Nigerian Journal of Cardiology

: 2019  |  Volume : 16  |  Issue : 1  |  Page : 38--42

Electrocardiographic abnormalities in sickle cell disease patients in Kano, Northwest Nigeria

Jamila Ado Yau1, Hadiza Saidu2, Ahmad Maifada Yakasai1,  
1 Department of Medicine, Public Health and Diagnostic Institute, Northwest University, Kano State, Nigeria
2 Department of Medicine, Murtala Muhammad Specialist Hospital, Bayero University Kano, Kano State, Nigeria

Correspondence Address:
Dr. Jamila Ado Yau
Public Health and Diagnostic Institute, Northwest University, Kano, Kano State


Background: Cardiovascular abnormalities are important causes of morbidity and mortality in sickle cell disease (SCD) patients. Data on electrocardiography (ECG) changes in SCD are lacking in Kano, Northwest Nigeria. This study, therefore, aimed to identify the pattern of ECG changes in steady state adult sickle cell patients. Methodology: A case–control cross-sectional study was conducted among SCD patients attending the sickle cell clinic in Murtala Muhammad Specialist Hospital, Kano. One hundred SCD patients were consecutively recruited and compared with 100 age- and sex-matched controls. All consenting participants had hemoglobin (Hb) electrophoresis and were subjected to electrocardiography. Results: The mean age of the cases is 20.98 ± 5.74 years, whereas that of the controls was 22.31 ± 3.27 years, P = 0.047. Among the cases, 57% were male, whereas in the control group, 55% were male (P = 0.443). The mean body mass index (BMI) for the cases was 18.14 ± 3.57 kg/m2, whereas that of the control was 22.74 ± 2.18 kg/m2, P < 0.001. The mean Hb concentration of the cases and the controls was 7.22 ± 0.94 g/dl and 12.00 ± 9.51 g/dl, respectively, P < 0.001. Nonspecific ST-T wave changes were the most common ECG abnormality detected in 76% of cases and 42% of controls, P < 0.0001. Other ECG abnormalities found among the SCD patients were right ventricular hypertrophy (64%), right atrial enlargement (24%), left atrial enlargement (4%), biatrial enlargement (8%), atrial ectopics (6%), premature ventricular contractions (1%), and prolonged PR interval (4%). An association was observed between low BMI and abnormal ECG findings among the cases (P = 0.006). Conclusion: ECG abnormalities are common in SCD patients and early identification would lead to early intervention to prevent cardiac events.

How to cite this article:
Yau JA, Saidu H, Yakasai AM. Electrocardiographic abnormalities in sickle cell disease patients in Kano, Northwest Nigeria.Nig J Cardiol 2019;16:38-42

How to cite this URL:
Yau JA, Saidu H, Yakasai AM. Electrocardiographic abnormalities in sickle cell disease patients in Kano, Northwest Nigeria. Nig J Cardiol [serial online] 2019 [cited 2020 Jul 13 ];16:38-42
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Full Text


Sickle cell disease (SCD) is an important medical problem with major economic and social implications in addition to multiple system organic problems.[1] Cardiovascular abnormalities have been well documented in SCD[2],[3],[4] and are a common cause of morbidity and mortality in SCD patients.

Reported ECG abnormalities are common and largely nonspecific. The most frequent ECG findings are first-degree atrioventricular block, right ventricular enlargement, conduction defects, and repolarization changes.[5],[6] In a study done by Holloman et al. on 87 adult SCD patients, nonspecific ST-T-wave abnormalities, left ventricular hypertrophy (LVH), J-point elevation (probable normal variant), prolonged Q-T interval, left atrial enlargement (LAE), and sinus tachycardia were found.[1] However, in this group of stable adult SCD patients findings indicative of right ventricular hypertrophy (RVH) or strain were absent.[1]

A previous study in the Southeast Nigeria conducted among SCD patients and controls found the following respective prevalence of ECG abnormalities: LVH (75% and 1.7%); LAE (40% and 0%); biventricular hypertrophy (11% and 0%); and ST-segment elevation (10% and 0%). Increased P-wave and corrected QT dispersions were also reported among SCD patients.[7] However, there are few data on ECG changes in SCD patients in Northwest Nigeria. Hence, this study aimed to determine the pattern of ECG abnormalities in SCD patients in comparison to healthy controls.


