Citations

Abstract Background: RUNX1 mutations are established high-risk features in acute myeloid leukemia (AML), associated with poor response to induction therapy and reduced overall survival (OS). Current prognostic models, including the ELN 2022 classification, incorporate RUNX1 mutation status but are based largely on cohorts of European ancestry. This raises concerns about their generalizability to underrepresented populations, particularly African American patients, who continue to experience worse outcomes in AML across treatment settings. Methods: We analyzed publicly available datasets, including TCGA-LAML, Beat AML, and a recent multi-omic study of 100 African American AML patients (Stiff et al., Nat Genet 2024). We evaluated RUNX1 mutation frequency, OS outcomes, and co-mutation patterns, stratified by race. To contextualize survival differences by ancestry, we performed a survival analysis of adult AML patients using the SEER 17 registries (2010–2020), accessed through SEER*Stat. Kaplan-Meier estimates and median OS were compared by race using disease-specific survival. Results: RUNX1 mutations were present in approximately 10–15% of AML cases and consistently associated with inferior OS (median 16–24 months) in both de novo and AML-MRC subsets. Co-mutations in DNMT3A and TET2 further worsened the prognosis. In the African American cohort described by Stiff et al., the frequency of RUNX1 mutations was similar to that in White patients; however, African American patients showed enrichment for IDH2, RAS, and WT1 mutations and lower incidence of NPM1 mutations. Despite comparable mutation rates, African American patients demonstrated significantly worse OS, even under standardized treatment. SEER 17 survival analysis of 5,932 AML cases (683 African American) confirmed shorter median OS in African American patients compared to non-African American patients (10.4 vs. 15.7 months, p<0.01).Conclusions: RUNX1 mutations confer adverse prognosis in AML, but current risk models may not adequately reflect risk in African American patients due to differing co-mutation patterns and underrepresentation in genomic datasets. These findings highlight the need for ancestry-aware risk stratification and inclusive genomic profiling to reduce disparities in AML outcomes. References: Lew-Derivry et al. Leukemia. 2023 Jalili et al. PMCID: PMC5980915 Stiff et al. Nat Genet. 2024 Bhatnagar et al. PMCID: PMC7933110 Tang et al. Blood. 2009 Mendler et al. JCO. 2012 He et al. Scand J Clin Lab Invest. 2020 Döhner et al. Blood. 2022. PMID: 35926292

Abstract Background Pirtobrutinib is a highly selective, non-covalent Bruton tyrosine kinase inhibitor (BTKi) approved for patients (pts) with relapsed/refractory (R/R) chronic lymphocytic lymphoma (CLL) who have previously received a covalent BTKi (cBTKi) and a BCL-2 inhibitor such as venetoclax. Pirtobrutinib monotherapy has demonstrated a median duration of response of 12.2 months in the BRUIN trial. Pirtobrutinib is increasingly being used as a second-line therapy after failure of a cBTK inhibitor without prior BCL-2 inhibitor exposure. We aim to characterize short-term survival outcomes and adverse events of pirtobrutinib in venetoclax-naïve versus venetoclax-exposed pts with R/R CLL. Methods We conducted a retrospective cohort study using TriNetX Global Collaborative Network, comprising data from 152 healthcare organizations. Adults (≥18 years) with R/R CLL who received pirtobrutinib after venetoclax were classified into the “V+P” cohort. Pts who received pirtobrutinib without prior venetoclax exposure were included in the “P” cohort. 1:1 propensity score matching (PSM) was performed, and the cohorts were balanced for gender and age. The primary outcome was all-cause mortality (ACM). Secondary outcomes assessed were anemia, neutropenia, sepsis, neutropenic fever, tumor lysis syndrome (TLS), and major adverse cardiovascular and cerebrovascular events (MACCE). Kaplan-Meier analysis and risk analysis were used to assess outcomes at 6 months and 1 year. Results We identified 200 pts in V+P and 172 pts in P, with 149 matched pts in each group after PSM. The mean age of pts in V+P and P was 72.4 +/- 8.6 years and 72.7 +/- 10.5 years, respectively. 