Cardiac Troponin “T” in Neonates with Severe and Moderate Persistent Pulmonary Hypertension
Shaimaa Yakoot Abd Elatif Yousif;
Abstract
Persistent pulmonary hypertension of the newborn (PPHN), a major clinical problem in the neonatal intensive care unit, can contribute significantly to morbidity and mortality in both term and preterm infants. (Steinhorn and Farrow, 2007)
PPHN induced circulatory failure further impairs oxygen delivery to the tissues and contributes to significant mortality and morbidity in newborn infants with PPHN. (Tourneux et al, 2008)
A comprehensive echocardiographic examination is an integral element of the initial evaluation of newborns with PPHN, both in order to exclude structural congenital heart disease, and to assess cardiac function. (Fraisse et al, 2004)
Cardiac troponins (cTnT) are highly specific cardiac markers, extremely sensitive and valuable in diagnostics of myocardial damage. (Agzew, 2009)
The aim of current study was to evaluate myocardial injury in moderate and severe persistent pulmonary hypertension of newborn (PPHN) in neonates using Echocardiography and measuring serum cardiac Troponin T (cTnT) levels in those patients.
This cross sectional study was carried out in the neonatal intensive care units (NICU) of Pediatrics department, Ain Shams University hospitals in the period from October 2012 to April 2014.
The study included 2 groups: Group I (gpI) included 30 full term (≥37wks) neonates with PPHN; they were 24 (80%) males and 6 (20%) females with a mean gestational age 37.63wk ± 1.05 days and Group II (gpII) included 30 apparently healthy age and sex matched neonates that served as a control group. They were 24 (80%) males and 6 (20%) females with a mean gestational age 37.867± 0.67 days.
The diagnosis of PPHN was based on the echocardiographic evidence of persistent pulmonary hypertension (right-to-left or bidirectional shunt shunting of blood across the ductus arteriosus and/or the foramen ovale) in newborns(Bassler et al, 2010); clinically postnatal period of cyanosis where the level of hypoxia is disproportionate to the degree of respiratory distress or respiratory distress which often with respiratory failure and the need for high ventilator pressures and increase oxygen requirements.(Evans et al, 1997)
Neonates with structural congenital heart diseases, primary parenchymal lung disease, sepsis and genetic syndrome or inborn error of metabolism were excluded from the study.
All gpI were subdivided into 2 groups: patients with moderate PPHN 56.4% and patients with severe PPHN 43.33% according estimated PAP, direction of shunting, orientation of ventricular septum and systolic function of the left ventricle.
All newborns included in this study were subjected to Fulldetailed history including: Perinatal history (perinatal asphyxia or hypoxia, maternal drug intake and maternal illness), Antenatal history (maternal chronic illnesses as DM and hypertension, history of maternal drug intake, maternal Parity and gravidity, history of premature rupture of membrane and mode of delivery), Natal history (APGAR 1 &5min, birth weight, gestational age and meconium staining of amniotic fluid or meconium in the trachea), Postnatal history (NICU admission, duration and management).
Detailed clinical assessment including: Anthropometric measures assessment (weight,length and body surface area), Gestational age assessment (the new Ballard scoring system),Vital signs assessment (respiratory rate, heart rate and mean blood pressure)and Systemicexamination (respiratory system, cardiovascular system and neurological examination).
Laboratory investigation:ABG (by the AVL OMNI 6 modulator system analyzer),CBC (by the Sysmex SF-3000 auto-analyzer system), CRP (by latex agglutination using BioMed-CRP latex reagent), and cTnT levels(by electrochemilunescence immunoassay (ECLIA).
Radiological investigation: Chest X-ray (postro-anterior view),M mode, 2D, colored, continuous wave, pulsed Doppler echocardiography(Vivid i; General Electric Medical Systems, Horten, Norway): For assessment of cardiac chamber size, pulmonary pressure, valvular status, cardiac systolic (EF). Right and Left ventricular functions were also assessed by Tissue Doppler imaging (TDI) (Sm, Em, Am, Em\Am), (ST, ET, AT, ET\AT),PEP/ET, Tei index, Strain and Strain rate.
The results of current study showed that, a significant increase was found in history of maternal DM, Hypertension,and presence of MAS in patient group (gpI)than controls (gpII) (P=0.012). Also, a highly significant increase was found in patients (gpI) delivered by CS than controls (gpII) (P= 0.009).
A highly significant decrease was found in Apgar score at 1min and 5min in gpI than gpII. (P=0.0009 and0.0003).
Moreover, comparison of vital signs in gpI and gpII revealed that a highly significant decrease was found in mean Blood pressure (Bp) values anda highly significant increase was found in mean Heart rate (HR) and mean Respiratory rate (RR)(P=0.0004, 0.000 and 0.000 respectively).
