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An elevated level of soluble suppression of tumorigenicity 2, but not galectin-3, is associated with the presence of coronary artery disease in hypertensive patients

A Comment to this article was published on 13 November 2024

Abstract

We investigated whether there were associations between coronary artery disease (CAD) and soluble suppression of tumorigenicity (sST2) and galectin-3 levels at the time of coronary artery computed tomography angiography (CCTA) for CAD screening. The subjects consisted of 429 patients who underwent CCTA examination. CAD was diagnosed when there was 50% or more stenosis in the coronary artery. Patient backgrounds were collected and plasma levels of sST2 and galectin-3 were measured. The presence or absence of CAD and factors that contributed to CAD were analyzed for all patients and for those with or without hypertension (HTN). The CAD group had significantly higher sST2 levels than the non-CAD group, whereas there was no significant difference in galectin-3 levels. The number of patients in the non-HTN and HTN groups was 174 and 255, respectively. In the HTN group, the CAD group was significantly older than the non-CAD group and had higher sST2 levels. Multivariate analysis showed that the factors that contributed to CAD in the HTN group were age and sST2 levels. On the other hand, in the non-HTN group, the CAD group was significantly older than the non-CAD group, and had a higher proportion of males and higher sST2 levels, while the contributing factors for the CAD group were age and male gender, but not sST2. In conclusion, a higher level of sST2, but not galectin-3, was a contributing factor for CAD in HTN patients. However, in non-HTN patients, a high level of sST2 was not a contributing factor for CAD.

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References

  1. Oshikawa K, Yanagisawa K, Tominaga S, Sugiyama Y. ST2 protein induced by inflammatory stimuli can modulate acute lung inflammation. Biochem Biophys Res Commun. 2002;299:18–24.

    Article  CAS  PubMed  Google Scholar 

  2. Schmitz J, Owyang A, Oldham E, Song Y, Murphy E, Mcclanahan TK, et al. IL-33, an interleukin-1-like cytokine that signals via the IL-1 receptor-related protein ST2 and induces T helper type 2-associated cytokines. Immunity. 2005;23:479–90.

    Article  CAS  PubMed  Google Scholar 

  3. Villacorta H, Maisel AS. Soluble ST2 testing: a promising biomarker in the management of heart failure. Arq Bras Cardiol. 2016;106:145–52.

    CAS  PubMed  PubMed Central  Google Scholar 

  4. Yancy CW, Jessup M, Bozkurt B, Butler J, Casey DJ, Drazner MH, et al. ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines. Circulation. 2013;128:e240–e327.

    PubMed  Google Scholar 

  5. Tymińska A, Kapłon-Cieślicka A, Ozierański K, Budnik M, Wancerz A, Sypień P, et al. Association of galectin-3 and soluble ST2 with in-hospital and 1-year outcomes in patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention. Pol Arch Intern Med. 2019;129:770–80.

    PubMed  Google Scholar 

  6. Sanada S, Hakuno D, Higgins LJ, Schreiter ER, McKenzie AN, Lee RT. IL-33 and ST2 comprise a critical biomechanically induced and cardioprotective signaling system. J Clin Invest. 2007;117:1538–49.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  7. Manzano-Fernández S, Mueller T, Pascual-Figal D, Truong QA, Januzzi JL. Usefulness of soluble concentrations of interleukin family member ST2 as predictor of mortality in patients with acutely decompensated heart failure relative to left ventricular ejection fraction. Am J Cardiol. 2011;107:259–67.

    Article  PubMed  PubMed Central  Google Scholar 

  8. Weinberg EO, Shimpo M, Hurwitz S, Tominaga S, Rouleau JL, Lee RT. Identification of serum soluble ST2 receptor as a novel heart failure biomarker. Circulation. 2003;107:721–26.

    Article  PubMed  Google Scholar 

  9. Sharma UC, Pokharel S, van Brakel TJ, van Berlo JH, Cleutjens JP, Schroen B, et al. Galectin-3 marks activated macrophages in failure-prone hypertrophied hearts and contributes to cardiac dysfunction. Circulation. 2004;110:3121–8.

    Article  CAS  PubMed  Google Scholar 

  10. Yu L, Ruifrok WP, Meissner M, Bos EM, van Goor H, Sanjabi B, et al. Genetic and pharmacological inhibition of galectin-3 prevents cardiac remodeling by interfering with myocardial fibrogenesis. Circ Heart Fail. 2013;6:107–17.

