Novel correlation among C3, h-CRP, and WBC in the pathogenesis of ST-elevation myocardial infarction

Subject Areas : Journal of Chemical Health Risks

Hassan Sarhan Sachit ¹ , Ali Mohammed Brakat ² , Gassan Jabbar Auda ³ , Raed Fanoukh Aboqader ^{4 *} , Adnan Taan Thamer ⁵

1 - Consultant Microbiologist, Department of Microbiology and Immunology College of Medicine Al-Ayen Iraqi University Thi-Qar, Iraq
2 - Consultant Microbiologist, Department of Microbiology and Immunology College of Medicine Al-Ayen Iraqi University Thi-Qar, Iraq
3 - Lecturer of Microbiology and Immunology Department of Microbiology and Immunology, College of Medicine Al-Ayen Iraqi University Thi-Qar, Iraq
4 - Al-Aouadi College of Medicine, Al-Ayen Iraqi University, AUIQ, An Nasiriyah, Iraq ORCID: 0009000123087714
5 - Professor Dr of Internal Medicine and Intervention Cardiology, Director of Al-Rabea Cardiac Center, Dean of College of Medicine – Al-Ayen Iraqi University, Thi-Qar, Iraq

Received: 2025-02-04 Accepted : 2025-04-15 Published : 2025-06-15

Keywords: C3, hs-CRP, WBC, LDL, STEMI,

Abstract :

ST-segment elevation myocardial infarction (STEMI) is a major contributor to global morbidity and mortality, necessitating a deeper understanding of its pathophysiology. This study aimed to evaluate the correlation among white blood cell (WBC) counts, complement component C3, high-sensitivity C-reactive protein (hs-CRP), and high and low-density lipoprotein levels in patients diagnosed with STEMI compared to a healthy control group. A total of 60 participants were included, with 30 individuals diagnosed with STEMI and 30 healthy controls, recruited from outpatient clinics in Nassiyria Province, Iraq, between January and December 2024. Blood samples were collected and analyzed for WBC counts, hs-CRP, C3, and LDL levels using standardized laboratory techniques, including ELISA and spectrophotometry. The results indicated a significant increase in hs-CRP, WBC, and LDL levels in the STEMI group compared to controls, with a notable decrease in C3 levels. These findings suggest that elevated inflammatory markers and lipid profiles may play a crucial role in the immunopathogenesis of STEMI. The study highlights the importance of monitoring these biomarkers in clinical settings, as they may provide insights into the inflammatory processes associated with myocardial infarction. Furthermore, the correlation among these markers could inform potential therapeutic strategies to mitigate inflammation and improve patient outcomes post-STEMI. Overall, this research contributes to understanding the complex interplay between lipid metabolism and inflammatory responses in the context of acute myocardial infarction, emphasizing the need for further investigation into targeted interventions for at-risk populations.

References:

References:
1. Reed GW, Rossi JE, Cannon CP (2017) Acute myocardial infarction. Lancet 389:197–210
2. Thygesen K, Alpert JS, White HD, Infarction JETF for the R of M (2007) Universal definition of myocardial infarction. J Am Coll Cardiol 50:2173–2195
3. Lucaci L (2022) ST segment elevation. Rom J Cardiol Vol 32:
4. Akbar H, Foth C, Kahloon R, Mountfort S (2024) Acute ST-Segment Elevation Myocardial Infarction (STEMI). StatPearls
5. Saleh M, Ambrose JA (2018) Understanding myocardial infarction. F1000Research 7:. https://doi.org/10.12688/f1000research.15096.1
6. Gomes DA, Paiva MS, Freitas P, et al (2024) Attainment of LDL-Cholesterol Goals in Patients with Previous Myocardial Infarction: A Real-World Cross-Sectional Analysis. Arq Bras Cardiol 121:e20230242
7. Bohula EA, Giugliano RP, Leiter LA, et al (2018) Inflammatory and cholesterol risk in the FOURIER trial. Circulation 138:131–140
8. Mortensen MB, Nordestgaard BG (2020) Elevated LDL cholesterol and increased risk of myocardial infarction and atherosclerotic cardiovascular disease in individuals aged 70–100 years: a contemporary primary prevention cohort. Lancet 396:1644–1652
9. Alloubani A, Nimer R, Samara R (2021) Relationship between hyperlipidemia, cardiovascular disease and stroke: a systematic review. Curr Cardiol Rev 17:52–66
10. Moldovan R, Ichim VA, Beliș V (2023) Recent perspectives on the early expression immunohistochemical markers in post-mortem recognition of myocardial infarction. Leg Med 64:102293
11. Wysoczynski M, Solanki M, Borkowska S, et al (2014) Complement component 3 is necessary to preserve myocardium and myocardial function in chronic myocardial infarction. Stem Cells 32:2502–2515
12. Damar İH, Eroz R (2022) Argyrophilic nucleolar organizer regions as new biomarkers in ST-Elevation myocardial infarction. J Cardiovasc Dev Dis 9:58
13. Santos-Gallego CG, Picatoste B, Badimón JJ (2014) Pathophysiology of Acute Coronary Syndrome. Curr Atheroscler Rep 16:401. https://doi.org/10.1007/s11883-014-0401-9
14. Onozato T, Wada H, Ogita M, et al (2024) Lower low-lipoprotein cholesterol level at the time of acute myocardial infarction is associated with increased cardiovascular events. Circulation 150:A4140089–A4140089
15. Patti G, Cumitini L, Bosco M, et al (2025) Impact of a personalized, strike early and strong lipid-lowering approach on LDL-cholesterol levels and cardiovascular outcome in patients with acute myocardial infarction. Eur Hear journal Cardiovasc Pharmacother. https://doi.org/10.1093/ehjcvp/pvaf004
16. Brzezinski RY, Banai S, Katz Shalhav M, et al (2024) The CRP troponin test (CTT) stratifies mortality risk in patients with non‐ST elevation myocardial infarction (NSTEMI). Clin Cardiol 47:e24256