This article is a continuation of the prior piece by Dr. Manu Mysore, expanding the discussion from risk awareness and work up of heart diseases to practical management in cancer. In this installment, we focus on the medications used to protect the heart during and after cancer treatment, as well as the surveillance strategies during survivorship. The goal is simple: treat the cancer effectively while preserving long-term cardiovascular health through proactive monitoring and timely intervention.
Question 1: Which cardioprotective medications (ACE inhibitors, ARBs, beta-blockers, statins) have the strongest evidence for primary prevention, and in which patients do you initiate them pre-emptively?
For primary prevention of cancer therapy–related cardiac dysfunction, the strongest evidence supports ACE inhibitors or ARBs and beta-blockers. Randomized and prospective studies, particularly in patients receiving anthracyclines or HER2-targeted therapies, show that starting an ACE inhibitor (like enalapril) or an ARB (like candesartan) before or early in therapy can reduce the risk of LVEF decline, especially in patients with high cumulative anthracycline doses, pre-existing cardiovascular risk factors such as hypertension or diabetes, or borderline baseline GLS or LVEF. Beta-blockers, particularly carvedilol or nebivolol, also demonstrate protective effects on myocardial function and subclinical injury, and are especially useful in patients with additional risk factors like hypertension, tachycardia, or prior cardiac disease. Statins have emerging data suggesting a potential protective effect through anti-inflammatory and antioxidant mechanisms, though the evidence is less robust; in practice, I consider initiating statins preemptively in patients who already have an indication for lipid lowering or in high-risk patients with multiple cardiovascular comorbidities. Overall, my approach is risk-stratified: patients at high risk receive prophylactic therapy upfront, while lower-risk patients are closely monitored with GLS, troponin, and natriuretic peptides, with therapy initiated promptly if early signs of dysfunction appear.
Question 2: How do you individualize cardioprotective therapy in patients with low blood pressure, renal dysfunction, or competing oncologic priorities?
Individualizing cardioprotective therapy in patients with low blood pressure, renal dysfunction, or competing oncologic priorities requires a careful balance between mitigating cardiotoxicity and maintaining tolerance for both cardiovascular and cancer treatments. For patients with low blood pressure, I am cautious with ACE inhibitors, ARBs, and beta-blockers; I often start at the lowest possible dose and titrate very slowly while monitoring symptoms, heart rate, and renal function, sometimes prioritizing a single agent rather than dual therapy. In patients with renal dysfunction, I pay close attention to baseline creatinine, eGFR, and potassium, choosing agents with the least nephrotoxic potential, avoiding combination RAAS blockade when possible, and monitoring labs frequently. Diuretics are used judiciously to prevent hypotension or volume depletion.
Question 3: At what threshold of cardiac dysfunction do you recommend holding, modifying, or continuing cancer therapy—and how do you communicate this risk to oncology teams?
In my practice, the decision to hold, modify, or continue cancer therapy is guided by the severity and trajectory of cardiac dysfunction, always in close collaboration with the oncology team. For subclinical dysfunction, such as a relative GLS decline ≥15% from baseline but preserved LVEF (≥50%), I typically continue cancer therapy while initiating or optimizing cardioprotective medications and increasing the frequency of imaging and biomarker surveillance. If there is a moderate decline in LVEF (typically a ≥10% drop to below 50%) or symptomatic heart failure, I engage in a multidisciplinary discussion about temporarily holding or modifying therapy while treating the cardiac issue. For severe dysfunction, such as LVEF <40%, overt heart failure, or rapid deterioration despite cardioprotective therapy, holding therapy is usually recommended until cardiac status stabilizes, with careful risk–benefit discussion with oncology. Communication with oncology is critical: I present objective data (serial LVEF, GLS trends, troponin/BNP changes, and symptoms), the anticipated risk of progression, and evidence-based thresholds for intervention.
Question 4: Which late cardiovascular complications are most commonly missed in survivorship care, and how can earlier diagnosis change outcomes?
In survivorship care, the late cardiovascular complications most commonly missed are subclinical left ventricular dysfunction progressing to heart failure, coronary artery disease, valvular disease, and arrhythmias, particularly atrial fibrillation. Patients who received anthracyclines, chest radiation, or HER2-targeted therapies are at risk for delayed cardiomyopathy, often years after therapy, and these changes can remain asymptomatic for a long time if routine surveillance is not maintained. Radiation can also accelerate atherosclerosis and lead to premature coronary artery disease, pericardial disease, or valvular thickening, which may be subtle initially on imaging. Arrhythmias, particularly atrial fibrillation, are often overlooked unless patients report palpitations, yet they carry substantial morbidity if untreated.
Earlier diagnosis through structured survivorship surveillance—using echocardiography with strain imaging, biomarkers, and clinical screening—allows intervention before symptoms develop or irreversible myocardial injury occurs. Initiating cardioprotective therapy, optimizing risk factors, or addressing early coronary or valvular disease can slow progression, prevent hospitalizations, and improve long-term survival. In practice, a systematic approach that combines risk stratification, longitudinal imaging, and biomarker monitoring can dramatically change outcomes by catching these silent complications before they manifest clinically.
Question 5: What is one evidence-based practice in cardio-oncology that you believe is still under-recognized or under-implemented across institutions?
A major challenge in cardio-oncology is identifying which patients truly need aggressive surveillance versus those who may safely undergo minimal or no routine cardiac screening, even under current HFA–ICOS (Heart Failure Association–International Cardio-Oncology Society) risk stratification thresholds. While HFA–ICOS provides a structured risk framework—categorizing patients as low, medium, high, or very high risk based on therapy type, cumulative dose, baseline CV risk, and comorbidities—real-world application can be tricky. Many “medium-risk” patients receive a one-size-fits-all imaging schedule that may be excessive for some or insufficient for others. Conversely, some “low-risk” patients are still subjected to frequent echocardiography or biomarker monitoring, which can burden patients and clinics without clear evidence of benefit.
Guest Contribution by Dr. Manu Mysore