Background Myocardial toxicity is a common side effect of chemotherapy and is associated with adverse outcomes in cancer patients. Sufficient prediction of chemotherapy-induced myocardiotoxicity (CIMC) is desirable. Therefore, we sought to develop a feasible scoring system to predict CIMC in cancer patients undergoing non-anthracycline chemotherapy. Methods We determined a scoring system, the “Cardiotoxicitiy Score” (the CardTox-Score), by multivariable regression of the parameters considered relevant to the development of CIMC, based on previously published data and current guidelines. Variables of the risk model consist of clinical (age, presence of cardiovascular risk conditionsconditions), blood tests (NT-proBNP), and echocardiographic parameters (left ventricular (LV) ejection fraction, LV strain analysis). The CardTox-Score was examined in an internal validation cohort by use of ROC and regression analysis. Results We prospectively investigated 225 patients (58.21 ± 6.3 years, 52.8% female) who received non-anthracycline myocardiotoxic anticancer agent as a derivation cohort. All patients underwent echocardiography before, during and after anticancer therapy. The mean follow-up duration was 25 ± 4 months. We found the CardTox-Score (>6 points) to be a strong independent predictor (AUC: 0.983, OR: 6.38, 95% CI: 1.6 2.8, p < 0.001) for the development of CIMC with high sensitivity (100%) and specificity (84.2%) in the validation cohort (n = 30, 59.2 ± 6.5 years, 57% female). Moreover, the CardTox-Score appropriately predicted all-cause mortality with high specificity (93.7%) and sensitivity (92.9%) as well (OR: 4.85, AUC: 0.978, p = 0.01). Conclusion The CardTox-Score offers a promising, feasible, and easy-to-handle scoring system for predicting CIMC in cancer patients undergoing non-anthracycline regimes, independent from the type of cancer.

Cardiotoxicity is a frequent side effect of chemotherapy leading to impaired outcomes in cancer survivors. Because of that cardiooncology has recently gained more importance in clinical practice. We aim to echocardiographically evaluate the development of cardiotoxicity and to detect early signs for preventing severe cardiomyopathies by repeated strain analysis. We included 80 patients (46.7 ± 14.7 years, 75% female) under diverse cardiotoxic chemotherapies (43.7% breast cancer, 43.7% haematological malignancy, 12.5% others). All patients underwent echocardiography before and during treatment. Follow-up echocardiography was performed approximately 5.5 ± 1.2 months after the first application of the chemotherapy. The apical four-chamber view was used to perform strain analysis employing dedicated and automated offline software as shown previously. Eight patients deceased due to oncological complications during follow up. Twelve patients showed significant reduced left ventricle ejection fraction (LVEFbaseline 63.2 ± 4.5%, LVEFFollow-up 48.6 ± 7.8%, p = 0.02) correlated with decrease in left ventricular global longitudinal strain (LV-GLSbaseline 17.1 ± 5.2%, LV-GLSFollow-up 9.7 ± 3.2%, p = 001). All of these patients presented heart failure symptoms, mostly with dyspnoea (85% functional NYHA class &gt; II) and oedema (65%). In 15 patients we found a reduction of left ventricular global longitudinal strain from &lt;5% without relevant reduction of LVEF. However, these patients showed also heart failure symptoms. During follow up 20 patients had to be admitted due to decompensated heart failure. Four patients deceased due to cardiovascular causes. Delta LV-GLS (LV-GLSbaseline – LV-GLSFollow-up) was found to be strongest independent predictor of mortality. Baseline LV-GLS &lt; 15% was found to be associated with mortality and frequent rehospitalisation. Solely LVEF is insufficient to detect cardiotoxicity and to estimate prognosis of patients under cardiotoxic chemotherapy. In our small patient collective we found baseline LV-GLS &lt;15% to be an adequate parameter for prognosis estimation and delta LV-GLS &gt; 5% a strongest independent predictor for mortality in patients with preserved LVEF under cardiotoxic chemotherapy.