Traditional and novel methods to assess and prevent chemotherapy-related cardiac dysfunction noninvasively.

The field of cardio-oncology is challenged to address an ever greater spectrum of cardiotoxicity associated with combination chemotherapy, greater dose intensity, extremes of age, and enhanced patient survival which exposes more protracted risk of developing congestive heart failure (CHF). Recent reports of chemotherapy-induced hypertension as a common adverse effect of angiogenesis inhibitors and immunosuppressants clarify the need for routine blood pressure (BP) monitoring and guideline-based management of hypertension as an integral strategy to preserve LV function. Serial monitoring of radionuclide left ventricular ejection fraction (LVEF) in adults and echocardiography in children continues to provide outcome based, cost-effective prevention of CHF in high risk patients receiving chemotherapy. To optimize treatment and monitoring strategies to eliminate late-onset LV dysfunction and CHF, traditional and novel candidate methods for assessment of chemotherapy-induced LV dysfunction are reviewed. These include serial assessment of LV volume indices by gated SPECT ERNA and gated SPECT MPI, 3D echocardiography and contrast 2D echocardiography; longitudinal strain imaging, diastolic functional parameters, (123)I-MIBG, (111)In-Antimyosin antibody imaging, and (99m)Tc-Annexin V apoptosis imaging, biomarkers including troponins and BNP; genetic markers, and both functional and tissue characterization techniques with T1 weighted and T2 weighted images with cardiac magnetic resonance imaging (CMR). In our quest to optimize strategies for long-term cancer survival and prevention of CHF for patients receiving chemotherapy, rigorous modality and guideline-specific clinical outcome trials are required. A new multi-modality monitoring approach is proposed, which integrates evidence-based strengths of CMR, echocardiography, ERNA, biomarkers, and BP management for surveillance and validation of cardiotoxicity and prevention of clinical heart failure in patients receiving a broad spectrum of cancer therapies.