1. Introduction
Cardiac troponins (troponin I and troponin T) are structural proteins integral to the contractile mechanism of cardiac muscle and are released into the bloodstream following myocardial injury [1]. They are widely regarded as the most sensitive and specific biomarkers for detecting myocardial damage and have become central to the diagnosis of acute coronary syndromes (ACS) [2]. The introduction of highsensitivity troponin assays has significantly improved the early detection of myocardial injury, enabling clinicians to identify even minor elevations that were previously undetectable [3].
Electrocardiography (ECG) remains a fundamental diagnostic tool in the initial assessment of patients presenting with chest pain or suspected cardiac events. Classical ECG changes, such as ST-segment elevation or depression and T-wave inversions, are critical for diagnosing myocardial ischemia and infarction [4]. However, it is well established that a normal ECG does not exclude the presence of ACS. Several studies have reported that a substantial proportion of patients with non-ST elevation myocardial infarction (NSTEMI) may initially present with normal or non-specific ECG findings [5].
The discordance between elevated troponin levels and normal ECG findings poses a diagnostic dilemma in clinical practice. Troponin elevation indicates myocardial injury but does not provide information regarding the underlying etiology . Apart from ischemic causes such as NSTEMl, elevated troponin levels can also be observed in conditions including myocarditis, pulmonary embolism, sepsis, renal failure, and heart failure [6]. This necessitates a comprehensive clinical evaluation to determine the exact cause and guide appropriate management.
Furthermore, elevated troponin levels have been shown to carry significant prognostic value. Even in the absence of diagnostic ECG changes, patients with raised troponin levels are at increased risk of adverse outcomes, including mortality and major adverse cardiac events (MACE) [7]. This highlights the importance of not dismissing troponin elevation solely based on a normal ECG.
Risk stratification tools such as the HEART score and TIMI score incorporate troponin levels along with clinical features and ECG findings to improve diagnostic accuracy and guide management decisions [8]. However, limited studies have specifically focused on the subgroup of patients with positive troponin and normal ECG, particularly in the context of comparative clinical outcomes.
Given this background, the present study aims to evaluate the clinical significance, etiological spectrum, and outcomes of patients presenting with elevated cardiac troponin levels in the presence of a normal ECG. Understanding this relationship is crucial for improving diagnostic accuracy, guiding treatment strategies, and ultimately enhancing patient outcomes.
2. Materials and Methodology
2.1. Study Design
This was a prospective comparative observational study.
2.2. Study Setting
The study was conducted in the Department of General Medicine and Emergency Medicine of a tertiary care hospital.
2.3. Study Duration
The study was carried out over a period of 12 months.
2.4. Sample Size
A total of 100 patients were included in the study.
2.5. Study Groups
The study population was divided into two groups: Group A: Patients with positive cardiac troponin and normal ECG (n = 50) Group B: Patients with either negative troponin or abnormal ECG findings (n = 50)
2.6. Inclusion Criteria
Patients aged years
Patients presenting with chest pain, dyspnea , or suspected cardiac symptoms
Patients who underwent cardiac troponin testing and ECG evaluation
2.7. Exclusion Criteria
Known cases of chronic ischemic heart disease History of recent myocardial infarction or cardiac surgery Patients with incomplete clinical or laboratory data Refusal to provide informed consent
2.8. Data Collection
Data were collected using a structured proforma and included: Demographic details (age, sex) Clinical presentation (chest pain, dyspnea , syncope) Risk factors (diabetes mellitus, hypertension, smoking, dyslipidemia) Cardiac troponin levels ECG findings at presentation Final diagnosis Clinical outcomes (ICU admission, complications, mortality, length of hospital stay)
2.9. Laboratory Assessment
Cardiac troponin levels were measured using a high-sensitivity assay. Values above the 99th percentile upper reference limit were considered positive.
2.10. Electrocardiographic Evaluation
A standard 12-lead ECG was performed at presentation. ECGs were interpreted by experienced clinicians and categorized as: Normal Abnormal (ST elevation, ST depression, T-wave inversion, arrhythmias)
2.11. Outcome Measures
Primary outcomes included: Diagnosis of acute coronary syndrome ICU admission Mortality
Secondary outcomes included: Length of hospital stay Development of complications such as heart failure
2.12. Statistical Analysis
Data were entered into Microsoft Excel and analyzed using SPSS version 26.0 (IBM Corp., Armonk, NY, USA) Continuous variables were expressed as mean standard deviation Categorical variables were expressed as percentages Chi-square test was used for comparison between groups A -value was considered statistically significant.
3. Results
A total of 100 patients were included in the study.
The study population was divided into two groups:
Group A: Patients with positive cardiac troponin and normal ECG (n = 50)
Group B: Patients with either negative troponin or abnormal ECG findings (n = 50)
Groups were compared and analysed.
