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Research Article | DOI: https://doi.org/10.31579/2690-8816/173
1Faculty of medical laboratory science, Federal university Otuoke, Bayelsa State.
2Department of Medical Laboratory Science Imo State University Owerri.
*Corresponding Author: Chinedu-Madu Jane Ugochi, Faculty of medical laboratory science, Federal university Otuoke, Bayelsa State.
Citation: Chinedu-Madu J.U., Nnodim Johnkennedy, (2025), Cardiomyopathic Parameters in Sickle Cell Anaemia, J Clinical Research Notes, 6(4); DOI:10.31579/2690-8816/173
Copyright: © 2025, Chinedu-Madu Jane Ugochi. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Received: 04 April 2025 | Accepted: 11 April 2025 | Published: 21 April 2025
Keywords: crp; troponin t; ck-mb; ldh; sickle cell anaemia
Serum levels of creatine kinase (CK-MB), lactate dehydrogenase (LDH), troponin T., and C-reactive protein (CRP) were assessed in sickle cell patients who were attending General Hospital Owerri, Nigeria. One hundred confirmed sickle cell patients (HbSS) between the ages of five and thirty were chosen. As a control, 100 healthy individuals (HbAA) between the ages of 5 and 30 were used. In sickle cell anemia, the levels of CRP, Troponin T., CK-MB, and LDH were considerably higher (p<0.05) than in the control group (HbAA). However, sickle cell disease had far greater levels of CRP, Troponin T, CK-MB, and LDH than HbAA. According to the findings, sickle cell anemia is associated with elevated levels of CRP, Troponin T, CK-MB, and LDH, all of which may raise the risk of cardiovascular disease. In sickle cell anemia, measurements of soluble CRP, Troponin T, CK-MB, and LDH may be useful indicators of an imminent coronary artery insult.
Sickle hemoglobin (HbS), an aberrant hemoglobin that polymerizes upon deoxygenation, is the cause of sickle cell disease (SCD), a collection of hereditary blood diseases. The majority of SCD children born in wealthy nations survive until adulthood with neonatal screening and extensive care, albeit with a markedly reduced life expectancy. The leading cause of death for adults with sickle cell disease is cardiopulmonary problems [1]. Elevated pulmonary artery pressures (PAPs), diastolic dysfunction, and heart chamber dilatation are often observed symptoms in sickle cell disease (SCD), although no single pathophysiologic cause has been identified. Diastolic dysfunction, left atrial dilatation, and left ventricular (LV) enlargement are the hallmarks of cardiomyopathy in sickle cell anemia (SCD). Often, systolic function is good, but myocardial fibrosis and poor perfusion reserve may also be present. A genetic disorder of red blood cell synthesis, sickle cell disease can impact the skeletal system by causing bone infarction and rapid hematopoiesis [2]. High levels of sickle cell hemoglobin are present in people with sickle cell anemia. The sickle cell disease red blood cells produce sickle cell hemoglobin (Hbs), an aberrant hemoglobin [3]. At least as good as cholesterol levels, CRP appears to indicate the likelihood of heart issues. According to one study, having high levels of C-reactive protein increases the chance of having a heart attack by three times. Skeletal and cardiac muscle contain the protein subunit troponin T, which is a component of the troponin complex. Its release into the bloodstream may be a sign of heart attack or injury. Proteins called troponin T (TnT), troponin I (TnI), and troponin C (TnC) combine to create the troponin complex, which is essential for heart and skeletal muscle contraction. The findings of a troponin test can verify that a cardiac attack has damaged the heart muscle. Troponin is released into the blood in greater amounts when the heart is damaged. Therefore, determining the blood's troponin level can also aid in estimating the extent of heart injury. A marker for heart injury, creatine kinase-MB is an isoenzyme of creatine kinase (CK), which is mostly found in heart muscle. It is especially useful for diagnosing or tracking myocardial infarction (heart attack) [4]. One type of enzyme that is mostly present in heart muscle cells is creatine kinase-MB (CK-MB). This test quantifies blood levels of CK-MB. The enzyme creatine kinase (CK) has three different forms, or isoenzymes, including CK-MB. Among these isoenzymes are CK-MM, which is present in the heart and skeletal muscles. Typically, a lactate dehydrogenase (LDH) test quantifies the amount of LDH present in a blood sample. LDH levels are occasionally assessed in bodily fluid samples. This involves testing the peritoneal fluid from the abdomen, the pleural fluid from the chest, and the cerebrospinal fluid from the spine [5].
Lactic acid dehydrogenase is another name for LDH. It's an enzyme. A protein called an enzyme quickens specific chemical reactions in your body. Your cells need LDH to produce energy. Almost every tissue in your body contains it. Your red blood cells, liver, kidneys, and muscles have the highest concentrations of LDH. Adults with SCD die primarily from cardiopulmonary problems, such as heart failure and arrhythmias [7]. According to reports, 25–30% of SCD patients die suddenly for no apparent reason; these deaths are most likely the result of cardiopulmonary events [8]. A worldwide understanding of the cardiac dysfunction in SCD is still inadequate, despite the fact that numerous research over the past 20 years have looked at the cardiac pathology and cardiac mortality in SCD and have identified risk factors for early mortality in SCD. The most reliable indicators of early mortality in people with sickle cell disease (SCD) are diastolic dysfunction, pulmonary hypertension (PH), and elevation of the tricuspid regurgitant jet velocity (TRV) as determined by echocardiography [9].
