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 Table of Contents  
Year : 2020  |  Volume : 27  |  Issue : 4  |  Page : 357-364

Electrocardiographic findings in human immunodeficiency virus-infected children in Benin City, Nigeria

1 Department of Child Health, University of Benin Teaching Hospital, Benin City, Nigeria
2 Department of Child Health, University of Benin Teaching Hospital; Department of Child Health, University of Benin, Benin City, Nigeria

Date of Submission21-Apr-2020
Date of Decision20-May-2020
Date of Acceptance27-Jul-2020
Date of Web Publication04-Nov-2020

Correspondence Address:
Prof. Wilson Ehidiamen Sadoh
Department of Child Health, University of Benin, PMB 1111, Benin City
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/npmj.npmj_92_20

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Background: Human immunodeficiency virus (HIV) infection is a global pandemic affecting mostly sub-Saharan Africa. It is a multisystem disease. Cardiovascular involvement detected by electrocardiogram (ECG) has been described mostly in adult populations with few studies on children. In this study, the ECG findings of HIV-infected as against HIV-uninfected children were evaluated. Subjects and Methods: This comparative cross-sectional study was conducted in two public hospitals in Benin City. Using convenience sampling, 200 each of HIV-positive children attending the HIV clinics of both hospitals and age- and sex-matched HIV-negative children attending follow-up clinics in the same hospitals were recruited. Biodata/sociodemographic information was obtained, while each participant underwent 12-channel ECG evaluation. Results: The prevalence of abnormal ECG findings in HIV-positive children was 34.5% compared to 4.5% in HIV-negative children (P < 0.0001). The mean PR, QRS and QT intervals in the participants were 0.13 ± 0.02 s, 0.11 ± 0.15 s and 0.41 ± 0.03, respectively. They were statistically significantly longer than controls, 0.12 ± 0.02 s, 0.08 ± 0.09 s and 0.40 ± 0.02 s, respectively, P < 0.05, in each case. The prevalence of prolonged PR, QRS and QTc was significantly higher in the patients, 5%, 3.5% and 3.5%, respectively, than controls, 05, 0% and 0%, respectively (P < 0.05 in each case). Conclusion: A third of the HIV-infected children in the study had abnormal ECG changes. It is recommended that ECG be included in their routine management of HIV-positive children so as to better supervise the affected children, retard the deterioration and improve their quality of health.

Keywords: Cardiovascular, children, electrocardiography, human immunodeficiency virus

How to cite this article:
Attamah CA, Sadoh WE, Ibadin MO, Omoigberale AI. Electrocardiographic findings in human immunodeficiency virus-infected children in Benin City, Nigeria. Niger Postgrad Med J 2020;27:357-64

How to cite this URL:
Attamah CA, Sadoh WE, Ibadin MO, Omoigberale AI. Electrocardiographic findings in human immunodeficiency virus-infected children in Benin City, Nigeria. Niger Postgrad Med J [serial online] 2020 [cited 2021 Feb 27];27:357-64. Available from: https://www.npmj.org/text.asp?2020/27/4/357/299919

  Introduction Top

Human immunodeficiency virus (HIV) infection is a pandemic, with more than 37.9 million people living with the virus globally. Of these, 1.7 million are children aged <15 years.[1] The HIV prevalence in Nigeria is 1.4% and an estimated 1.9 million Nigerians are living with HIV. Among children 0–14 years, the prevalence is 0.2%.[2] All systems of the body are affected by HIV, and the clinical and pathologic findings in various organ systems have been described.[3] In the cardiovascular system, the manifestations include pericarditis, myocarditis, cardiomyopathies, pulmonary hypertension and increased incidence of vascular diseases including coronary artery disease and pulmonary vascular diseases.[4] These result from various events ranging from direct myocardial invasion, chronic inflammatory immune response, endothelial cell dysfunction and/or injury and autoimmune response to the viral infection. Also implicated are the effects of the use of highly active antiretroviral therapy (HAART).[5]