Table 1. Demographic and Risk Factor Profile
| Variable | Group A (Troponin +, Normal ECG) (n=50) | Group B (Control) (n=50) | P-value |
|---|---|---|---|
| Mean Age (years) | 0.21 | ||
| Male | 32 (64%) | 30 (60%) | 0.68 |
| Diabetes Mellitus | 22 (44%) | 15 (30%) | 0.04 |
| Hypertension | 28 (56%) | 20 (40%) | 0.03 |
| Smoking | 18 (36%) | 14 (28%) | 0.39 |
Patients in Group A had a higher prevalence of cardiovascular risk factors. Diabetes (44% vs 30%) and hypertension (56% vs 40%) were significantly more common (), indicating that troponin-positive patients with normal ECG often belong to a higher-risk population.
Table 2. Etiological Spectrum of Troponin Elevation
| Diagnosis | Group A (n=50) | Group B (n=50) | p-value |
|---|---|---|---|
| NSTEMI | 21 (42%) | 10 (20%) | 0.01 |
| Myocarditis | 8 (16%) | 3 (6%) | 0.04 |
| Pulmonary Embolism | 6 (12%) | 4 (8%) | 0.51 |
| Sepsis-related Injury | 7 (14%) | 6 (12%) | 0.77 |
| Non-cardiac causes | 8 (16%) | 27 (54%) | 0.001 |
NSTEMI was significantly higher in Group A (42% vs 20%, ), demonstrating that normal ECG does not exclude myocardial infarction. Myocarditis was also significantly higher (16%, ). Non-cardiac causes were significantly more common in controls ().
Table 3. Clinical Outcomes
| Outcome | Group A (n=50) | Group B (n=50) | p-value |
|---|---|---|---|
| ICU Admission | 18 (36%) | 10 (20%) | 0.04 |
| Heart Failure | 12 (24%) | 6 (12%) | 0.05 |
| Mortality | 5 (10%) | 2 (4%) | 0.23 |
| Hospital Stay days | 20 (40%) | 12 (24%) | 0.04 |
Patients with positive troponin and normal ECG had worse outcomes:
ICU admission significantly higher (36% vs 20%, )
Prolonged hospital stay higher (40% vs 24%, )
Mortality higher (10% vs 4%) though not statistically significant
This indicates higher morbidity even with normal ECG findings.
4. Discussion
The present study demonstrates that elevated cardiac troponin in the presence of a normal ECG is clinically significant and associated with adverse outcomes. A major finding was that 42% of patients in Group A were diagnosed with NSTEMI highlighting that ECG alone cannot reliably exclude myocardial infarction.
Similar findings have been reported in previous studies where a significant proportion of NSTEMI patients presented without diagnostic ECG changes. This reinforces the concept that troponin is a more sensitive indicator of myocardial injury than ECG [9, 10].
High-sensitivity troponin assays have revolutionized the detection of myocardial injury by identifying even minimal cardiomyocyte damage. However, this increased sensitivity also introduces diagnostic complexity, as elevated troponin may occur in a variety of non-ischemic conditions [11].
In our study, myocarditis (16%), pulmonary embolism (12%), and sepsis (14%) contributed to troponin elevation. These findings are consistent with previous literature indicating that troponin elevation is not specific to coronary artery disease but reflects myocardial injury of diverse etiologies [12, 13].
The higher prevalence of diabetes and hypertension in Group A aligns with established cardiovascular risk profiles. These comorbidities are known to contribute to endothelial dysfunction and microvascular ischemia, increasing susceptibility to myocardial injury.
Importantly, our study showed significantly higher ICU admissions and prolonged hospital stays among troponin-positive patients. This is supported by earlier studies demonstrating that elevated troponin is an independent predictor of adverse outcomes, including mortality and heart failure [14, 15, 16].
Recent meta-analyses have also highlighted the prognostic value of troponin elevation across various clinical conditions, including stroke and chronic coronary artery disease, where it is associated with increased mortality. This further supports our findings that troponin elevation, irrespective of ECG findings, is clinically meaningful.
The diagnostic challenge lies in distinguishing between ischemic and non-ischemic causes of troponin elevation. Clinical correlation, serial troponin measurements, imaging modalities such as echocardiography, and risk stratification tools are essential for accurate diagnosis.
Our findings emphasize that a normal ECG should not reassure clinicians in the presence of elevated troponin levels. Instead, such patients should undergo thorough evaluation and close monitoring to prevent missed diagnoses and adverse outcomes.
5. Conclusion
Positive cardiac troponin in patients with a normal ECG is a significant clinical finding that should not be overlooked. A substantial proportion of these patients have underlying myocardial infarction or other serious conditions and are at increased risk of adverse outcomes. Comprehensive evaluation and early intervention are essential to improve prognosis and reduce morbidity.