Introduction: AMI is the leading cause of death for both men and women all over the world. Acute myocardial infarction is myocardial necrosis resulting from acute obstruction of coronary artery. Calcium ions are involved in myocardial contraction, and during acute myocardial infarction. The disruption of blood flow to the heart muscle can lead to an imbalance in calcium levels. This disruption can cause calcium overload with myocardial cells, leading to cellular injury and dysfunction. Magnesium has properties of myocardial cryoprotection, the pathophysiological explanations of which in açute myocardial infarction include prevention of arrythmia, antiplatelet effect, prevention of reperfusion injury and coronary vasodilation. Increased serum uric acid (SUA) levels have been associated with various pathologic processes such as increased oxidative stress, inflammation and endothelial dysfunction. Troponin I is highly specific to cardiac muscle so its presence in the blood stream is a reliable indicator of heart muscle damage. The Elevation in troponin I levels is used as a diagnostic marker for AMI.
Material and Methods:A comparative and cross-sectional study was conducted in the Department of Biochemistry in Rangaraya Medical College, Kakinada over a period of 4 months. Sampling Type: Casual sampling of newly diagnosed AMI patients attending the OPD. Controls are recruited from healthy individuals attending the OPD for health checkup. Sample Size: 50 newly diagnosed AMI patients constitute group 1, 50 age and sex matched healthy individuals in group 2. Results: The Group 1 has a higher mean age (54.36±6.70 years) compared to Group 2 (51.3±7.98 years), suggesting that on average, participants in Group 1 are older than those in Group 2. The higher mean calcium level in Group 2 (9.276±1.24 mg/dl) compared to Group 1 (8.548±1.73 mg/dl) suggests that, on average, participants in Group 2 have higher calcium levels than those in Group 1. Comparing the two groups:- Group 2 has a higher mean magnesium level (2.062 mg/dl) compared to Group 1 (1.892 mg/dl). The standard deviation for magnesium levels is smaller in Group 2 (0.41) compared to Group 1 (0.71), indicating that magnesium levels in Group 2 are less variable around the mean compared to Group 1. Group 1 has a mean uric acid level of 7.824 mg/dl with a standard deviation of 5.95 mg/dl. Group 2 has a mean uric acid level of 6.188 mg/dl with a standard deviation of 2.10 mg/dl. Group 1 has a mean Troponin I level of 4463 pg/ml with a standard deviation of 5226.92 pg/ml. Group 2 has a mean Troponin I level of 10.048 pg/ml with a standard deviation of 14.03 pg/ml. Conclusion: Acute MI is the 3rd largest cause of death in the population. If untreated it causes necrosis of the myocardium and finally death of the patient. Magnesium has cytoprotective properties, anti-platelet effect, prevents arrhythmias and reperfusion injury and coronary vasodilation. So it should be estimated. Calcium ions are involved in myocardial contraction. It plays a role in coagulation cascade. It forms blood clots that obstruct blood flow so medications targeting calcium channel to reduce myocardial oxygen load and improve coronary circulation. Uric acid may be a marker for increased cardiovascular risk. Troponin I is highly specific and diagnostic of acute MI.
