Left ventricular mass in newborn with perinatal asphxia: Assessment of allometric relations and impact of birth weight

Abstract

BACKGROUND

Utero-placental insufficiency seen in perinatal asphyxia may adversely affect left ventricular (LV) geometry.

AIM

To document the LV mass values in perinatal asphyxia and to elicit associated factors.

METHODS

This was a cross-sectional study conducted in a tertiary health facility among newborns with perinatal asphyxia. Echocardiography was used to compare the LV mass of 84 new-borns with perinatal asphyxia with the LV mass of 48 new-borns without perinatal asphyxia matched for age. The data was analysed using SPSS version 25 (IBM, United States).

RESULTS

The mean LV mass (7.9 ± 2.3 g) of perinatal asphyxia is lower than control (10.1 ± 0.7 g) P = 0.001. New-borns with severe perinatal asphyxia had the lowest mean LV mass (7.1 ± 1.5), while the moderate group had the highest (8.8 ± 2.5), with the Analysis of Variance (ANOVA) result of F = 1.26 and P = 0.289. The mean LV mass was highest on day 1 (8.1 ± 2.5) and slightly lower on days 2 and 3 (both 7.7 ± 1.9 and 7.7 ± 2.0, respectively). Though ANOVA result (F = 2.47, P = 0.7282) indicates no significant relationship between the age of the newborn and LV mass, a weak positive correlation was observed between LV mass and gestational age which is statistically significant (r = 0.269 P = 0.028). A moderate positive correlation between the LV mass and birth weight of newborn was observed. This is statistically significant (r = 0.610, P = 0.001). There was weak negative correlation (r = -0.10, P = 0.752), between LV mass and age of the newborn without perinatal asphyxia but a moderate positive correlation (r = 0.69, P = 0.015) was observed, between LV mass and weight in non-asphyxiated newborn.

CONCLUSION

This study showed that the LV mass in perinatal asphyxia was significantly lower than those without asphyxia. There was a direct correlation between LV mass and birth weight of neonates with perinatal asphyxia. Early detection of the cardiac disease, appropriate management and sustained reduction of birth asphyxia, and improved intra-partum quality of care are key.

Key Words: Left ventricular mass; Newborn; Perinatal asphyxia; Birthweight; Left ventricular

Core Tip: Perinatal asphyxia may cause possible insults from hypoxic ischaemic damage to the myocardium especially of the left ventricle. This changes may affect left ventricular contractility. Hypoxic- ischemic- damage of the cardiac muscles may also cause increase in peripheral vascular resistance, leading to blood flow compromise to the left ventricle.

INTRODUCTION

The centre for disease control defined birth asphyxia as a failure to initiate and sustain spontaneous respiration at birth[1]. Perinatal asphyxia is clinical scenario with a fetal sequela if not appropriately managed[2,3]. About 3% of 120 million new-borns from developing countries develop birth asphyxia[4]. Previous study has assessed the association between left ventricular (LV) mass, perfusion and serum cardiac troponin in infants with severe perinatal asphyxia[5]. They noted increases in serum cardiac troponin with a markedly low coronary flow and reduced LV mass and LV output Gebauer et al[6] also documented that in newborn with severe asphyxia, the LV output was reduced to 67% of the usual post-hypothermic levels[6]. Hypoxic- ischemic-induced increases in peripheral vascular resistance, blood flow compromise to the left ventricle may explain these changes noted in reduced LV output.

During fetal circulation, there is change from a high-resistance to a low-resistance pulmonary circulation. These changes in the circulatory system, including the switch from the right to the left heart dominance, is enhanced by a reduction in thromboxanes, increase in secretion of nitric oxide which lowers the peripheral vascular resistance, with a resultant enhancement of the LV function[6]. Changes accompanying the first respiratory response at birth is crucial for a smooth transition of the fetus to neonatal circulation. Certain diseases such as perinatal asphyxia, which may lead to utero-placental insufficiency may adversely affect LV geometry. This stems from the fact that the left ventricle is the main ventricle that initiates a systemic perfusion after birth. Perinatal asphyxia leads to a compromise in the LV and coronary artery blood flow[6].

It is pertinent to note that the left ventricle is the harbinger and bears all the brunt in perinatal asphyxia. The use of inotropes and drugs that enhance perfusion may be valuable in the management of such babies.

