If you have been through cancer treatment — chemotherapy, radiation, or targeted therapy — and you are now in remission, the conversation you likely had with your oncologist on discharge focused on surveillance for cancer recurrence. Scans at six months. Tumour markers. The things that confirm the cancer has not returned.

Here is what that conversation probably did not cover: your heart.

A 2026 review of the Australian cardio-oncology landscape, published in Current Treatment Options in Oncology, documents something that is counterintuitive until you read the data — and then becomes difficult to unsee. Among Australia’s more than 1.2 million cancer survivors, cardiovascular disease has now surpassed cancer recurrence as the leading cause of late mortality. In those who survive five years past their initial cancer diagnosis, 27% of deaths are attributed to CVD. That figure is equivalent to 56% of all non-cancer deaths in this population.

The word for this is cardiotoxicity. The mechanism has been understood for decades. What has changed is the scale.

The both-and

Australian cancer survival rates have improved substantially. That improvement has created a population of long-term survivors who are carrying a cardiovascular load that the health system has not organised itself to monitor. Hold both.

The cardiotoxicity picture. A Lancet Regional Health Western Pacific study found that more than half of Australian cancer patients receiving active treatment are exposed to potentially cardiotoxic medicines. The agents with the strongest CV signal include anthracyclines (doxorubicin, epirubicin — used widely in breast, lymphoma, and leukaemia regimens), trastuzumab (Herceptin — used in HER2-positive breast cancer), immune checkpoint inhibitors (pembrolizumab, nivolumab — now first-line in multiple cancer types), and radiation to the chest wall or mediastinum.

These agents damage the myocardium through different mechanisms — anthracyclines cause dose-dependent cardiomyocyte loss through oxidative stress; trastuzumab induces reversible contractile dysfunction; immune checkpoint inhibitors can trigger immune-mediated myocarditis. Chest radiation accelerates atherosclerosis in the vessels closest to the treatment field. The cumulative effect on the coronary circulation, myocardial function, and peripheral vasculature is measurable — and in many patients, progressive — over years.

For breast cancer specifically: five-year survival in Australia now exceeds 90%. A 2026 NSW population-wide data linkage study found that breast cancer survivors carry a CVD death risk almost twice that of the general population, with elevated risk evident as early as seven years post-diagnosis and higher among those who received anthracycline-containing chemotherapy. The population of Australian women who are alive, in remission from breast cancer, and carrying an unmonitored cardiovascular load is not small.

The system gap. Cardio-oncology as a subspecialty exists in Australia. Several major metropolitan hospitals — including the Baker Heart and Diabetes Institute, the Victorian Heart Institute, and services in NSW — have dedicated cardio-oncology clinics. But access is concentrated in major metropolitan centres and largely absent in rural, remote, and regional areas. For most cancer survivors outside a major city, cardiovascular surveillance after cancer treatment is not systematically conducted.

The clinical gap is compounded by a structural one: oncology and cardiology operate in largely separate pathways. The oncologist manages the cancer. The cardiologist manages the heart. The GP is, in practice, the person most likely to be seeing a breast cancer survivor at five years post-treatment — and also the person least likely to have had a formal cardio-oncology briefing on what surveillance should look like.

2 cents

The monitoring question is practical and answerable. If you have completed cancer treatment involving anthracyclines, trastuzumab, immune checkpoint inhibitors, or chest radiation — and you are in remission — cardiovascular surveillance is worth raising explicitly at your next GP or oncology follow-up.

The surveillance picture generally includes: blood pressure measurement and trend review, fasting lipid profile and glucose, a discussion of any new cardiorespiratory symptoms (dyspnoea, reduced exercise tolerance, palpitations, chest discomfort), and — depending on the treatment received and risk factors — consideration of echocardiography to assess left ventricular function. These are not exotic investigations. They are the standard metabolic and cardiovascular checks that get done routinely in other contexts, and which fall off the agenda in cancer follow-up because the frame is oncological.

The conversation to have is this: “I’ve had [treatment]. What cardiovascular monitoring should I have, and when?” A GP comfortable with this question can structure the surveillance. If they are not — a referral to a cardiologist or, where available, a dedicated cardio-oncology service is a reasonable next step.

This is general information. The individual cardiovascular risk after cancer treatment depends heavily on the specific agents used, cumulative doses, your pre-existing cardiovascular risk factors, age, and current symptoms. That individual picture is what a clinical consultation unpacks — not an article.

Verdict

Verdict: maybe — watch this space, and ask the question now.

The science on cardiotoxicity is not contested. CVD surpassing cancer recurrence as the leading late cause of death in Australian cancer survivors is a documented pattern, not a hypothesis. What remains unresolved is the systematic implementation of surveillance — who does it, in what pathway, with what frequency, and at what cost. The cardio-oncology field is building the answer in real time. In the meantime, the question you can ask at your next follow-up visit is concrete and actionable. That is a maybe that tilts toward yes for anyone who has been through treatment.

After cancer, the next risk is your heart — and it's being underdetected

The both-and

2 cents

Verdict

Sources cited