The introduction of HAART regimens has significantly modified the course of HIV disease, leading to improved survival rates and enhanced patients' quality of life. The use of HAART has also raised concerns about increases in peripheral and coronary artery diseases and myocardial infarction. Prolonged use of HAART, especially protease inhibitors, increases the risk of these cardiovascular complications.[4],[6] For example, zidovudine-cardiotoxicity is associated with dilated cardiomyopathy.[7],[8] However, a recent study in the USA showed higher left ventricular fractional shortening in HAART-exposed children compared to HAART-naïve ones. The study also demonstrated that cardiac function and structure were better with longer HAART exposure duration.[9]

Cardiovascular diseases in HIV-infected individuals are usually subclinical, and they often go unrecognised. Electrocardiography (ECG) is an inexpensive, easily operable and readily available clinical investigative tool for the evaluation of cardiovascular diseases.[10] Specific ECG changes are predictive of specific cardiovascular diseases. The ECG changes can precede echocardiographic findings and overt clinical abnormalities.[10]

There are varied reports on the prevalence of ECG changes in HIV-infected individuals. Pongprot et al.[11] in 2004 in Thailand reported 88.0% prevalence of ECG changes among HIV-infected children. Lubega et al.[12] in 2005 in Uganda reported a prevalence of 26.5% among children. In Nigeria, Sani et al.[10] in 2004 in Jos reported a prevalence of 65.0% among adults, while Ige et al.[13] only studied the QT interval in HIV-infected children. There is paucity of studies on comprehensive ECG findings in children with HIV, especially those in the sub-Saharan Africa where the burden of the disease is marked. This study evaluated the prevalence and pattern of ECG findings in children with HIV/AIDS and in HIV-negative children seen in the University of Benin Teaching Hospital (UBTH) and Central Hospital, Benin (CHB), both in Benin City, Nigeria. The relationships between ECG findings and use of antiretroviral drugs were also explored.

  Subjects And Methods Top

The study was carried out at the paediatric HIV outpatient clinics of the two major hospitals providing paediatric HIV care in Benin City: UBTH and CHB, between January and June 2014. Paediatric HIV care in both centres is supported by 'Achieving Health Nigeria Initiative', and patients are enrolled after testing positive for HIV. UBTH is a tertiary centre, whereas CHB is a secondary-level facility. The study is a comparative cross-sectional and descriptive one. Ethical clearance was obtained from the Ethics and Research Committee of the UBTH, Benin City, with protocol number AMD/E22/A/VOL.VII/871 and dated 04 December 2013. Written informed consent was obtained from the parent(s)/guardian(s) of each participant. Where appropriate, assent was also obtained from each child aged >10 years. Parents/guardians of HIV-negative children were offered pre- and post-test counselling for HIV testing.

The sample size was determined using the formula described by Araoye:[14]

where n = minimum sample size of the study population

Z = normal standard deviation for the defined confidence level of 95% = 1.96

P = Estimated prevalence or known prevalence of cardiovascular abnormalities in HIV-positive children as determined by ECG from a previous study of 26.5%.[12]

q = 1 – p = 1–0.26.5 = 0.735

d = margin of error to be tolerated (fixed at 5% or 0.05).


Subsequently, the sample size was determined for the study population <10,000.[14]

where nf= the desired sample size of a study when population is <10,000.

N = the estimate of the population over the past year (total number of new and old patients who attended the clinic in the last 1 year = 606).

n = the desired sample size of study when population is <10,000.

A minimum sample size of 200 was calculated from the above formula.

The study participants were recruited using convenience sampling method. Consecutive HIV-positive and HIV-negative children who met the study criteria in the clinics were recruited. Otherwise eligible study participants were excluded from the study if they were known to have congenital or acquired cardiovascular diseases (as previously documented in their medical records) or detected at enrolment and if they had comorbidities such as recognisable or confirmed genetic/chromosomal anomalies because of their known accompaniment with cardiovascular manifestations. Also excluded were those receiving medications with known cardiovascular effects such as digoxin, propranolol and salbutamol. Others were those with diarrhoea because of possible electrolyte derangement and those receiving in-patient care.

