Immunological alterations in cancer patients have been discovered by recent study, which may assist determine which people are more vulnerable to harmful cardiac side effects from immune checkpoint inhibitors, which are cancer medications. This study suggests they could be key in mediating the heart damaging effects of immune checkpoint inhibitor cancer drug.
Assistant Professor Pilar Martin, group leader at CIBER-CV and head of the Regulatory Molecules of Inflammation Lab at the Spanish National Centre for Cardiovascular Research (CNIC), oversaw the work.
She explained, “Immune checkpoint inhibitors have revolutionised cancer treatment, but they can also damage the hearts of some patients. In this study, we monitored how levels of immune cells, which are known to be involved in the development of heart diseases, change after treatment.”
“We were surprised to see an early and rapid loss of protective immune cells, called regulatory T cells, after cancer patients started treatment. This suggests a window of vulnerability early in treatment.” Assistant Professor Martin continued.
The new research is being presented at European Cardio-Oncology 2025, a scientific congress of the European Society of Cardiology.
Immune checkpoint inhibitors are medications that target cancer cells by using the patient’s immune system. Regretfully, some patients may have adverse consequences such as cardiotoxicity or heart damage. Myocarditis is a potentially fatal cardiac problem that affects around 1 in 100 people using these medications.
Researchers found that patients with lower levels of a blood biomarker, called CD69 and found in protective immune cells, experienced a greater decrease in protective immune cells and a resulting increase in destructive pro-inflammatory immune cells. Such a decline in protective immune cells has previously been associated with a greater risk of developing cardiovascular complications such as myocarditis.
“We put patients into two groups based on their levels of a protective biomarker called CD69, and saw these groups had very different response to the cancer treatments. Those who had lower levels of CD69 before starting treatment had a more negative immune response which puts them at much greater risk of heart damage,” Professor Martin stated.
“More work is needed to validate this biomarker and fully understand the immune changes that are taking place, but testing patients for this biomarker with a blood test is relatively cheap and easy and has the potential to help doctors identify which patients are at greatest risk of complications. This could allow doctors to monitor these patients more closely, and in time I hope we can develop new treatments to prevent the immune dysregulation we see in these patients,” Professor Martin continued.
Blood samples from 215 cancer patients belonging to the Spanish Immunotherapy Registry of Cardiovascular Toxicity (SIR-CVT)2 were examined by researchers prior to treatment, as well as 24 weeks, 1012 weeks, 6 months, and 1 year following immune checkpoint inhibitor treatment. The patients received various immune checkpoint inhibitor therapies, such as anti-PD1, PDL1, and CTLA4, for a variety of malignancies, including skin, breast, and lung cancer.
Depending on the level of a particular protective T-cell biomarker (CD69) in their blood, patients were divided into two groups, and variations in the immune cell populations’ levels were tracked over time.
While both patient groups experienced some decline in levels of a specific type of a protective immune cell (CD69 positive regulatory T cells) in response to treatment, those patients with low starting levels of the protective biomarker had a much larger decrease. These patients also had an increase in immune cells with a role to kill other cells and others that have a role in inflammation.
Regulatory T cells are found in the blood and are important to maintain immune balance and stop the immune system damaging healthy tissues, including the heart and blood vessels. Previous research has shown how the wrong levels of these cells can result in damage to blood vessels and the heart, and this study suggests they could be key in mediating the heart damaging effects of immune checkpoint inhibitor cancer drugs.
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