It is unclear what pathophysiology and mechanisms underlie inexplicable consequences such arrhythmias and sudden death and connect these risk factors to the cardiac phenotype of SCD. This disease has a significant impact on society [6]. Even though sickle cell disease may be killing a lot of people, Nigeria hasn't done much research to improve knowledge, diagnosis, and treatment. This study was conducted to assess the status of CRP, Troponin T., CK-MB, and LDH in sickle cell anemia in light of the aforementioned information. This study was conducted with the intention of improving our understanding of sickle cell anemia by the knowledge gathered from the research.
One hundred HbSS diagnosed by haemoglobin electrophoresis, aged 5 - 30 years were selected for the study. One hundred HbAA normal subjects were used as control. Both male and female were equal.
Blood sample: In all subjects, 5ml of venous blood was collected into a non - anticoagulated tubes. The sample were spun in a Wisterfuge (model 684), centrifuge at 1000g for 10 minutes and the serum collected into a clean dry bijou bottle. The Serum CRP, Troponin T., CK-MB, LDH were measured by enzyme linked immunoabsorbent assay (ELIZA) using standard commercial kits (Bachem UK). Informed consent of the participants was obtained and was conducted in line with the ethical approval of the hospital.
The results were expressed as mean ± standard deviation. The statistical evaluation of data was performed by using students t- test. The level of significance was calculated at P<0>
| Parameters | HbSS | HbAA |
| CRP (mg/L) | 87.10 ±12.43* | 31.11 ±14.15 |
| Troponin T (ng/L) | 89.83 ±14.50* | 36.22 ±15.23 |
| CK-MB (ng/mL) | 48.13 ±11.3* | 27.16 ±10.41 |
| LDH (U/L) | 289.21 ±23.51* | 211.53 ±21.35 |
* Significantly increased when compared with the control at p<0>
Table 1. CRP, Troponin T., CK-MB, LDH levels in sickle cell anaemia and control
A rare but serious side effect of sickle cell disease (SCD) is hypercoagulability, which is a hereditary trait that increases the risk of thromboembolic events [10]. In this study, sickle cell anemia was found to have higher levels of CRP, Troponin T, CK-MB, and LDH than the control group. The stimulation of the vascular endothelium in sickle cell anemia may be the cause of this rise. It is becoming more widely acknowledged that endothelial dysfunction is one of the early signs of vascular disease. Since endothelium damage is the primary cause of sickle cell anemia's onset and progression, endothelial abnormality indicators are implicated [11]. In sickle cell anemia, inflammation may be connected to the rise in CRP. Although it cannot identify the exact origin or location, a rise in C-reactive protein (CRP) suggests inflammation in the body, possibly brought on by an infection, trauma, or chronic illness. Similarly, compared to the control, sickle cell anemia showed a markedly elevated Troponin T level. This might most likely be the result of inflammatory events. Muscle fibers are bound to troponin proteins via troponin T [12].
After an injury, like a heart attack, the heart releases troponin I and troponin T into the circulation. Generally speaking, elevated troponin levels indicate a recent heart attack. Myocardial infarction is the medical term for this attack. Significantly elevated troponin levels are a clear sign of a heart damage, especially if they increase and decrease over several hours. Extremely elevated troponin levels usually signify a heart attack, which can happen when the blood flow to a portion of the heart muscle is abruptly cut off. Lower but still increased troponin levels could indicate a different diagnosis [13]. According to this study, sickle cell anemia patients had higher levels of CK-MB than the control group. One type of enzyme that is mostly present in heart muscle cells is creatine kinase-MB (CK-MB). Every time there is muscular damage, CK is released from the muscle cells and can be found in the blood. CK-MM makes up the majority of the tiny amount of CK that is typically present in the blood. CK-MB is usually only seen in considerable quantities when the heart is injured, whereas CK-BB hardly ever enters the blood. A CK test does not differentiate between the three isoenzymes; instead, it assesses the total level. The CK-MB test can be used to identify whether an elevated level of CK in the blood is caused by heart damage or is more likely to be attributable to skeletal muscle injury. To ascertain whether an elevated creatine kinase (CK) is the result of skeletal muscle injury or cardiac damage, a creatine kinase-MB (CK-MB) test may be performed as a follow-up test. If a person feels chest pain or if their diagnosis is unclear—for example, if they have nonspecific symptoms like nausea, dizziness, shortness of breath, or excessive fatigue—the test is most likely to be ordered [14].
The troponin test, which is more specific for cardiac injury, has largely supplanted the CK and CK-MB tests that were originally the main assays ordered to identify and track heart attacks [15]. When a troponin test is unavailable and a heart attack is suspected, the CK test may occasionally be utilized. A CK-MB test may be performed as a follow-up test in this situation to ascertain whether the high CK is the result of skeletal muscle or cardiac injury [15]. Additionally, compared to the control, sickle cell anemia patients had higher levels of LDH. Nearly every bodily tissue has the enzyme lactate dehydrogenase (LDH), which is essential for the synthesis of energy and whose levels can reveal illness or tissue damage. The enzyme lactate dehydrogenase is found in practically every bodily tissue. Liver illness, anemia, heart attacks, bone fractures, muscular damage, malignancies, and infections including HIV, encephalitis, and meningitis can all result in elevated LDH levels in the blood. Another non-specific indicator of tissue turnover, a typical metabolic process, is LDH. Increases in LDH levels or one of its isozymes are common in several malignancies [16]. As a result, it might not be a distinct tumor marker that can be used to determine the type of cancer. Since routine isozyme testing is typically not available in clinical laboratories and LDH is non-specific.
That sickle cell anemia is linked with increased CRP, Troponin T., CK-MB, LDH level which could lead to increased risk of cardiovascular risk in Sickle cell anaemia. Measurement of soluble CRP, Troponin T., CK-MB, LDH may be helpful marker of impending coronary artery insult in sickle cell anaemia
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