|Year : 2023 | Volume
| Issue : 1 | Page : 111-114
Estimation of serum uric acid in patients of acute myocardial infarction
Devendra Nath Mishra1, Rajesh Kumar Singh1, Hari Prasad2, Anuj Dwivedi3
1 Department of Biochemistry, TSM Medical College and Hospital, Lucknow, Uttar Pradesh, India
2 Department of Anatomy, TSM Medical College and Hospital, Lucknow, Uttar Pradesh, India
3 Department of Physiotherapy, TSM Medical College and Hospital, Lucknow, Uttar Pradesh, India
|Date of Submission||23-Mar-2022|
|Date of Acceptance||14-Jun-2022|
|Date of Web Publication||21-Jan-2023|
Dr. Devendra Nath Mishra
Department of Biochemistry, TSM Medical College and Hospital, Lucknow - 226 008, Uttar Pradesh
Source of Support: None, Conflict of Interest: None
BACKGROUND: Acute myocardial infarction (AMI), often known as a heart attack, is a medical emergency that is the top cause of mortality for both men and women worldwide. Recent evidence suggests that it is caused by the sudden blockage of a coronary artery by a blood clot, also known as coronary thrombosis. Due to the regional impending of blood supply, heart muscles become damaged. Uric acid has been shown in large cohort studies to be an important independent risk factor for cardiovascular mortality. As serum uric acid (SUA) is an early predictor hence study will help to devise a better remedy for AMI.
AIM: This study aims to study the levels of SUA in patients with AMI as compared to the control.
OBJECTIVE: The primary goal of this study is to examine SUA levels in patients with AMI and to correlate uric acid levels with associated mortality in AMI. The secondary goal is to predict AMI early diagnosis, better management and treatment, and prognosis.
METHODS: The current study was conducted at the department of biochemistry and the central investigation laboratory at our institute, in partnership with the department of medicine, intense cardiac care units, medical intensive care units, and emergency and private hospitals. A total of 100 patients were investigated. There were 50 instances of AMI and 50 age-matched healthy controls. The Microlab 300 analyzers (semi-autoanalyzer) were used to assess SUA concentrations, and the comparisons between the two groups were examined using an unpaired t-test. A P < 0.05 was deemed statistically significant.
RESULTS: There was a substantial rise in the mean level of SUA in cases on the 0, 3rd, and 7th days were 8.503 + 2.976 mg/dl, 5.472 + 2.683 mg/dl, and 4.992 + 1.707 mg/dl day, respectively, which were higher than controls group (3.976 + 0.947 mg/dl). Comparison between control and AMI SUA on 0 and 3rd days was found to be more significant than the 7th day. There was a substantial rise in blood uric acid levels in cases when compared to healthy controls (P < 0.005).
CONCLUSION: Thus, the study shows that blood uric acid levels play a significant role in the diagnosis and therapy of AMI.
Keywords: Acute myocardial infarction, heart attack, serum uric acid
|How to cite this article:|
Mishra DN, Singh RK, Prasad H, Dwivedi A. Estimation of serum uric acid in patients of acute myocardial infarction. Indian J Health Sci Biomed Res 2023;16:111-4
|How to cite this URL:|
Mishra DN, Singh RK, Prasad H, Dwivedi A. Estimation of serum uric acid in patients of acute myocardial infarction. Indian J Health Sci Biomed Res [serial online] 2023 [cited 2023 Jan 28];16:111-4. Available from: https://www.ijournalhs.org/text.asp?2023/16/1/111/368317
| Introduction|| |
Acute myocardial infarction (AMI), also known as a heart attack, is a medical emergency that is the leading cause of death for both men and women worldwide.
AMI is a serious cardiovascular event that is associated with significant morbidity and mortality. In patients with coronary artery disease, total white blood cell count has been identified as an independent predictor of death or myocardial infarction.
Recent evidence suggests that uric acid is a potent antioxidant that may protect against cardiovascular disease and certain cancers. High serum uric acid (SUA) level has been linked to a higher risk of coronary heart disease (CHD) than other risk factors such as hypertension, diabetes, dyslipidemia, and obesity.