Using proportionate distribution, 120 (60.0% of the target population of 200 HIV-positive children) children were recruited from UBTH, while the remaining 80 were recruited from CHB. Corresponding numbers of apparently healthy HIV-negative children were recruited from both centres. Using a structured questionnaire, information on the sociodemographics was obtained from parent(s)/guardian(s) of each participant. The HIV-positive children were examined and their respiratory rates and blood pressure (BP) were determined. Heart rate was counted using the ECG machine. The BP was measured with a mercury sphygmomanometer using standard guidelines as prescribed in the Fourth Report.[15] Diagnoses of symptomatic HIV infection were made according to the WHO clinical staging criteria for HIV/AIDS.[16]

The weights of children <2 years of age were measured using a Bassinet scale with a precision of 0.1 kg, whereas those >2 years were weighed using a Seca weighing scale made by Seca Grubh and Co (Hammer Steindamm, Hamburg, Germany). (Model 220 CE 0123). Both instruments had a sensitivity of 0.1 kg (100 g). The scales were calibrated on each clinic day using a known weight. The length of children aged 18 months to 2 years was measured with a non-distensible tape, while the height of children aged above 2 years was determined using a stadiometer. The measurements were made in accordance with standard recommendations.[17] The weight and height measurements of the patients and controls were used to calculate the children's body mass index (BMI).[18]


All the study participants had standard 12-lead surface ECG recording. Each ECG was read with a convenient ECG ruler using standard guidelines.[19],[20]

Determination of human immunodeficiency virus status and CD4+

The HIV status of controls was determined according to the WHO standardised serial testing algorithm.[21]

Follow-up care

Results of the ECG were immediately communicated to the parents/caregivers. Those with significant ECG changes were referred to the Cardiology Clinic of UBTH for follow-up while they maintained their routine appointments at the paediatric HIV clinics.

Statistical analysis

Data were analysed using IBM-Statistical Package for Scientific Solution (SPSS) version 21.0 IBM-SPSS version 21.0. Armonk, NY:IBM Corp. Student's t-test was used to compare means derived from continuous variables. Chi-square test was used to compare categorical variables, but its variant, the Fisher's exact test, was used when any cell value was <5. The level of significance was set at P < 0.05 at a confidence level of 95%.

  Results Top

Two hundred each of HIV-positive children and age- and sex-matched HIV-negative children were recruited for the study.

Sociodemographic characteristics of the patients and controls

[Table 1] shows the sociodemographic characteristics of the study participants. The mean age of the HIV-positive children of 8.30 ± 3.92 years was comparable to that of HIV-negative children (8.41 ± 3.99 years) (P = 0.78). The gender and socioeconomic class distribution of the HIV-positive and HIV-negative children is shown in [Table 1].
Table 1: Sociodemographic characteristics of the study participants

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Anthropometry and blood pressure of patients and controls

The mean weight, length/height and BMI of the HIV-positive and HIV-negative children were comparable. No differences were observed in the systolic BP and diastolic BP between the two groups [Table 2].
Table 2: Anthropometric measurements and blood pressure values of the study participants

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Prevalence of electrocardiography changes and mean values of electrocardiography parameters in human immunodeficiency virus-positive and human immunodeficiency virus-negative children

ECG changes in the study were noted in 69 (34.5%) HIV-positive children and nine (4.5%) HIV-negative children, P = 0.0001. The mean values of ECG parameters in the study participants are shown in [Table 3]. The mean heart rate was higher in HIV-positive children compared to HIV-negative children (95.60 ± 17.11 beats/min [bpm] vs. 87.36 ± 13.94 bpm, P = 0.0001). The mean P wave duration, PR interval, QRS and QTc interval in HIV-positive children were also statistically significantly longer in HIV-positive children compared to HIV-negative children (P = 0.031, P = 0.002, P = 0.045 and P = 0.003, respectively).
Table 3: Comparison of mean electrocardiogram parameters in human immunodeficiency virus-positive and human immunodeficiency virus-negative children