The estimation of the LV mass in babies with perinatal asphyxia may help in the diagnosis of LV hypertrophy. This is important for clinical care in children with perinatal asphyxia as it will help the clinician to initiate early intervention when the values are noted to be compromised[7].

LV mass is very important issue in perinatal asphyxia because an altered LV mass is a harbinger for an underlying cardiac insults. This may predict higher odds for cardiovascular morbidity and mortality[7]. Perinatal asphyxia may cause a direct LV dysfunction, which may influence clinical outcomes[7-9]. Perinatal asphyxia is a major cause of hypoxia which activates the pentose phosphate pathway, giving rise to and lactic acidosis, redistribution of blood to vital organs with attendant myocardial ischemia and injury the LV musculatures[8,9]. The myocardial damage which causes hypoxic insult on myocardial cells may also activate an increase in cardiac troponin, an important biomarker for cell death The damaged cardiac muscles may lead to reduced stroke volume, impaired LV contractility and decreased LV output[9-12]. Reduced LV output reduces blood flow to vital organs such as liver, kidneys and the gut, causing multi-organ dyssfunction, a serious sequel of perinatal asphyxia[9,10].

The specific clinical gap the study aims to fill included the fact that there is a dearth of established normative reference values for LV mass index using appropriate pediatric scales[13]. It is crucial to note that while the cardiovascular effects of asphyxia are well-documented, a persistent gap such as absence of reliable pediatric reference data coupled with the fact that it is not known if specific LV mass parameters in perinatal asphyxia can predict long-term cardiovascular outcomes accurately, which may help to stratify risk and guide therapeutic interventions[13]. Furthermore, few studies provide normative LVM values or examine allometric relationships in asphyxiated neonates[13].

This study elicited LV mass values in perinatal asphyxia by echocardiography. The importance of estimation of the LV mass in perinatal asphyxia cannot be overemphasized. Studies on LV hypertrophy among infants with hypertension, congenital heart defect, acute kidney injury abound but only very few studies have elicited the pattern and distribution of LV mass values in babies with perinatal asphyxia. This is the very first work on LV mass in perinatal asphyxia published in this vicinity. This work is therefore aimed to document the mean LV mass of perinatal asphyxia and to correlate it with the severity of perinatal asphyxia.

MATERIALS AND METHODS

Study area and study population

This study was conducted in Enugu State University Teaching Hospital, Enugu, Nigeria using a total of 84 new-borns with perinatal asphyxia. The hospital provides specialized services and serves as a referral centre for the management of new-borns with various kinds of disease and also reviews new-borns who came for follow-up after being managed for any neonatal illness. Newborn babies with perinatal asphyxia, aged first day of life to third day of life and who fulfilled the inclusion criteria were consecutively recruited until the required sample size was reached. Perinatal asphyxia aged first day of life to third day of life who had only birth asphyxia without any other systemic illnesses were included in the study. Newborn babies with any renal disease or inborn errors of metabolism or those born to mothers with any chronic illnesses, newborn babies who had echocardiographic diagnosis of congenital cardiac defects were also excluded from the study. Besides, new-born with suspected raised blood pressure were also excluded. The control is made of 48 new-borns matched for age and gender who had no birth asphyxia.

Study design and sampling

This was a hospital-based cross-sectional study of asphyxiated neonates at Enugu State University Teaching Hospital, Enugu, conducted between June and December 2024. The clinical history of all the newborn babies admitted in the hospital of study was reviewed. Information on maternal age, gestational age, baby’s weight and mode of delivery was documented.

Study instrument

Newborn babies who fulfilled the inclusion criteria had echocardiographic ultrasound Imaging. The echocardiographic images were viewed after the newborn baby was supported with a soft bedding to enable the baby stay in the left lateral position. All the images and the M–mode recording were derived from the 2-dimensional images. The study was done by the principal investigator, so inter-observer variability testing was not necessary[14,15]. Anthropometric measurements were also documented. Weight was measured in kilograms using a standard weighing scale. The research was done over a 5-month period, from July to November 2024.

Apgar score and grading of severity of perinatal asphyxia

Each component is scored 0, 1, or 2[16]. The score is assigned at 1 minute and 5 minutes after birth in all neonates with expanded recording at 5 minutes’ intervals up to 20 minutes for infants who scored 7 or less at 5 minutes, and in those requiring resuscitation as a method for monitoring response. Studies revealed that the 5-minute score correlates best with degree of asphyxia and is the most predictive in terms of adverse outcomes[16]. Scores greater than 7 are considered reassuring; scores of 6 to 7 are mild asphyxia; scores of 4 to 5 are moderate asphyxia; and scores of 0 to 3 are severe asphyxia[16].