Recent evidence suggests that it is caused by heart muscle death caused by the sudden blockage of a coronary artery by a blood clot, also known as coronary thrombosis. Uric acid has been shown in large cohort studies to be an important independent risk factor for cardiovascular mortality. High SUA levels increase platelet reactivity, which mediates inflammation and enhances smooth muscle cell proliferation, likely worsening acute thrombosis., SUA levels have been linked to all major types of cardiovascular disease death, including acute, subacute, and chronic coronary artery disease, heart failure, and stroke.
| Methods|| |
The current study was conducted in collaboration with the department of medicine, departments of biochemistry, and central research laboratory. The study was approved by the institutional ethical committee. Informed consent was obtained from participants. The research was carried out from January 2021 to January 2022. The study includes patients with AMI and healthy controls. Ethical Clearance was obtained from Institutional Ethical Committee of TSM Medical College and Hospital, on 3rd January 2020 with Ref no- TSMMC&H/Admin/784/2020/MEU.
Based on inclusion and exclusion criteria, a total of 100 participants were chosen for the current study. There were 50 patients with AMI and 50 age-matched healthy controls among the 100 participants.
The study covers AMI patients aged 30–75 years who were referred to our institute by various intense cardiac care units, medical intensive care units, and emergency and private hospitals.
Criteria for myocardial infarction refer (at least two must be present):
- Typical (ischemic) symptoms of long-lasting chest pain
- Changes in serial electrocardiograms (ECGs).
- Progression from no Q wave to obvious Q wave
- Lesser Q wave progression mixed with growing ST-segment depression and emerging ST-segment elevation
- Consistent ST-segment elevation with gradual T-wave inversion in daily ECGs
- (3) Cardiac enzyme levels Creatinine Kinase-Megabyte twice the limit of normal.
The age group of 50 normal healthy subjects without major illnesses from the same socioeconomic status were belonging to the same age group as in cases.
The following patients will be excluded from the study:
- Patients suffering from sexually transmitted infections
- Rheumatoid arthritis patients
- Patients suffering from rheumatic fever
- Patients suffering from inflammatory bowel illness
- Patients suffering from neoplastic illness
- Renal failure patients with gout and bacterial infections.
Collection of blood sample
About 3–5 ml of venous blood was collected in a vacutainer by means of a sterile needle, from the anterior antecubital vein. It was allowed to clot for a few minutes and was subjected to centrifugation for 10 min at 3000 rpm to separate the serum and kept at −20°C until analysis was carried out.
The concentration of SUA was tested using the uricase technique on the 0th, 3rd, and 7th days after myocardial infarction using a Microlab 300 analyzer (semi-autoanalyzer).
| Results|| |
The current investigation was conducted at the tertiary hospital's department of biochemistry. A total of 100 people were investigated, with 50 serving as cases (AMI patients) and 50 serving as controls (age matched).
From [Table 1], it is clear that the total sample comprise 50 cases and 50 controls. Among cases, 42 were male which constitute 84% and 8 were female, which constitute 16%. Out of 50 controls, 41 were male which constitute 82%, whereas nine were female which constitute 18%. The mean age of cases and controls were 56.53 ± 8.68 years and 51.90 ± 10.39 years, respectively. This is statistically significant P < 0.02 [Table 2].
It is clear form [Table 3] that 41 (82%) of 50 AMI cases had risk factors such as hypertension, diabetes mellitus, and smoking habits. Out of 41 participants with risk factors, 18 (43.9%) had hypertension, 13 (31.7%) had diabetes mellitus, and 10 (24.3%) were smokers.