We conducted a descriptive cross-sectional study among 100 SCD patients in a steady state. These patients were sampled from patients 16 years and above attending the outpatient sickle cell clinic of Murtala Muhammad Specialist Hospital, Kano State, Nigeria. An equal number of age- and sex-matched hemoglobin (Hb) genotype AA individuals who were selected from patient relatives and hospital staff served as controls. The inclusion criteria for the controls were as follows: age ≥16 years, Hb AA genotype, absence of congenital or acquired heart diseases, absence of pregnancy and intercurrent illness, and hematocrit level >30%. Exclusion criteria for the cases were as follows: the presence of SCD crisis, age <16 years, Hb genotype AA, and presence of congenital and acquired heart diseases. The steady state is defined as the absence of any crisis in the preceding 4 weeks and/or absence of any symptoms or sign attributable to acute illness.[7] Informed consent was obtained from all the participants and those <18 years consent was obtained from their parents or guardians.

All the participants were evaluated by electrocardiography. Resting 12-lead ECG was performed on all participants using Zoncare Model ZQ-1203G electrocardiography machine at a paper speed of 25 mm/s and standardized at a 0.1 mv/mm. A cardiologist analyzed the electrocardiogram. The measurements of the heart rate, cardiac axis, PR-interval, QRS duration, and QTc interval were done in the standard fashion.[8] Randomly selected electrocardiograms were cross-checked for accuracy independently by another cardiologist. ECG reference values for the dark skinned population proposed by Araoye were used as cutoff values for the duration of electrocardiographic deflections and intervals.[8] LVH diagnosis was based on Sokolow–Lyon voltage criteria,[9] whereas RVH diagnosis was based on the Allenstein and Mori criteria.[10] Left atrial enlargement (LAE) diagnosis was based on the criteria described by Macruz et al. validated in the Negro population by Araoye et al.[11],[12]

The ST segment was taken as the interval between the J point (or end of the QRS complex) and the beginning of the T wave (defined as the point of maximum abrupt deflation after the ST segment).[9] Elevation or depression of the ST segment by 2 mm or more from the isoelectric line was considered abnormal.[9] QTc was computed using Bazett formula, while QTc prolongation was defined as values >440 ms in males and >460 ms in females.[13] In addition, measurements of parameters of the electrocardiogram were made in milliseconds in Leads II and V1 for the following: P-wave, P-R, QRS, and QT intervals as well as heart rate. Arrhythmias and specific ECG abnormalities were also recorded.

Data analysis

Data were collected from all the 200 participants in data sheets, and then explored for skewness and analyzed using the Statistical Packages for Social Sciences (SPSS Inc., Chicago, Illionios) software version 19. The median with interquartile ranges, Chi-square, Fisher's exact probability, Student's t-test, and Mann–Whitney U-tests were used to compare categorical and continuous variables as appropriate. Value of P ≤ 0.05 was considered to be statistically significant.


A total of 100 SCD patients were recruited into the study and compared with 100 age- and sex-matched controls. The mean age of the cases in years was 20.98 ± 5.74, whereas that of the controls was 22.3 ± 3.27, P = 0.047 Among cases, 57% were male, whereas in the control group, 55% were male and 45% were female (P = 0.443). The mean body mass index (BMI) (kg/m2) for the cases was 18.14 ± 3.57, whereas that of the control is 22.74 ± 2.18, P < 0.001. The mean Hb concentration (g/dl) of the cases is 7.22 ± 0.94, whereas that of the control is 12.00 ± 9.51, P < 0.001.

