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Risk stratification analysis of recurrent myocardial infarction in Indian population using inflammatory, lipid,
Ritu Singh1, Sana Tasnim1, Sudhir Chandra1
1Department of Biochemistry, Lady Hardinge Medical College, Connaught Place, New Delhi, India.
Insights
Recurrent myocardial infarction (MI) is linked to inflammation, endothelial adhesion, and extracellular matrix remodeling markers. Non-lipid factors offer key insights into plaque instability and predicting recurrent MI events.
Area of Science:
- Cardiovascular Medicine
- Biomarker Discovery
- Atherosclerosis Research
Background:
- Atherosclerosis involves lipid imbalance and arterial inflammation, leading to plaque rupture and myocardial infarction (MI).
- Despite managing risk factors like hypertension and dyslipidemia, adverse events post-MI remain high, necessitating research into plaque instability determinants.
- This study investigates inflammation, extracellular matrix (ECM) remodeling, thrombosis, and lipid markers in first-time versus recurrent MI (RMI).
Observation:
- Serum levels of tumor necrosis factor-alpha (TNF-α), vascular cell adhesion molecule-1 (VCAM-1), matrix metalloproteinase-9 (MMP-9), pappalysin-A (PAPP-A), and paraoxonase-1 (PON-1) were significantly upregulated in RMI patients.
- First-time MI patients exhibited higher serum levels of interleukin-6 (IL-6) and D-dimer compared to RMI patients.
- Multivariate logistic regression identified proteomic indicators for RMI risk categorization.
Findings:
- Recurrent MI is associated with elevated markers of inflammation (e.g., TNF-α), endothelial adhesion (VCAM-1), ECM remodeling (MMP-9, PAPP-A), and the antioxidant enzyme PON-1.
- Specific inflammatory and thrombotic markers (IL-6, D-dimer) were higher in first-time MI cases.
- Non-lipid biomarkers are crucial for understanding plaque instability and predicting recurrent events.
Implications:
- Non-lipid factors significantly contribute to understanding atherosclerotic plaque instability.
- Inflammation, thrombosis, ECM remodeling markers, and PON-1 are reliable indicators for predicting recurrent myocardial infarction.
- These findings can inform risk stratification and therapeutic strategies for patients post-MI.
Objective:
Atherosclerosis is a chronic condition characterized by impaired lipid homeostasis and chronic inflammatory pathology in large and mid-sized arteries. Myocardial infarction is caused by coronary artery thrombosis in a ruptured or unstable atherosclerotic plaque. Despite the emphasis on known triggering factors, such as hypertension and dyslipidemia, adverse events following MI, such as recurrence and mortality, are still high. Therefore, it is imperative to assess potential determinants of plaque instability. We evaluated markers of inflammation, extracellular matrix (ECM) remodeling, thrombosis, and lipids in first-time and recurrent MI (RMI).
Methods:
Two hundred patients diagnosed with MI within the first 24 h of the event were included in the study and categorized as first-time or recurrent MI. Serum levels of NF-κB, hs-CRP, TNF-α, IFN γ, IL-6, VCAM-1,MMP-9, stromelysin, TIMP-1, MCP-1, PAPP-A, vWF, D-dimer, PLA2, PON-1, Apo-B, Apo-A1, ox-LDL, and anti-oxidized LDL antibodies were analyzed by ELISA. We performed a multivariate logistic regression analysis for risk stratification.
Results:
The mean age of first-time MI patients was 52.4 ± 25 years and that of recurrent MI patients was 55.9 ± 24.6 years. RMI patients showed significant (p¡0.05) upregulation of markers of inflammation (TNF-α), endothelial adhesion (VCAM-1), ECM remodeling (MMP-9, PAPP-A), and antioxidant PON-1 enzyme. First-time MI patients had significantly higher serum IL-6 and D-dimer levels than RMI patients. Risk categorization for RMI was determined at 0.5 cut-off utilizing proteomic indicators at 95% confidence interval.
Conclusion:
Non-lipid factors provide substantial insights into plaque instability. Multiple markers of inflammation, thrombosis, extracellular matrix remodeling, and paroxonase-1 are reliable indicators of recurrent myocardial infarction.
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