AMI is the leading cause of death for both men and women all over the world. Acute myocardial infarction is myocardial necrosis resulting from acute obstruction of coronary artery. [1] Symptoms include chest discomfort with or without dyspnea, nausea and diaphoresis. Diagnosis is by ECG and the presence or absence of biomarkers. Treatment is with antiplatelets, anticoagulants, nitrates, beta-blockers, statins and reperfusion therapy. [2] For ST segment elevation Myocardial infarction emergency reperfusion is via fibrinolytic drugs, percutaneous intervention or coronary artery Bypass graft Surgery. [3]
Calcium plays a crucial role in several processes. Calcium ions are involved in myocardial contraction, and during acute myocardial infarction. The disruption of blood flow to the heart muscle can lead to an imbalance in calcium levels. [4] This disruption can cause calcium overload with myocardial cells, leading to cellular injury and dysfunction. Additionally, calcium plays a role in imitating the coagulation cascade, contributing to the formation of blood clots that can further obstruct blood flow to the heart. [5] Management strategies for AMI often involve medications that target calcium channels to reduce myocardial oxygen demand and improve coronary blockers. [6]
Magnesium has properties of myocardial cytoprotection, the pathophysiological explanations of which in açute myocardial infarction inculde prevention of arrythmia, antiplatelet effect, prevention of reperfusion injury and coronary vasodilation. [7] Although several studies have evaluated the role of magnesium administration in patients with acute myocardium infartion, the clinical impact of such a therapy in this condition has been controversial largely as a result of conflicting data from randomised controlled trials. [8] The data available to date do not favor the routine administration of intravenous magnesium in patients with myocardial infraction, but this should not preclude magnesium administration to replenish low serum magnesium concentrations or use of magnesium Sulfate for treatment of torsades de pointes in patients with myocardial infarction. [9]
Increased serum uric acid (SUA) levels have been associated with various pathologic processes such as increased oxidative stress, inflammation and endothelial dysfunction. Recent epidemiological evidence suggests that increased SUA maybe related to acute myocardial infraction. [10] Uric acid levels tend to rise during acute myocardial infractions due to increased cellular breakdown, particularly of nucleic acids. This increase in uric acid Levels has been associated with worse outcomes in heart attack patients, potentially due to its role in inflammation and oxidative stress. Elevated uric acid levels during a heart attack might indicate a more severe myocardial injury and could be a marker for increased cardiovascular risk. [11]
Troponin I is highly specific to cardiac muscle so its presence in the blood stream is a reliable indicator of heart muscle damage. The Elevation in troponin I levels is used as a diagnostic marker for AMI. Troponin I level begin to rise within hours of the onset of a heart attack peaking around 24-48hrs afterward. [12]
Aim:
The present study aims to assess Uric Acid, Magnesium, Calcium and Troponin I levels in Acute MI patients
A comparative and cross-sectional study was conducted in the Department of Biochemistry in Rangaraya Medical College, Kakinada over a period of 4 months.
Inclusion Criteria:
Exclusion Criteria:
Controls Selection
Sampling Type: Casual sampling of newly diagnosed AMI patients attending the OPD. Controls are recruited from healthy individuals attending the OPD for health checkup. Sample Size: 50 newly diagnosed AMI patients constitute group 1, 50 age and sex matched healthy individuals in group 2.
Data Collection
Statistical Analysis:
SPSS software is used for data analysis after taking for normal distribution of data. Normal variables mean +/- SD is used to summarise this data. ANOVA and students t test are used for comparison of means among the different variables for detection of significant difference. P value less than 0.05 is used for identification of statistically significant difference of variables among groups. Pearson’s correlation test is used for calculation of r value to determine strength of association between variables.
Informed Consent: Oral and written informed consent is taken from the study participants.
Table 1: Distribution of Gender
|
Group 1 |
Group 2 |
||
Gender |
Frequency |
Percentage |
Frequency |
Percentage |
Male |
30 |
60 |
31 |
62 |
Female |
20 |
40 |
19 |
38 |
Total |
50 |
100 |
50 |
100 |
In table 1 shows the gender distribution within each group both in terms of frequencies and percentages of the total respondents.
For Group 1:
- Total number of respondents: 50
- Male respondents: 30
- Female respondents: 20
For Group 2:
- Total number of respondents: 50
- Male respondents: 31
- Female respondents: 19
Table 2: Mean Age group
Age |
Group 1 |
Group 2 |
Mean±SD |
54.36±6.70 |
51.3±7.98 |
In table 2 (mean) and (standard deviation) of ages within each group. Group 1 has a higher mean age (54.36±6.70 years) compared to Group 2 (51.3±7.98 years), suggesting that on average, participants in Group 1 are older than those in Group 2. The standard deviation indicates the variability or spread of ages around the mean within each group.
Table 3: Distribution of Mean Calcium Levels
Biochemical Parameters |
Group 1 Mean±SD |
Group 2 Mean±SD |
Calcium (mg/dl) |
8.548±1.73 |
9.276±1.24 |
In table 3, the higher mean calcium level in Group 2 (9.276±1.24 mg/dl) compared to Group 1 (8.548±1.73 mg/dl) suggests that, on average, participants in Group 2 have higher calcium levels than those in Group 1. The standard deviations show that calcium levels in Group 1 have higher variability compared to Group 2, where the values are more tightly clustered around the mean.
