ANALYSIS OF CHARACTERISTICS OF LIPID METABOLISM DISORDERS IN PATIENTS WITH ACUTE CORONARY SYNDROME AND THEIR ASSOCIATION WITH THYROID FUNCTION
DOI:
https://doi.org/10.11603/1811-2471.2024.v.i1.14390Keywords:
acute coronary syndrome, myocardial infarction, unstable angina, thyroid function, hypothyroidism, subclinical hypothyroidism, thyroid-stimulating hormone, lipid metabolismAbstract
SUMMARY. The paper presents the results of a study of characteristics of lipid metabolism in patients with acute coronary syndrome (ACS) and their association with thyroid-stimulating hormone (TSH) levels.
The aim – to study the characteristics of lipid metabolism disorders in patients with ACS and their association with the TSH levels.
Material and Methods. The study includes 125 patients with ACS aged 36 to 81 (mean age – 60,98± 0,81 years old). The patients were divided into two groups according to thyroid function. Group one (I) included 51 individuals (40.8 %) – hypothyroid patients (TSH level>4 μIU/ml), mean age – 62.51±1.18 years old. Group II included 74 individuals (59.2 %) – euthyroid patients (TSH level 0.4-4 μIU/ml), mean age – 59.93±1.08 years old. The proportion of patients with unstable angina (UA), among all examined individuals, was 28.8 %, and with myocardial infarction (MI) – 71.2 %. More specifically, in Group I, the proportion of patients with UA was 23.53 %, and with MI – 76.47 %. In Group II, the proportion of patients with UA was 32.43 %, and with MI – 67.57 %, p>0.05 between Groups I and II. The proportion of women in Group I was 27.45 % (n=14), and the proportion of men – 72.55 % (n=37). In Group II, the proportions were 29.73 % (n=22) and 70.27 % (n=52) respectively.
The following indicators of lipid metabolism were determined: total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (TG), and non-high-density lipoprotein cholesterol (non-HDL-C). The TSH level was determined to assess thyroid function in the patients examined.
Results. At the study initiation, mean TC, LDL-C, TG, and non-HDL-C levels were significantly higher in Group I patients compared to Group II patients: TC – by 25.17 % (5.76±1.19 mmol/l (I) vs 4.31±1.30 (ІІ), р<0.001), LDL-C – by 31.64 % (3.54±1.10 mmol/l (І) vs 2.42±1.08 (ІІ), р<0.001), TG – by 21.95 % (2.05±1.61 mmol/l (І) vs 1.60±1.24 (ІІ), р<0.05), and non-HDL-C – by 25.78 % (4.46±1.18 mmol/l (І) vs 3.31±1.31 (ІІ) р<0.001) respectively.
The proportion of individuals with TC, LDL-C, and non-HDL-C levels above target ones was also significantly higher in hypothyroid individuals (I): by 39.46 % (92.16±3.76 vs 52.70±5.80 %), 16.96 % (98.04±1.94 vs 81.08±4.55 %), and 10.34 % (94.12±3.29 vs 83.78±4.28 %) respectively as compared to euthyroid patients (II).
The assessment of the association of the mean TSH levels with lipid metabolism indicators shows a moderate direct correlation between the TSH and TC levels (correlation coefficient (r)=0.335, p<0.05), and TSH and LDL-C levels (r=0.384, p<0.01) in the group of hypothyroid patients (I). Such changes were not observed in euthyroid individuals (II).
Conclusions. Mean lipid (TC, LDL-C, TG, and non-HDL-C) major pro-atherogenic fraction levels were significantly higher, by 20–30 %, in the group of hypothyroid patients with ACS (I) compared to euthyroid patients (II). The proportion of individuals with TC, LDL-C, and non-HDL-C levels above target ones was significantly higher among patients with ACS and TSH above 4.0 μIU/ml (I) compared to those with TSH below 4.0 μIU/ml (II) by 39.46 %, 16.96 %, and 10.34 % respectively. A moderate direct correlation was established between the TSH and TC levels (correlation coefficient (r)=0.335, p<0.05), and TSH and LDL-C levels (r=0.384, p<0.01) in the group of hypothyroid patients (I). Such changes were not observed in euthyroid individuals (II).
References
Liu, X.L., He, S., Zhang, S.F., Wang, J., Sun, X.F., Gong, C.M., Zheng, S.J., Zhou, J.C., & Xu, J. (2014). Alteration of lipid profile in subclinical hypothyroidism: a meta-analysis. Medical science monitor : international medical journal of experimental and clinical research, 20, 1432-1441. DOI: 10.12659/MSM.891163.
Delitala, A.P., Fanciulli, G., Maioli, M., & Delitala, G. (2017). Subclinical hypothyroidism, lipid metabolism and cardiovascular disease. European journal of internal medicine, 38, 17-24. DOI: 10.1016/j.ejim.2016.12.015.
Kuusi, T., Taskinen, M.R., & Nikkilä, E.A. (1988). Lipoproteins, lipolytic enzymes, and hormonal status in hypothyroid women at different levels of substitution. The Journal of clinical endocrinology and metabolism, 66(1), 51-56. DOI: 10.1210/jcem-66-1-51.
O'Brien, T., Dinneen, S.F., O'Brien, P.C., & Palumbo, P.J. (1993). Hyperlipidemia in patients with primary and secondary hypothyroidism. Mayo Clinic proceedings, 68(9), 860-866. DOI: 10.1016/s0025-6196(12)60694-6.