    Article  CAS  PubMed  Google Scholar 

  11. Rumberger JA. Coronary calcium, as determined by electron beam computed tomography, and coronary disease on arteriogram. Eff Patient’s Sex Diagnosis Circulation. Circulation. 1995;91:1363–67.

    Article  CAS  PubMed  Google Scholar 

  12. Achenbach S. Detection of coronary stenoses by multidetector computed tomography: it’s all about resolution. J Am Coll Cardiol. 2004;43:840–1.

    Article  PubMed  Google Scholar 

  13. Vanhoenacker PK, Heijenbrok-Kal MH, Van Heste R, Decramer I, Van Hoe LR, Wijns W, et al. Diagnostic performance of multidetector CT angiography for assessment of coronary artery disease: meta-analysis. Radiology. 2007;244:419–28.

    Article  PubMed  Google Scholar 

  14. Stephen S. Cardiac computed tomography: indications, applications, limitations, and training requirements: Report of a Writing Group deployed by the Working Group Nuclear Cardiology and Cardiac CT of the European Society of Cardiology and the European Council of Nuclear Cardiology. Eur Heart J. 2008;29:531–56.

    Article  Google Scholar 

  15. Mitsutake R, Miura S, Kawamura A, Saku K. Are metabolic factors associated with coronary artery stenosis on MDCT? Circ J. 2009;73:132–8.

    Article  PubMed  Google Scholar 

  16. Mitsutake R, Miura S, Zhang B, Saku K. HDL-associated factors provide additional prognostic information for coronary artery disease as determined by multi-detector row computed tomography. Int J Cardiol. 2010;143:72–8.

    Article  PubMed  Google Scholar 

  17. Mitsutake R, Miura S, Shiga Y, Uehara Y, Saku K. Association between hypertension and coronary artery disease as assessed by coronary computed tomography. J Clin Hypertens (Greenwich). 2011;13:198–204.

    Article  PubMed  Google Scholar 

  18. Shiga Y, Miura S, Mitsutake R, Kawamura A, Uehara Y, Saku K. Significance of serum high-density lipoprotein cholesterol levels for diagnosis of coronary stenosis as determined by MDCT in patients with suspected coronary artery disease. J Atheroscler Thromb. 2010;17:870–8.

    Article  CAS  PubMed  Google Scholar 

  19. Shiga Y, Miura S, Mitsutake R, Yamagishi S, Saku K. Significance of plasma levels of pigment epithelium-derived factor as determined by multidetector row computed tomography in patients with mild chronic kidney disease and/or coronary artery disease. J Int Med Res. 2011;39:880–90.

    Article  CAS  PubMed  Google Scholar 

  20. Nakamura A, Miura S, Shiga Y, Norimatsu K, Miyase Y, Suematsu Y, Mitsutake R, et al. Is pentraxin 3 a biomarker, a player, or both in the context of coronary atherosclerosis and metabolic factors? Heart Vessels. 2015;30:752–61.

    Article  PubMed  Google Scholar 

  21. Norimatsu K, Miura S, Suematsu Y, Shiga Y, Miyase Y, Nakamura A, et al. Associations between glycated albumin or hemoglobin A1c and the presence of coronary artery disease. J Cardiol. 2015;65:487–93.

    Article  PubMed  Google Scholar 

  22. Yano M, Miura S, Shiga Y, Miyase Y, Suematsu Y, Norimatsu K, et al. Association between smoking habits and severity of coronary stenosis as assessed by coronary computed tomography angiography. Heart Vessels. 2016;31:1061–8.

    Article  PubMed  Google Scholar 

  23. Norimatsu K, Kuwano T, Miura S, Shimizu T, Shiga Y, Suematsu Y, et al. Significance of the percentage of cholesterol efflux capacity and total cholesterol efflux capacity in patients with or without coronary artery disease. Heart Vessels. 2017;32:30–8.

    Article  PubMed  Google Scholar 

  24. Ueda Y, Shiga Y, Idemoto Y, Tashiro K, Motozato K, Koyoshi R, et al. Association between the presence or severity of coronary artery disease and pericardial fat, paracardial fat, epicardial fat, visceral fat, and subcutaneous fat as assessed by multi-detector row computed tomography. Int Heart J. 2018;59:695–704.

