Myeloperoxidase as a Potential Biomarker of Acute-Myocardial-Infarction-Induced Depression and Suppression of the Innate Immune System
Abstract
:1. Introduction
1.1. Depression and Myocardial Infarction
1.2. Depression, Myocardial Infarction and Inflammation
1.3. Links of Proinflammatory Cytokines and the Hyperactivity of the HPA Axis
1.4. Depression and the Innate Immune System
1.5. Myeloperoxidase (MPO) as a Biomaker of the Activity of the Innate System
2. Objectives
3. Methods and Materials
3.1. Methods
3.2. Diagnosis of AMI
3.3. Psychiatric Diagnoses
3.4. Sociodemographic Characteristics
3.5. Clinical Characteristics of the AMI Patients
- Cardiac status at the time of AMI: type of AMI (STEMI/NSTEMI), Killip class stratification (=mortality risk after AMI).
- Severity of myocardial infarction: Troponin T, creatine kinase MB (CK-MB), maximum creatinine kinase (CK max) within the first three days after AMI. CK values were measured at least once daily within the first 3 days after AMI.
- Percutaneous coronary intervention (PCI): coronary artery disease, coronary flow before PCI (TIMI Score), coronary flow after PCI (TIMI Score), as well as single=versus-multivessel PCI.
- In-hospital outcome: AMI-related death, reinfarction, severe bleeding and left-ventricular rejection fraction (LVR %).
- Cardiological risk factors at the time of the AMI: body-mass index (BMI); insulin-dependent diabetes mellitus, arterial hypertension and hyperlipidemia.
- Pre-existing psychiatric morbidity; addictions.
3.6. Laboratory Analyses
3.7. Statistical Analyses
4. Results
4.1. Sociodemographic Characteristics
4.2. Depression
4.3. Interleukin 6 (IL-6) and Depression
4.4. MPO and AMI
4.5. MPO and Type of AMI
4.6. MPO and Severity of AMI
4.7. MPO and Depression
4.8. MPO and Severity of Depression
4.9. Multivariate Analyses
5. Discussion
6. Limitations
7. Conclusions
Supplementary Materials
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Conflicts of Interest
References
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Category | Total Sample (n = 109) | p | Depression (n = 57/109; 52.3%) | No Depression (n = 52/109; 47.7%) | p | |
---|---|---|---|---|---|---|
Sociodemographic Characteristics | ||||||
Age | mean (±SD) | 60.3 (±11.33) | - | 59.84 (±12.50) | 60.84 (±9.99) | t = 0.460, df = 107 p = 0.646 a |
Sex | ||||||
Male | n (%) | 90 (82.6%) | χ² = 46.248, df = 1, p < 0.001 b | 42 (73.7%) | 48 (92.3%) | χ² = 6.553, df = 1 p = 0.010 b |
Female | n (%) | 19 (17.4%) | 15 (26.3%) | 4 (7.7) | ||
Clinical Characteristics | ||||||
Type of Acute Myocardial Infarction | ||||||
NSTEMI | n (%) | 44 (40.4%) | χ² = 2.440, df = 2, p = 0.295 b | 23 (40.4%) | 21 (40.4%) | χ² = 0.135, df = 2, p = 0.935 b |
