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Greener
Journal of Human Physiology and Anatomy
Vol. 3(1), pp. 01-10, 2021
ISSN: 2354-2314
Copyright ©2021, the copyright of this article is
retained by the author(s)
https://gjournals.org/GJHPA
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Increased Heart Rate
and Steady State Among Sickle Cell Patients Seen in Sokoto, North-West Nigeria
1Michael I.
Ikedue;
2Frank B.O. Mojiminiyi; 3Muhammad A. Ndakotsu;
4Simeon A. Isezuo; 5Adamu J. Bamaiyi
1MSc, Department of Physiology. Usmanu
Danfodiyo University, Sokoto, Nigeria.
2PhD, Professor,
Department of Physiology, Usmanu Danfodiyo University, Sokoto, Nigeria.
3MBBS, FMCPath, Associate Professor of
Haematology and Consultant Haematologist Haematology Department, Usmanu
Danfodiyo University, Sokoto, Nigeria.
4MBBS, FMCP, Professor of Medicine and
Consultant Cardiologist, Internal Medicine Department, Usmanu Danfodiyo
University, Sokoto, Nigeria.
5MBBS, PhD, Senior Lecturer, Department of
Physiology, Usmanu Danfodiyo University, Sokoto, Nigeria.
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ARTICLE INFO
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ABSTRACT
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Article No.: 071021064
Type: Research
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Background: Sickle cell
anaemia (SCA) remains a major cause of morbidity and mortality among patients
homozygous for the traits. However, some patients homozygous for the disease
do not have vaso-occlusive crisis as much as others, and the reason for this
is not yet clear.
Objectives: The present study
aimed to assess haemodynamic and haematological parameters among adult SCA
patients (with crisis or in steady state) attending clinics and compared same
with normal adults.
Methods: One hundred and six consenting consecutive
subjects were recruited under the groups; Steady (n = 53) or Crisis (n = 53)
and compared the results with 40 apparently healthy genotype AA adults.
Results: We report that, the steady group, has
significantly less Packed cell volume (PCV) compared to the normal group
(27.39 ±4.36% Vs 33.44 ±1.80%, p <0.00005), but showed higher values of
PCV compared to the crisis group (27.39 ±4.36% Vs 25.67 ± 4.23%, p
<0.0422). The steady group compared to the crisis group, also demonstrated
enhanced heart rate (HR) (84.19 ± 16.53 bpm Vs 78.96 ± 15.90 bpm, p = 0.019)
and longer QTc (429.00 ± 37. 33 Vs 416.15 ±35.10, p = 0.0060).
Conclusions:
Enhanced HR, rate pressure product (RPP) and optimum systolic phase of
the cardiac cycle (QTc) in the steady state sub-group, may result in better
ventricular functions and cardiac output. Therefore, whole blood or
intravenous fluid infusion in SCA patients may improve the chronotropic and
inotropic properties of the heart, enhance tissue perfusion and oxygen
delivery that will help reduce crisis in the patients.
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Accepted: 15/07/2021
Published: 31/07/2021
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*Corresponding Author
Dr Adamu Jibril Bamaiyi
E-mail: adamu,jibril
@udusok.edu,ng; abamaiyi@ yahoo.com
Phone: +2348030925695
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Keywords: Sickle cell anaemia; Homozygous trait; Vaso-occlusive
crisis; Steady state; Heart rate; Whole blood; Intravenous infusion; Cardiac
output; Inotropic; Chronotropic
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REFERENCES
1. Chirico
EN, Faës C, Connes P, Canet-Soulas E, Martin C, Pialoux V. Role of
Exercise-Induced Oxidative Stress in Sickle Cell Trait and Disease. Sports Med.
2016;46(5):629-39.
2. Adeyemo
T, Ojewunmi O, Oyetunji A. Evaluation of high performance liquid chromatography
(HPLC) pattern and prevalence of beta-thalassaemia trait among sickle cell
disease patients in Lagos, Nigeria. The Pan African medical journal.
