Myocardial infarction (MI) remains the leading cause of mortality and morbidity worldwide. It is caused by a thrombotic occlusion of coronary vessel/s that leads to cardiomyocyte death. As a response, inflammatory and fibrotic responses are initiated to replace the necrotic tissue and remodel the heart. However, in most cases, these responses are excessively activated, which accentuates the injury and causes adverse cardiac remodeling, often leading to heart failure. This is highly attributed to the dysregulated repair mechanism brought by reduced regenerative capacity of the adult heart, chronic inflammation, and other patient factors, such as comorbidities, diet, and lifestyle. Because of the negative consequences of excessive inflammation and fibrosis in post-MI responses, inhibiting factors associated with these processes are one of the major approaches in MI management. Several therapies have been developed to broadly and/or selectively inhibit inflammation- and fibrosis-associated proteins over the past decades and have shown promise in addressing post-MI complications. However, challenges (e.g., off-targets, problems with drug delivery, dosage, route, and cost) and efficacy of these interventions in the clinical setting remain. Hence, alternative approaches to optimally alleviate these post-MI processes are still much needed. In this review, we discuss the possible use of plasmapheresis, a technique that involves extracorporeal replacement of blood plasma, as a treatment for MI. We provide an overview of the inflammatory and fibrotic responses after MI and focus on how plasmapheresis can be an approach to target these pathways.
Restricted accessEditorialFirst published August, 2025pp. 157-157
