On the occasion of Heart Month, this blog aims to highlight what cardio-oncology truly offers to both physicians and patients, specifically in terms of cardiac assessment and surveillance. Today, there are millions of cancer survivors living with short- and long-term cardiovascular complications related to their cancer therapies. Caring for this growing population is no longer optional. The ability to appropriately screen, monitor, and manage cardiovascular risk before, during, and after cancer treatment has become a core component of modern medical care. While cardio-oncology plays a central role, the responsibility does not rest with one specialty alone—primary care physicians, oncologists, cardiologists, and allied health professionals must all participate in early recognition and shared management of cardiovascular disease in patients with cancer. Through a question-and-answer format, this series aims to simplify complex concepts while preserving clinical nuance, offering insight into the real-world decision-making that guides cardiovascular care before and during cancer treatment. In this first part, we focus on the foundational cardiovascular workup and surveillance strategies. Part 2 will address treatment approaches and long-term survivorship surveillance.
Manu Mysore, MD is an Assistant Professor of Medicine at the University of Maryland School of Medicine and serves as Co-Medical Director of the Cardio-Oncology Program at the University of Maryland Medical Center. He completed his Bachelor of Science in Chemistry at Duke University, earned his MD from Louisiana State University Health Sciences Center, trained in internal medicine at the University of Virginia Health System, and completed his cardiovascular medicine fellowship at the University of Maryland Medical Center and the Baltimore VA Medical Center. Dr. Mysore’s clinical expertise lies in preventive cardiology, non-invasive cardiac imaging, and cardio-oncology, with a rigorous, detail-oriented approach to cardiovascular risk stratification and surveillance in patients undergoing cancer therapy. He plays a central role in multidisciplinary collaboration with hematologists and oncologists at the Marlene and Stewart Greenbaum Comprehensive Cancer Center. Widely regarded as a kind and compassionate physician, Dr. Mysore is also a wonderful mentor to students and trainees and an outstanding clinician dedicated to delivering precise, patient-centered cardio-oncology care.
Question 1: How do you screen patients before starting potentially cardiotoxic cancer therapy? How does it influence treatment?
Before starting potentially cardiotoxic cancer therapy, I routinely perform structured risk stratification to identify patients at higher risk of cardiac complications and tailor monitoring and management. One of the most validated tools I use is the HFA-ICOS risk score, which incorporates age, baseline LVEF, cardiovascular comorbidities, prior cardiotoxic therapy, and other risk factors to categorize patients as low, intermediate, high, or very high risk. The exact approach depends on the cancer type and the specific chemotherapy or targeted therapy planned, since anthracyclines, HER2-targeted agents, and immune checkpoint inhibitors carry different patterns and timing of cardiotoxicity. Low-risk patients generally proceed with standard baseline echocardiography and routine follow-up, whereas high- or very high-risk patients may benefit from preemptive cardioprotective therapy with ACE inhibitors or beta-blockers, more frequent cardiac imaging, and tighter optimization of cardiovascular risk factors.
Question 2: What baseline cardiovascular testing is truly essential versus optional before initiating anthracyclines, HER2-targeted therapy, or immune checkpoint inhibitors?
Before initiating potentially cardiotoxic cancer therapy, baseline cardiovascular testing should be risk-adapted and therapy-specific. For anthracyclines, essential testing includes a thorough history and physical exam, baseline ECG, and transthoracic echocardiography (TTE) to assess left ventricular ejection fraction (LVEF), as these agents carry dose-dependent risk of cardiomyopathy. Optional assessments, particularly for higher-risk patients, include cardiac biomarkers such as troponin or NT-proBNP. For HER2-targeted therapy like trastuzumab, baseline LVEF assessment by TTE is mandatory, along with history, physical, and ECG; Biomarkers should be considered in high-risk individuals. In contrast, immune checkpoint inhibitors generally require a history, physical exam, and baseline ECG, while baseline TTE is reserved for patients with preexisting cardiac disease or high-risk features including dual immune checkpoint inhibitor use, use with co-existing cardiotoxic chemotherapy. Biomarkers such as troponin and NT-proBNP may be considered in higher-risk patients to facilitate early detection of myocarditis, and cardiology involvement is guided by underlying cardiac comorbidity or abnormal baseline studies. Across all therapies, the intensity of baseline testing and monitoring increases with age, cardiovascular risk factors, prior cardiotoxic therapy, or planned high-dose regimens, ensuring that therapy is both effective and as safe as possible from a cardiac standpoint.
Question 3: How do you integrate global longitudinal strain (GLS) into routine surveillance, and what absolute or relative change prompts intervention in your practice?
In routine cardio-oncology surveillance, I integrate global longitudinal strain (GLS) as a complementary, early marker of myocardial dysfunction alongside LVEF, with a strong emphasis on longitudinal comparison. A baseline GLS is obtained before initiation of potentially cardiotoxic therapy using consistent acquisition and vendor-specific software whenever possible. Follow-up GLS is then incorporated into scheduled surveillance imaging during treatment—typically every few cycles of anthracyclines or at three-month intervals during HER2-targeted therapy—and sooner if symptoms, biomarker elevations, or equivocal LVEF changes arise. GLS is always interpreted in context, considering image quality, heart rate, blood pressure, and concurrent clinical or biomarker data rather than as a single isolated value.