The characteristics of all the study participants are depicted in [Table 1], whereas characteristics of SCD patients based on ECG status are depicted in [Table 2].{Table 1}{Table 2}


This study examined the ECG abnormalities in SCD patients in comparison with healthy controls. The study demonstrated ECG abnormalities are significantly higher in the SCD patients in comparison with age- and sex-matched controls. It also showed the association of abnormal ECG findings in sickle cell patients with low BMI.

In this study, RVH was observed to be the most common ECG abnormality seen in 64% of SCD patients and this is in keeping with previous studies that showed a high incidence of right-sided heart disease.[6],[14],[15] Similarly, right atrial enlargement was more common among SCD patients compared to the controls. RVH has been associated with recurrent in situ vaso-occlusive crisis in the pulmonary vascular bed with resultant pulmonary hypertension.[16],[17] However, SCD patients in steady state without pulmonary hypertension were reported to have dilated right heart chambers without significant right ventricular dysfunction.[18]

LVH was uncommon among the current study population. Previous studies have, however, demonstrated a higher prevalence of LVH of 22% as reported by Holloman et al. and 75% as reported by Oguanobi et al.[1],[7] This difference could be explained by the difference in the age of the SCD patients in this study group (21 years) compared with those in the other studies (27 years and 28 years, respectively).[1],[7] Increasing age was reported to be directly proportional to increasing left ventricular (LV) filling.[19] LV stroke volume increases with significant dilatation of the LV as a result of chronic anemia and a subsequent increase in cardiac output.[20] The degree of LV dilatation is directly proportional to the degree of anemia.[21]

In this study, nonspecific ST-T changes were significantly higher in SCD patients compared to the controls (76% vs. 42%, P = 0.001). Similarly, previous studies have shown a high prevalence of nonspecific ST-T-wave changes.[1],[6] Repolarization abnormalities are frequent in SCD[1],[6] as well as in chronic anemia.[3] It has been suggested that the ST-T wave abnormality might be an index of myocardial ischemia (MI);[1],[7] however, no clear evidence of myocardial infarction was demonstrated by this study as the patients were in steady state with no specific complaint.

There was no significant difference in QTc interval between the SCD patients and the controls. This finding is similar to a study by Odia[22] who found no difference between age- and sex-matched controls, but at variance with the study by Oguanobi et al.[7] and Adebayo et al.[23] PR interval was significantly higher in the cases compared to the controls (4% and 0%, respectively, P = 0.027). This is comparable to findings by Akinola (9.1%)[24] but at variance with findings reported by Oguanobi et al. (23%),[7] Uzsoy (29%),[3] and Klinefelter (50%).[25] ST-segment changes, abnormal rhythm, prolonged QTc interval, T-wave abnormalities, and prolonged PR interval are recognized features of MI.[26]

In the short term, patchy microvascular occlusion will lead to areas of hypoperfusion, myocardial injury from ischemia with or without infarction, and impaired myocardial function, as demonstrated by several authors.[27],[28] de Montalembert et al. reported an improvement in myocardial perfusion among their patients with evidence of myocardial ischemia after the administration of hydroxyurea.[28] Nevertheless, caution should be exercised when administering hydroxyurea to sickle cell anemia patients who already have features of MI.[29] In the long term, recurrent episodes of ischemia might have detrimental effects on myocardial performance, especially as that organ also has to cope with the stress of chronic anemia, since severe ischemia can predispose to sudden death during sickle cell crises, as such early detection may be lifesaving. Thus, the availability of a simple screening tool becomes invaluable, especially in resource poor settings.