[Table 4] demonstrates that males were more likely than females in the case group. The highest number of men were 14 (28%) in age groups 41-50 years, followed by 12 (24%) in age groups 51-60 years, and 7 (14%) in age categories above 61 years. In the case group, the majority of males were between the ages of 30 and 40. In instances, the largest number of females were 5 (10%) who were 51-60 years old, followed by 3 (6%) females who were 41-50 years old. While 2 (4%) females were between the ages of 30 and 40, and 2 (4%) were beyond the age of 61 years.
|Table 4: Age- and sex-wise distribution of acute myocardial infarction in case and control|
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As shown in [Table 5], mean SUA in patients with AMI group measured on 0, 3rd and 7th days were 8.503 + 2.976 mg/dl, 5.472 + 2.683 mg/dl, and 4.992 + 1.707 mg/dl day, respectively, which were higher than controls group (3.976 + 0.947 mg/dl). Comparison between control and SUA on 0 and 3rd days was found to be more significant than that of 7th day. Unpaired t-test showed that there was a significant increase in SUA level in cases as compared to controls (P < 0.005).
|Table 5: Comparison of serum uric acid at 0 day, 3rd day, and 7th day in case and control group|
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The comparison of mean SUA levels between controls and cases was also presented graphically in [Bar Diagram 1].
| Discussion|| |
Uric acid is an independent predictor of major adverse cardiovascular events in patients with coronary artery disease. High SUA levels increase platelet reactivity, which mediates inflammation and stimulates smooth muscle cell proliferation, likely exacerbating acute thrombosis., We attempted to assess SUA levels in AMI patients in this study.
The current study was carried out to look into the possible role of SUA in patients with AMI. Our study included 50 cases and 50 controls. There were 42 male cases (84%) and 8 female cases (16%). Out of 50 controls, 41 (82%) were male and 9 were female (18%) [Table 1]. The mean age of cases and controls were 56.53 ± 8.68 years and 51.90 ± 10.39 years, respectively. This is statistically significant [Table 2].
Our result correlated well with findings shown by Nadkar and Jain Agrawal et al., Baruah et al., Saab et al., Badiger et al., and Chaithra and Harsha Gosar et al.
As shown in [Table 3], that 41 (82%) of 50 AMI cases had risk factors such as hypertension, diabetes mellitus, and smoking habits. Out of 41 participants with risk factors, 18 (43.9%) had hypertension, 13 (31.7%) had diabetes mellitus, and 10 (24.3%) smoked.
[Table 4] this shows that males in the case group were more likely than females. The most men 14 (28%) were in the age groups 41-50 years, followed by 12 (24%) in the age groups 51-60 years, and 7 (14%) in the age groups over 61 years. The majority of the males in the case group were between the ages of 30 and 40. In some cases, 5 (10%) of the females were 51-60 years old, followed by 3 (6%) females 41-50 years old. While 2 (4%) of females were between the ages of 30 and 40, and 2 (4%) were over the age of 61 years. Our result correlated well with findings showed by Kulkarni et al. (2020).
In our study, mean uric acid levels in cases on 0, 3rd, and 7th days were 8.503 ± 2.976 mg/dl, 5.472 ± 2.683 mg/dl, and 4.992 ± 1.707 mg/dl day, respectively, which were higher than the controls group (3.976 ± 0.947 mg/dl). Comparison between control and SUA on 0 and 3rd days was found to be more significant than the 7th day. Unpaired t-test showed that there was a significant increase in SUA level in cases as compared to controls (P < 0.005). Our study correlated with Gosar et al. and Kulkarni et al.
Under ischemic conditions, xanthine oxidase activity and uric acid synthesis are increased in vivo, and thus elevated SUA may act as a marker of underlying tissue myocardial ischemia. Endothelial dysfunction, oxidative metabolism, platelet adhesiveness, hemorheology, and aggregation are all negatively impacted by hyperuricemia. According to the evidence, high uric acid is a poor prognostic factor in patients with mild-to-severe heart failure., Jacobs, in his study, discovered that hyperuricemia was a strong risk factor for MI.,
The reasons for high uric acid levels in tissue ischemia are as follows:
- Adenosine synthesized locally by vascular smooth muscle in cardiac tissue is rapidly degraded by the endothelium to uric acid, which undergoes rapid efflux to the vascular lumen due to low intracellular pH and negative membrane potential (Kroll et al.,).
- Xanthine oxidase activity and uric acid synthesis are increased in vivo under ischemic conditions (Kogure K et al., 1999).