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[Table 4] shows the prevalence of various ECG changes in the study participants. Ten (5.0%) HIV-positive children and one (0.5%) HIV-negative child had first-degree heart block (Fisher's exact test, P = 0.011, odds ratio [OR] = 10.4, 95% confidence interval [CI] = 1.32–82.60). Prolonged QTc interval was seen in seven (3.5%) HIV-positive children, whereas none of the HIV-negative children had prolonged QTc interval (P = 0.015, OR = 15.5, 95% CI = 1.84–2.25). Seventeen (8.5%) HIV-positive children had ST-segment changes compared to only one (0.05%) HIV-negative child.
Table 4: Prevalence of electrocardiogram changes in human immunodeficiency virus-positive and human immunodeficiency virus-negative children

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Thirteen (6.5%) and 17 (8.5%) HIV-positive children had right and left ventricular hypertrophy, respectively, whereas right and left ventricular hypertrophy were each found in 3 (1.5%) HIV-negative children (Fisher's exact test; P = 0.019, OR = 4.5, 95% CI = 1.28–16.27, and P = 0.002, OR = 6.1, 95% CI = 1.75–21.15, respectively, for right and left ventricular hypertrophy).

The mean values of ECG parameters in the HIV-positive children in accordance with HAART status are depicted in [Table 5]. The mean PR interval of the HAART-experienced HIV-positive children of 0.13 ± 0.02 s was significantly longer than that obtained in HAART-naive HIV-positive children (0.12 ± 0.02 s) (t = 2.67, 95% CI = 0.00–0.02, P = 0.008).
Table 5: Mean electrocardiogram parameters of the human immunodeficiency virus-positive children according to highly active antiretroviral therapy status

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Of the 200 HIV-positive children, 64 (32.0%) were classified as clinical Stage I and 84 (42.0%) and 52 (26.0%) were classified, respectively, as clinical Stages II and III [Table 6]. The prevalence of ECG changes such as sinus tachycardia; prolonged PR, QRS and QTc intervals; right ventricular hypertrophy; left ventricular hypertrophy and multiple ECG changes increased progressively among HIV-positive children as the clinical staging worsened though the relationships were not statistically significant.
Table 6: Occurrence of electrocardiogram changes in relation to human immunodeficiency virus clinical staging among the study participants

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  Discussion Top

The prevalence of ECG changes among HIV-positive children of 34.5% was significantly higher than 4.5% obtained in HIV-negative children. The higher prevalence of ECG findings in HIV-positive children may have been due to the influence of HIV infection and HAART therapy on the heart. The prevalence of ECG changes in this study of 34.5% was higher than the 26.5% reported by Lubega et al.[12] in HIV-infected Ugandan children. The higher prevalence in this study may be due to the higher number of HIV-positive children (83%) on HAART in this study (10.2%) that received protease inhibitors compared to the study by Lubega et al.[12] where only 0.43% of the children received HAART and none received protease inhibitor. HAART, especially protease inhibitors, has been reported to cause cardiovascular diseases in HIV-infected individuals.[4],[12] Our value of 34.5% was, however, lower than the 93.0% documented by Lipshultz.[5] The use of 24 h ambulatory ECG recordings in the Lipshultz study may have accounted for the higher value in that study.

The spectrum of ECG changes reported in this study was similar to those reported by other workers.[5],[12] Sinus tachycardia was the most common finding in this study (18.5%). Our value of 18.5% is higher than the 9.0% reported by Ige et al.[13] in Jos, North-central Nigeria, in 2014. Perhaps, the changes may be ascribed to autonomic impairment and neuropathies with unopposed sympathetic stimulation and left ventricular systolic dysfunction, both of which have been documented in children with HIV infection.[13],[22] Autonomic impairment and neuropathy progress with worsening HIV disease are thought to be present early in HIV infection though the exact cause(s) remains unclear.[22] Sinus tachycardia was higher among HAART-experienced individuals compared to HAART-naive individuals (19.9% vs. 11.8%). Incidences of lipodystrophy/lipoartophy, increase in LDL and HDL which lead to increase in arterial disease and myocardial infarction are the basis of HAART induced cardiovascular disease in HIV infected subjects.[23]