The BMI of SCD patients in this study was lower than the control group. Furthermore, abnormal ECG correlated with low BMI as demonstrated in the current study. Early data, indicating lower than normal anthropometric measurements in adult and adolescent SCD patients,[30],[31] have been confirmed by recent evidence,[32] and this reduction in body habitus is reported to be more pronounced in males than females. Elevated protein turnover and energy expenditure have been reported in SCD adults, suggesting increased protein and energy requirements.[33] Protein metabolism consumes approximately 30% of energy at rest, and recent data indicate that the high resting energy expenditure in SCD is determined primarily by energy needs for cardiac compensation and increased protein metabolism.[34] These reports have confirmed the need for additional need for macronutrient supplementation as normal diet is inadequate due to additional demand for increased erythropoiesis for red cell replacement.[35] This highlights the importance of nutrition in the management of SCD.

This study is not without limitations and it should be noted that echocardiography was not performed to confirm the presence of some of these abnormalities. Furthermore, cardiac enzymes assessment was not done to confirm the absence of MI. However, the strength of the study is that a sizeable number of SCD patients were compared with healthy controls.


It is therefore suggested that ECG should be carried out periodically among these patients and those found with abnormalities should undergo echocardiography and appropriate management. A prospective study on the impact of proper nutrition on cardiovascular abnormalities in Sickle cell disease is recommended considering the relationship between BMI and ECG abnormalities observed in this study.


This study provides additional data on the occurrence of ECG abnormalities most especially the ST-T wave changes in steady state Sickle cell disease patients, which might be an index of myocardial ischaemia (MI).[1],[7] Further studies in Sickle cell disease patients in crisis is suggested as sudden cardiac death seen in the aging Sickle cell disease patients are attributed to cardiopulmonary complications.[36]