6-month ACM was 15.5% in V+P, and 12.7% in P. However, the odds ratio of ACM at 6 months, in pts in V+P when compared to P was 1.259 (95% CI 0.654 to 2.425, p = 0.490) and was not statistically significant. At 6 months, the odds ratios of the secondary outcomes in the V+P pts were higher when compared to P pts, but were not statistically significant; anemia 1.614 (95% CI 0.617 to 4.225, p = 0.327), neutropenia 1.445 (95% CI 0.599 to 3.486, p = 0.411), sepsis 1.196 (95% CI 0.477 to 2.998, p = 0.703), neutropenic fever 1.353 (95% CI 0.573 to 3.195, p = 0.490), TLS 1.180 (95% CI 0.474 to 2.939, p = 0.722), and MACCE 1.046 (95% CI 0.541 to 2.024, p = 0.893). 1 year ACM was 18.75% in V+P vs. 10.55% in P (OR 1.96; 95% CI 1.03-3.71; p=0.038) and was statistically significant. However, the secondary outcomes were clinically significant but statistically insignificant in V+P pts when compared to P pts- anemia 1.614 (95% CI 0.617 to 4.225, p = 0.327), neutropenia 1.269 (95% CI 0.568 to 2.834, p = 0.561), sepsis 1.077 (95% CI 0.438 to 2.650, p = 0.872), neutropenic fever 1.24 (95% CI 0.589 to 2.607, p = 0.571), TLS 1.180 (95% CI 0.474 to 2.939, p = 0.722), and MACCE 1.338 (95% CI 0.724 to 2.472, p = 0.352). Conclusion Pirtobrutinib use in venetoclax-exposed pts was associated with a statistically significant higher odds of all-cause mortality at 1 year, which was not present at 6 months. Although adverse event rates of anemia, neutropenia, TLS, sepsis, and neutropenic fever were numerically higher in the venetoclax-exposed cohort, these differences did not reach statistical significance. These findings suggest early survival benefit of pirtobrutinib in venetoclax-naïve patients and aligns with existing evidence supporting its role as a second-line therapy following covalent BTK inhibitor failure, including results from the BRUIN trial. Prospective studies are needed to validate these preliminary observations.

Abstract Background: Patients with myelodysplastic syndromes (MDS) are highly susceptible to infections, with sepsis being a major cause of hospitalization and death. While gender differences in sepsis outcomes have been described in broader populations, their impact among patients with MDS remains poorly defined. Methods: We performed a retrospective cohort study using the National Inpatient Sample (NIS) from 2016 to 2022 to identify adult hospitalizations with co-diagnoses of MDS and sepsis. Patients were stratified by sex: male (n = 47,170) and female (n = 31,365). Multivariable logistic regression was used to evaluate the association between female sex and key outcomes: respiratory failure, encephalopathy, disseminated intravascular coagulation (DIC), Clostridioides difficile infection (CDI), fungal sepsis, and in-hospital mortality. Models were adjusted for demographics, comorbidities, and hospital characteristics. Results: Female sex was independently associated with increased odds of respiratory failure (OR 1.05, 95% CI 1.01–1.08, p = 0.011) and encephalopathy (OR 1.07, 95% CI 1.02–1.12, p = 0.010). There was a nonsignificant trend toward higher odds of CDI (OR 1.14, p = 0.086). No significant sex-based differences were observed for DIC (OR 0.84, p = 0.103), fungal sepsis (OR 0.89, p = 0.598), or in-hospital mortality (OR 0.98, p = 0.653). Conclusion: In this large national analysis of MDS patients hospitalized with sepsis, female patients were more likely to experience respiratory failure and encephalopathy, but sex was not significantly associated with mortality, DIC, or fungal infections. These findings suggest that while certain complications may differ by sex, overall in-hospital survival remains comparable between male and female patients with MDS and sepsis.Keywords: Myelodysplastic syndromes, sepsis, gender disparities, mortality, respiratory failure, encephalopathy, NIS

Abstract Background: Cryoprecipitate is indicated for bleeding patients with hypofibrinogenemia, typically when fibrinogen levels fall below 100–150 mg/dL. Despite established national transfusion guidelines, inappropriate use remains a persistent issue in clinical practice, especially in community hospitals where formal transfusion oversight may be limited. Unnecessary transfusions can expose patients to avoidable risks and contribute to increased healthcare costs. As part of a hospital-wide quality improvement initiative, we conducted a retrospective review of cryoprecipitate use at our institution to assess adherence to transfusion guidelines and identify areas for improvement. Methods: We performed a retrospective review of all cryoprecipitate transfusions at Landmark Medical Center, a 