Key result
MINOCA linked to ~21% lower dityrosine levels vs. MI-CAD despite similar inflammation.
Why the study?
Patients without occlusive coronary artery stenosis can also present with myocardial infarction (MINOCA), prompting an evaluation of oxidative stress and inflammatory responses compared to patients with MI and CAD.
Do oxidative stress markers and systemic inflammatory indices differ between patients presenting with MINOCA versus those with MI-CAD?
Cross-Sectional (n=88)
No
Do oxidative stress markers and systemic inflammatory indices differ between patients presenting with MINOCA versus those with MI-CAD?
Oxidative stress biomarkers (dityrosine, malondialdehyde, kynurenine, and lipid hydroperoxide) are significantly lower in MINOCA than in obstructive MI-CAD despite comparable systemic inflammation, suggesting utility in differentiating MI pathophysiology and assessing myocardial cellular damage.
May support MINOCA as distinct from MI-CAD; leaves open diagnostic or prognostic utility in prospective studies.
Myocardial infarction (MI) is defined as a clinical event in which myocardial damage is evidenced in the setting of myocardial ischemia. However, patients without occlusive coronary artery stenosis can also have myocardial infarction, which is titled Myocardial Infarction with Non-Obstructive Coronary Arteries (MINOCA). In our study, we aimed to evaluate oxidative stress and inflammation responses between MINOCA and MI with coronary artery disease (CAD) patients. In this prospective, cross-sectional study, patients with elevated cardiac markers who were admitted to the cardiology clinic between March 2024 and May 2024 with the preliminary diagnosis of acute coronary syndrome were included. Patients were consecutively collected as those with an occlusive lesion on coronary angiography and those without. Routine blood samples and oxidative stress parameters were obtained and compared between groups. A total of 88 patients, including 44 MINOCA and 44 MI-CAD patients, were included in the study. The MINOCA group was significantly younger than the MI-CAD group (56.2 ± 12.5, vs. 64.7 ± 9.3, p: 0.001). While inflammatory parameters were similar between groups, dityrosine (5708 FU/mL (5311–6417) vs. 4488 FU/mL (3641–5238), p < 0.001), lipid hydroperoxide (3.6 nmol/mL (3.4–3.9) vs. 3.4 nmol/mL (3.1–3.9), p: 0.023), kynurenine (3814 ± 621 FU/mL vs. 3319 ± 680 FU/mL, p: 0.001), and malondialdehyde (17.4 nmol/mL (13.7–19.1) vs. 13.1 nmol/mL (12–14.9), p < 0.001) levels were higher in the MI-CAD group than in the MINOCA group. Although inflammation parameters did not differ between MI-CAD and MINOCA patients, oxidative stress parameters were higher in the MI-CAD group. Regardless of the presence and severity of inflammation, oxidative markers can help to assess the level of myocardial cell damage, risk stratification, and diagnosis of myocardial infarction.
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Koç et al. (2025) conducted a cross-sectional in Acute coronary syndrome (MINOCA vs. MI-CAD) (n=88). Myocardial Infarction with Non-Obstructive Coronary Arteries (MINOCA) vs. Myocardial Infarction with Obstructive Coronary Artery Disease (MI-CAD) was evaluated on Dityrosine levels (FU/mL) and other oxidative stress markers (lipid hydroperoxide, kynurenine, malondialdehyde) (p=<0.001). MINOCA patients exhibited significantly lower oxidative stress marker levels, including dityrosine (4488 vs. 5708 FU/mL, p<0.001) and malondialdehyde (13.1 vs. 17.4 nmol/mL, p<0.001), than MI-CAD patients despite similar inflammatory indices.
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