PPHN induced circulatory failure further impairs oxygen delivery to the tissues and contributes to significant mortality and morbidity in newborn infants with PPHN. (Tourneux et al, 2008)
A comprehensive echocardiographic examination is an integral element of the initial evaluation of newborns with PPHN, both in order to exclude structural congenital heart disease, and to assess cardiac function. (Fraisse et al, 2004)
Cardiac troponins (cTnT) are highly specific cardiac markers, extremely sensitive and valuable in diagnostics of myocardial damage. (Agzew, 2009)
The aim of current study was to evaluate myocardial injury in moderate and severe persistent pulmonary hypertension of newborn (PPHN) in neonates using Echocardiography and measuring serum cardiac Troponin T (cTnT) levels in those patients.
This cross sectional study was carried out in the neonatal intensive care units (NICU) of Pediatrics department, Ain Shams University hospitals in the period from October 2012 to April 2014.
The study included 2 groups: Group I (gpI) included 30 full term (≥37wks) neonates with PPHN; they were 24 (80%) males and 6 (20%) females with a mean gestational age 37.63wk ± 1.05 days and Group II (gpII) included 30 apparently healthy age and sex matched neonates that served as a control group. They were 24 (80%) males and 6 (20%) females with a mean gestational age 37.867± 0.67 days.
The diagnosis of PPHN was based on the echocardiographic evidence of persistent pulmonary hypertension (right-to-left or bidirectional shunt shunting of blood across the ductus arteriosus and/or the foramen ovale) in newborns(Bassler et al, 2010); clinically postnatal period of cyanosis where the level of hypoxia is disproportionate to the degree of respiratory distress or respiratory distress which often with respiratory failure and the need for high ventilator pressures and increase oxygen requirements.(Evans et al, 1997)
Neonates with structural congenital heart diseases, primary parenchymal lung disease, sepsis and genetic syndrome or inborn error of metabolism were excluded from the study.
All gpI were subdivided into 2 groups: patients with moderate PPHN 56.4% and patients with severe PPHN 43.33% according estimated PAP, direction of shunting, orientation of ventricular septum and systolic function of the left ventricle.
All newborns included in this study were subjected to Fulldetailed history including: Perinatal history (perinatal asphyxia or hypoxia, maternal drug intake and maternal illness), Antenatal history (maternal chronic illnesses as DM and hypertension, history of maternal drug intake, maternal Parity and gravidity, history of premature rupture of membrane and mode of delivery), Natal history (APGAR 1 &5min, birth weight, gestational age and meconium staining of amniotic fluid or meconium in the trachea), Postnatal history (NICU admission, duration and management).
Detailed clinical assessment including: Anthropometric measures assessment (weight,length and body surface area), Gestational age assessment (the new Ballard scoring system),Vital signs assessment (respiratory rate, heart rate and mean blood pressure)and Systemicexamination (respiratory system, cardiovascular system and neurological examination).
Laboratory investigation:ABG (by the AVL OMNI 6 modulator system analyzer),CBC (by the Sysmex SF-3000 auto-analyzer system), CRP (by latex agglutination using BioMed-CRP latex reagent), and cTnT levels(by electrochemilunescence immunoassay (ECLIA).
Radiological investigation: Chest X-ray (postro-anterior view),M mode, 2D, colored, continuous wave, pulsed Doppler echocardiography(Vivid i; General Electric Medical Systems, Horten, Norway): For assessment of cardiac chamber size, pulmonary pressure, valvular status, cardiac systolic (EF). Right and Left ventricular functions were also assessed by Tissue Doppler imaging (TDI) (Sm, Em, Am, Em\Am), (ST, ET, AT, ET\AT),PEP/ET, Tei index, Strain and Strain rate.
The results of current study showed that, a significant increase was found in history of maternal DM, Hypertension,and presence of MAS in patient group (gpI)than controls (gpII) (P=0.012). Also, a highly significant increase was found in patients (gpI) delivered by CS than controls (gpII) (P= 0.009).
A highly significant decrease was found in Apgar score at 1min and 5min in gpI than gpII. (P=0.0009 and0.0003).
Moreover, comparison of vital signs in gpI and gpII revealed that a highly significant decrease was found in mean Blood pressure (Bp) values anda highly significant increase was found in mean Heart rate (HR) and mean Respiratory rate (RR)(P=0.0004, 0.000 and 0.000 respectively).
Other data
| Title | Cardiac Troponin “T” in Neonates with Severe and Moderate Persistent Pulmonary Hypertension | Other Titles | مستوى تروبونين القلب "T" فى حديثى الولاده الذين يعانون من ارتفاع شديد الى متوسط فى ضغط الدم الرئوى المستمر | Authors | Shaimaa Yakoot Abd Elatif Yousif | Issue Date | 2014 |
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