• Users Online: 175
  • Print this page
  • Email this page


 
 
Table of Contents
ORIGINAL ARTICLE
Year : 2021  |  Volume : 18  |  Issue : 3  |  Page : 230-234

The prognostic value of serum uric acid in ST-segment elevation myocardial infarction


1 Azadi Teaching Hospital, Duhok, Iraq
2 Department of Medicine, College of Medicine, University of Duhok, Kurdistan Region, Iraq

Date of Submission03-Apr-2021
Date of Acceptance29-Jul-2021
Date of Web Publication29-Sep-2021

Correspondence Address:
Sulaiman Yaseen Mohammed
Azadi Teaching Hospital, Duhok.
Iraq
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/MJBL.MJBL_23_21

Get Permissions

  Abstract 

Background and Objective: Acute myocardial infarction is the leading cause of mortality and morbidity across the world. Acute myocardial infarction with ST-segment elevation has been considered a common cardiac emergency and has considerable morbidity and mortality. The role of uric acid (UA) in the mortality rate of ST-segment elevation myocardial infarction (STEMI) was examined in the present study. Materials and Methods: In this prospective study, 107 patients diagnosed with STEMI aged 18 years and older in the coronary care unit at Azadi Teaching Hospital, Duhok, Iraq from April 20, 2017 to December 20, 2017 were followed up for 1 month to determine the 30-day mortality in relation to serum UA level. Results: The mean age of patients was 55.27±13.59 years. The inferior type of STEMI was the most prevalent one among the patients (45.1%). Serum UA was not significantly different in both the groups (P > 0.05). Conclusion: The study did not show UA as a risk factor for mortality in patients with STEMI.

Keywords: Mortality rate, risk factor, ST-elevated myocardial infarction, uric acid


How to cite this article:
Mohammed SY, Rasool MT. The prognostic value of serum uric acid in ST-segment elevation myocardial infarction. Med J Babylon 2021;18:230-4

How to cite this URL:
Mohammed SY, Rasool MT. The prognostic value of serum uric acid in ST-segment elevation myocardial infarction. Med J Babylon [serial online] 2021 [cited 2021 Dec 3];18:230-4. Available from: https://www.medjbabylon.org/text.asp?2021/18/3/230/327032




  Introduction Top


Acute myocardial infarction (MI) is defined as a myocardial necrosis event in which unstable ischemic syndrome is a causative factor.[1] Acute MI is the leading cause of mortality and morbidity across the world. Acute MI with or without ST-segment elevation MI (STEMI or non-STEMI) is considered to be a common cardiac emergency and has considerable morbidity and mortality.[2] STEMI happens when a major epicardial coronary vessel is obstructed due to thrombus formation or other factors. STEMI is a life-threatening condition and must be diagnosed and managed quickly through coronary revascularization such as percutaneous coronary intervention.[3] Practically, acute MI is diagnosed through clinical evaluation, electrocardiogram (ECG), biochemical indicators, pathological evolution, and imaging techniques.[2]

Since the past three to four decades, epidemiological features of acute MI have been changed substantially. Currently, low- and middle-income countries have been shifted to have considerable global burden of cardiovascular and acute MI.[4]

Rupture or erosion in a vulnerable, fatty, and atherosclerotic coronary plaque has been shown to be an initial mechanism for acute MI. This mechanism leads to circulating blood exposure to highly thrombogenic core and matrix materials in the plaque.[5] Currently, the number of cases due to erosion is increasing compared with the cases due to rupture factor.[6] Total occlusion due to thrombus leads to STEMI.[7] A partial occlusion, or occlusion in the presence of collateral circulation, leads to non-STEMI or unstable angina.[8]

STEMI is one type of MI that the myocardium of heart muscle has died owing to blood supply obstruction. The ST-segment backs to the flat section in an ECG reading representing the interval between jagged heartbeats. This segment will appear abnormally elevated during MI.[9] STEMI is a clinical syndrome depicted by characteristic symptoms of myocardial ischemia in relation to more than 20 min ST elevation (STE) and subsequent release in biomarkers of myocardial necrosis.[7],[10]

Significance of the study

Cardiac myocytes produce adenosine which is responsible for vasodilation of arteries. Under some circumstances, the adenosine level is raised substantially which results in hypoxia and tissue ischemia.[11] Consequently, endothelium degrades adenosine to uric acid (UA) quickly. Due to the increase in UA concentrations and decrease in intracellular pH, UA effluxed to the vascular lumen.[12] Therefore, it may be that the UA level is an indicator of ischemia severity and tissue hypoxia. The higher concentration of UA level has been shown to be a risk factor for coronary artery disease (CAD) or a prognostic factor for mortality and morbidity in patients with CAD. Some investigators showed the higher concentration of UA in STEMI mortality.[13],[14]

New therapeutic methods are established for those patients who develop heart failure following STEMI, and the aim is to reduce STEMI mortality. It is highly important to examine the role of serum UA to reduce mortality in STEMI patients. The role of serum UA in the 30-day mortality rate of STEMI was examined in the present study.


