When the heart's muscle is weakened or injured due to a heart attack, it can make it hard for the heart to pump enough blood to meet the body's needs. Over time, it can lead to heart failure, where the heart's function drops below 40%. The condition affects an estimated 6.7 million people over the age of 20 in the United State, according the Centers for Disease Control and Prevention. Approximately 50% of patients with heart failure die within five years of developing the condition, and there's no cure to stop this disease from progressing.
"For the last 25 to 35 years, we've used the same medications for heart failure, but none of the current medicines alter disease progression. The reason for that is we really don't understand the underlying mechanisms that leads to this progressive cardiac dysfunction," said Shyam Bansal, associate professor of medicine at Penn State College of Medicine and vice chair for basic science research at Penn State Heart and Vascular Institute.
Now, Bansal and a team of researchers from Penn State College of Medicine have revealed that the culprit may be the body's own defense system doing more harm than good. Specifically, they found that a type of immune cell, called helper T cells, usually involved in healing wounds and fighting infections becomes overly activated in failing human hearts, causing damage. The researchers explained that this activation of T cells - the first time it's been seen in human hearts - highlights the impact of inflammation and immune dysfunction in heart failure and reveals potential therapeutic targets that could be used to design new drugs to treat heart failure. The team published their work in the Journal of Molecular and Cellular Cardiology.
