Prostate cancer treatments can cause side effects in a part of the body that might be unexpected— the heart. Here's how one expert believes patients can mitigate them.
While prostate cancer treatment can cause cardiovascular-related side effects, patients can take certain steps to mitigate those risks, according to Dr. Neal D. Shore, medical director of the Carolina Urologic Research Center.
In an interview with OncLive®, CURE®’s sister publication, Shore recently discussed the role that general health-related interventions such as regular exercise and bloodwork play in keeping the risk of treatment-related cardiovascular toxicity low. Shore also touched on the idea that the choice of therapy could impact these risks in a positive way, based on the results of the recent HERO trial, which examined the use of the hormone-suppressing drug relugolix in this patient population.
Yeah, that's a very important question. The whole field of cardio oncology, across all the different oncology or cancer disease states, has gotten so much more traction. As we know, where we give testosterone suppression, we basically create what's described as this quasi-metabolic syndrome, where we see central adiposity (excessive body weight). We see, potentially, with LHR agonists — and it's in their label — a warning as it relates to arrythmia and potential QT prolongation (heart rhythm irregularities). We didn't see that with relugolix.
But what are the things that we can do? We can make sure that patients are following a better, heart-healthy diet, that they're regularly exercising (and) having their lipid panels and their cholesterol checked. If they have diabetes, they're under really tight glucose management, monitoring their hemoglobin A1C. And so, these are some factors, (including) avoidance of smoking (and) avoidance of a sedentary lifestyle; there are these classic, sort of ABCDE outlines that people can be thinking about.
I'm really happy and proud of our HERO trial, because this adds to a strategy to avoid cardiovascular toxicity, and yet at the same time achieve what we're trying to achieve, which is rapid T (testosterone) suppression and rapid PSA (prostate-specific antigen) corollary declines. We had really excellent results in our T levels that went below 20, even though less than 50 nanograms per deciliter is the pharmacologic endpoint for approval.
So, yes, we can be a lot more proactive in our cardio-oncology strategies, as well as in our prostate cancer therapeutic selections.