214-bed community hospital in Rhode Island, between January 2021 and June 2025. Transfusion episodes were identified through blood bank records. For each episode, we extracted the number of units ordered and administered, pre-transfusion fibrinogen levels, documented clinical indication in the electronic medical record (EMR), and any product wastage. Each transfusion was assessed based on institutional criteria aligned with national guidelines, which recommend cryoprecipitate only in cases of active bleeding with fibrinogen <100–150 mg/dL. Results: Twenty patients received cryoprecipitate in 23 transfusion episodes involving 32 units. Of these, 28 units were administered and 4 were wasted. The majority of patients were female (65%), and 40% were between ages 61 and 75. Only 10 of 23 episodes (43%) met established transfusion criteria. Nine episodes (39%) were given when fibrinogen levels ranged between 100–200 mg/dL, and two episodes (9%) occurred with levels >200 mg/dL. One transfusion was administered without a documented fibrinogen level. Additionally, 8 episodes (35%) lacked a clearly documented indication in the EMR. Three episodes (13%) involved product wastage, including one with no documentation and another where an order was placed but the unit was not administered. Conclusion: This review revealed that more than half of cryoprecipitate transfusions did not meet guideline-based criteria. The findings point to deficiencies in provider knowledge, inconsistent documentation, and limited transfusion oversight contributing to inappropriate use. These results highlight the need for targeted interventions, including: (1) provider education on transfusion thresholds, (2) EMR-based decision support requiring lab values prior to ordering, and (3) routine audits with feedback. Strengthening transfusion practices through structured quality improvement efforts can reduce unnecessary use, improve patient safety, and preserve limited blood product supplies for those who truly need them.

Abstract Background In patients with myelofibrosis (MF) undergoing allogeneic hematopoietic cell transplantation (allo-HCT), graft-versus-host disease (GVHD) prophylaxis has traditionally included a calcineurin inhibitor (CNI) plus methotrexate (MTX). We conducted a retrospective study comparing the safety and efficacy of post-transplant cyclophosphamide (PTCy)-based GVHD prophylaxis to CNI-based regimens. Methods This study was approved by the Mayo Clinic IRB. Patients with myelofibrosis who underwent allo-HCT after 2016 at Mayo Clinic in Arizona and Florida were included. Categorical variables were compared using Chi-square or Fisher's exact tests. Overall survival (OS) was defined from transplant to death, and progression-free survival (PFS) from transplant to relapse or death. OS and PFS were estimated using Kaplan-Meier methods; univariate differences were assessed with log-rank tests. The cumulative incidence of acute and chronic GVHD and time to neutrophil and platelet engraftment were analyzed using competing risk models, with death as a competing event; differences were tested using Gray's test. Cox proportional hazards models were used to estimate adjusted hazard ratios (HRs). Results A total of 110 patients were included. 53 patients received PTCy-based prophylaxis (43 PTCy/Tac/MMF, 1 PTCy/CSA/MMF, 9 PTCy/Siro/MMF), while 57 received non-PTCy regimens (54 Tac/MTX +/- 39 T-cell depletion, 2 CSA/MMF, 1 Tac/MMF). Median age at transplant was 63 (range: PTCy 40-76; others 38-74) years in both groups; 59 were male (58.5% PTCy vs 49.1% others). Median Karnofsky Performance Status (KPS) and HCT–Comorbidity Index (HCT-CI) in patients receiving PTCy vs non-PTCy were 90 vs 80 and 1 vs 3, respectively. Conditioning intensity was similar: 22.6% myeloablative vs 21.7%, and 77.4% reduced-intensity vs 76.7% in PTCy and non-PTCy, respectively (p=1.000). Stem cell source was peripheral blood in all patients except one in the non-PTCy group who received bone marrow. 