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- Cardiac surgery
- heart transplant
- transplantation
- coronary artery disease
- heart failure
- imaging and diagnostics
- cellular physiology
- cardiovascular pharmacology
- ischaemia reperfusion
- cell biology
In about 30% of patients undergoing coronary revascularisation by planned percutaneous coronary intervention (PCI), the procedure itself results in peri-procedural myocardial necrosis.1 This form of PCI-related myocardial injury, which is often clinically silent, can be detected as an increase in serum cardiac enzymes above the 99th centile upper reference limit.2 Peri-procedural myocardial necrosis following PCI, as measured by raised levels of serum troponin, has been shown to be associated with higher major adverse cardiac events (MACE), with a twofold and threefold increased risk of overall death and subsequent myocardial infarction, respectively.3 MACE are further amplified in the 15% of patients who experience peri-procedural myocardial infarction (PMI) during the PCI procedure (termed type 4a myocardial infarction and defined as an elevation of cardiac biomarkers more than three times the 99th centile upper reference limit).2
The cause of PMI during PCI is multifactorial and includes distal coronary artery embolisation, side-branch occlusion, coronary dissection, occlusion of collaterals and epicardial or microvascular spasm (see figure 1).1 PMI following PCI can be visualised using cardiac MRI as discrete areas of late gadolinium enhancement, the extent of which correlates with the increase in serum cardiac enzymes.4 A wide variety of factors confer greater susceptibility to PMI during PCI. These …
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Linked article 302252.
Competing interests None.
Provenance and peer review Commissioned; internally peer reviewed.