Scientific background

scientific background

Scientific background

Upon AMI, the first medical action is to restore blood flow in the affected blood vessel(s) to limit the damage to the heart muscle (e.g. percutaneous coronary intervention; PCI). However, directly following AMI an inevitable inflammatory response and dilatation of the heart is initiated, in an attempt of the body to compensate for the damage. In addition, unwanted fibrotic changes in functional areas of the heart may also occur that will further decrease cardiac function, a process called reactive fibrosis. This process of maladaptive changes of the heart (adverse remodeling) is actually leading to chronic heart failure. At the basis of this process are several ‘danger signals’ generated in the heart upon AMI. Production of danger molecules causes attraction and activation of inflammatory cells, which clear damaged heart tissue and cause tissue destruction. In addition, danger molecules signal resident cells to form scar tissue (fibrosis) outside the infarcted area, which impairs the contractile performance of the heart. As a result, the heart is less able to pump blood, leading to cardiac failure. At present time, no interventions are available to prevent this damaging process to the heart. There is clearly an urgent need for new treatment options.

AMI explanation

Chronic heart failure develops after post-MI remodeling