    Article  CAS  PubMed  Google Scholar 

  25. Nose D, Shiga Y, Ueda Y, Idemoto Y, Tashiro K, Suematsu Y, et al. Association between plasma levels of PCSK9 and the presence of coronary artery disease in Japanese. Heart Vessels. 2019;34:19–28.

    Article  PubMed  Google Scholar 

  26. Leipsic J, Abbara S, Achenbach S, Cury R, Earls JP, Mancini GJ, et al. SCCT guidelines for the interpretation and reporting of coronary CT angiography: a report of the Society of Cardiovascular Computed Tomography Guidelines Committee. J Cardiovasc Comput Tomogr. 2014;8:342–58.

    Article  PubMed  Google Scholar 

  27. Gensini GG. A more meaningful scoring system for determining the severity of coronary heart disease. Am J Cardiol. 1983;51:606.

    Article  CAS  PubMed  Google Scholar 

  28. Dubois D, Dubois EF. A formula to estimate the approximate surface area if height and weight be known. Arch Intern Med. 1916;17:863–71.

    Article  CAS  Google Scholar 

  29. Vianello E, Dozio E, Tacchini L, Frati L, Corsi Romanelli MM. ST2/IL-33 signaling in cardiac fibrosis. Int J Biochem Cell Biol. 2019;116:105619.

    Article  CAS  PubMed  Google Scholar 

  30. Ojji DB, Opie LH, Lecour S, Lacerda L, Adeyemi OM, Sliwa K. The effect of left ventricular remodelling on soluble ST2 in a cohort of hypertensive subjects. J Hum Hypertens. 2014;28:432–7.

    Article  CAS  PubMed  Google Scholar 

  31. Cuspidi C, Rescaldani M, Sala C, Negri F, Grassi G, Mancia G. Prevalence of electrocardiographic left ventricular hypertrophy in human hypertension: an updated review. J Hypertens. 2012;30:2066–73.

    Article  CAS  PubMed  Google Scholar 

  32. Wei P, Liu L, Wang X, Zong B, Liu X, Zhang M, et al. Expression of soluble ST2 in patients with essential hypertension and its relationship with left ventricular hypertrophy. ESC Heart Fail. 2023;10:303–10.

    Article  PubMed  Google Scholar 

  33. Coglianese EE, Larson MG, Vasan RS, Ho JE, Ghorbani A, McCabe EL, et al. Distribution and clinical correlates of the interleukin receptor family member soluble ST2 in the Framingham Heart Study. Clin Chem. 2012;58:1673–81.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  34. Wu AH, Wians F, Jaffe A. Biological variation of galectin-3 and soluble ST2 for chronic heart failure: implication on interpretation of test results. Am Heart J. 2013;165:995–9.

    Article  CAS  PubMed  Google Scholar 

  35. Zhang Q, Hu M, Ma S. Association of soluble suppression of tumorigenicity with no-reflow phenomenon and long-term prognosis in patients with non-ST-segment elevation acute coronary syndrome after percutaneous coronary intervention. J Atheroscler Thromb. 2021;28:1289–97.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  36. Chen D, Untaru R, Stavropoulou G, Assadi-Khansari B, Kelly C, Croft AJ, et al. Elevated soluble suppressor of tumorigenicity 2 predict hospital admissions due to major adverse cardiovascular events (MACE). J Clin Med. 2023;12:2790.

    Article  PubMed  PubMed Central  Google Scholar 

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Correspondence to Shin-ichiro Miura.

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SM has received honoraria from Daiichi Sankyo, Otsuka Pharma, and Novartis Pharma, scholarships from Abbott Medical and Sumitomo Pharma, and research grants from AMGEN, Bayer Yakuhin, Novo Nordisk Pharma, and MSD.

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Miura-Takahashi, E., Tsudome, R., Suematsu, Y. et al. An elevated level of soluble suppression of tumorigenicity 2, but not galectin-3, is associated with the presence of coronary artery disease in hypertensive patients. Hypertens Res 48, 650–661 (2025). https://doi.org/10.1038/s41440-024-01934-x

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  • DOI: https://doi.org/10.1038/s41440-024-01934-x

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