  Patients and Methods Top


Study design

In the prospective cohort study, 107 patients between 25 and 83 years were included. They have been diagnosed with STEMI in the Internal Medicine Department at Azadi Teaching Hospital in Duhok, Iraq.

Inclusion criteria

The patients met the eligibility criteria if they were 18 years and older, male or female, and met the diagnostic criteria of STEMI, including resting chest pain lasting for more than 30 min; having typical ischemic ST-elevation in ECG leads; and rise in cardiac troponins.

Exclusion criteria

In this study, the patients with following characteristics were excluded:

  • Patients diagnosed with acute non-STEMI;


  • Impaired renal function;


  • Hypothyroidism;


  • Malignancy;


  • Gout;


  • Inflammatory diseases;


  • Those using corticosteroid or cytotoxic drugs.


  • Data collection methods

    The questionnaire of collecting data consisted of three following sections: The first section had sociodemographic factors and clinical history including age, gender, risk factors, and disease types. The second section consisted of biochemical indicators, including troponin, UA, creatinine, random blood sugar, total cholesterol (TC), and triglyceride (TG). In the last or third section, the mortality of patients was recorded following 1 month of hospital admission.

    Measurement and diagnostic criteria

    The general characteristics of the patients listed in the following were collected: age in year; gender as male or female; hypertension; diabetes mellitus; smoking; dyslipidemia; and family history of CAD.

    The diagnosis of acute STEMI was established based on signs, symptoms, and biochemical indicators, according to the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.[7] Diagnostic STE is defined as new STE at the J-point in at least two contiguous leads >2 mm (0.2 mV) in men or >1.5 mm (0.15 mV) in women in leads V2-V3 and/or >1 mm (0.1 mV) in other contiguous chest or limb leads.[1],[15]

    Laboratory measurements

    Venous blood samples were taken from the patients in the morning in a fasting status. Serum UA, TC, and TG were measured with a 7600 Automatic Biochemistry Analyzer (Hitachi Limited Corporation, Germany). Baseline serum uric acid ≥7 mg/dL for men and ≥6 mg/dL for women was diagnosed with hyperuricemia.[16]

    Dyslipidemia was assessed through the biochemical measurement in the hospital according to the American Association of Clinical Endocrinologists and American College of Endocrinology Guidelines (AACE)[17] as follows:

  • TC: desirable < 200 mg/dL, borderline high 200–239 mg/dL, high > 239 mg/dL.


  • High-density lipoprotein-cholesterol: dyslipidemia low < 40 mg/dL in males and < 50 mg/dL in females.


  • Low-density lipoprotein-cholesterol: optimal < 100 mg/dL, near optimal 100–129 mg/dL, borderline high 130–159 mg/dL, high 160–189 mg/dL, very high > 189 mg/dL.


  • TG: normal < 150 mg/dL, high 150–199 mg/dL.


  • Statistical methods

    The frequency percentage and mean standard deviation were used for descriptive purposes of the study such as mortality rate. The independent t-test, one-way analysis of variance (ANOVA), and Fisher’s exact tests were performed for statistical difference of UA in sample size. The level of less than 0.05 was considered as statistically significant difference. Statistical Package for Social Sciences (SPSS) version 23.00 (IBM) was used for statistical calculations.

    Ethical considerations

    The ethical approval of the present study was obtained from the Iraqi Board. The participation was completely optional. The current study did not apply any intervention on the patients.


