With a lot of improvements in cancer therapies recently, cancer survivorship amongst patients has been increasing and we found that in these cancer patients that are surviving longer and longer, they have an increased risk of cardiovascular disease. A lot of this is due in part directly to the cancer therapies they’ve received and others we’re not exactly sure why some people develop cardiovascular disease and others don’t develop cardiovascular disease...
With a lot of improvements in cancer therapies recently, cancer survivorship amongst patients has been increasing and we found that in these cancer patients that are surviving longer and longer, they have an increased risk of cardiovascular disease. A lot of this is due in part directly to the cancer therapies they’ve received and others we’re not exactly sure why some people develop cardiovascular disease and others don’t develop cardiovascular disease. And a lot of the work I’ve done with my research mentor, Dr Jennifer Kwan, has been with CHIP or clonal hematopoiesis of indeterminate potential. And these are mutations in blood cells in the bone marrow, like hematopoietic stem cells. And these mutations are in epigenetic regulators like TET2, DNMT3A that give these cells a survival advantage. They allow them to go into the peripheral blood and clonally expand into larger populations and these populations have been shown to have increased pro-inflammatory effects. They’ve been shown to be associated with increased all-cause mortality in the general population and also increased cardiovascular disease like accelerated atherosclerosis. The paper that I’m presenting at ESC today is about CHIP’s risk with diastolic dysfunction. Diastolic dysfunction itself is associated with increased stiffness, decreased relaxation of the left ventricle of the heart. And we found that there’s not many, it’s not entirely understood why diastolic dysfunction occurs in the heart. Many people have hypothesized that inflammatory mechanisms underlie this development of diastolic dysfunction. And given CHIP’s pro-inflammatory effects, we thought this would be a natural cause and effect. And in our work, we did find that it’s an independent risk factor for the development of diastolic dysfunction in cancer patients. And going forward, it’s yet to be seen the reasons why we might want to screen cancer patients for CHIP. Is there any yield for it? We know that it increases the risk for different diseases, but the downstream things that would make this more beneficial would be understanding, are there anything actionable that we can do in these patients? For instance, is there anything other than closer monitoring for these patients that we can do?
This transcript is AI-generated. While we strive for accuracy, please verify this copy with the video.