Table 4: Distribution of Mean Magnesium Levels
Biochemical Parameters |
Group 1 Mean±SD |
Group 2 Mean±SD |
Magnesium (mg/dl) |
1.892±0.71 |
2.062±0.41 |
In table 4, Comparing the two groups:- Group 2 has a higher mean magnesium level (2.062 mg/dl) compared to Group 1 (1.892 mg/dl). The standard deviation for magnesium levels is smaller in Group 2 (0.41) compared to Group 1 (0.71), indicating that magnesium levels in Group 2 are less variable around the mean compared to Group 1. Therefore, on average, participants in Group 2 tend to have higher magnesium levels compared to those in Group 1, and the variability in magnesium levels is lower in Group 2.
Table 4: Distribution of Mean Uric Acid Levels
Biochemical Parameters |
Group 1 Mean±SD |
Group 2 Mean±SD |
Uric Acid (mg/dl) |
7.824±5.95 |
6.188±2.10 |
In table 4, Group 1 has a mean uric acid level of 7.824 mg/dl with a standard deviation of 5.95 mg/dl. Group 2** has a mean uric acid level of 6.188 mg/dl with a standard deviation of 2.10 mg/dl.
Group 2 has a lower mean uric acid level (6.188 mg/dl) compared to Group 1 (7.824 mg/dl). The standard deviation for uric acid levels is smaller in Group 2 (2.10 mg/dl) compared to Group 1 (5.95 mg/dl), indicating that uric acid levels in Group 2 are less variable around the mean compared to Group 1. Therefore, on average, participants in Group 2 tend to have lower uric acid levels compared to those in Group 1, and the variability in uric acid levels is lower in Group 2 as well.
Table 5: Distribution of Mean Troponin I Levels
Biochemical Parameters |
Group 1 Mean±SD |
Group 2 Mean±SD |
Troponin I (pg/ml)
|
4463.99±5226.92 |
10.048±14.03 |
In table 5, Group 1 has a mean Troponin I level of 4463 pg/ml with a standard deviation of 5226.92 pg/ml. Group 2 has a mean Troponin I level of 10.048 pg/ml with a standard deviation of 14.03 pg/ml.
Comparing the two groups:- Group 1 has a higher mean Troponin I level (4463.99 pg/ml) compared to Group 1 (10.048 pg/ml). The standard deviation for Troponin I levels is much smaller in Group 2 (14.03 pg/ml) compared to Group 1 (5226.92 pg/ml), indicating that Troponin I levels in Group 2 are much less variable around the mean compared to Group 1.
Therefore, on average, participants in Group 1 tend to have higher Troponin I levels compared to those in Group 2, and the variability in Troponin I levels is significantly lower in Group 2.
In our study, the higher mean calcium level in Test Group (9.276±1.24 mg/dl) compared to Control Group (8.548±1.73 mg/dl) suggests that, on average, participants in Group 2 have higher calcium levels than those in Group 1. The standard deviations show that calcium levels in Group 1 have higher variability compared to Group 2, where the values are more tightly clustered around the mean. The main finding of this study is that serum calcium concentrations were significantly decreased in patients with newly diagnosed AMI.
In our study, compared to patients without first incident AMI, serum calcium was significantly decreased in patients with first incident AMI. Our results were consistent with previous findings. Our results were also similar to parts of results from the Tromso study, although serum calcium levels were higher in men with a history of AMI. [13] The Tromso study revealed the relationship between serum calcium and history of AMI but not AMI, which may account for the different results. [13] The relationship between low serum calcium levels and first incident AMI was further detected in patients grouped by sex and age after full adjustment.
Serum calcium exists in the free or ionized form, which regulates cell function and systems physiology, about 40% binds to albumin, which reflects the serum albumin levels, and the remaining 10% is bound to anions such as phosphate, bicarbonate, and lactate. [14] Although low serum calcium concentrations might increase first incident AMI, the mechanisms remain unclear. Possible mechanisms were described in detail. Serum calcium tightly tied to cardiovascular risk factors. First of all, the serum calcium concentrations of the hypertensive group were lower than that of the normotensive group in older men in East China. [15] Serum calcium participates in vascular smooth muscle cell contractility and inhibits renin secretion, which mediates blood pressure. High serum calcium has a protective function in hypertension. The presence of classical independent risk factors, such as Lp (a), hypertension, DM, smoking, and hyperlipidemia, increases the incidence of AMI. [16]
In our study, comparing the two groups:- Group 2 has a higher mean magnesium level (2.062 mg/dl) compared to Group 1 (1.892 mg/dl). The standard deviation for magnesium levels is smaller in Group 2 (0.41) compared to Group 1 (0.71), indicating that magnesium levels in Group 2 are less variable around the mean compared to Group 1. Therefore, on average, participants in Group 2 tend to have higher magnesium levels compared to those in Group 1, and the variability in magnesium levels is lower in Group 2.