      Results Top


    The study found that of the 107 patients recruited in the study, more than two-thirds of them (75.7%) were males and remaining 24.3% were female patients. Hypertension and smoking were the most prevalent risk factors, 15.9% and 14.0%, respectively. Close to half of them had multiple risk factors for MI (45.8%). The mean of the patients was 55.27 (SD:13.59) years. The most common type of STEMI was inferior type (45.1%), followed by lowest was lateral (1.0%) and inferior and septal (1.0%). In the study sample size, mortality rate was 4.7%, as shown in [Table 1].
    Table 1: Baseline characteristics of patients

    Click here to view


    The mean serum of UA and random blood sugar were 6.15 (SD: 1.96) mg/dL and 187.50 (SD: 111.72) mg/dL, respectively. The mean values of TC and TG were 205.52 (SD: 77.76) mg/dL and 211.21 (SD: 103.89) mg/dL, respectively. The median and interquartile values of serum creatinine were 0.86 and 0.38 mg/dL, respectively [Table 2].
    Table 2: Biochemical indicators of patients

    Click here to view


    The impact of serum UA on mortality rate was examined in [Table 3]. The study did show that mortality has not been affected by serum UA (P=0.435). The mean value of UA in deceased patients following 1 month was 6.89±1.98 mg/dL and the mean value of UA in live patients was 6.11±196 mg/dL.
    Table 3: Impact of serum UA on mortality in patients with STEMI

    Click here to view


    Similarly, the study showed that means of UA in different STEMI types were comparable (P=0.679) [Table 4].
    Table 4: Level of UA in patients with different types of STEMI

    Click here to view



      Discussion Top


    This study showed that the mortality rate is 4.7% following 1 month of hospital admission. In addition, the investigator did not find UA as a risk factor for mortality in STEMI patients. Similar levels of UA were found in patients with different STEMI types.

    Other investigators have examined the effect of UA on mortality and morbidity among patients with STEMI as well. For instance, Hajizadeh et al.[18] enrolled 608 patients with STEMI in a prospective cohort study between December 21, 2012 and February 10, 2014 to find out the effect of UA on patients’ mortality, morbidity, left ventricular ejection fraction, and atrial and ventricular arrhythmia. They showed that those patients with higher serum UA level have higher Killip class after STEMI. In agreement with the current study, they did not find that short- and mid-term mortality is associated with UA (P=0.31). Their finding is congruent with some other studies as well.[13],[19],[20],[21],[22]

    In our study, we examined the role of UA on short-term mortality (1 month) and found no significant association between UA and mortality in patients with STEMI. The long-term mortality has also been investigated by Hajizadeh et al.[18] and found no substantial relationship with UA. However, some other studies have shown a substantial serum UA and an increase in mortality in patients with STEMI. For example, Kojima et al.[23] divided the study patients into four groups according to the serum UA level. They showed that the patients with serum UA level more than 4.5 mg/dL have 3.5 times higher mortality rate when compared with those with serum UA below 3.0 mg/dL. However, the mean of their patients was 67 years, significantly different from our study (55.27 years). In addition, Omidvar et al.[24] showed that serum UA concentration of 7 mg/dL or greater plays a prognostic role for short-term and in-hospital mortality (30-day) in male hyperuricemic patients only with odds ratio of 3.76 for short-term mortality, but not for female patients, similar to some other studies.[25]

    In contrast to those studies showed higher serum UA as a risk factor for STEMI or not, the studies have shown that it is an independent risk factor for short- or long-term adverse events in patients with STEMI.[26] It is significantly associated with cardiovascular disease and increase in mortality and occurrence of CAD in clinical and epidemiological investigations.[27],[28],[29]

    By taking into account the wide variety of studies conducted on UA role in STEMI patients mortality, it is evident that its role as a prognostic factor is controversial. However, the Framingham Heart study as one of the most important studies did not show this association.[30] Therefore, most of the medical societies do not consider serum UA as a risk factor of short- or long-term mortality in patients with STEMI.[30]

    It is recommended that future attempts focus on average hospital stay in STEMI patients with hyperuricemia in comparison to patients with non-hyperuricemia. Different cut-off values for serum UA have been considered in these kinds of studies. Still, there is no internationally accepted normal range for male and female populations making hard to establish a between-study comparison.

    Limitations of the study

    The findings reported in the present study must be traced in the light of study design and sampling methods. The study investigators were unable to follow the patients for longer than 1 month. Possibly, long-term follow-up with larger sample size is required to get the better picture of impact of UA on the cardiovascular system. In addition, the severity of disease has not been measured through Killip class to predict the mortality risk owing to time limitation of the present study.


      Conclusions and Recommendations Top


    The present study shows 4.7% of mortality rate in patients with STEMI. In addition, the study did not show any association between serum UA levels and mortality rate in STEMI patients. It is recommended that clinicians attempt to reduce the level of UA in STEMI patients as it may lead to other medical conditions. Clinicians must trace the mortality expectation of STEMI patients in other risk factors such as smoking and dietary behaviors.



