Key result
Copeptin and its hs-cTnI interaction fail to differentiate ACS from non-cardiac chest pain.
Why the study?
Acute coronary syndrome remains a leading cause of morbidity and mortality worldwide, necessitating quick and accurate diagnosis using biomarkers like high-sensitivity troponin and copeptin for early detection.
Does the combination of copeptin and high-sensitivity troponin I improve early diagnosis of acute coronary syndrome in patients presenting with acute chest pain?
Case-Control (n=100)
Single-blind
No
Does the combination of copeptin and high-sensitivity troponin I improve early diagnosis of acute coronary syndrome in patients presenting with acute chest pain?
Absolute Event Rate: 298.92% vs 288.45%
p-value: p=0.45
The addition of copeptin to high-sensitivity troponin I did not significantly improve the early diagnosis of acute coronary syndrome in this cohort, likely due to systemic stress attenuating copeptin's specificity.
Copeptin levels did not differ in ACS; does not support routine addition to HS-troponin; leaves open validation in larger cohorts.
Acute Coronary Syndrome (ACS) is still the main reason of malady and death world-wide, highlighting needs for quick andaccurate diagnosis. Biomarkers such as high-sensitivity troponin and copeptin have been known to improve early detection. This study aims to evaluate the levels and clinical significance of copeptin and high-sensitivity troponin I in patients presenting with acute coronary syndrome. A prospective observational study enrolled patients presenting with acute chest pain, who were categorized into ACS and non-ACS groups. The relationship between high-sensitivity troponin (HS-troponin) and copeptin was examined. In the total of 100 participants included 62 for ACS group and 38 for non-ACS group. Patients with ACS were significantly older (52.6 vs 44.1 years, p = 0.0010) and more often overweight (51.6% vs. 23.7%, p = 0.0461). Lipid abnormalities were markedly higher in ACS patients, including elevated total cholesterol (48.4% vs 2.6%, p < 0.0001).), low density lipoprotein (37.1% vs 0%, p < 0.0001).), low high density lipoprotein (93.6% vs 60.5%, p < 0.0001).), and high triglycerides (79.0% vs 15.8%, p < 0.0001). Clinically, dyspnea (96.8% vs 73.7%, p = 0.0009), arm pain radiation (67.7% vs 28.9%, p = 0.0002), and nausea/vomiting (59.7% vs 26.3%, p = 0.0012) were significantly more common in ACS. However, copeptin levels and the HS-troponin × copeptin interaction didn’t vary significantly between groups (p = 0.4516). Similarly, no significant variation was observed across lipid categories. While traditional risk factors, symptoms, and lipid abnormalities were strongly associated with ACS, these findings suggest that in high-stress, comorbid clinical settings, copeptin's biomarker specificity is attenuated by systemic physiological demand. In conclusion, evaluation of copeptin and high-sensitivity troponin I shows a critical knowledge in early acute coronary syndrome triage. However, due to the systemic stress attenuates copeptin specificity, localized reference intervals are recommended for accurate clinical assessment.
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Asaad et al. (2026) conducted a case-control in Acute Coronary Syndrome (n=100). Copeptin and High-Sensitivity Troponin I vs. Non-ACS patients was evaluated on Copeptin levels and HS-troponin I × copeptin interaction (p=0.45). Copeptin levels and the high-sensitivity troponin I by copeptin interaction did not vary significantly between patients with acute coronary syndrome and those with non-cardiac chest pain.
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