Modified Sarnat score in the assessment of neonatal encephalopathy

The Sarnat score is an essential clinical tool used in the evaluation and assessment of the severity of neonatal encephalopathy following perinatal asphyxia[17]. It provides a standardized approach to systematic neurological examination and documentation of pertinent neurological findings[17]. It uses 6 clinical parameters to classify encephalopathy as mild (stage 1), moderate (stage 2), or severe (stage 3)[17]. There are four neurological items, one autonomic nervous system item, and one item related to the presence or absence of seizure. The strength of this score is that it provides a clear picture of the infant’s neurological status. It has been widely accepted both nationally and internationally[17].

The original paper on the Sarnat score was based on 21 term newborns suffering from perinatal asphyxia. Stage 1 has a duration of less than 24 hours and consists of hyperalertness with a normal moro, normal stretch reflexes, normal sympathetic effects and a normal electroencephalogram (EEG)[17]. Stage 2 infants are obtunded, hypotonic, with strong distal flexion, and multifocal seizures. Persistence of stage 2 for more than 7 days or failure of the EEG to revert to normal was associated with later neurological impairment or death. Stage 3 infants are stuporous, flaccid, with suppressed brain stem reflexes, depressed autonomic functions[17].

Sample size determination

The desired sample size was calculated using Cochran formula[18] to yield a representative sample for proportions of large population as shown below: n = Z²(p)(q)/e². Where n = sample size, Z = the standard normal coefficient, usually set at 1.96 (corresponds to 95% confidence interval). P = prevalence of study in question = (prevalence of asphyxia from recent ESUTH SCBU data) = 28.6% = 0.29. q = (1 - p) = (1 - 0.29) = 0.71. e² = desired level of precision (standard error) = 5% = (0.05)². Therefore, n = (1.96)² × 0.29 × 0.71/ (0.05)². n = 316. To correct the sample size when the study population is less than 10000 (i.e., finite population) is as shown below: Nf = n/[1 + (n/N)][19]. Where nf = final sample size. n = sample size when study population is greater than 10000; n = 316. N = study population size, which is 100 (recent ESUTH SCBU data). Therefore, nf = 316/[1 + (316/100)] = 75.96 = 76. An attrition of 10% was added to give a total sample size of 76 + 7.6 = 83.6 = 84. Hence a minimum sample size of 84 was judged to have sufficient power to address the hypotheses of the study. However, we used 48 new-borns without birth asphyxia as control.

Ethical considerations

This was obtained from the Ethics and Research Committee of the Enugu State University Teaching Hospital, Enugu before the commencement of the study. In addition, an informed written consent was also obtained from the parents/caregivers of the newborn babies with birth asphyxia. The code number for the ethical clearance is ESUTHP/C-MAC/RA/034/201.

Echocardiographic determination of LV mass

Given the importance of LVM in newborns with perinatal asphyxia, it is crucial to have a reliable method to avoid conflicting results[20,21]. Left ventricular mass was estimated in this study by the use of the E2-model portable Sonoscape Medical Corp 2019 Cardiac Ultrasound Imaging[22]. This was measured in end-diastole by means of linear measurements of the interventricular septum, LV wall thickness, and LV internal diameter derived M-mode[23-26]. The Devereux formula, which assumes an ellipsoid shape of the LV in the ratio of 1:2 was used[26]. The current European Association of Cardiovascular Imaging Chamber Quantification Guidelines was applied in the measurement of LV mass in this study. If M-mode in a parasternal long axis view proved difficult based on the baby’s position or in a restless child, a short axis view was used. In this view, the cursor cuts through the mid-papillary level at end-diastole[26]. Echocardiography was used to compare the LV mass of 84 new-borns with perinatal asphyxia with the LV mass of 48 new-borns without perinatal asphyxia matched for age.

Statistical analysis

The data was analysed using SPSS v25 (IBM, United States). Frequencies, percentages, mean and standard deviation was used to summarize the data. Pearson’s correlation was used to assess the relationship between LV mass with neonatal and maternal characteristics. The Analysis of Variance (ANOVA) was used to assess the difference in mean LV mass and severity of asphyxia and the distribution of LV mass and socio-economic class. The independent t-test was used to assess the mean LV mass and mode of delivery. A P value less than 0.05 was determined as statistically significant for all interferential analyses.

