Prognostic value of inflammatory markers in acute coronary syndrome in a population with premature cardiovascular disease (RCD code: VIII)
Introduction: Inflammation plays a significant role in the development of atherosclerosis, and inflammatory markers could be used in risk assessment of patients with ischaemic heart disease. The use of such markers could be beneficial in younger patients, since in this group, prevention is more effective than treatment of myocardial infarctions, as long‐term prognoses are often unfavourable. Aim: Our goal was
to examine the value of inflammatory biomarkers as an assessment tool for cardiovascular risk in a population with a premature ischaemic heart disease. Materials and Methods: We analysed laboratory test results of 100 consecutive patients hospitalized in the John Paul II Hospital in Krakow, Poland between 2014–2017. Inclusion criteria was cardiovascular disease diagnosed in coronarography under the age of
55 years for women and 45 years for men. We excluded patients with incomplete data and acute infections. The remaining 90 patients were divided into groups based on the reason of admission (myocardial infarction or elective diagnostics). Results: White blood cell count (median of 6.990 × 10 3 per/μl in comparison to 8.535 × 10 3 /μl) and absolute neutrophil count (median of 4060 × 10 3 /μl and 5360 × 10 3 /μl ) were lower in the group admitted for diagnostics. Although inflammatory biomarkers (platelet distribution width, white blood cells) were within normal ranges, we observed higher values (above the medians for studied population) in the group admitted to hospital due to acute coronary syndrome. Conclusion: Inflammatory biomarkers could be useful in the assessment of cardiovascular risk in patients with a premature ischaemic heart disease. Since the measured values of the inflammatory biomarkers were within normal range in the examined population, further studies should be conducted to determine appropriate cut‐off values. JRCD 2019; 4 (2): 37–41
Singh RB, Mengi SA, Xu YJ. Pathogenesis of atherosclerosis: A multifactorial process. Exp Clin Cardiol 2002; 7: 40–53.
Weber C, Noels H. Atherosclerosis: current pathogenesis and therapeutic options. Nat Med 2011; 17: 1410–1422.
Coppinger JA, Cagney G, Toomey S, et al. Characterization of the proteins released from activated platelets leads to localization of novel platelet proteins in human atherosclerotic lesions. Blood 2004; 103: 2096–2104.
Gawaz M, Langer H, May AE. Platelets in inflammation and atherogenesis. J Clin Invest 2005; 115: 3378–3384.
Gordon T, Castelli W, Hjortland M, et al. High density lipoprotein as a protective factor against coronary heart disease. Am J Med 1977; 62: 707–714.
Pearson TA, Mensah GA, Alexander RW, et al. Markers of Inflammation and cardiovascular disease application to clinical and public health practice: a statement for healthcare professionals from the Centers for Disease Control
and Prevention and the American Heart Association. Circulation 2003; 107: 499–511.
Rankin JA. Biological mediators of acute inflammation. AACN Clin Issues 2004; 15: 3–17.
Bhat T, Teli S, Rijal J, et al. Neutrophil to lymphocyte ratio and cardiovascular diseases: a review. Expert Rev Cardiovasc Ther 2013; 11: 55–59.
Casas JP, Shah T, Hingorani AD, et al. C‐reactive protein and coronary heart disease: a critical review. J Intern Med 2008; 264: 295–314.
Alvitigala BY, Azra MAF, Kottahachchi DU, et al. A study of association between platelet volume indices and ST elevation myocardial infarction. Int J Cardiol Heart Vasc 2018; 21: 7–10.
Choudhury L, Marsh JD. Myocardial infarction in young patients. Am J Med 1999; 107: 254–261
Global Health Observatory (GHO) data. Top 10 causes of death, situation and trends. http://origin.who.int/gho/mortality_burden_disease/causes_death/ top_10/en/ (03.06.2019).
Maroszyńska‐Dmoch EM, Wożakowska‐Kapłon B. Choroba wieńcowa w populacji młodych dorosłych: skala problemu, czynniki ryzyka i rokowanie — przegląd literatury. Folia Cardiologica 2014; 9: 267–274.
Choudhury L, Marsh JD. Myocardial infarction in young patients. Am J Med. 1999; 107: 254–261.
Sproston NR, Ashworth JJ. Role of C‐Reactive Protein at Sites of Inflammation and Infection. Front Immunol 2018; 9: 754.
Bairey Merz CN, Johnson BD, Sharaf BL, et al. Hypoestrogenemia of hypothalamic origin and coronary artery disease in premenopausal women: a report from the NHLBI‐sponsored WISE study. J Am Coll Cardiol 2003; 41: 413–419.
Koopman RJ, Mainous III AG, Diaz VA, et al. Changes in age at diagnosis of type 2 diabetes mellitus in the United States, 1988 to 2000. Ann Fam Med 2005; 3: 60–63.
Song SH. Complication characteristics between young‐onset type 2 versus type 1 diabetes in a UK population. BMJ Open Diabetes Research and Care 2015; 3: e000 044.
Pura AM, Wilk M, Kuczyńska G, et al. Acute myocardial infarction risk factors among population with premature cardiovascular disease. Arterial Hypertension 2018; 22: 81–86.
Forget P, Khalifa C, Defour JP, et.al. What is the normal value of the neutrophil‐to‐lymphocyte ratio? BMC Res Notes 2017; 10: 12.
Dong CH, Wang ZM, Chen SY. Neutrophil to lymphocyte ratio predict mortality and major adverse cardiac events in acute coronary syndrome: A systematic review and meta‐analysis. Clin Biochem 2018; 52: 131–136.
Guo TM, Cheng B, Ke L, et.al. Prognostic Value of Neutrophil to Lymphocyte Ratio for In‐hospital Mortality in Elderly Patients with Acute Myocardial Infarction. Curr Med Sci 2018; 38: 354–359.
Paquissi FC. The role of inflammation in cardiovascular diseases: the predictive value of neutrophil–lymphocyte ratio as a marker in peripheral arterial disease. Ther Clin Risk Manag 2016; 12: 851–860.
- There are currently no refbacks.