58 patients had primary MF (54.7% PTCy vs 50.9% others), and 52 had secondary MF (45.3% PTCy vs 49.1% others), including essential thrombocythemia (28.3% PTCy vs 31.6% others), polycythemia vera (17.0% vs 15.8%), and MPN-NOS (0% vs 1.8%). Median follow-up was 26.2 months (95% CI: 20.7-52.7) in the PTCy and 60.6 months (95% CI: 53.1-70.6) in the non-PTCy cohort. CD3 and CD33 donor chimerism ≥95% at day +100 was 66.7% and 86.7% in PTCy vs 63.6% and 92.7% in others, respectively (p=0.50); day +100 driver molecular mutations were present in 32.1% of PTCy and 32.0% of others (p>0.99). Rates of acute GVHD grades ≥2 and ≥3 were not statistically significant, in the PTCy group (37.7% vs 49.1% p=0.229 and 17.0% vs 22.8% p=0.445, respectively). Chronic GVHD (any grade) occurred in 42.3% of PTCy vs 38.2% of others (p=0.664), while moderate-to-severe cGVHD was lower with PTCy (21.2% vs 27.3% p=0.461). Platelet engraftment was significantly delayed in the PTCy group (median 33 vs 21 days, p=0.030). Median time to neutrophil engraftment was also delayed in the PTCy group (20 vs 17 days, adjusted p=0.025). Age-adjusted HR for time to platelet engraftment was 0.60 (95% CI: 0.41–0.90; p=0.014), and for neutrophil engraftment 0.65 (95% CI: 0.44–0.95; p=0.025), indicating significantly delayed hematopoietic recovery with PTCy. Graft failure occurred in 9.4% vs 5.3% (p = 0.48); primary 7.5% vs 3.5%, secondary 1.9% vs 1.8% in PTCy vs non-PTCy groups, respectively. Relapse or progression occurred in 11.3% of PTCy vs 17.5% of others (p=0.355); four patients in the non-PTCy group progressed to AML post-transplant, versus none in the PTCy group (p=0.119). 1-year TRM was 22.6% in the PTCy group and 14.0% in the non-PTCy group, p = 0.324. Median OS was 72.8 months in the PTCy group (95% CI: 49.9 months, upper limit not estimable [NE]) and 93.4 months in the non-PTCy group (95% CI: 48.5 months, upper limit NE), although the difference was not statistically significant (p=0.739). After adjusting for age and HCT-CI, there were no significant differences in PFS (adjusted HR 1.37; 95% CI: 0.73–2.56; p=0.331) or OS (adjusted HR 1.27; 95% CI: 0.64–2.51; p=0.498). Conclusions In myelofibrosis patients undergoing allo-HCT, PTCy-based GVHD prophylaxis showed similar rates of grade ≥2 acute and moderate-severe chronic GVHD compared to non-PTCy regimens. Engraftment was significantly delayed, while OS and PFS were comparable. PTCy appears to be a safe and viable alternative to CNI-based prophylaxis.

817 Background: Cancer screening ingastrointestinal (GI) malignancies has translated into an improvement in overall survival due to detection at an earlier stage. The majority of survivors (up to 67%) are over the age of 65. The impact of metabolic profiles on cerebrovascular events amongst this population of cancer survivors is unclear. Methods: Data from the NIS database from 2016 to 2020 were reviewed for patients with seven GI malignancies. Analysis was performed based on the presence or absence of prediabetes using ICD-10 codes. Baseline characteristics, comorbidities, and cerebrovascular outcomes were studied in these 2 cohorts. Results: 1,532,250 hospitalizations of patients with seven GI malignancies, namely colorectal cancer (CRC), pancreatic cancer, hepatocellular carcinoma (HCC), gastric cancer, small intestinal cancer, cholangiocarcinoma, and esophageal cancer, were evaluated and divided into two subgroups: prediabetics (15,610) and non-prediabetics (1,516,640). Prediabetics with GI malignancies as compared to non-prediabetics with GI malignancies were noted to be older (67.7 years vs. 65.64 years), with higher total hospitalization charges (USD 87,267 vs. USD 80,173), greater rates of elective admissions (34.92% vs. 25.89%) but a lower length of stay (6.018 days vs. 6.53 days). Prediabetic patients with GI malignancies were noted to have a higher prevalence of obesity (18.64% vs. 7.69%), dyslipidemia (52.99% vs. 26.16%), and hypertension (49.59% vs. 39.37%). Prediabetics with CRC, as compared to non-prediabetics, had higher adjusted odds ratios (aORs) of occlusion/stenosis of precerebral or cerebral arteries not leading to cerebral infarction, and cerebral infarction, with aORs of 2.03 (95% CI 1.24-3.30, p 0.004), and 1.63 (95% CI 1.01-2.63, p 0.045) respectively. Additionally, prediabetics with pancreatic cancer had a higher aOR of cerebral infarction as compared to non-prediabetics, with aOR of 2.42 (95% CI 1.70-3.44, p<0.001). Conclusions: Prediabetic patients with CRC had higher aORs of cerebral infarction and occlusion/stenosis of precerebral arteries not leading up to cerebral infarction, and prediabetics with pancreatic cancer had twice the risk of cerebral infarction as compared to non-prediabetics. This study highlights the impact of prediabetes, a modifiable risk factor, on cerebrovascular outcomes in patients with GI malignancies.