RESULTS

Table 1 showed the socio-demographic variables of newborn with perinatal asphyxia. The highest age of presentation is among neonates who are 1 day old and the modal maternal age is among mothers who were between the age of 25-34 years and the modal gestational age is among mothers who are between 37-40 weeks’ gestation. Tables 2 and 3 shows that the mean LV mass (7.9 ± 2.3 g) of perinatal asphyxia is lower than control (10.1 ± 0.7 g) P = 0.001. Fifty-three (63%) of the perinatal asphyxia had left ventricular mass lower than that obtained in normal babies (10.1 ± 0.7 g). The table above shows the difference in mean LV mass between male and female in both groups is not statistically significant. Table 4 showed the comparison of mean LV mass by severity of asphyxia. Using the Sanat criteria, the severe group had the lowest mean LV mass (7.1 ± 1.5), while the moderate group had the highest (8.8 ± 2.5), with an ANOVA result of F = 1.26 and P = 0.289. The mean LV mass was highest on day 1 (8.1 ± 2.5) and slightly lower on days 2 and 3 (both 7.7 ± 1.9 and 7.7 ± 2.0, respectively). Though ANOVA result (F = 2.47, P = 0.7282) indicates no significant relationship between the age of the newborn and LV mass. Tables 5 and 6 shows the mean LV mass was 7.6 ± 2.2 in the upper class, 8.1 ± 2.5 in the middle class, and 7.8 ± 2.1 in the lower class. The ANOVA result (F = 0.10, P = 0.905) confirms no significant association between social class and LV mass. The mean LV mass for spontaneous vaginal delivery (SVD) was 7.7 ± 2.4, while for caesarean section (CS), it was slightly higher at 8.1 ± 2.2. The t-test result (-0.86, P = 0.391) indicates that the difference is not statistically significant.

Table 1 Socio-demographic variables of the new-borns with perinatal asphyxia.

Variables	n	(%)
Child’s age in days
1	38	45.2
2	34	40.5
3	12	14.3
Gender
Male	46	54.8
Female	38	45.2
Maternal age (years)
< 25	9	10.7
25-34	60	71.4
35-44	15	17.9
Gestational age (weeks)
37-40	76	90.5
40-42	8	9.5
Social class
Upper	5	5.9
Middle	34	40.5
Lower	45	53.6

Table 2 Mean left ventricular mass and gender comparison between perinatal asphyxia with those without perinatal asphyxia.

Comparison of LV mass	Asphyxia	Control
Mean	7.9	10.1
SD	2.3	0.7
t-test (P value)	6.9 (0.001)a

^aP < 0.05.

LV: Left ventricular.

Table 3 Mean left ventricular mass and gender comparison between perinatal asphyxia with those without perinatal asphyxia.

Comparison of LV mass by gender	Male	Female	t-test (P value) (95%CI)
With asphyxia	8.4 ± 2.4	7.5 ± 2.1	1.57 (0.120)
Without asphyxia	9.4 ± 1.4	9.9 ± 0.6	1.17 (0.520)

LV: Left ventricular.

Table 4 Comparison of age of new-born and mean left ventricular mass by severity of asphyxia.

Severity of asphyxia	LV mass, mean ± SD (95%CI)	ANOVA
Severity by Sanat
Mild	7.8 ± 2.3	F = 1.26, P = 0.289
Moderate	8.8 ± 2.5
Severe	7.1 ± 1.5

ANOVA: Analysis of Variance; LV: Left ventricular.

Table 5 Comparison of age of new-born and mean left ventricular mass by severity of asphyxia.

Age of newborn (days)	LV mass, mean ± SD, (95%CI)	ANOVA
1	8.1 ± 2.5	F = 2.47, P = 0.7282
2	7.7 ± 1.9
3	7.7 ± 2.0

ANOVA: Analysis of Variance; LV: Left ventricular.

Table 6 Comparison of left ventricular mass by socioeconomic class.

Social class	LV mass, mean ± SD (95%CI)	ANOVA
Upper	7.6 ± 2.2	F = 0.10, P = 0.905
Middle	8.1 ± 2.5
Lower	7.8 ± 2.1
Mode of delivery
SVD	7.7 ± 2.4
CS	8.1 ± 2.2
t-test (P value)	-0.86 (0.391)

ANOVA: Analysis of Variance; SVD: Spontaneous vaginal delivery; CS: Caesarean section; LV: Left ventricular.

