Measurement of Lipid Profile, LDH, Spo2 and Heart Rate in COVID-19 Patients Associated with Cardiovascular Problems in Thi Qar Province

• Mohammed Mahdi abd

  Ministry of Education, Thi-Qar Education Directorate, Thi-Qar

The study aims to investigate the physiological characteristics of COVID-19 patients, considering demographic factors such as gender, age, infection severity, and associated cardiovascular complications. This is particularly relevant as several clinical trials have established a correlation between COVID-19 and cardiovascular disease, a grave illness that has impacted individuals globally. The study recruited 142 COVID-19 patients and 50 control individuals from hospitals and isolation centers in Thi Qar Province. Patients were categorized based on infection severity, with 54 moderate, 53 severe, and 35 critical cases. The findings reveal that 60.6% of patients were male, and the majorities (50%) were between 50-69 years old. Patients experienced various cardiovascular complications, including myocardial infarction (5.6%), arrhythmia (4.2%), heart failure (2.8%), and pulmonary embolism (2.8%), with 3.5% experiencing more than one adverse event.Compared to the control group, COVID-19 patients had significantly higher lactate dehydrogenase (LDH) concentrations and heart rates, but lower levels of total cholesterol (TC), high-density lipoprotein (HDL), low-density lipoprotein (LDL), triglycerides (TG), and oxygen saturation (SPO2). The study also identified gender and age-related differences in these parameters, highlighting the importance of considering individual characteristics when assessing the impact of COVID-19 on cardiovascular health.

Highlights: 

1. COVID-19 patients showed increased LDH and heart rates but lower cholesterol and oxygen saturation levels.
2. Gender, age, and infection severity influenced cardiovascular health outcomes in patients.
3. The study emphasizes personalized approaches to manage COVID-19-related cardiovascular risks.

Keywords: COVID, LDH, Lipid Profile, Spo2, Cardiovascular Disease.

[1] A. P. S. Akshay, V. S. M. Veena, K. B. Teja, and S. J. Tomar, "Emerging human viral diseases, Volume I: respiratory and haemorrhagic fever," in Springer Nature Singapore, Singapore, 2023, pp. 157–187.

[2] E. Bilehjani, S. Fakhari, H. Farzin, A. Tajlil, and N. D. Nader, "Diagnosis and treatment of cardiovascular manifestations of COVID-19: a narrative review," Acta Cardiologica, vol. 78, no. 5, pp. 1–7, 2023.

[3] N. Vishwakarma, R. B. Goud, M. P. Tirupattur, and L. C. Katwa, "The eye of the storm: investigating the long-term cardiovascular effects of COVID-19 and variants," Cells, vol. 12, no. 17, p. 2154, 2023.

[4] H. F. Okab, M. B. Salih, and B. A. Jarulla, "Immunopathy of COVID-19 patients without chronic disease: proinflammatory and anti-inflammatory cytokines attributable to disease severity," Laboratory Research in Clinical Practice, vol. 13, no. 1, pp. 47–59, 2024.

[5] S. H. Tveit, P. L. Myhre, and T. Omland, "The clinical importance of high-sensitivity cardiac troponin measurements for risk prediction in non-cardiac surgery," Expert Rev. Mol. Diagn., vol. 23, no. 6, pp. 535–544, 2023.

[6] E. Cojocaru, C. Cojocaru, C. E. Vlad, and L. Eva, "Role of the renin-angiotensin system in long COVID’s cardiovascular injuries," Biomedicines, vol. 11, no. 7, p. 2004, 2023.

[7] F. H. Fadhil, "Association between the demographic characteristics of patients and the severity of COVID-19," University of Thi-Qar Journal of Science, vol. 10, no. 2, pp. 92–97, Dec. 2023.

[8] J. Hippisley-Cox et al., "Risk of severe COVID-19 disease with ACE inhibitors and angiotensin receptor blockers: cohort study including 8.3 million people," Heart, vol. 106, no. 19, pp. 1503–1511, 2020.