e16342 Background: Pancreatic cancer poses a major challenge due to its high mortality rates and is known as one of the deadliest cancers. The increasing mortality in addition to the aggressive nature of the tumor may be due to major cardiovascular and cerebrovascular events (MACCE). The key to mitigating the risk of pancreatic cancer as well as MACCE, is primary prevention of common risk factors including tobacco use, obesity, dietary factors, alcohol use, and physical activity. Understanding that many of these factors are directly and indirectly influenced by income status, this study aims to explore the relationship between household income on MACCE in pancreatic cancer patients. Methods: Using ICD-10 codes, patients with pancreatic cancer were identified from National Inpatient Sample 2019 database. We included all-cause in-hospital mortality (ACIHM), acute myocardial infarction (AMI), arrythmia, cerebrovascular accident (CVA), and sudden cardiac death (SCD) as MACCE for the outcomes. Baseline characteristics including demographics, comorbidities; and MACCE outcomes were studied using chi-square for categorical or ANOVA for continuous data (statistical significance determined as p-value < 0.05) and results were stratified based on median household income quartiles. Results: Of the 114,235 patients identified with pancreatic cancer who were admitted to the hospital, 25% (28,570) belonged to the first income quartile ($1-47,999), 23.8% (27,235) belonged to the second income quartile ($48,000-60,999), 26.38% (30,135) belonged to the third income quartile ($61,000-81,999), and 24.76% (28,295) belonged to the fourth income quartile ($82,000+). When compared to the patients in the fourth quartile, the adjusted odds ratio (aOR) was found to be higher for all MACCE outcomes for patients in first quartile. The aOR for ACIHM in the first quartile was found to be 1.24 (95% CI 1.06-1.46, p = 0.006) as compared to patients in the fourth quartile. Additionally, the aOR for AMI, was found to be statistically significant in patients belonging to the first quartile at 1.30 (95% CI 1.01-1.70, p = 0.047). Similarly, the aORs for both arrhythmia and SCD were also higher in the population from the first quartile at 3.67 (95% CI 1.10-12.28, p = 0.03) and 1.45 (95% CI 1.01-2.09, p = 0.049). https://docs.google.com/document/d/1v84LyPoGL406_7SDxO1N-wKxwujSgFpf/edit?usp = sharing&ouid = 110330426831507953030&rtpof = true&sd = true. Conclusions: As compared to patients in fourth income quartile, the aOR was found to be higher for all MACCE outcomes for patients in the first income quartile, indicating a vast variation based on income strata. This hints towards a complex interplay of healthcare disparities including but not limited to difficult access to quality healthcare including subspecialities. Further research may be pertinent to explore the causes of this clear disparity to ensure equitable healthcare for all patient population.

