Chemotherapy Related Cardiotoxicity Evaluation-A Contemporary Review with a Focus on Cardiac Imaging

Abstract

The long-term survivorship of patients diagnosed with cancer has improved due to accelerated detection and rapidly evolving cancer treatment strategies. As such, the evaluation and management of cancer therapy related complications has become increasingly important, including cardiovascular complications. These have been captured under the umbrella term "cardiotoxicity" and include left ventricular dysfunction and heart failure, acute coronary syndromes, valvular abnormalities, pericardial disease, arrhythmia, myocarditis, and vascular complications. These complications add to the burden of cardiovascular disease (CVD) or are risk factors patients with cancer treatment are presenting with. Of note, both pre- and newly developing CVD is of prognostic significance, not only from a cardiovascular perspective but also overall, potentially impacting the level of cancer therapy that is possible. Currently, there are varying recommendations and practices regarding CVD risk assessment and mitigating strategies throughout the cancer continuum. This article provides an overview on this topic, in particular, the role of cardiac imaging in the care of the patient with cancer. Furthermore, it summarizes the current evidence on the spectrum, prevention, and management of chemotherapy-related adverse cardiac effects.

Keywords: cardiac imaging; cardio-oncology; cardiotoxicity; chemotherapy; echocardiography.

Figure 1

Graphical depiction of cardiac investigations involved in the baseline assessment, surveillance, and monitoring of cancer patients at risk of cancer therapy-related cardiac dysfunction. BNP, brain natriuretic peptide; NT-proBNP, N-terminal-proBNP; MRI, magnetic resonance imaging; PET, positron emission tomography; SPECT, single-photon emission computed tomography; MUGA, multigated acquisition scan; PYP, technetium-99 m pyrophosphate scintigraphy; CT, computed tomography.

Figure 2

Flow chart of suggested baseline risk assessment for all cancer patients prior to receiving potentially cardiotoxic cancer therapy. Surveillance for cancer therapy-related cardiac dysfunction (CTRCD) is suggested based on stratification of baseline risk. This figure has been adapted from the 2022 ESC Guidelines on cardio-oncology [15]. ECG, electrocardiogram; BNP, brain natriuretic peptide; TTE, transthoracic echocardiogram; LVEF, left ventricular ejection fraction; ACEi, angiotensin-converting enzyme inhibitor.

Figure 3

Flow chart of suggested cardiovascular monitoring for cancer patients receiving cardiotoxic cancer therapy, separated by baseline risk assessment and chemotherapeutic agent. (A) Anthracycline therapy. (B) Human epidermal growth factor receptor 2 (HER2) targeted therapies. This figure has been adapted from the 2022 ESC Guidelines on cardio-oncology [15]. TTE, transthoracic echocardiogram; BNP, brain natriuretic peptide; TnI, troponin I.

Figure 4

Global longitudinal strain (GLS) images of a 63-year-old female with Grade 1 invasive ductal carcinoma of the breast, estrogen receptor (ER)/progesterone receptor (PR)/human epidermal growth factor receptor-2 (HER2) receptor positive. She was treated with lumpectomy and adjuvant trastuzumab. (A) Baseline transthoracic echocardiogram (TTE) with normal GLS and left ventricular ejection fraction (LVEF), prior to receiving trastuzumab. (B) First surveillance TTE after commencement of trastuzumab therapy showed a decline in LVEF of 8% (less than the 10% cutoff for cardiotoxicity), an absolute decline in GLS of 6%, and a relative decline in GLS of 27%, consistent with mild CTRCD. (C) Second surveillance TTE after commencement of trastuzumab showing further reduction in LVEF to 49% and GLS to 14%. Patient was accordingly commenced on guideline-directed medical therapy (GDMT), including beta-blocker and angiotensin receptor blocker, and advised for cessation of alcohol (which she was taking in excess). No interruption in trastuzumab therapy was needed, as LVEF did not drop further with these measures. (D) TTE 6 months after GDMT and on completion of trastuzumab therapy with improvement in both LVEF and GLS.