Abstract Body (Do not enter title and authors here):
Intro
Tyrosine Kinase inhibitors (TKI) have been an effective treatment option for multiple cancer types. Unfortunately, TKIs have shown to have off-target Kinase binding to cardiac tissue. The examination of these cardiotoxic side effects have not been sufficiently explored in minority populations and studies such as DASISION and ENESTnd with high NAA homogeneous demographics reflect this issue. AA tend to have higher rates of HTN and HF at baseline, so further evaluation of TKI cardiotoxicity in this population is warranted.

Methods
A total of 181 patients (pts) charts were reviewed in this study, who were exposed to either Ibrutinib, Imatinib and Sorafenib. First, Patients’ demographic data, such as age, gender, race, malignancy type were obtained along with their corresponding exposure to TKIs discussed above. Next, each patient (pt) chart was examined for any cardiotoxic etiologies after starting a TKI, such as arrhythmias, new- onset heart failure (nOHF) , cardiac arrest (CA), and Myocardial infarction (MI). Echocardiography reports were examined for Ejection fraction ( EF). In summary, this is an observational study looking at Cardiotoxicity secondary to TKI use in the AA population.
Results
This study's demographics consisted of 149 AA and 32 NAA (non- african american), with the average age of 64.2, and had 128 males and 53 females. A total of 89 pts were on imatinib, 57 on Ibrutinib, 35 on sorafenib. In our population, 64 pts received cardiac echography while on TKIs, with 9 of them demonstrating nOHF. In terms of cardiac arrhythmias, a total of 67 pts experienced this while on TKI, with about 34% (51/149) of AA compared to 50% (16/32) of NAA. A total of 18 pts in the study required hospital management as a sequelae of their cardiotoxicity.
Conclusion
There were a few trends that diverged from most studies regarding cardiotoxicity associated with TKIs in our study. When looking at individual items, such as rate of Atrial Fibrillation (AF), seen commonly in patients on Ibrutinib, our rate seen is 4.6% which is lower compared to earlier pooled homogenous population studies (6-7%). Earlier clinical trials of Sorafenib had a 2 % rate of HF in mostly homogenous NAA populations, and our study had 0% rate in total. Overall, several cardiotoxicity trends seen with the TKIs in this observational study warrant need for future studies to enable improved cardiac surveillance strategies post treatment in heterogeneous populations.