The fibrotic response after a myocardial infarction (MI) can be classified into two types of fibrosis:
1-Replacement or reparative fibrosis at the infarcted area (scar formation)
2- Reactive fibrosis outside the infarcted area usually after the replacement fibrosis
The replacement fibrosis or fibrosis healing phase (takes 4 to 6 weeks post MI) is a pivotal process to prevent the rupturing of the ventricular wall after an ischemic insult. However, is it wrong if we disrupt this process?
I would be grateful if you could give me anything about this topic.
The best approach hypothetically will be regeneration of cardiomyocites
Free wall rupture generally occurs early (days) in the 4-6 period week post myocardial infarction and is often associated with late presentation and transmural infarct.
See here for details: http://heart.bmj.com/content/83/5/499
Presumably any attempt to disrupt the replacement fibrosis healing phase refers to patients who have sustained an infarct with LV dysfunction with the aim of preventing negative remodelling. See here for details: Article Mechanisms of Post-Infarct Left Ventricular Remodeling
It is important to note this distinction when moving forward.
Hope this helps!
In response to myocardial infarction we have two mechanisms - reparative and reactive cardiac fibrosis. This article will be helpful!
Article Cardiac fibrosis in myocardial infarction-from repair and re...
Hypoxiainduced cardiomyocyte death leads to the activation of myofibroblasts and a reparative fibrotic response in the injured area. Right top In adult mammals, the fibrotic scar formed at the infarcted area is permanent and promotes reactive fibrosis in the uninjured myocardium. Right bottom In
Very interesting data...
After MI, Fb are activated throughout the LV, presumably through TGF-β1 in response to increased wall stress and/or inflammation. Additional regional specific signaling leads to interstitial fibrosis via collagen cross-linking in MIadjacent. Local LOX activity could be stimulated by higher mechanical load imposed by tethering to the infarct or signals could diffuse from the scar. Identifying specific signaling cues to maintain the mature state of MyoFb phenotype in the scar tissue may open new perspectives in targeting the MyoFb reversibility in interstitial fibrosis without damaging existing scar tissue.
https://www.nature.com/articles/s41598-017-09790-1
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