Canaris, G.J., Manowitz, N.R., Mayor, G., & Ridgway, E.C. (2000). The Colorado thyroid disease prevalence study. Archives of internal medicine, 160(4), 526-534. DOI: 10.1001/archinte.160.4.526.
Vierhapper, H., Nardi, A., Grösser, P., Raber, W., & Gessl, A. (2000). Low-density lipoprotein cholesterol in subclinical hypothyroidism. Thyroid : official journal of the American Thyroid Association, 10(11), 981-984. DOI: 10.1089/ thy.2000.10.981.
Efstathiadou, Z., Bitsis, S., Milionis, H.J., Kukuvitis, A., Bairaktari, E.T., Elisaf, M.S., & Tsatsoulis, A. (2001). Lipid profile in subclinical hypothyroidism: is L-thyroxine substitution beneficial?. European journal of endocrinology, 145(6), 705-710. DOI: 10.1530/eje.0.1450705.
Caraccio, N., Ferrannini, E., & Monzani, F. (2002). Lipoprotein profile in subclinical hypothyroidism: response to levothyroxine replacement, a randomized placebo-controlled study. The Journal of clinical endocrinology and metabolism, 87(4), 1533-1538. DOI: 10.1210/jcem.87.4.8378.
Walsh, J.P., Bremner, A.P., Bulsara, M.K., O'leary, P., Leedman, P.J., Feddema, P., & Michelangeli, V. (2005). Thyroid dysfunction and serum lipids: a community-based study. Clinical endocrinology, 63(6), 670-675. DOI: 10.1111/ j.1365-2265.2005.02399.x.
Monzani, F., Caraccio, N., Kozàkowà, M., Dardano, A., Vittone, F., Virdis, A., Taddei, S., Palombo, C., & Ferrannini, E. (2004). Effect of levothyroxine replacement on lipid profile and intima-media thickness in subclinical hypothyroidism: a double-blind, placebo-controlled study. The Journal of clinical endocrinology and metabolism, 89(5), 2099-2106. DOI: 10.1210/jc.2003-031669.
Iqbal, A., Jorde, R., & Figenschau, Y. (2006). Serum lipid levels in relation to serum thyroid-stimulating hormone and the effect of thyroxine treatment on serum lipid levels in subjects with subclinical hypothyroidism: the Tromsø Study. Journal of internal medicine, 260(1), 53-61. DOI: 10.1111/j.1365-2796.2006.01652.x.
Torun, A.N., Kulaksizoglu, S., Kulaksizoglu, M., Pamuk, B. O., Isbilen, E., & Tutuncu, N.B. (2009). Serum total antioxidant status and lipid peroxidation marker malondialdehyde levels in overt and subclinical hypothyroidism. Clinical endocrinology, 70(3), 469-474. DOI: 10.1111/ j.1365-2265.2008.03348.x.
Hak, A.E., Pols, H.A., Visser, T.J., Drexhage, H.A., Hofman, A., & Witteman, J.C. (2000). Subclinical hypothyroidism is an independent risk factor for atherosclerosis and myocardial infarction in elderly women: the Rotterdam Study. Annals of internal medicine, 132(4), 270-278. DOI: 10.7326/0003-4819-132-4-200002150-00004.
Hernández-Mijares, A., Jover, A., Bellod, L., Bañuls, C., Solá, E., Veses, S., Víctor, V.M., & Rocha, M. (2013). Relation between lipoprotein subfractions and TSH levels in the cardiovascular risk among women with subclinical hypothyroidism. Clinical endocrinology, 78(5), 777-782. DOI: 10.1111/cen.12064.
Santos-Palacios, S., Brugos-Larumbe, A., Guillén-Grima, F., & Galofré, J.C. (2013). A cross-sectional study of the association between circulating TSH level and lipid profile in a large Spanish population. Clinical endocrinology, 79(6), 874-881. DOI: 10.1111/cen.12216.
Erem, C. (2006). Blood coagulation, fibrinolytic activity and lipid profile in subclinical thyroid disease: subclinical hyperthyroidism increases plasma factor X activity. Clinical endocrinology, 64(3), 323-329. DOI: 10.1111/j.1365- 2265.2006.02464.x.
Thayakaran, R., Adderley, N.J., Sainsbury, C., Torlinska, B., Boelaert, K., Šumilo, D., Price, M., Thomas, G.N., Toulis, K.A., & Nirantharakumar, K. (2019). Thyroid replacement therapy, thyroid stimulating hormone concentrations, and long term health outcomes in patients with hypothyroidism: longitudinal study. BMJ (Clinical research ed.), 366, l4892. DOI: 10.1136/bmj.l4892.
Biondi, B., Bartalena, L., Cooper, D.S., Hegedüs, L., Laurberg, P., & Kahaly, G.J. (2015). The 2015 European Thyroid Association Guidelines on Diagnosis and Treatment of Endogenous Subclinical Hyperthyroidism. European thyroid journal, 4(3), 149-163. DOI: 10.1159/000438750.
Pearce, S.H., Brabant, G., Duntas, L.H., Monzani, F., Peeters, R.P., Razvi, S., & Wemeau, J.L. (2013). 2013 ETA Guideline: Management of Subclinical Hypothyroidism. European thyroid journal, 2(4), 215-228. DOI: 10.1159/ 000356507.
Pesic, M.M., Radojkovic, D., Antic, S., Kocic, R., & Stankovic-Djordjevic, D. (2015). Subclinical hypothyroidism: association with cardiovascular risk factors and components of metabolic syndrome. Biotechnology, biotechnological equipment, 29(1), 157-163. DOI: 10.1080/13102818. 2014.991136.
