Background: Tumour necrosis factor-alpha (TNF-alpha) converting enzyme (TACE) plays an essential role in the TNF-alpha shedding process, which could affect the outcome of acute myocardial infarction (AMI). However, it remains unclear whether it originates from the ruptured plaque or represents a systemic process. This study analysed TACE-mediated TNF-alpha shedding at the site of ruptured plaques in AMI patients and compared them with a systemic mechanism.
Materials and methods: The study included 60 patients with AMI who underwent percutaneous coronary intervention (PCI) and 21 patients with stable angina pectoris (SA). Local samples from the site of plaque were taken from AMI using aspiration catheter treatment. Systemic samples were also taken from the aorta in all patients with AMI and SA.
Results: Systemic levels of TACE and TNF-alpha were higher in AMI patients than in SA patients. In AMI patients, these levels were higher in local samples than in systemic samples. A positive correlation was seen between local TACE and TNF-alpha levels in AMI patients. Thrombus material removed from the ruptured plaque showed immunostainings of TACE and TNF-alpha in infiltrating macrophages. By six months follow-up study, local TACE levels remained the only significant independent predictors of adverse cardiac events in AMI patients.
Conclusions: This study demonstrates that local expression of TACE is related to TNF-alpha shedding at the site of ruptured plaques in AMI patients. In addition, local TACE expression at the site of ruptured plaques may play an important role in poor outcomes in patients with AMI.