     
      References Top

    1.
    Thygesen K, Alpert JS, Jaffe AS, Simoons ML, Chaitman BR, White HD, et al; Writing Group on the Joint ESC/ACCF/AHA/WHF Task Force for the Universal Definition of Myocardial Infarction; ESC Committee for Practice Guidelines (CPG). Third universal definition of myocardial infarction. Eur Heart J 2012;33:2551-67.  Back to cited text no. 1
        
    2.
    Anderson JL, Morrow DA. Acute myocardial infarction. N Engl J Med 2017;376:2053-64.  Back to cited text no. 2
        
    3.
    Healio. Coronary Artery Disease—STEMI Topic Review Web: Healio; 2010. Available from: https://www.healio.com/cardiology/learn-the-heart/cardiology-review/topic-reviews/coronary-artery-disease-stemi. [Last accessed on 20 Oct 2019].  Back to cited text no. 3
        
    4.
    Murray CJ, Barber RM, Foreman KJ, Ozgoren AA, Abd-Allah F, Abera SF, et al. Global, regional, and national disability-adjusted life years (DALYs) for 306 diseases and injuries and healthy life expectancy (HALE) for 188 countries, 1990–2013: Quantifying the epidemiological transition. Lancet 2015;386:2145-91.  Back to cited text no. 4
        
    5.
    Libby P. Mechanisms of acute coronary syndromes and their implications for therapy. N Engl J Med 2013;368:2004-13.  Back to cited text no. 5
        
    6.
    Libby P, Bornfeldt KE, Tall AR. Atherosclerosis: Successes, surprises, and future challenges. Circ Res 2016;118:531-4.  Back to cited text no. 6
        
    7.
    O’Gara PT, Kushner FG, Ascheim DD, Casey DE Jr, Chung MK, de Lemos JA, et al; CF/AHA Task Force. 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction: Executive summary: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2013;127:529-55.  Back to cited text no. 7
        
    8.
    Amsterdam EA, Wenger NK, Brindis RG, Casey DE Jr, Ganiats TG, Holmes DR Jr, et al; ACC/AHA Task Force Members; Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons. 2014 AHA/ACC Guideline for the Management of Patients with Non-ST-Elevation Acute Coronary Syndromes: Executive Summary: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation 2014;130:2354-94.  Back to cited text no. 8
        
    9.
    Fogoros RN. ST-segment elevation myocardial infarction, the most severe type of heart attack 2017. Available from: https://www.verywell.com/stemi-st-segment-elevation-myocardial-infarction-1746032. [Last accessed on 20 Oct 2019].  Back to cited text no. 9
        
    10.
    Hwang C, Levis JT. ECG diagnosis: ST-elevation myocardial infarction. Perm J 2014;18:e133.  Back to cited text no. 10
        
    11.
    Raatikainen MJ, Peuhkurinen KJ, Hassinen IE. Contribution of endothelium and cardiomyocytes to hypoxia-induced adenosine release. J Mol Cell Cardiol 1994;26:1069-80.  Back to cited text no. 11
        
    12.
    Kroll K, Bukowski TR, Schwartz LM, Knoepfler D, Bassingthwaighte JB. Capillary endothelial transport of uric acid in guinea pig heart. Am J Physiol 1992;262:H420-31.  Back to cited text no. 12
        
    13.
    Chen L, Li XL, Qiao W, Ying Z, Qin YL, Wang Y, et al. Serum uric acid in patients with acute ST-elevation myocardial infarction. World J Emerg Med 2012;3:35-9.  Back to cited text no. 13
        
    14.
    Car S, Trkulja V. Higher serum uric acid on admission is associated with higher short-term mortality and poorer long-term survival after myocardial infarction: Retrospective prognostic study. Croat Med J 2009;50:559-66.  Back to cited text no. 14
        
    15.
    Harrigan RA, Chan TC. What is the ECG differential diagnosis of ST segment elevation? In: Brady WJ, Truwit JD, editors. Critical Decisions in Emergency and Acute Care Electrocardiography. Chichester: Wiley-Blackwell; 2009. p. 417-27.  Back to cited text no. 15
        
    16.
    Kanbay M, Solak Y, Dogan E, Lanaspa MA, Covic A. Uric acid in hypertension and renal disease: The chicken or the egg? Blood Purif 2010;30:288-95.  Back to cited text no. 16
        
    17.
    Jellinger PS, Handelsman Y, Rosenblit PD, Bloomgarden ZT, Fonseca VA, Garber AJ, et al. American Association of Clinical Endocrinologists and American College of Endocrinology Guidelines for Management of Dyslipidemia and Prevention of Cardiovascular Disease. Endocr Pract 2017;23:1-87.  Back to cited text no. 17
        