[9] J. Mohammadshahi et al., "Role of lipid profile and its relative ratios to predict in-hospital mortality COVID-19," J. Lipids, 2023.

[10] H. F. Okab, M. B. Salih, and B. A. Jarulla, "Evaluation of CXCL 10 and IL-10 in COVID-19 pneumonia," University of Thi-Qar Journal of Science, vol. 10, no. 2, pp. 92–97, Dec. 2023.

[11] A. Bellia et al., "Atherogenic dyslipidemia on admission is associated with poorer outcome in COVID-19," Diabetes Care, vol. 44, no. 9, pp. 2149–2157, 2021.

[12] J. S. Whittle et al., "Respiratory support for adult patients with COVID‐19," J. Am. Coll. Emerg. Physicians Open, vol. 1, no. 2, pp. 95–101, 2020.

[13] R. Sami et al., "A one-year hospital-based prospective COVID-19 open-cohort study," PLoS One, vol. 15, no. 11, p. e0241537, 2020.

[14] R. A. Raxmatjon o'g'li, "Anatomical properties of the heart and physiological basis of the heart," Int. Multidiscip. J. Res. Dev., vol. 10, no. 12, 2023.

[15] N. Makris, Z. Kotsialou, and S. Gall, "Origin and regulation of the normal heartbeat," Anaesth. Intensive Care Med., 2024.

[16] S. S. Rathore et al., "Myocarditis associated with COVID‐19," Int. J. Clin. Pract., vol. 75, no. 11, p. e14470, 2021.

[17] A. Farhana and S. L. Lappin, "Biochemistry, lactate dehydrogenase," StatPearls Publishing, 2020.

[18] G. S. Gupta, "The lactate and the lactate dehydrogenase in inflammatory diseases," Inflammation, vol. 45, no. 6, pp. 2091–2123, 2022.

[19] S. M. Michienzi and M. E. Badowski, "Can vitamins and/or supplements provide hope against coronavirus?," Drugs Context, vol. 9, 2020.

[20] B. Fialek et al., "Diagnostic value of lactate dehydrogenase in COVID-19: A systematic review," Cardiol. J., vol. 29, no. 5, pp. 751–758, 2022.

[21] H. K. Hussain et al., "Prediction of blood lactate levels in children," in Proc. 3rd Int. Conf. Artif. Intell. Smart Energy (ICAIS), pp. 1163–1169, 2023.

[22] A. A. Alsaidan et al., "The potential role of SARS‐CoV‐2 infection in acute coronary syndrome," Immun. Inflamm. Dis., vol. 11, no. 3, p. e798, 2023.

[23] D. McGuone et al., "COVID-19 outcomes in patients with pre-existing cardiovascular disease," Br. J. Card. Nurs., vol. 19, no. 1, pp. 1–13, 2024.

[24] S. Pujhari et al., "Clotting disorder in severe acute respiratory syndrome coronavirus 2," Rev. Med. Virol., vol. 31, no. 3, p. e2177, 2021.

[25] M. Levi and T. Iba, "COVID-19 coagulopathy: is it disseminated intravascular coagulation?," Intern. Emerg. Med., vol. 16, pp. 309–312, 2021.

[26] P. Tandon et al., "Unraveling links between chronic inflammation and long COVID: Workshop report," J. Immunol., vol. 212, no. 4, pp. 505–512, 2024.

[27] W. Wang and P. M. Kang, "Oxidative stress and antioxidant treatments in cardiovascular diseases," Antioxidants, vol. 9, no. 12, p. 1292, 2020.

[28] L. Yu, Y. Liu, and Y. Feng, "Cardiac arrhythmia in COVID‐19 patients," Ann. Noninvasive Electrocardiol., vol. 29, no. 2, p. e13105, 2024.

[29] S. Babapoor-Farrokhran et al., "Arrhythmia in COVID-19," SN Compr. Clin. Med., vol. 2, pp. 1430–1435, 2020.

[30] S. H. Yoon et al., "Assessment of the proarrhythmic effects of repurposed antimalarials," Front. Pharmacol., vol. 14, p. 1220796, 2023.