Figure 1A shows scatter diagram (Pearson correlation) between LV mass and gestational age. A weak positive correlation (r = 0.269, P = 0.028) was observed, which is statistically significant. Figure 1B shows scatter diagram (Pearson correlation) between LV mass and maternal age. There is a weak negative correlation between LV mass and maternal age, though no significant correlation was observed (r = -0.058, P = 0.64). However, 7 (8.3%) of the perinatal asphyxia whose LV mass were below that seen in control (10.1 ± 0.7 g), were mainly born to mothers less than 25 years of age, while 33 (39.3%) of the perinatal asphyxia whose LV mass were below that seen in control (10.1 ± 0.7 g), were mainly born to mothers aged 25-34 years and 12 (14.3%) of the perinatal asphyxia whose LV mass were below that seen in control (10.1 ± 0.7 g), were born to mothers above 35 years. Figure 1C shows a weak negative correlation the correlation between LV mass and age of the newborn and this was not statistically significant (r = -0.074, P = 0.552). Figure 1D shows a moderate positive correlation between the LV mass and birth weight of newborn which is statistically significant (r = 0.610, P = 0.001). A moderate positive correlation (r = 0.69, P = 0.015) was observed, which is statistically significant (Figure 1E). No meaningful correlation (r = -0.10, P = 0.752), and the result was not statistically significant (Figure 1F).

Figure 1 Scatter diagram. A: Correlation of left ventricular (LV) mass and gestational age; B: Correlation of LV mass and maternal age; C: Correlation of LV mass and age of newborn; D: Correlation of LV mass and weight of newborn; E: Correlation of LV mass and weight of new-born without asphyxia; F: Correlation of LV mass and age of newborn without asphyxia. LV: Left ventricular.

DISCUSSION

This work is aimed to document the mean LV mass of perinatal asphyxia and to correlate it with the severity of perinatal asphyxia. It also elicited the relationship between LV mass of perinatal asphyxia with their mothers age and gestational age. Besides it also documented gender association with LV mass and other associated factors.

This study showed that the LV mass in perinatal asphyxia was significantly lower than those without asphyxia. Furthermore, this study showed that 63% of the babies with perinatal asphyxia had mean LV mass lower than that obtained in the controls. This was at variance with the study of Vijayashankar et al[27] who noted compromised LV mass and LV function in new-borns with perinatal asphyxia. The definition of perinatal asphyxia, the methods used in grading severity of perinatal asphyxia and the sample used in both studies may explain the varying results. Cardiac abnormalities in perinatal asphyxia create a huge impact on the systemic ventricles. This included mitral regurgitation, transient myocardial ischemia and wall motion abnormalities of the left ventricle. Ischemic hypoxic changes and utero-placental insufficiency, can adversely affect the LV mass and LV function. This they do by causing systemic hypo-perfusion with attendant compromise of arterial peripheral vascular resistance, loss of arterial wall stiffness and compliance[6]. Management consists of ventilatory support, nitric oxide and extracorporeal membrane oxygenation for severe cases. Cardiac abnormalities in babies with perinatal asphyxia are often underdiagnosed and require a high index of suspicion[27].

Using Pearson correlation variable, the study showed that perinatal asphyxia showed increases of LV mass with gestational age. Findings from various studies had shown that babies born at lower gestational age, had higher odds of having LV abnormalities[28-30]. This might be due to poor lung surfactant, with immature lungs and poor respiratory muscles and hypoxic changes in the myocardium from birth asphyxia[7-11,27]. Similarly, a study had followed the gestational age of new-borns for three months using echocardiography on fifth day of life, and then at three months. They noted that gestational age varied inversely with ventricular diameters, ventricular wall thicknesses, and LV mass, but no differences in systolic and diastolic functioning[31].

In addition, the mean LV mass was highest on the first day of life and slightly lower on second and third day of life. Perinatal asphyxia causes more damage to the left ventricle as the newborn gets older. This may be due to prolonged and cumulative hypoxic-ischaemic changes to the muscles of the left ventricle as the day goes by.

There was a direct correlation between LV mass and birth weight of neonates with perinatal asphyxia. This shows that the size of the LV chamber varies directly with the weight of infants. A study noted that birth weight is the most reliable predictor of LV mass and LV dimension[29]. Abushaban et al[29] also noted that asphyxiated babies are known to have early and mild cardiovascular dysfunction compared to controls, and this was strongly associated with birthweight[30].