2014;18:71-.
3. Aliyu
ZY, Kato GJ, Taylor Jt, Babadoko A, Mamman AI, Gordeuk VR, et al. Sickle cell
disease and pulmonary hypertension in Africa: a global perspective and review
of epidemiology, pathophysiology, and management. Am J Hematol.
2008;83(1):63-70.
4. Makani
J, Williams TN, Marsh K. Sickle cell disease in Africa: burden and research
priorities. Ann Trop Med Parasitol. 2007;101(1):3-14.
5. Platt
OS, Brambilla DJ, Rosse WF, Milner PF, Castro O, Steinberg MH, et al. Mortality
in sickle cell disease. Life expectancy and risk factors for early death. The
New England journal of medicine. 1994;330(23):1639-44.
6. Mueller
BU, Martin KJ, Dreyer W, Bezold LI, Mahoney DH. Prolonged QT interval in
pediatric sickle cell disease. Pediatr Blood Cancer. 2006;47(6):831-3.
7. Lamers
L, Ensing G, Pignatelli R, Goldberg C, Bezold L, Ayres N, et al. Evaluation of
left ventricular systolic function in pediatric sickle cell anemia patients
using the end-systolic wall stress-velocity of circumferential fiber shortening
relationship. Journal of the American College of Cardiology.
2006;47(11):2283-8.
8. Manwani
D, Frenette PS. Vaso-occlusion in sickle cell disease: pathophysiology and
novel targeted therapies. Blood. 2013;122(24):3892-8.
9. World
Medical A. World Medical Association Declaration of Helsinki: ethical
principles for medical research involving human subjects. Jama.
2013;310(20):2191-4.
10. Kumar
P, Clark M. In: Kumar P, Clark M, editors. Kumar and Clark's Clinical Medicine:
Elsevier; 2016.
11. Ballas
SK, Smith ED. Red blood cell changes during the evolution of the sickle cell
painful crisis. Blood. 1992;79(8):2154-63.
12. Perloff
D, Grim C, Flack J, Frohlich ED, Hill M, McDonald M, et al. Human blood
pressure determination by sphygmomanometry. Circulation. 1993;88(5 Pt
1):2460-70.
13. Sokolow
M, Lyon TP. The ventricular complex in left ventricular hypertrophy as obtained
by unipolar precordial and limb leads. 1949. Ann Noninvasive Electrocardiol.
2001;6(4):343-68.
14. Ogunlade
O, Akintomide AO. Assessment of voltage criteria for left ventricular
hypertrophy in adult hypertensives in south-western Nigeria. J Cardiovasc Dis
Res. 2013;4(1):44-6.
15. Azeem
T, Vassallo M, Samani NJ. Rapid Review of ECG Interpretation. CRC press, Boca
Raton: Manson Publishing; 2005. 127 p.
16. Bachorik
PS. Collection of blood samples for lipoprotein analysis. Clinical chemistry.
1982;28(6):1375-8.
17. Sperber
GH. Clinically Oriented Anatomy. J Anat. 2006;208(3):393-.
18. Mannheimer
PD. The light-tissue interaction of pulse oximetry. Anesthesia and analgesia.
2007;105(6 Suppl):S10-S7.
19. Batchelder
PB, Raley DM. Maximizing the laboratory setting for testing devices and
understanding statistical output in pulse oximetry. Anesthesia and analgesia.
2007;105(6 Suppl):S85-S94.
20. Brendorp
B, Elming H, Jun L, Køber L, Malik M, Jensen GB, et al. Qtc interval as a guide
to select those patients with congestive heart failure and reduced left
ventricular systolic function who will benefit from antiarrhythmic treatment
with dofetilide. Circulation. 2001;103(10):1422-7.
21. Dahou
A, Toubal O, Clavel MA, Beaudoin J, Magne J, Mathieu P, et al. Relationship
Between QT Interval and Outcome in Low‐Flow Low‐Gradient Aortic Stenosis
With Low Left Ventricular Ejection Fraction. Journal of the American Heart
Association.5(10):e003980.