[31] N. G. Kounis et al., "SARS-CoV-2 infection affects the human cardiovascular system: a narrative review," Balkan Med. J., vol. 41, no. 1, p. 7, 2024.

[32] H. M. van Goor et al., "Circadian patterns of heart rate in COVID-19 patients," PLoS One, vol. 17, no. 7, p. e0268065, 2022.

[33] M. Prokop et al., "CO-RADS: a categorical CT assessment scheme for COVID-19," Radiology, vol. 296, no. 2, pp. E97–E104, 2020.

[34] J. Kozakiewicz et al., "Pulmonary embolism: pathophysiology, diagnosis and unusual cases," Qual. Sport, vol. 39, p. 58909, 2025.

[35] I. Safiriyu et al., "Impact of COVID-19 infection on the clinical outcomes of pulmonary embolism hospitalizations,"

[36] F. Al-Ani, S. Chehade, and A. Lazo-Langner, "Thrombosis Risk Associated With COVID-19 Infection: A Scoping Review," Thrombosis Research, vol. 192, pp. 152–160, 2020.

[37] R. Root-Bernstein, "COVID-19 Autoimmune Coagulopathies and Myocarditis," International Journal of Molecular Sciences, vol. 24, no. 3, p. 3001, 2023.

[38] P. P. Nigade, S. S. Dhanagar, and V. S. Nikam, "Venous Thromboembolism in Infectious Diseases," Comparative Clinical Pathology, pp. 1–17, 2025.

[39] T. Zhao et al., "Altered Lipid Profile in COVID-19 Patients and Metabolic Reprogramming," Frontiers in Microbiology, vol. 13, p. 863802, 2022.

[40] J. T. Sun et al., "Lipid Profile Features and Their Associations With Disease Severity," Frontiers in Cardiovascular Medicine, vol. 7, p. 584987, 2020.

[41] M. A. Perrone et al., "Effects of Reduced Physical Activity on the Lipid Profile During COVID-19 Lockdown," International Journal of Environmental Research and Public Health, vol. 18, no. 16, p. 8858, 2021.

[42] J. Malik et al., "Effect of COVID-19 on Lipid Profile and Its Correlation With Acute Phase Reactants," medRxiv, 2021.

[43] I. Zitnanova et al., "Sex Differences in LDL and HDL Subfractions," Clinical Biochemistry, vol. 79, pp. 9–13, 2020.

[44] Y. Chang et al., "Association of Triglyceride/HDL-C Ratio With Severe Complications of COVID-19," Heliyon, 2023.

[45] J. E. Tanner and C. Alfieri, "The Fatty Acid Lipid Metabolism Nexus in COVID-19," Viruses, vol. 13, no. 1, p. 90, 2021.

[46] J. A. Fried et al., "The Variety of Cardiovascular Presentations of COVID-19," Circulation, vol. 141, no. 23, pp. 1930–1936, 2020.

[47] G. D. Mironova, N. V. Belosludtseva, and M. A. Ananyan, "Regulators of Oxidative Stress in COVID-19," European Review for Medical and Pharmacological Sciences, vol. 24, no. 16, 2020.

[48] A. I. Alayash, "The Impact of COVID-19 on Oxygen Homeostasis," Frontiers in Physiology, vol. 12, p. 711976, 2021.

[49] A. Masumoto et al., "Impact of Serum LDH on the Prognosis of COVID-19," Journal of Cardiology, vol. 79, no. 4, pp. 501–508, 2022.

[50] H. Liu et al., "IL-6, Ferritin, and LDH With Venous Thromboembolism in COVID-19," BMC Infectious Diseases, vol. 24, no. 1, pp. 1–13, 2024.

[51] E. Poggiali et al., "LDH and CRP as Predictors of Respiratory Failure in COVID-19," Clinica Chimica Acta, vol. 509, pp. 135–138, 2020.

[52] T. Mokhtari et al., "COVID-19 and Multiorgan Failure: A Narrative Review," Journal of Molecular Histology, vol. 51, pp. 613–628, 2020.