Acute Coronary Syndrome (ACS) remains a major cause of morbidity and mortality worldwide over the past decade. Despite advances in risk management, morbidity and mortality rates are still not optimally controlled. To improve ACS prevention and management, it is essential to identify key risk factors that can trigger heart attacks.^1-4

Stress is recognized as an important risk factor for acute coronary events.^5-7 It is a common condition in daily life, with estimates suggesting that in the past two weeks, two-thirds of the population experienced stress, and about 50% reported moderate to high levels.¹ This stress burden is significantly associated with overall health status.⁸

Physiologically, stress induces vasoconstriction, which reduces blood flow.⁹ This reduction in perfusion can precipitate ACS.⁹ Furthermore, impaired microvascular blood flow increases the likelihood of red blood cell entrapment, contributing to vascular occlusion.¹⁰ Although coronary artery occlusion is relatively rare, when it does occur and is not promptly treated, it can lead to life-threatening ACS. Therefore, early detection is crucial to prevent such outcomes.¹¹

Stress experienced by individuals with ACS can trigger heart attacks, with chest pain being the most common presenting symptom.¹² Although chest pain is typical, other symptoms such as nausea, palpitations, and shortness of breath may also occur.¹³ In addition to physical symptoms, biomarker changes are observed in the blood, characterized by elevated levels of cardiac enzymes that indicate myocardial injury, such as troponin and CK-MB (Creatine Kinase Myocardial Band).^14,15

This study aimed to analyze the correlation between stress, physical complaints (specifically chest pain), electrocardiographic changes, and alterations in cardiac enzyme levels among patients presenting with ACS in the hospital emergency department.

The results of the study describe the characteristics of the respondents, including general demographic data and the health history of patients with ACS. In addition to respondent characteristics, the study also presents the findings of correlation and multivariate analyses between variables. The characteristics of the 105 respondents in this study are summarized in Table 1.

Table 1 illustrates that ACS patients are predominantly male (79%). The majority of respondents were older than 46 years (92.5%), and more than half (55.2%) were self-employed. Regarding health history, most patients reported a history of smoking (70.5%). Hypertension and diabetes mellitus were the two most common comorbidities, each affecting more than 60% of patients. Within the past year, most patients experienced a single heart attack (79%). In the past week, the majority reported severe stress (76.2%). Upon admission to the emergency department with complaints of heart attack, patients most frequently presented with moderate to severe chest pain, and the most common electrocardiographic finding was STEMI (58.1%).

Table 2 shows that the stress score was significantly associated with chest pain, CKMB levels, troponin levels, and ECG findings in ACS patients, with p-values of <0.001 for each variable. In terms of correlation strength, the relationship between stress score and chest pain was very strong (r = 0.852). Meanwhile, the correlations between stress score and CKMB levels (r = 0.390) and troponin levels (r = 0.472) were moderate. The relationship between stress score and ECG findings also demonstrated statistical significance (p < 0.001) with a moderate correlation strength (r = 0.339). These results are further illustrated in the Central Figure.

Table 3 shows that the chest pain scale was significantly associated with increases in troponin levels, CKMB levels, and ECG findings in ACS patients, with p-values of <0.001 for each variable. In terms of correlation strength, the relationship between the chest pain scale and troponin levels was moderate (r = 0.443), while the correlation with CKMB levels was also moderate (r = 0.501). The relationship between the chest pain scale and ECG findings demonstrated a weaker, though still significant, correlation (r = 0.359).

Based on Table 4, it was found that ACS patients who experienced severe pain and very severe or uncontrolled pain during the electocardiogram were mostly associated with ST elevation patterns.

Table 5 illustrates that troponin and CKMB levels in ACS patients are affected by chest pain felt by patients (p-value = 0.031; p-value = 0.001). Meanwhile, stress and frequency of recurrence that occurred in patients had no effect on troponin and CKMB levels.

Table 6 shows that both troponin and CK-MB levels were higher at the onset of attacks occurring within 6 hours, with mean rank values of 64.72 and 67.63, respectively. Table 7 demonstrates that troponin and CK-MB levels differed significantly between attack onset within six hours and beyond six hours.

In this study, stress experienced by ACS patients in the past month was found to be significantly associated with the chest pain symptoms reported. Moreover, stress was also linked to elevated troponin and CK-MB levels. These findings are consistent with previous studies that identified emotional stress as a factor triggering chest pain in patients with acute myocardial infarction.¹² Other studies have shown that stress increases the intensity of chest pain in patients undergoing cardiac rehabilitation programs.¹⁶ Stress induces ischemia in the heart muscle, and this study further revealed that female patients with a history of myocardial infarction had twice the likelihood of stress-induced myocardial ischemia.¹⁷ This increased risk is attributed to abnormal vasoreactivity and microvascular inflammation in such patients.¹⁸

Patients presenting to the emergency room with chest pain can determine whether the cause is cardiac or non-cardiac by undergoing cardiac enzyme testing. Cardiac biomarkers, particularly troponin, are key indicators that chest pain is of cardiac origin.¹⁹ Ischemia resulting from insufficient oxygen supply to the heart muscle leads to myocardial damage, which can be detected through elevated levels of cardiac enzymes such as troponin I and T.²⁰ This study found that ACS patients had significantly higher troponin levels when the onset of attack occurred within six hours compared to attacks beyond six hours. Similarly, CKMB levels were also significantly elevated in patients with attack onset within 6 hours. These findings suggest that increases in troponin and CK-MB levels are most pronounced during the early hours of a myocardial infarction, serving as important indicators of myocardial injury.

The rise in troponin and CK-MB levels was proportional to the severity of chest pain reported. Patients experiencing severe or uncontrolled chest pain were more likely to show ST elevation on ECG. Acute ST elevation occurs due to coronary artery occlusion, which causes transmural myocardial ischemia and leads to myocardial injury or necrosis.^21-23 Severe chest pain, often described as intense pressure, burning sensations, or accompanied by shortness of breath, typically reflects acute myocardial infarction. This pain may radiate to the left shoulder, neck, or arm, and can be triggered by stress or physical exertion, though it may also occur without a clear precipitating factor.²² In contrast, patients with NSTEMI or Unstable Angina Pectoris (UAP) more commonly reported moderate chest pain, while NSTEMI patients were also found to experience mild pain.

Stress experienced by ACS patients is significantly associated with chest pain, ECG changes, and alterations in cardiac enzyme levels. Among patients who presented with STEMI patterns on ECG, the majority reported severe chest pain. Chest pain complaints were found to have a significant impact on elevated troponin and CK-MB levels in ACS patients.

The practical implication of these findings is that treatment should be comprehensive, addressing not only the physical symptoms of ACS but also the psychological aspects. Incorporating stress management interventions may help reduce chest pain episodes and improve patient outcomes, with the goal of preventing further myocardial cell damage.