22. Husby
MP, Soliman EZ, Goldberger JJ, Liu K, Lloyd-Jones D, Durazo-Arvizu R, et al.
The Association between the PR Interval and Left Ventricular Measurements in
the Multiethnic Study of Atherosclerosis. Cardiol Res Pract. 2015;2015:193698-.
23. Nikolaidou
T, Pellicori P, Zhang J, Kazmi S, Goode KM, Cleland JG, et al. Prevalence,
predictors, and prognostic implications of PR interval prolongation in patients
with heart failure. Clin Res Cardiol. 2018;107(2):108-19.
24. Akinbami
A, Dosunmu A, Adediran A, Oshinaike O, Phillip A, Vincent O, et al. Steady
state hemoglobin concentration and packed cell volume in homozygous sickle cell
disease patients in Lagos, Nigeria. Caspian J Intern Med. 2012;3(2):405-9.
25. West
MS, Wethers D, Smith J, Steinberg M. Laboratory profile of sickle cell disease:
a cross-sectional analysis. The Cooperative Study of Sickle Cell Disease. J
Clin Epidemiol. 1992;45(8):893-909.
26. Porter
WB, JamesIII GW. The Heart in Anemia. Circulation. 1953;8:111–6.
27. Sugimoto
T, Sagawa K, Guyton A. Effect of tachycardia on cardiac output during normal
and increased venous return. American Journal of Physiology-Legacy Content.
1966;211(2):288-92.
28. Pakkam
ML, Brown KN. Physiology, Bainbridge Reflex.
StatPearls. Treasure Island (FL): StatPearls Publishing LLC.; 2020.
29. Crystal
GJ, Salem MR. The Bainbridge and the "reverse" Bainbridge reflexes:
history, physiology, and clinical relevance. Anesthesia and analgesia.
2012;114(3):520-32.
30. Reinier
K, Narayanan K, Uy-Evanado A, Teodorescu C, Chugh H, Mack WJ, et al.
Electrocardiographic Markers and the Left Ventricular Ejection Fraction have
Cumulative Effects on Risk of Sudden Cardiac Death. JACC Clin Electrophysiol.
2015;1(6):542-50.
31. Grassi
G. Heart Rate as Marker of Cardiovascular Risk. E-Journal of Cardiology
Practice. 2007;5(21).
32. Lang
CC, Gupta S, Kalra P, Keavney B, Menown I, Morley C, et al. Elevated heart rate
and cardiovascular outcomes in patients with coronary artery disease: clinical
evidence and pathophysiological mechanisms. Atherosclerosis. 2010;212(1):1-8.
33. Hall
AS, Palmer S. The heart rate hypothesis: ready to be tested. Heart.
2008;94(5):561-5.
34. Böhm
M, Schumacher H, Teo KK, Lonn EM, Mahfoud F, Ukena C, et al. Resting heart rate
and cardiovascular outcomes in diabetic and non-diabetic individuals at high
cardiovascular risk analysis from the ONTARGET/TRANSCEND trials. European heart
journal. 2020;41(2):231-8.
35. Chen
X-j, Barywani SB, Hansson P-O, Östgärd Thunström E, Rosengren A, Ergatoudes C,
et al. Impact of changes in heart rate with age on all-cause death and
cardiovascular events in 50-year-old men from the general population. Open
heart. 2019;6(1):e000856.
36. Tian
J, Yuan Y, Shen M, Zhang X, He M, Guo H, et al. Association of resting heart
rate and its change with incident cardiovascular events in the middle-aged and
older Chinese. Scientific Reports. 2019;9(1):6556.
37. Odesina
V. Intravenous support for the patient in sickle cell crisis. J Intraven Nurs.
2001;24(1):32-7.
38. Wethers
DL. Sickle cell disease in childhood: Part II. Diagnosis and treatment of major
complications and recent advances in treatment. Am Fam Physician.
2000;62(6):1309-14.