This study demonstrated that prolonged PR interval was significantly associated with HIV disease. It was significantly higher among HIV-positive children compared to their HIV-negative counterparts (5% vs. 0.5%), and the mean PR interval was also significantly longer in HIV-positive children compared to the HIV-negative ones. A longer PR interval may indicate increased predisposition to first-degree arterioventricular block and is associated with a 20.0%–30.0% increased risk of atrial fibrillation according to a report by Nielson et al.[24] in 2013 in Copenhagen, Denmark. Prolonged PR interval has similarly been reported by other workers.[25] Deteriorating clinical stage of HIV disease and direct myocardial invasion by HIV virus have been suggested as possible means by which cardiovascular diseases such as prolonged PR interval arise in HIV-infected children.[26]

The prevalence of prolonged QTc was higher among the HIV-positive than HIV-negative children, and the mean QTc interval of HIV-positive children was significantly longer than that of the HIV-negative children (0.41 ± 0.03 vs. 0.40 ± 0.02 s; P = 0.003). A longer QTc interval induces prolonged ventricular depolarisation and repolarisation, hence they may lead to arrhythmia.[27] The prevalence of prolonged QTc of 3.5% noted in this study is lower than the 18.0% reported in children by Ige et al.[13] in 2014 in Jos. The low prevalence in the study may have been due to the inclusion of non-symptomatic HIV-positive children in the extant study unlike in the case of Ige et al.,[13] who included children with Stage IV disease (AIDS) as participants. Prolonged QTc interval may be due to myocarditis, subclinical cardiomyopathy, autonomic neuropathy and myocardial ischemia that are known to occur in HIV-infected children.[28],[29]

The mean QTc interval was noted to be longer, whereas prolonged QTc interval was also noted to be more common in HAART-exposed HIV-positive children compared to those who were HAART naive. Similar finding had been reported by Ige et al.[13] among HAART-experienced children in Jos, Nigeria, in 2014 and by Idris et al.[25] among Indonesian HIV-infected children in 2016. Prolonged QTc interval in HIV-infected patients is associated with a higher risk of sudden death from fatal arrhythmias,[13],[27] and it is a predictor of cardiovascular mediated mortality even in the absence of overt heart disease.[12] Depressed ST segment which is suggestive of ischaemic heart disease[30] was significantly high in HIV-positive than HIV-negative children. Thirty-nine per cent of the HIV-positive children had ST-segment changes in a similar study carried out by Pongprot et al.,[11] who studied a very small number of individuals (n = 48). This may have accounted for the difference in prevalence between the two studies.

Right ventricular hypertrophy was also significantly more common in HIV-positive than HIV-negative children. Our figure is, however, lower than the 13.9% reported by Lubega et al.[12] Unlike what obtained in this study, Lubega et al.[12] recruited individuals who had other comorbidities such as congenital heart diseases. This may have accounted for why slightly more children had right ventricular hypertrophy in their study compared to the extant one. Right ventricular hypertrophy was more common in HAART-exposed children compared to HAART-naive ones. Similar finding had previously been documented.[22] Pulmonary hypertension has been implicated as the probable cause of right ventricular hypertrophy.[31] Both events confer poor prognosis and diminished survival chances on HIV-infected patients.[32]

The prevalence of left ventricular hypertrophy was significantly higher in HIV-positive children compared to the HIV-negative ones. A comparable prevalence of 5.6% was reported by Lubega et al.[12] The finding of LVH on ECG may be a pointer to the onset of possible cardiomyopathy in the near future[33] with attendant poor prognosis and reduced survival.[28] This report underscores the need for routine cardiovascular evaluation in HIV-infected patients using ECG.

Multiple ECG changes (MEC) describe the occurrence of more than one type of ECG changes in a study participant, thus the possibility of more than one type of cardiovascular disease in a particular participant. This study found that MEC was significantly more prevalent in HIV-positive than HIV-negative children, and this was particularly so in HIV-infected children on HAART (12.0%) compared to those who were HAART naive (5.9%). There is paucity of studies on MEC in HIV-infected children or adults.

Two main limitations are identified in this study. The duration of HAART exposure and duration of HIV infection were not factored in the study. It is possible that the duration of both HAART exposure and HIV infection could have influenced the prevalence of the ECG changes seen in HIV-infected children.