STEMI (anterior) | n (%) | 33 (30.3%) | 18 (31.6%) | 15 (28.84%) | ||
STEMI (posterior) | n (%) | 32 (29.4%) | 16 (28.1%) | 16 (30.8%) | ||
Killip Class Stratification | ||||||
Killip Class I | n (%) | 85 (78.0%) | χ² = 199.71, df = 3, p < 0.001 b | 43 (82.7%) | 42 (91.3%) | χ² = 2.798, df = 3, p = 0.42 b |
Killip Class II | n (%) | 7 (6.4%) | 4 (7.7%) | 3 (6.5%) | ||
Killip Class III | n (%) | 4 (3.7%) | 3 (5.8%) | 1 (2.2%) | ||
Killip Class IV | n (%) | 2 (1.8) | 2 (3.8%) | 0 (0%) | ||
Severity of the AMI | ||||||
Maximum Creatinine Kinase (CK max) | Median, IQR | 314 U/L, 714.0 | - | 376 U/L, 732.5 | 243 U/L, 643.0 | Mann-Whitney-U= 1321.0, p = 0.329 d |
Creatine Kinase MB (CK-MB) | Median, IQR | 32.5 U/L, 69.5 | - | 43.0 U/L, 88.0 | 30.0 U/L, 62.0 | Mann-Whitney-U= 702.5, p = 0.109 d |
Troponin T | Median, IQR | 784 pg/mL, 2153 | - | 849.0 pg/mL, 2546.0 | 725.5 pg/mL, 2133.25 | Mann-Whitney-U= 1375.0, p = 0.518 d |
Percutaneous Coronary Intervention (PCI)-Related Parameters | ||||||
Coronary Flow before PCI (TIMI Score e) | ||||||
0-I e | n (%) | 82 (75.2%) | χ² = 107.540, df = 2 p < 0.001 b | 40 (78.4%) | 42 (85.7%) | χ² = 1.886, df = 2 p = 0.389 b |
II e | n (%) | 13 (11.9%) | 7 (13.7%) | 6 (12.2%) | ||
III e | n (%) | 5 (4.6%) | 4 (7.8%) | 1 (2.0% | ||
Coronary Flow after PCI (TIMI Score e) | ||||||
0-I e | n (%) | 4 (3.7%) | χ² = 151.264, df = 2 p < 0.001 b | 0 (0%) | 4 (7.7%) | χ² = 10.977, df = 2 p = 0.004 b |
II e | n (%) | 7 (6.4%) | 7 (13.0%) | 0 (0%) | ||
III e | n (%) | 95 (87.2%) | 47 (87.0%) | 48 (92.3%) | ||
Multivessel PCI | n (%) | 23 (22.5%) | - | 14 (25.9%) | 9 (18.8%) | χ² = 0.749, df = 1 p = 0.387 b |
Coronary Artery Disease—Number of Affected Vessels | Mean (±SD) | 1.85 (±0.82) | 1.89 (±0.86) | 1.81 (±0.77) | t = −0.555, df = 107 p = 0.580 a | |
In-Hospital Outcome | ||||||
Severe Bleeding | n (%) | 0 (0%) | - | 0 (0%) | 0 (0%) | - |
Reinfarction | n (%) | 2 (1.8%) | - | 0 (0%) | 2 (3.8%) | p = 0.234 c |
LVEF (%) | Mean (SD) | 53.05 (±10.893) | - | 53.78 (±11.96) | 52.21 (±9.59) | t = −0.615, df = 72 p = 0.541 c |
Cardiological Risk Factors | ||||||
Body Mass Index | Mean (±SD) | 28.21 (±3.87) | - | 27.93 (±4.03) | 28.51 (±3.70) | t = 0.752, df = 100, p = 0.454 a |
IDDM | n (%) | 2 (1.8%) | - | 2 (3.5%) | 0 (0%) | p = 0.496 c |
Arterial Hypertension | n (%) | 98 (89.9%) | - | 49 (94.2.7%) | 49 (86.0%) | χ² = 2.048, df = 1 p = 0.152 b |
Hyperlipidemia | n (%) | 55 (50.5%) | - | 33 (57.9%) | 22 (44.9%) | χ² = 1.783, df = 1 p = 0.182 b |
Previous Mental Illness | ||||||
Previous Mental Illness (Adjustment Disorder, Burn-out Syndrome)—not present at the time of the AMI | n (%) | 10 (9.2%) | - | 8 (14.0%) | 2 (3.8%) | p = 0.097 c |