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1Holloman KL, Johnson CS, Haywood LJ. Electrocardiogram analysis in adult patients with sickle cell disease. J Natl Med Assoc 1987;79:809-14.
2Rees DC, Williams TN, Gladwin MT. Sickle-cell disease. Lancet 2010;376:2018-31.
3Uzsoy NK. Cardiovascular findings in patients with sickle cell anemia. Am J Cardiol 1964;13:320-8.
4Falk RH, Hood WB Jr. The heart in sickle cell anemia. Arch Intern Med 1982;142:1680-4.
5Mulet M, Kaufman JM. The electrocardiogram in 50 cases of sickle-cell anaemia. East Afr Med J 1962;39:232-4.
6Windsor T, Burch GE. The electrocardiogram and cardiac state in active sickle cell anemia. Am Heart J 1945;29:685-96.
7Oguanobi NI, Onwubere BJ, Ike SO, Anisiuba BC, Ejim EC, Ibegbulam OG. Electocardiographic findings in adult Nigerians with sickle cell anaemia. Afr Health Sci 2010;10:235-41.
8Araoye MA. Left ventricular hypertrophy by electrocardiography: A code system applicable to Negroes. Nig Postgrad Med J 1996;3:92-7.
9Sokolow M, Lyon TP. The ventricular complex in left ventricular hypertrophy as obtained by unipolar precordial and limb leads. Am Heart J 1949;37:161-86.
10Allenstein BJ, Mori H. Evaluation of electrocardiographic diagnosis of ventricular hypertrophy based on autopsy comparison. Circulation 1960;21:401-12.
11Macruz R, Perloff JK, Case RB. A method for the electrocardiographic recognition of atrial enlargement. Circulation 1958;17:882-9.
12Araoye MA, Oladigo OG, Omotoso AB. Appraisal of the electrocardiographic signs of left a trial enlargement. Nig Postgrad Med J 1999;6:161-6.
13Bazett HC. An analysis of the time relations of electrocardiograms. Heart 1918-1920;7:353-70.
14Lindo CL, Doctor LR. The electrocardiogram in sickle-cell anemia. Am Heart J 1955;50:218-24.
15Ng ML, Liebman J, Anslovar J, Gross S. Cardiovascular findings in children with sickle cell anemia. Dis Chest 1967;52:788-99.
16Oguanobi NI, Ejim EC, Anisiuba BC, Onwubere BJ, Ike SO, Ibegbulam OG, et al. Clinical and electrocardiographic evaluation of sickle-cell anaemia patients with pulmonary hypertension. ISRN Hematol 2012;2012:768718.
17Trenko L. Heart disease in sickle cell anaemia. Mod Med 1956;55:234-44.
18Sachdev V, Machado RF, Shizukuda Y, Rao YN, Sidenko S, Ernst I, et al. Diastolic dysfunction is an independent risk factor for death in patients with sickle cell disease. J Am Coll Cardiol 2007;49:472-9.
19Lester LA, Sodt PC, Hutcheon N, Arcilla RA. Cardiac abnormalities in children with sickle cell anemia. Chest 1990;98:1169-74.
20Mueller BU, Martin KJ, Dreyer W, Bezold LI, Mahoney DH. Prolonged QT interval in pediatric sickle cell disease. Pediatr Blood Cancer 2006;47:831-3.
21Lippman SM, Niemann JT, Thigpen T, Ginzton LE, Laks MM. Abnormal septal Q waves in sickle cell disease. Prevalence and causative factors. Chest 1985;88:543-8.
22Odia OJ. Electrocardiographic observations in patients with sickle cell diseases. Trop Cardiol 1990;16:135-8.
23Adebayo RA, Balogun MO, Akinola NO, Akintomide AO. The clinical, electrocardiographic and self-paced walking exercise features of Nigerians with sickle cell anaemia presenting at OAUTHC, ile-ife. Niger J Med 2002;11:170-6.
24Akinola NO. Cardiovascular Status of Nigerian Individuals with Sickle Cell Anaemia. National Postgraduate Medical College of Nigeria. FMCP Dissertation; 1994.
25Klinefelter HF. The hearts in sickle cell anaemia. Am J Med Sci 1942;203:34-51.
26Park MK, Guntheroth WG. Basic measurements. In: Park MK, Guntheroth WG, editors. How to Read Pediatric ECGs. St Louis, MO: Mosby Year Book; 1992.
27Norris S, Johnson CS, Haywood LJ. Sickle cell anemia: Does myocardial ischemia occur during crisis? J Natl Med Assoc 1991;83:209-13.
28de Montalembert M, Maunoury C, Acar P, Brousse V, Sidi D, Lenoir G. Myocardial ischaemia in children with sickle cell disease. Arch Dis Child 2004;89:359-62.
29Fattori A, de Souza RA, Saad ST, Costa FF. Acute myocardial infarction in sickle cell disease: A possible complication of hydroxyurea treatment. Hematol J 2005;5:589-90.
30Ashcroft MT, Serjeant GR, Desai P. Heights, weights, and skeletal age of Jamaican adolescents with sickle cell anaemia. Arch Dis Child 1972;47:519-24.
31Ashcroft MT, Serjeant GR. Body habirus of Jamaican adults with sickle cell anemia. South Med J 1972;65:579-82.
32Mitchell MJ, Carpenter GJ, Crosby LE, Bishop CT, Hines J, Noll J. Growth status in children and adolescents with sickle cell disease. Pediatr Hematol Oncol 2009;26:202-15.
33Badaloo A, Jackson AA, Jahoor F. Whole body protein turnover and resting metabolic rate in homozygous sickle cell disease. Clin Sci (Lond) 1989;77:93-7.
34Hibbert JM, Creary MS, Gee BE, Buchanan ID, Quarshie A, Hsu LL. Erythropoiesis and myocardial energy requirements contribute to the hypermetabolism of childhood sickle cell anemia. J Pediatr Gastroenterol Nutr 2006;43:680-7.
35Hyacinth HI, Gee BE, Hibbert JM. The role of nutrition in sickle cell disease. Nutr Metab Insights 2010;3:57-67.
36Gladwin MT, Sachdev V. Cardiovascular abnormalities in sickle cell disease. J Am Coll Cardiol 2012;59:1123-33.