In an Indian study, the comparison between the serum magnesium level between the control group and the acute myocardial infarction group showed that the mean level of serum magnesium among the group of patients was 1.01 with a range of 0.42-1.56, and it was considerably lower (P<0.01) compared to the control group (2.2 mEq/L). [17] Although we did not compare our findings among AMI patients with the control group, the findings showed that AMI patients experienced a low level of serum magnesium, which was in agreement with the previous study. [18]
According to a report, low magnesium may be caused by a number of things, including insufficient magnesium intake, ongoing stress, malabsorption, and medications such as diuretics. [19] This was in agreement with our findings as we found that a significantly higher proportion of AMI patients were administrating diuretics when assessing their history.
It was reported that individuals managed by intravenous magnesium post infarction were at a significantly lower risk of dying from ischemic heart disease-related complications. [20] However, there were no mortality cases reported in our study. Additionally, a study by Akila et al. conducted on AMI patients revealed that those patients with low magnesium levels were more predisposed to get arrhythmia. [21] Also, there were no arrhythmia cases reported in our study.
The study showed that the MI risk and all-cause mortality depended on both Serum uric acid exposure and on the time course of Serum uric accumulation. The relationship between Serum uric acid and MI has been debated with conflicting results in previous studies. The AMORIS study16 and the Rotterdham study15 have been demonstrated a significant association between Serum uric acid & MI. In contrast, the Tromso study25 and the NHANES (National Health and Nutrition Examination Survey) III study26 have failed to establish an independent association between Serum uric acid and MI.
First, Serum uric acid is a product of xanthine oxidoreductase, which is known to be one of the most important sources of reactive oxygen species, High Serum uric acid is therefore associated with increased vascular endothelial function, vascular smooth muscle cell proliferation and oxidative stress thereby increasing the risk of MI and all-cause mortality. 27,28 Second, high Serum uric acid exerts a plethora of deleterious effects in cells and thus may be directly involved in the pathophysiological characteristics of MI and all-cause mortality. 29 Third, high Serum uric acid is correlated with almost all known cardiovascular risk factors, such as metabolic syndrome 30 and chronic kidney disease thus, a higher level of Serum uric acid may be seen as correlation of cardiovascular risk or an epiphenomenon of coexisting cardiometabolic risk factor.
In this study, Group 1 has a mean Troponin I level of 4463 pg/ml with a standard deviation of 5226.92 pg/ml. Group 2 has a mean Troponin I level of 10.048 pg/ml with a standard deviation of 14.03 pg/ml. Comparing the two groups:- Group 1 has a higher mean Troponin I level (4463.99 pg/ml) compared to Group 1 (10.048 pg/ml). The standard deviation for Troponin I levels is much smaller in Group 2 (14.03 pg/ml) compared to Group 1 (5226.92 pg/ml), indicating that Troponin I levels in Group 2 are much less variable around the mean compared to Group 1. Therefore, on average, participants in Group 1 tend to have higher Troponin I levels compared to those in Group 2, and the variability in Troponin I levels is significantly lower in Group 2.
The main etiology of MI is a lack of oxygen supply—acute ischemia of cardiac tissue. [22] The development of acute ischemia leads to cardiomyocyte necrosis, the destruction of cell membranes and organelles, and the subsequent release of cell proteins into the blood. This results in a considerable increase of Troponin concentration in blood that typically reaches its peak at 10–20 hours in patients with reperfusion of occluded coronary arteries or 24–50 hours in patients with no reperfusion after the beginning of acute ischemia. [23
Acute MI is the 3rd largest cause of death in the population. If untreated it causes necrosis of the myocardium and finally death of the patient. Magnesium has cytoprotective properties, anti-platelet effect, prevents arrhythmias and reperfusion injury and coronary vasodilation. So it should be estimated. Calcium ions are involved in myocardial contraction. It plays a role in coagulation cascade. It forms blood clots that obstruct blood flow so medications targetting calcium channel to reduce myocardial oxygen load and improve coronary circulation. Uric acid may be a marker for increased cardiovascular risk. Troponin I is highly specific and diagnostic of acute MI