    18.
    Hajizadeh R, Ghaffari S, Salehi R, Mazani S, Aghavali S. Association of serum uric acid level with mortality and morbidity of patients with acute ST-elevation myocardial infarction. J Cardiovasc Thorac Res 2016;8:56-60.  Back to cited text no. 18
        
    19.
    Homayounfar S, Ansari M, Kashani KM. Evaluation of independent prognostic importance of hyperuricemia in hospital death after acute myocardial infarction. Saudi Med J 2007;28:759-61.  Back to cited text no. 19
        
    20.
    Lazzeri C, Valente S, Chiostri M, Sori A, Bernardo P, Gensini GF. Uric acid in the acute phase of ST elevation myocardial infarction submitted to primary PCI: Its prognostic role and relation with inflammatory markers: A single center experience. Int J Cardiol 2010;138:206-9.  Back to cited text no. 20
        
    21.
    Akpek M, Kaya MG, Uyarel H, Yarlioglues M, Kalay N, Gunebakmaz O, et al. The association of serum uric acid levels on coronary flow in patients with STEMI undergoing primary PCI. Atherosclerosis 2011;219:334-41.  Back to cited text no. 21
        
    22.
    Basar N, Sen N, Ozcan F, Erden G, Kanat S, Sokmen E, et al. Elevated serum uric acid predicts angiographic impaired reperfusion and 1-year mortality in ST-segment elevation myocardial infarction patients undergoing percutaneous coronary intervention. J Investig Med 2011;59:931-7.  Back to cited text no. 22
        
    23.
    Kojima S, Sakamoto T, Ishihara M, Kimura K, Miyazaki S, Yamagishi M, et al; Japanese Acute Coronary Syndrome Study (JACSS) Investigators. Prognostic usefulness of serum uric acid after acute myocardial infarction (the Japanese Acute Coronary Syndrome Study). Am J Cardiol 2005;96:489-95.  Back to cited text no. 23
        
    24.
    Omidvar B, Ayatollahi F, Alasti M. The prognostic role of serum uric acid level in patients with acute ST elevation myocardial infarction. J Saudi Heart Assoc 2012;24:73-8.  Back to cited text no. 24
        
    25.
    Wasserman A, Shnell M, Boursi B, Guzner-Gur H. Prognostic significance of serum uric acid in patients admitted to the department of medicine. Am J Med Sci 2010;339:15-21.  Back to cited text no. 25
        
    26.
    Kaya MG, Uyarel H, Akpek M, Kalay N, Ergelen M, Ayhan E, et al. Prognostic value of uric acid in patients with ST-elevated myocardial infarction undergoing primary coronary intervention. Am J Cardiol 2012;109:486-91.  Back to cited text no. 26
        
    27.
    Baker JF, Krishnan E, Chen L, Schumacher HR. Serum uric acid and cardiovascular disease: Recent developments, and where do they leave us? Am J Med 2005;118:816-26.  Back to cited text no. 27
        
    28.
    Brodov Y, Chouraqui P, Goldenberg I, Boyko V, Mandelzweig L, Behar S. Serum uric acid for risk stratification of patients with coronary artery disease. Cardiology 2009;114:300-5.  Back to cited text no. 28
        
    29.
    Bae MH, Lee JH, Lee SH, Park SH, Yang DH, Park HS, et al. Serum uric acid as an independent and incremental prognostic marker in addition to N-terminal pro-B-type natriuretic peptide in patients with acute myocardial infarction. Circ J 2011;75: 1440-7.  Back to cited text no. 29
        
    30.
    Feig DI, Kang DH, Johnson RJ. Uric acid and cardiovascular risk. N Engl J Med 2008;359:1811-21.  Back to cited text no. 30
        



     
     
        Tables

      [Table 1], [Table 2], [Table 3], [Table 4]



     

    Top
     
      Search
     
        Similar in PUBMED
       Search Pubmed for
       Search in Google Scholar for
     Related articles
        Access Statistics
        Email Alert *
        Add to My List *
    * Registration required (free)  

     
      In this article
    Abstract
    Introduction
    Patients and Methods
    Results
    Discussion
    Conclusions and ...
    References
    Article Tables

     Article Access Statistics
        Viewed90    
        Printed8    
        Emailed0    
        PDF Downloaded12    
        Comments [Add]    

    Recommend this journal