Chemotherapy is an effective treatment for many forms of cancer, including leukemias, lymphomas, and breast cancer. However, a class of chemotherapy called anthracyclines can cause toxic effects on the heart in approximately 10% of patients, leading to heart failure. These toxic effects, known as cardiac toxicity, are particularly dangerous for older patients with pre-existing cardiovascular disease. Currently, doctors do not have reliable ways to predict which patients are at risk for cardiac toxicity or to detect it in its early stages.
Researchers at the Beth Israel Deaconess Medical Center (BIDMC) have identified a protein that may be linked to the onset of cardiac toxicity in patients receiving anthracycline chemotherapy. The protein, called hemopexin, was found to be associated with increased cardiac toxicity in two studies of women undergoing treatment for breast cancer. Mice studies also showed that hemopexin has heart-protective properties. These findings, published in Science Advances, suggest that the body produces hemopexin as a defense mechanism against chemotherapy-induced cardiac toxicity. If this is the case, doctors may be able to use a simple blood test to monitor patients receiving anthracycline chemotherapy for abnormal heart function by measuring levels of hemopexin in the blood.
“Given the increasing burden of both heart failure and cancer in the aging population, the development of new biomarkers and heart-protective strategies is essential to minimizing the impact of cancer therapy-associated cardiac toxicity,” said Dr. Aarti Asnani, a cardiologist and the director of the Cardio-Oncology Program at BIDMC. “This study identifies the induction of circulating hemopexin as a heart-protective mechanism relevant to patients treated with anthracyclines.”
In the studies, researchers monitored a group of 30 and then 31 women diagnosed with breast cancer and scheduled to receive anthracycline chemotherapy. Blood samples, echocardiograms, and questionnaires were collected from the participants at baseline and every three months during treatment. At three months after starting chemotherapy, the scientists observed a decline in heart function in all of the participants, with six patients developing heart failure within a year. The researchers analyzed 1,317 proteins in the participants’ blood plasma and found changes in 39 proteins, with increases in hemopexin being most strongly linked to early heart toxicity.
Further research is needed to confirm the role of hemopexin in cardiac toxicity and to determine the best way to use it as a biomarker. However, these findings offer hope for the development of new strategies to protect the hearts of cancer patients receiving chemotherapy.