Addiction to Alcohol | n (%) | 1 (0.9%) | - | 1 (1.8%) | 0 (0%) | p = 0.388 c |
Addiction to Nicotine | n (%) | 50 (45.9%) | - | 26 (45.6%) | 24 (46.2%) | χ² = 0.003, df = 1 p = 0.955 b |
Addiction to Illicit Drugs | n (%) | 0 (0%) | - | 0 (0%) | 0 (0%) | - |
Step 1 (Model 1) DV = Depression (Yes/No) | B | S.E. | WALD | df | Exp (B) | p |
---|---|---|---|---|---|---|
Constant | 1.404 | 0.617 | 5.181 | 1 | 4.073 | 0.023 |
MPO at the time of AMI | −0.003 | 0.001 | 4.922 | 1 | 0.997 | 0.027 |
R2 COX &Snell): 0.051 Omnibus: χ² = 5.728, df = 1, p = 0.017 Hosmer–Lemeshow Test: χ² = 9.607, df = 8, p = 0.294 | ||||||
Step 2 (Model 2) DV = Depression (Yes/No) | B | S.E. | WALD | df | Exp (B) | p |
Constant | 3.759 | 1.614 | 5.424 | 1 | 42.926 | 0.020 |
MPO at the time of AMI | −0.003 | 0.001 | 5.013 | 1 | 0.997 | 0.025 |
Sex (male = 1) | −1.440 | 0.621 | 5.372 | 1 | 0.237 | 0.020 |
Age | −0.026 | 0.020 | 1.675 | 1 | 0.974 | 0.196 |
Coronary artery disease (number of affected vessels) | 0.322 | 0.265 | 4.646 | 1 | 1.380 | 0.224 |
R2 COX &Snell): 0.122 Omnibus: χ² = 14.165, df = 4, p = 0.007 Hosmer-Lemeshow-Test: χ² = 8.872, df = 8, p = 0.795) |
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Baranyi, A.; Enko, D.; Meinitzer, A.; Von Lewinski, D.; Rothenhäusler, H.-B.; Harpf, L.; Traninger, H.; Obermayer-Pietsch, B.; Harb, B.M.; Schweinzer, M.; et al. Myeloperoxidase as a Potential Biomarker of Acute-Myocardial-Infarction-Induced Depression and Suppression of the Innate Immune System. Antioxidants 2022, 11, 2083. https://doi.org/10.3390/antiox11112083
Baranyi A, Enko D, Meinitzer A, Von Lewinski D, Rothenhäusler H-B, Harpf L, Traninger H, Obermayer-Pietsch B, Harb BM, Schweinzer M, et al. Myeloperoxidase as a Potential Biomarker of Acute-Myocardial-Infarction-Induced Depression and Suppression of the Innate Immune System. Antioxidants. 2022; 11(11):2083. https://doi.org/10.3390/antiox11112083
Chicago/Turabian StyleBaranyi, Andreas, Dietmar Enko, Andreas Meinitzer, Dirk Von Lewinski, Hans-Bernd Rothenhäusler, Leonhard Harpf, Heimo Traninger, Barbara Obermayer-Pietsch, Birgit M. Harb, Melanie Schweinzer, and et al. 2022. "Myeloperoxidase as a Potential Biomarker of Acute-Myocardial-Infarction-Induced Depression and Suppression of the Innate Immune System" Antioxidants 11, no. 11: 2083. https://doi.org/10.3390/antiox11112083
APA StyleBaranyi, A., Enko, D., Meinitzer, A., Von Lewinski, D., Rothenhäusler, H. -B., Harpf, L., Traninger, H., Obermayer-Pietsch, B., Harb, B. M., Schweinzer, M., Platzer, M., & Zelzer, S. (2022). Myeloperoxidase as a Potential Biomarker of Acute-Myocardial-Infarction-Induced Depression and Suppression of the Innate Immune System. Antioxidants, 11(11), 2083. https://doi.org/10.3390/antiox11112083