The progression of heart failure following a heart attack is driven by sustained levels of chronic inflammation. Researchers have now demonstrated the importance of inflammation in this case through the targeted removal of a critical population of T cells in mice, cells that become inappropriately inflammatory after injury to heart tissue. This selected destruction of immune cells produces a reversal of detrimental remodeling of heart muscle, as well as improvement in other inflammation-linked aspects of heart failure, such as fibrosis in heart tissue. Interestingly, this approach seems to result in lasting effects, as the replacement T cells, newly generated by the body, do not provoke further inflammation. All in all, this is a very promising set of data.
A heart attack triggers an acute inflammatory response, followed by resolution of inflammation and wound healing. A severe heart attack, however, can cause chronic and sustained inflammation that leads to heart failure and death. Researchers have found that a group of immune cells called regulatory T-lymphocyte cells, or T-regs, appear to go rogue in heart failure. Instead of their normal job to resolve inflammation, the dysfunctional T-reg cells become pro-inflammatory and prevent the growth of new capillaries. Experimental