In practice, the primary threshold that prompts concern is a relative decline in GLS of 15% or greater from baseline, even when LVEF remains preserved. This degree of change is treated as evidence of subclinical LV dysfunction and generally triggers initiation of cardioprotective therapy, most commonly with an ACE inhibitor or ARB and a beta-blocker, along with closer imaging surveillance, while cancer therapy is usually continued. If GLS decline is accompanied by a significant drop in LVEF (typically ≥10% to a value below 50%), this is managed as overt cardiotoxicity with guideline-directed heart failure therapy and multidisciplinary discussion regarding cancer treatment modification. Overall, GLS functions as an early, actionable signal that allows intervention before irreversible reductions in LVEF occur.
Question 4: When echocardiography is limited, how do you decide between cardiac MRI, MUGA, or CT for functional assessment?
When echocardiographic assessment is suboptimal, I base the choice between cardiac MRI, MUGA, and CT on the specific clinical question, whether tissue characterization is needed, patient-related considerations, and how likely the patient is to require repeat imaging. Cardiac MRI is my first choice whenever it is practical, as it offers the most reliable and reproducible measurements of ventricular volumes and ejection fraction, along with added diagnostic value from tissue characterization using T1/T2 mapping and late gadolinium enhancement. This is especially helpful in cardio-oncology when myocarditis, myocardial edema, or fibrosis is a concern. I tend to use MRI when clinical symptoms do not align with echocardiographic findings, when highly accurate quantification is needed to inform treatment decisions, or when GLS trends raise concern but TTE image quality is insufficient, assuming there are no contraindications and the patient can tolerate the study.
Question 5: What are the biggest differentials for cardiomyopathy apart from CTRCD? What imaging features help differentiate cancer-therapy–related cardiomyopathy from ischemic or hypertensive heart disease?
Beyond cancer-therapy–related cardiac dysfunction (CTRCD), the major differentials for cardiomyopathy in oncology patients include ischemic cardiomyopathy, hypertensive heart disease, valvular cardiomyopathy, infiltrative processes such as amyloidosis or sarcoidosis, inflammatory cardiomyopathy including myocarditis (viral or immune-checkpoint–inhibitor related), stress-induced cardiomyopathy, tachycardia-mediated cardiomyopathy, and less commonly genetic or metabolic cardiomyopathies unmasked by cancer therapy. Volume overload states from anemia, renal dysfunction, or high-output physiology should also be considered, particularly in patients with advanced malignancy.
Imaging plays a central role in distinguishing CTRCD from these entities. CTRCD typically presents with a global, rather than regional, reduction in systolic function and a diffuse decline in GLS without a coronary distribution. On echocardiography, wall thickness is usually normal early, and diastolic dysfunction may be mild or absent initially. Cardiac MRI often shows the absence of focal late gadolinium enhancement (LGE) or, in later stages, diffuse interstitial fibrosis reflected by elevated native T1 and extracellular volume rather than discrete scar. In contrast, ischemic cardiomyopathy is characterized by regional wall-motion abnormalities on TTE and subendocardial or transmural late gadolinium enhancement in a coronary artery distribution on MRI. Hypertensive heart disease typically demonstrates concentric left ventricular hypertrophy, impaired relaxation with preserved or mildly reduced ejection fraction early on, and relatively preserved GLS with predominant basal strain reduction; MRI may show mid-wall fibrosis in advanced disease rather than the diffuse interstitial pattern seen with CTRCD.
Additional imaging clues can further refine the diagnosis. Myocarditis often presents with regional or global dysfunction accompanied by myocardial edema on T2-weighted or T2-mapping sequences and patchy, nonischemic LGE. Infiltrative cardiomyopathies are suggested by increased wall thickness, biatrial enlargement, abnormal strain patterns such as apical sparing in amyloidosis, and characteristic diffuse subendocardial or transmural LGE with markedly elevated extracellular volume on MRI. Taken together, the pattern of ventricular dysfunction, strain abnormalities, wall thickness, and LGE distribution allows differentiation of CTRCD from ischemic, hypertensive, and other non-therapy–related cardiomyopathies in most cases.
Question 6: What is the role of high-sensitivity troponin and natriuretic peptides in early detection of cardiotoxicity, and how often should they be checked during treatment?
High-sensitivity troponin and natriuretic peptides play a complementary role to imaging in the early detection of cardiotoxicity, with troponin serving primarily as a marker of myocardial injury and natriuretic peptides reflecting hemodynamic stress and evolving ventricular dysfunction. High-sensitivity troponin is most useful for identifying early, often subclinical injury during exposure to cardiotoxic therapies—particularly anthracyclines and HER2-targeted agents—where persistent or recurrent elevations are associated with subsequent declines in GLS and LVEF. Natriuretic peptides are less sensitive for very early injury but are helpful for identifying patients developing increased filling pressures or overt heart failure physiology, especially later in the treatment course.
In practice, while some protocols advocate frequent biomarker surveillance, real-world logistics often limit how often testing can realistically be performed. Given this, I use biomarkers selectively rather than universally. I obtain baseline troponin and natriuretic peptide levels before initiating higher-risk therapies, then repeat testing at key inflection points—such as after completion of anthracyclines, early during HER2 therapy, or when there is a concerning change in GLS, LVEF, blood pressure, or symptoms—rather than at every cycle. For patients at particularly high risk or those with rising but subthreshold imaging abnormalities, I will check troponin intermittently during treatment, but I do not require routine, frequent testing in low-risk or clinically stable patients.
Overall, biomarkers are most valuable when integrated with imaging and clinical assessment rather than used in isolation. A rising troponin or natriuretic peptide level in conjunction with a GLS decline or new symptoms lowers my threshold for initiating cardioprotective therapy or increasing surveillance, whereas stable biomarkers in an asymptomatic patient with reassuring imaging allow a more pragmatic, less burdensome testing strategy that reflects the realities of patient access and adherence.
Part 2 will be published soon….
Guest contribution by Dr. Manu Mysore.