  Conclusion Top

The prevalence of ECG changes was significantly higher in children with HIV infection compared to controls, suggesting perhaps that the risk of cardiovascular disease is higher in non-symptomatic HIV-infected children compared to HIV-negative children. Cardiovascular diseases in HIV-infected children as revealed by ECG worsened with progression of the HIV disease clinical stage.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Joint United Nations Programme on HIV/AIDS (UNAIDS) Global and Regional HIV Statistics: UNAIDS Fact Sheet; 2019. Available from: https://www.unaids.org/sites/default/files/media_asset/UNAIDS_FactSheet_en.pdf. [Last accessed on 2020 Jun 12].  Back to cited text no. 1
Joint United Nations Programme on HIV/AIDS (UNAIDS) Press Release. New Survey Results Indicate that Nigeria has a Prevalence of 1.4%. Available from: https://www.unaids.org/en/resources/presscentre/pressreleaseandstatementarchive/2019/march/20190314_nigeria. [Last accessed 2020 Jun 12].  Back to cited text no. 2
Lepage P, Spira R, Kalibala S, Pillay K, Giaquinto C, Castetbon K, et al. Care of human immunodeficiency virus-infected children in developing countries. International Working Group on Mother-to-Child Transmission of HIV. Pediatr Infect Dis J 1998;17:581-6.  Back to cited text no. 3
Barbaro G. Cardiovascular manifestations of HIV infection. Circulation 2002;106:1420-5.  Back to cited text no. 4
Lipshultz SE, Chanock S, Sanders SP, Colan SD, Perez-Atayde A, McIntosh K. Cardiovascular manifestations of human immunodeficiency virus infection in infants and children. Am J Cardiol 1989;63:1489-97.  Back to cited text no. 5
Iloeje UH, Yuan Y, L'italien G, Mauskopf J, Holmberg SD, Moorman AC, et al. Protease inhibitor exposure and increased risk of cardiovascular disease in HIV-infected patients. HIV Med 2005;6:37-44.  Back to cited text no. 6
Chariot P, Perchet H, Monnet I. Dilated cardiomyopathy in HIV-infected patients. N Engl J Med 1999;340:732.  Back to cited text no. 7
Herskowitz A, Willoughby SB, Baughman KL, Schulman SP, Bartlett JD. Cardiomyopathy associated with antiretroviral therapy in patients with HIV infection: A report of six cases. Ann Intern Med 1992;116:311-3.  Back to cited text no. 8
Lipshultz SE, Wilkinson JD, Thompson B, Cheng I, Briston DA, Shearer WT, et al. Cardiac effects of highly active antiretroviral therapy in perinatally HIV-infected children: The CHAART-2 study. J Am Coll Cardiol 2017;70:2240-7.  Back to cited text no. 9
Sani MU, Okeahialam BN, Ukoli CO. Electrocardiographic abnormalities in Nigerian AIDS patients. Trop Cardiol 2004;30:3-33.  Back to cited text no. 10
Pongprot Y, Sittiwangkul R, Silvilairat S, Sirisanthana V. Cardiac manifestations in HIV-infected Thai children. Ann Trop Paediatr 2004;24:153-9.  Back to cited text no. 11
Lubega S, Zirembuzi GW, Lwabi P. Heart disease among children with HIV/AIDS attending the paediatric infectious disease clinic at Mulago Hospital. Afr Health Sci 2005;5:219-26.  Back to cited text no. 12
Ige O, Oguche S, Yilgwan C, Abdu H, Bode-Thomas F. The QT interval in human immunodeficiency virus-positive Nigerian children. J Med Trop 2014;16:61-5.  Back to cited text no. 13
  [Full text]  
Araoye MA. Research Methodology with Statistics for Health and Social Sciences. Nathdex Publishers Ilorin; 2004. p. 115-22.  Back to cited text no. 14
National High Blood Pressure Education Program Working Group on High Blood Pressure in Children and Adolescents: Fourth report on the diagnosis, evaluation and treatment of high blood pressure in children and adolescents. Paediatrics 2004;114:555-66.  Back to cited text no. 15
