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[Mechanism of troponin and CK-MB release after percutaneous coronary interventions]
Annalisa Mongiardo1, Alessandro Ferraro, Roberto Ceravolo
1U.O. di Cardiologia Interventistica, Università degli Studi Magna Graecia, Catanzaro. indolfi@unicz.it
Insights
Cardiac troponin levels can increase after percutaneous coronary interventions, especially with stenting. Cardiac troponin I remains a specific marker for myocardial injury in these cases.
Area of Science:
- Cardiology
- Biomarkers
- Interventional Cardiology
Background:
- Cardiac troponins are sensitive and specific biomarkers for detecting myocardial injury.
- Elevated cardiac troponin occurs in 5-40% of patients post-percutaneous coronary interventions (PCI).
- Troponin elevation is more common after stenting compared to balloon angioplasty alone.
Discussion:
- Myocardial necrosis during angioplasty results from plaque embolization, side branch occlusion, intimal dissection, or temporary vessel occlusion.
- Factors like complex lesions, diabetes, and plaque instability increase troponin elevation risk.
- Prolonged procedure times in interventions and atherectomy can also cause myocardial necrosis.
Key Insights:
- Minor troponin elevation is possible even after successful PCI.
- Cardiac troponin I is a highly specific indicator of myocardial injury in the context of PCI.
- Understanding these mechanisms aids in accurate patient assessment and risk stratification.
Outlook:
- Further research into minimizing troponin release during PCI.
- Developing strategies to differentiate procedural elevation from significant myocardial infarction.
- Optimizing patient selection and procedural techniques to reduce cardiac troponin increase.
Abstract:
Cardiac troponins are highly sensitive and specific markers of early detection of myocardial injury. The incidence of cardiac troponin increase is of 5-40% after percutaneous coronary interventions and is significantly higher in patients undergoing stenting than in patients with balloon angioplasty only. Four mechanisms are responsible for myocardial necrosis during coronary angioplasty: 1) distal embolization of small fragments of the atherosclerotic plaque; 2) side branch occlusion; 3) intimal dissection, and 4) temporary vessel occlusion. The multiple and/or complex lesions, the diabetic status and plaque instability increase the probability of troponin elevation during coronary angioplasty. Moreover, the long time needed for interventional as well as atherectomy procedures may induce myocardial necrosis. In conclusion, after successful percutaneous coronary interventions, minor elevation of troponin may occur. In this setting cardiac troponin I is a highly specific marker of myocardial injury.