Though there is a weak negative correlation between LV mass and maternal age of newborn with perinatal asphyxia, however, 8.3% of the perinatal asphyxia whose LV mass were below that seen in control, were mainly born to mothers less than 25 years of age, while 39.3% of the perinatal asphyxia whose LV mass were below that seen in control, were mainly born to mothers aged 25-34 years and 14.3% of the perinatal asphyxia whose LV mass were below that seen in control, were born to mothers above 35 years. A study on a large population-based cohort showed that infants born to mothers greater than 40 years of age had smaller LV internal diameters and decreased stroke volume compared to new-borns of mothers in their early thirties. There is evidence that advanced maternal age is associated with overt neonatal cardiac anomalies[32,33]. In our setting, a good number of pregnancies occur at advanced maternal age (> 35 years). This is a risk factor for complications in pregnancy. Pregnancy is a hyper-dynamic state and require massive hemodynamic adaptations such as increased blood volume and cardiac output[34].

Male perinatal asphyxia was found to have higher LV mass than their female counterparts as seen in this study (though this was not statistically significant). Gardin et al[35] also corroborated these findings. They noted that gender of the infant is a significant predictor of left ventricular internal diameter in diastole. Besides they also noted that males appear to have larger LV dimensions than females. Goble et al[36] among his subjects also noted that males have an increased LV mass compared to females. Besides, Dai et al[37] on 678 healthy children also showed male predominance. Sørensen et al[38] among three hundred and thirty-four healthy participants, aged 6 years to 23 years also noted that left ventricular hypertrophy was higher in males than females. The higher LV mass in male neonates with perinatal asphyxia compared with their female counterpart may be due to sex difference in myocardial mass and the number of myocytes that was programmed in early life, differential cardiac muscle proliferation with respect to hypertrophy of myocytes during development in males[39].

Using the Sanat criteria for grading severity of perinatal asphyxia, new-borns with severe asphyxia had the lowest mean LV mass compared with those with mild and moderate asphyxia. Severe asphyxia causes severe infarcts and thrombotic lesions on the heart, especially the left ventricle. Transient acute dilatation of the right ventricle, D-shaping of the LV, early changes in ventricular chamber shape and mass, septal flattening and decrease in LV end-diastolic area have been reported in an experimental porcine study[40].

The majority of mothers (61.9%) delivered perinatal asphyxia whose LV mass were smaller than control. Antepartum risk factors such as severe maternal hypertensive diseases[41], antepartum haemorrhage[42], less than four antenatal care visits[41-43], prolonged second stage of labour[41-43], home delivery[43], obstructed labour, maternal anaemia and low educational status of the mother have been linked with small LV mass in newborn babies with perinatal asphyxia.

There was no statistical difference when the mean LV mass of babies with perinatal asphyxia delivered by SVD were compared with those delivered by CS. However, a study has described an inverse association between elective caesarean section and birth asphyxia[42]. Kiyani et al[42] reported that perinatal asphyxia occurs in 44.4% of newborn delivered by SVD when comparted to 32.14% seen in babies delivered by caesarean section.

Though the LV mass of new-borns with perinatal asphyxia was larger (8.1 ± 2.5) amongst babies delivered by mothers of the middle socioeconomic class, ANOVA test did not detect any statistical significance when the three classes of social classification were compared. Laitinen et al[43] in a cohort study of 1871 participants, reported that low family socio-economic class was associated with increased LV mass and impaired diastolic function. Measures on cardiovascular disease prevention should include the family environment of the newborn[43].

Limitation of the study

A study design that involve a very large cohort of newborn with perinatal asphyxia drawn from a large sample population may yield a better result. The effect of maternal characteristics (such as maternal weight, obesity, blood pressure and diabetes mellitus) on LV mass were not included in this study. This would make the study worthwhile.

CONCLUSION

This study showed that the LV mass in perinatal asphyxia was significantly lower than those without asphyxia using Pearson correlation variable, the study showed that perinatal asphyxia showed increases of LV mass with gestational age. There was a direct correlation between LV mass and birth weight of neonates with perinatal asphyxia. There is a weak negative correlation between LV mass and maternal age. Early detection of the cardiac disease, appropriate management and sustained reduction of perinatal asphyxia, and improved intrapartum quality of care are key.

ACKNOWLEDGEMENTS

We are grateful to the statistician who did the analysis.