Acute inflammation is a protective response of the body’s immune system to danger signals, including infections and damaged cells, to eliminate infection and repair damaged tissues. Inflammation leads to increased blood flow and permeability of blood vessels so that immune cells can access the site of infection or damage. Following tissue repair and elimination of the danger signal, it is vital that the initial inflammatory and reparative response be switched off. This is usually a result of the accumulated inflammatory cells undergoing cell death by apoptosis and their uptake by macrophages via efferocytosis, a process which induces an anti-inflammatory response, terminating the inflammation. A failure of this off switch results in ongoing chronic inflammation, which is seen in many disorders including heart failure.
One of the factors predisposing people to heart failure is older age. It is widely recognized that ageing is associated with an increase in low grade background inflammation, which, in turn, appears to result from a failure of efferocytosis of apoptotic cells. The effect of chronic inflammation in the heart is an increase in cell death of cardiomyocytes (heart muscle cells) and increased fibrogenesis (the laying down of scar tissue). The result is reduced heart function due to the weakening and stiffening of the heart muscle.