Rapid progression of non-culprit vessels (NCVs) post-PCI in acute myocardial infarction: Causes and current research status

Acute myocardial infarction (AMI) remains a major cause of morbidity and mortality globally, with percutaneous coronary intervention (PCI) serving as the primary treatment for revascularization of culprit vessels. However, non-culprit vessels (NCVs), which harbor significant atherosclerosis but are not directly responsible for acute ischemic events, have gained increasing attention owing to their role in future cardiovascular risks. Recent studies have highlighted the rapid progression of post-PCI, driven by factors such as inflammation, endothelial dysfunction, and hemodynamic changes. This progression is linked to adverse outcomes, including recurrent myocardial infarction and cardiovascular mortality. Inflammation, particularly activation of the NLRP3 inflammasome, plays a critical role in plaque vulnerability within NCVs, and is exacerbated by systemic responses following PCI. Endothelial dysfunction, characterized by reduced nitric oxide availability and oxidative stress, further accelerates atherosclerotic progression in NCVs. Imaging technologies such as optical coherence tomography and intravascular ultrasound allow for a detailed assessment of these vessels, enabling the identification of high-risk plaques. Pharmacological interventions, such as high-intensity statins, PCSK9 inhibitors, and anti-inflammatory therapies targeting IL-1β, are emerging as promising strategies to mitigate NCV progression. Complete revascularization, addressing both culprit and NCVs, may improve the long-term outcomes in patients with AMI. Future research should focus on understanding the pathophysiology of NCVs, optimizing therapeutic strategies, and personalizing treatment approaches based on patient risk profiles to enhance the management and prognosis of patients with AMI.