Thus, in AMI as duration progresses, there are different levels of ischemia. This could lead to different levels of uric acids.
| Conclusion|| |
Thus, the study concludes that evaluation of SUA in serum play an important role in the diagnosis and management of AMI.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Thygesen K, Alpert JS, Jaffe AS, Simoons ML, Chaitman BR, White HD, et al
. Third Universal Definition of Myocardial Infarction. J Ame Coll Cardiol 2012;16:1581-98.
Khan HA, Alhomida AS, Sobki SH, Al Moghairi A. Significant increases in monocyte counts and serum creatine kinase in acute myocardial infarction versus general infections. Indian J Pathol Microbiol 2012;55:474-7.
] [Full text]
Gandiah P, Venkateshwarlu N, Naveen Kumar M, Indira G, Sivarajappa P. Serum uric acid estimation in acute myocardial infarction – A prognostic indicator. Int J Recent Trends Sci Tech 2013;9:199-204.
Gosar P, Singh AP, Gosar P, Rani B. Role of serum uric acid as a marker of short-term mortality in acute myocardial infarction. Int J Contemp Med Res 2020;7:1-4.
Baruah M, Nath CK, Chaudhury B, Devi R, Ivvala AS. A study of serum uric acid and C-reactive protein in acute myocardial infarction. Int J Basic Med Sci Pharm 2012;2:21-4.
Padma V, Banupriya A. Serum uric acid levels in acute myocardial infarction. Int J Adv Med 2017;4:1-4.
Bickel C, Rupprecht HJ, Blankenberg S, Rippin G, Hafner G, Daunhauer A, et al.
Serum uric acid as an independent predictor of mortality in patients with angiographically proven coronary artery disease. Am J Cardiol 2002;89:12-7.
Akgul O, Uyarel H, Pusuroglu H, Gul M, Isiksacan N, Turen S, et al.
Predictive value of elevated uric acid in Turkish patients undergoing primary angioplasty for ST elevation myocardial infarction. Acta Cardiol Sin 2014;30:119-27.
Tiongco RH, Te CG Jr, Punzalan FE, Uy CC, Gonda VM. High sensitive CRP and short-term cardiovascular risk among patients with acute myocardial infaraction. ACTA Medicaphilippina 2012;46:64-8..
Joshi P, Islam S, Pais P, Reddy S, Dorairaj P, Kazmi K, et al.
Risk factors for early myocardial infarction in South Asians compared with individuals in other countries. JAMA 2007;297:286-94.
Gosar P, Singh AP, Gosar P, Rani B. Evaluating serum uric acid levels in patients with acute myocardial infarction. Int J Adv Med 2020;7:1256-9.
Nadkar MY, Jain VI. Serum uric acid in acute myocardial infarction. J Assoc Physicians India 2008;56:759-62.
Agrawal S, Aundhkar SC, Patange A, Panpalia NG, Jain S, Garg R. Evaluate the role of serum uric acid in acute myocardial infarction as a prognostic marker. Int J Health Sci 2014;4:120-8.
Saab G, Whooley MA, Schiller NB, Ix JH. Association of serum phosphorus with left ventricular mass in men and women with stable cardiovascular disease: Data from the heart and soul study. Am J Kidney Dis 2010;56:496-505.
Badiger RH, Dinesha V, Hosalli A, Ashwin SP. Hs-C reactive protein as an indicator for prognosis in acute myocardial infarction. J Sci Soc 2014;41:118-21. [Full text]
Chaithra SP, Harsha MM. High sensitive C-reactive protein in acute MI and its correlation with one year mortality. J Evol Med Dent Sci 2013;2:5293-7.
Kulkarni MR. Assessment of serum uric acid levels in patients with acute myocardial infarction. Academia J Med 2020;3:46-48.
Ochiai ME, Barretto AC, Oliveira MT Jr., Munhoz RT, Morgado PC, Ramires JA. Uric acid renal excretion and renal insufficiency in decompensated severe heart failure. Eur J Heart Fail 2005;7:468-74.
Jacobs D. Hyperuricaemia and myocardial infarction. S Afr Med J 1972;46:367-9.
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.
Kogure K, Ishizaki M, Nemoto M, et al
. Evaluation of serum uric acid changes in different forms of hepatic vascular inflow occlusion in human liver surgeries. Life Sci.1999; 64:305-13
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]