloon aortic valvoplasty (BAV) and surgical aortic valvotomy (SAV) are palliative procedures in patients with non-critical congenital valve stenosis. The aim of the study was to evaluate long-term BAV and SAV results after up to 24 years of follow-up. From 1987 to 2013, 74 consecutive interventions were performed in patients with aortic stenosis, and 62 were included in the study (39 BAVs and 23 SAVs). Age of BAV patients was 1.3 months to 17 years, and of SAV patients 1.2 months to 15 years. Although BAV patients were older, there was no difference between groups according to sex, valve function/morphology, and early/late follow-up results, with exception to hospitalization period. Significant pressure gradient reduction and aortic regurgitation increment were registered after procedures. Three patients did not survive early period after surgery. Follow-up period was 7.0 ± 5.4 and 9.0 ± 8.0 years after BAV and SAV, respectively (p = 0.242). Follow-up pressure gradient rose only in the BAV group, and was emphasized after 10-year-follow-up (p = 0.020). Significant aortic insufficiency progression was registered after 15 years of follow-up in both groups (p = 0.007 and p = 0.009, respectively). Mean reintervention-free survival was 12.0 years in the BAV and 14.5 years in the SAV group (p = 0.733), and mean survival without aortic valve replacement was 15.2 and 17.4 years, respectively (p = 0.877). BAV and SAV in patients with congenital aortic stenosis are very comparable in both early and late follow-up results.

Predictive value of biochemical, echocardiographic and electrocardiographic markers in non-surviving and surviving asphyxiated full-term newborns.

Severe perinatal asphyxia can cause multiple organ dysfunction and early neonatal mortality. This prospective study was conducted at the Regional University Hospital Neonatology Center in Serbia. The aim of this study was to compare fullterm asphyxiated newborn infants (n=55) with (n=13) and without (n=42) mortality outcome and healthy full-term newborns (n=36) regarding biochemical (cardiac troponin I, creatine kinase (total and MB fraction) and C-reactive protein), echocardiographic (ejection fraction, fractional shortening, mitral regurgitation, significant tricuspid regurgitation, and patent ductus arteriosus) and electrocardiographic (ST segment elevation/depression, T wave inversion and corrected QT interval) markers of myocardial damage in order to assess their predictive value in the clinical outcome. Statistically significant differences in the majority of the tested markers of ischemic myocardial lesion were found between perinatal asphyxia survivors and the control group. However, among the biochemical indicators, only the level of cardiac troponin I was significantly higher in the group of neonates who died compared to the group of asphyxiated neonates who survived (p: 0.000), with an area under the receiver operating characteristic curve of 0.821 and cutoff value for lethal outcome of 0.135 µg/L (sensitivity 0.85; specificity 0.69). In addition, differences in ejection fraction, fractional shortening and significant tricuspid regurgitation (≥2+) were also found between the two subgroups of asphyxiated newborns. Cardiac troponin I is the most sensitive ischemic myocardial lesion biochemical marker in the prediction of early mortality in perinatal asphyxia patients.

The role of biochemical markers as early indicators of cardiac damage and prognostic parameters of perinatal asphyxia.

BACKGROUND/AIM: In recent years, the focus of interest of the scientific community is the application of heart markers as early indicators and prognostic parameters of perinatal asphyxia (PA). The aim of this study was to evaluate the significance of clinical application of heart markers in term newborns with perinatal asphyxia. METHODS: During a 3-year period we analyzed 91 full-term newborns (55 with and 36 without perinatal asphyxia). In all the subjects within the first 24-48 h after birth, we simultaneously determined serum concentrations of cardiac troponin I, brain natriuretic peptide, MB fraction of creatine kinase (CK-MB) and C-reactive protein. RESULTS: In the group of full-term neonates with PA significantly higher levels of cardiac tropon-inI (p = 0.000), CK-MB fraction (p = 0.000), brain natriuretic peptide (p = 0.003) and C-reactive protein (p = 0.017) were found, compared to the group of healthy full-term newborns. In merged group (n = 91) cardiac troponin I level correlated with the fifth minute Apgar score (r = -0.637, p = 0.000) and the serum lactate concentration in the first 12h after birth (r = 0.529, p = 0.000). Early increase in cardiac troponin I > 0.135 microg/L predicted the risk of death with the sensitivity of 84.6% and specificity of 85.9%, while the increase in CK-MB fraction, brain natriuretic peptide and C-reactive protein did not have a predictive value with respect to a mortality outcome. CONCLUSION: Among the tested cardiac markers, cardiac troponin I is the most sensitive and the only reliable early predictor of mortality in full-term neonates with perinatal asphyxia.

Risk factors for thrombosis in Serbian children.

Venous and arterial thromboses are increasingly encountered in the pediatric population. We present results of a case-control study of inherited and acquired risk factors for thrombosis in 129 pediatric patients from the first day of life to 18 years. The aims of study were to determine the importance of thrombophilic risk factors and comorbidity as a cause of thrombosis in children. Single thrombophilic risk factor was found in 24.4% (n = 21), whereas combined thrombophilic factors were found in 15.1% (n = 13) patients. A total of 87.2% of the children had recognized thrombophilic risk factors for thrombosis and/or additional comorbid risk factors. The single independent risk factors for thrombosis were mutation of factor V Leiden (P = 0.021), lupus anticoagulant antibodies (P = 0.028), and comorbidity (P = 0.000). Mutation of factor V Leiden [odds ratio (OR), 6.2 (95% confidence interval, CI 1.1-38.1, P = 0.048] was found to be a risk factor for venous thrombosis. Lupus anticoagulant antibodies were related to both venous (P = 0.008) and arterial thrombosis (P = 0.016). The frequency of inherited thrombophilic factors were the same in neonates and adolescents (23%). The prothrombotic gene mutations were present in 18.6% (n = 8) of asymptomatic children. Our study confirms that thrombosis in children is a multifactorial disorder, and associated most with the underlying medical disease (comorbidity) for vein thrombosis [OR, 18.6 (95% CI 3.7-93.4), P = 0.000] and for arterial thrombosis [OR, 10.5 (95% CI 2.2-49.9) P = 0.003]. Inherited thrombophilic disorders contributed to the development of thrombosis in children.