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Published on: June 14, 2015
Plasmapheresis as a Potential Generalizable Therapy for Myocardial Infarction
Joana Marie C Cruz1,2, Javier Lozano-Gerona3, Al James A Manua3
1Department of Bioengineering and QB3 Institute, University of California, Berkeley, California, USA.
Insights
Plasmapheresis, a blood plasma filtering technique, may offer a novel approach to manage myocardial infarction (MI) complications. This method targets excessive inflammation and fibrosis, common issues following heart attacks that can lead to heart failure.
Area of Science:
- Cardiology
- Immunology
- Regenerative Medicine
Background:
- Myocardial infarction (MI) is a leading global cause of death, characterized by cardiomyocyte death due to coronary occlusion.
- Post-MI healing involves inflammation and fibrosis, which can become excessive, leading to adverse cardiac remodeling and heart failure.
- Current therapies targeting inflammation and fibrosis post-MI face challenges in efficacy, delivery, and cost.
Purpose of the Study:
- To review inflammatory and fibrotic responses following myocardial infarction.
- To explore plasmapheresis as a potential therapeutic strategy for managing post-MI inflammation and fibrosis.
- To discuss the potential of plasmapheresis in mitigating adverse cardiac remodeling and improving outcomes after MI.
Main Methods:
- Review of existing literature on myocardial infarction pathophysiology, inflammatory and fibrotic pathways.
- Analysis of plasmapheresis, a procedure involving extracorporeal blood plasma replacement.
- Discussion of plasmapheresis's potential mechanisms for targeting inflammation and fibrosis post-MI.
Main Results:
- Inflammatory and fibrotic responses are critical but often dysregulated post-MI, contributing to heart failure.
- Plasmapheresis has the capacity to remove circulating inflammatory mediators and other harmful plasma components.
- Targeting these pathways with plasmapheresis could offer a novel therapeutic avenue for MI management.
Conclusions:
- Excessive inflammation and fibrosis exacerbate myocardial infarction injury and contribute to heart failure.
- Plasmapheresis presents a promising, yet under-explored, therapeutic option for modulating these detrimental post-MI processes.
- Further research is warranted to investigate the clinical efficacy and safety of plasmapheresis in MI patients.
Abstract:
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.
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