Cancer can definitely cause heart failure, a complex challenge that has led to the emergence of the specialized field of Cardio-Oncology. Heart failure occurs when the heart muscle cannot pump blood efficiently enough to meet the body’s needs. The connection between cancer and heart dysfunction is two-fold: damage can arise from the malignancy itself or, more commonly, as a side effect of the therapeutic interventions used to fight the cancer. The study of this intersection is now a major focus in medicine, recognizing that cardiovascular health is deeply intertwined with cancer survival and quality of life.
How Cancer Directly Affects the Heart
Cancer can directly weaken the heart muscle and surrounding structures through several non-treatment related mechanisms. The systemic effects of an active malignancy generate profound stress on the cardiovascular system. This often involves chronic, low-grade inflammation driven by the release of pro-inflammatory signaling molecules called cytokines, which can directly injure heart cells and promote tissue remodeling.
Another direct mechanism is the development of cancer cachexia, a severe wasting syndrome characterized by significant loss of skeletal muscle and fat. This systemic wasting can extend to the heart, leading to a degenerative form of cardiomyopathy where the ventricular walls become thinner, impairing function. In rare instances, the cancer may physically involve the heart through direct invasion or the metastasis of tumor cells to the heart muscle (myocardium) or the sac surrounding the heart (pericardium). Certain blood cancers, such as multiple myeloma, can also cause cardiac amyloidosis, where abnormal proteins deposit in the heart tissue, making the muscle stiff and dysfunctional.
Treatment Related Cardiotoxicity
The most common cause of heart dysfunction in cancer patients is cardiotoxicity resulting from cancer treatments. The therapies designed to destroy rapidly dividing cancer cells can inadvertently damage healthy, non-dividing cardiac cells. This damage is categorized based on the type of treatment used and the specific mechanism of harm to the heart.
Chemotherapy agents like anthracyclines (e.g., doxorubicin) are well-known for their dose-dependent cardiotoxic effects. Anthracyclines cause Type I cardiotoxicity, characterized by irreversible damage and loss of heart muscle cells (cardiomyocytes) through oxidative stress and DNA damage. This leads to a permanent reduction in the heart’s ability to pump blood. Conversely, targeted therapies like trastuzumab typically cause Type II cardiotoxicity, involving dysfunction in the heart muscle’s contraction without cell death. The damage is often reversible if the drug is stopped early.
Radiation therapy directed at the chest poses a significant risk due to its effect on the heart and surrounding vessels. The damage is often delayed, sometimes appearing years or even decades after treatment completion. Radiation can cause fibrosis or scarring of the heart muscle, leading to restrictive cardiomyopathy, or it can damage the coronary arteries, resulting in accelerated coronary artery disease. It can also affect the heart valves and the pericardium, leading to valvular disease or constrictive pericarditis.
Newer treatments, including targeted therapies and immunotherapies, also carry unique risks. Certain tyrosine kinase inhibitors (TKIs) can cause hypertension and suppress levels of nitric oxide necessary for vascular health, leading to strain on the heart. Immune checkpoint inhibitors can sometimes cause a severe, life-threatening inflammation of the heart muscle called myocarditis by directing the immune response against the heart cells.
Identifying the Symptoms of Heart Dysfunction
Recognizing the signs of developing heart dysfunction is challenging because the symptoms often overlap with the general side effects of cancer and its treatments. The most common symptoms of heart failure include shortness of breath, which may be worse when lying flat, and excessive fatigue. Other physical signs include swelling (edema) in the legs, ankles, or feet due to fluid retention, and a rapid or irregular heartbeat (arrhythmia).
Patients undergoing chemotherapy frequently experience profound fatigue and generalized weakness, which can mask the early signs of heart failure. A patient might attribute increasing breathlessness to being out of shape or the effects of their cancer treatment, delaying diagnosis. Clinicians rely on objective diagnostic tools to identify heart dysfunction, such as echocardiograms, which provide images of the heart’s structure and pumping function. They also use blood tests for specific biomarkers like B-type natriuretic peptide (BNP), which is released when the heart is under stress. Reporting any new or worsening symptoms like a persistent cough, sudden weight gain, or an unusual feeling of fullness in the abdomen should prompt a prompt evaluation.
Prevention and Monitoring Strategies
Proactive strategies are implemented to mitigate the risk of cardiotoxicity, involving close collaboration between oncology and cardiology teams. Before starting potentially cardiotoxic therapy, a comprehensive assessment is performed, including a detailed medical history and a baseline echocardiogram to measure the heart’s pumping efficiency, known as the left ventricular ejection fraction (LVEF). Managing pre-existing cardiovascular risk factors like high blood pressure, diabetes, and high cholesterol is a fundamental preventive step, as these conditions significantly increase the likelihood of cardiac damage from cancer therapy.
During treatment, ongoing monitoring is essential, particularly for patients receiving high-risk agents like anthracyclines. This surveillance often involves scheduled follow-up echocardiograms to detect any asymptomatic decline in heart function before it becomes symptomatic heart failure. In some high-risk patients, cardioprotective medications may be used preventatively. Drugs like angiotensin-converting enzyme (ACE) inhibitors or beta-blockers have shown modest benefit in preserving LVEF in selected patients. For certain anthracycline regimens, the drug dexrazoxane is the only approved agent specifically shown to provide robust cardioprotection. The long-term surveillance of cancer survivors emphasizes a heart-healthy lifestyle and regular follow-up to address delayed cardiac complications.