Inflammation and repair in the ischaemic myocardium

2015 ◽  
Vol 35 (01) ◽  
pp. 34-36 ◽  
Author(s):  
F. K. Swirski

SummaryShortly after myocardial infarction, various circulating leukocyte subsets accumulate in the heart. Leukocyte recruitment is highly coordinated and relies on cell production in the bone marrow, mobilization to the blood, and chemokine-mediated infiltration to the destination tissue. Neutrophils, which are phagocytic and inflammatory, are among the first leukocytes to accumulate in large numbers. Within a day, neutrophils disappear and are replaced by a subset of monocytes that further contribute to inflammation and phagocytosis. After a few days, monocyte-derived reparative macrophages accrue, quell inflammation, and foster angiogenesis and tissue remodelling. Studies suggest a wellbalanced response comprising these three waves is essential to optimal infarct healing.


2011 ◽  
Vol 7 (4) ◽  
pp. 280
Author(s):  
Ali Ghodsizad ◽  
Mina Farag ◽  
Matthias Loebe ◽  
Eric Lumsden ◽  
Christoph Phiechaczek ◽  
...  

Cell transplantation for myocardial regeneration has been shown to have beneficial effects on cardiac function after myocardial infarction. Here, we discuss the application of CD 271+ bone marrow-derived stem cells (BMCs) as novel markers for the enrichment of mesenchymal somatic stem cells. Injection of BMCs into ischaemic myocardium during surgery has been shown to be both feasible and safe. This novel approach might hold promise as an alternative to medical management in patients with severe ischaemic heart failure who are ineligible for conventional revascularisation.



Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 396
Author(s):  
Wolf-Stephan Rudi ◽  
Michael Molitor ◽  
Venkata Garlapati ◽  
Stefanie Finger ◽  
Johannes Wild ◽  
...  

Aims: Angiotensin-converting-enzyme inhibitors (ACE inhibitors) are a cornerstone of drug therapy after myocardial infarction (MI) and improve left ventricular function and survival. We aimed to elucidate the impact of early treatment with the ACE inhibitor ramipril on the hematopoietic response after MI, as well as on the chronic systemic and vascular inflammation. Methods and Results: In a mouse model of MI, induced by permanent ligation of the left anterior descending artery, immediate initiation of treatment with ramipril (10 mg/k/d via drinking water) reduced cardiac inflammation and the number of circulating inflammatory monocytes, whereas left ventricular function was not altered significantly, respectively. This effect was accompanied by enhanced retention of hematopoietic stem cells, Lin−Sca1−c-Kit+CD34+CD16/32+ granulocyte–macrophage progenitors (GMP) and Lin−Sca1−c-Kit+CD150−CD48− multipotent progenitors (MPP) in the bone marrow, with an upregulation of the niche factors Angiopoetin 1 and Kitl at 7 d post MI. Long-term ACE inhibition for 28 d limited vascular inflammation, particularly the infiltration of Ly6Chigh monocytes/macrophages, and reduced superoxide formation, resulting in improved endothelial function in mice with ischemic heart failure. Conclusion: ACE inhibition modulates the myeloid inflammatory response after MI due to the retention of myeloid precursor cells in their bone marrow reservoir. This results in a reduction in cardiac and vascular inflammation with improvement in survival after MI.





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