World Health Organization: WHO Case Definition of HIV for Surveillance and Revised Clinical Staging and Immunological Classification of HIV Related Diseases in Adults and Children. Geneva: World Health Organization; 2007. Available from: http://www.who.int /hiv/pub/ guidelines/HIV staging 2010. [Last accessed 2016 Mar 20].  Back to cited text no. 16
National Health and Nutritional Examination Survey (NHANES); Anthropometric Procedures Manual; 2014. Available from: http://www.cdc.gov/nehs/data/nhanes/nhanes_07_08/manual_an.pdf. [last accessed 2016 Mar 19].  Back to cited text no. 17
Center for Disease Control, National Center for Health Statistics. Available from: http://www.cdc.gov/growth charts/2010. [last accessed on 2016 Apr 05].  Back to cited text no. 18
Myung KP, Warren GG. How to Read Paediatric ECG. 4th ed. Philadelphia, Pennsylvania, USA: Mosby-Elsevier USA; 2006. p. 8-115.  Back to cited text no. 19
Davingnon A, Rautaharju P, Burselle E, Soumis F, Megelas M. Normal ECG standards for infants and children. Pediatr Cardiol 1979;1:133-52.  Back to cited text no. 20
WHO/CDC: Guidelines for Appropriate Evaluations of HIV Testing Technologies in Africa. Oxford University Press; 2003. Available from: https://www.who.int/hiv/pub/vct/testing_africa/en/). [Last accessed on 2016 Mar 07].  Back to cited text no. 21
Issenberg HJ, Charytan M, Rubenstein A. Cardiac involvement in children with acquired immune deficiency syndrome. Am Heart J 1985;110:710-15.  Back to cited text no. 22
Behrens G, Schmidt H, Meyer D, Stoll M, Schmidt RE. Vascular complications associated with use of HIV protease inhibitors. Lancet 1998;351:1958.  Back to cited text no. 23
Nielsen JB, Pietersen A, Graff C, Lind B, Struijk JJ, Olesen MS, et al. Risk of atrial fibrillation as a function of the electrocardiographic PR interval: Results from the Copenhagen ECG Study. Heart Rhythm 2013;10:1249-56.  Back to cited text no. 24
Idris NS, Cheung MH, Grobbee DE, Burgner DD, Kurniati N, Djer MM, et al. Effects of paediatric HIV infection on electrical conduction of the heart. Open Heart 2016;3:340-46.  Back to cited text no. 25
Lewis W, Grody WW. AIDS and the heart: Review and consideration of pathogenetic mechanisms. Cardiovasc Pathol 1992;1:53-64.  Back to cited text no. 26
Moss AJ. Measurement of the QT interval and the risk associated with QTc interval prolongation: A review. Am J Cardiol 1993;72:23B-5B.  Back to cited text no. 27
Grody WW, Cheng L, Lewis W. Infection of the heart by the human immunodeficiency virus. Am J Cardiol 1990;66:203-6.  Back to cited text no. 28
Plein D, Van Camp G, Cosyns B, Alimenti A, Levy J, Vandenbossche JL. Cardiac and autonomic evaluation in a pediatric population with human immunodeficiency virus. Clin Cardiol 1999;22:33-6.  Back to cited text no. 29
Pollehn T, Brady WJ, Perron AD, Morris F. The electrocardiographic differential diagnosis of ST segment depression. Emerg Med J 2002;19:129-35.  Back to cited text no. 30
Sitbon O, Lascoux-Combe C, Delfraissy JF, Yeni PG, Raffi F, De Zuttere D, et al. Prevalence of HIV-related pulmonary arterial hypertension in the current antiretroviral therapy era. Am J Respir Crit Care Med 2008;177:108-13.  Back to cited text no. 31
Chetty R. Vasculitis associated with human immunodefficiency virus infection. J Clin Pathol 2001;4:275-8.  Back to cited text no. 32
van Leth F, Phanuphak P, Stroes E, Gazzard B, Cahn P, Raffi F, et al. Nevirapine and efavirenz elicit different changes in lipid profiles in antiretroviral-therapy-naive patients infected with HIV-1. PLoS Med 2004;1:e19.  Back to cited text no. 33


  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]


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