e13102 Background: Hereditary mutations of the homologous recombination (HR), the key DNA double-strand break repair pathway, are one of the well-known causes of breast and ovarian cancers. Few reports exist on these mutations and the utilization of PARP inhibitors in the Middle Eastern region. Methods: This is a single-center retrospective study of breast and ovarian cancer patients who underwent genetic testing for g BRCA and HR defects (HRD) respectively between August 2021 and May 2023. Data was summarized using descriptive statistics and compared using counts and percentages. Response to treatment was assessed using RECIST criteria. Results: The prevalence of pathogenic mutations was 22.8%, with 26.3% of breast cancers harboring g BRCA mutations and 24% of ovarian cancers showing HRD positivity. Middle Eastern patients comprised 40% of the g BRCA-positive breast cancer group, while Asians accounted for 66% of the HRD-positive ovarian cancer patients. In mutated breast cancer, 53.3% had a positive family history of cancer. 33.3% of mutated breast cancer group and 66.6% of the ovarian cancer group received PARPis. Objective response to PARPi was 40% and 100% in breast and ovarian cancers, respectively. Conclusions: Our study revealed a high prevalence of g BRCA mutations (26.3%) in breast cancer and HRD positivity (24%) in ovarian cancer). Ethnic profiles differed between these cancers, with Middle Eastern and Southeast Asian patients dominating the breast and ovarian groups, respectively. Interestingly, the TNBC rate in breast cancer remained around 20% regardless of g BRCA status. While disparities between HRD groups were more pronounced in ovarian cancer, as expected, unexpected trends emerged in breast cancer. Further research with larger cohorts is needed to confirm these findings. [Table: see text]

e19076 Background: Non-Hodgkin Lymphoma (NHL) is the seventh most prevalent cancer and has sixth highest malignancy mortality in United States. Owing to the advances in treatment of NHL including targeted therapies, the survival of NHL patients has increased over the past decades. However, inequalities may exist in the access to advanced care, clinical trials, and subspecialist appointments in certain patient populations. We aim to study the racial disparities in major cardiovascular and cerebrovascular events (MACCE) in NHL patients. Methods: Using ICD-10 codes, patients with NHL were identified from National Inpatient Sample 2019 database. We included all-cause in-hospital mortality (ACIHM), acute myocardial infarction (AMI), atrial fibrillation (AF), cerebrovascular accident (CVA), and sudden cardiac death (SCD) as MACCE for the outcomes. Baseline characteristics including demographics, comorbidities; and MACCE outcomes were studied using chi-square for categorical or ANOVA for continuous data (statistical significance determined as p-value <0.05) and results were stratified based on patient’s races. Results: Out of the total sample size of 205220 patients admitted with a diagnosis of NHL, 74.94% (153785) were White, 8.95% (18370) were Black, 9.46% (19415) were Hispanic, 3.48% (7140) were Asian/Pacific Islander, 0.42% (875) were Native American, while 2.75% (5635) belonged to other races. When compared to White patients, ACIHM was significantly higher in Black patients with adjusted odds ratio (aOR) of 1.294 (95% CI 1.099-1.523, p=0.002) and Asian/Pacific Islander patients (aOR 1.279, 95% CI 1.005-1.628, p=0.045). Risk of AMI was lower in Black patients (aOR 0.751, 95% CI 0.587-0.96, p=0.023) as compared to White patients. AF risk was significantly lower in Black, Hispanic, and Other race patients compared to White patients. The odds of developing CVA are higher in Asian/Pacific Islander patients (aOR 1.285, 95% CI 1.002-1.649, p=0.048) and of having SCD are higher in Black patients (aOR 2.052, 95% CI 1.5-2.806, p<0.001) when compared to White patients. Conclusions: In patients with NHL, Black patients had higher ACIHM and SCD while Asian/Pacific Islander patients had higher ACIHM and CVA when compared to White patients. Although the reason of disparity is likely multifactorial, the findings of this study highlight the need for development of healthcare strategies stratified by race which may aid to mitigate the increased risk of MACCE in certain races. Further research involving possible genetic influences and social determinants of health contributing to poorer outcomes in Black and Asian/Pacific Islander patients with NHL becomes imperative.

e13740 Background: Hepatocellular carcinoma (HCC) ranks as the 6th most common cancer and as the 3rd leading cause of cancer-related mortality. With immunotherapy improving survival rates, the relevance of major adverse cardiovascular and cerebrovascular events (MACCE) is increasing. We aim to explore the racial disparities in MACCE among patients with HCC, thus leading to a better understanding of the interplay of these conditions with social determinants of health. Methods: Using ICD-10 codes, patients with HCC were identified from National Inpatient Sample 2019 database. We included all-cause in-hospital mortality (ACIHM), acute myocardial infarction (AMI), atrial fibrillation (AF), cerebrovascular accident (CVA), and sudden cardiac death (SCD) as MACCE for the outcomes. Baseline characteristics including demographics, comorbidities; and MACCE outcomes were compared using chi-square for categorical or ANOVA for continuous data (statistical significance determined as p-value <0.05) and results were stratified based on patient’s races. Results: Out of the total sample size of 89,615 patients admitted with a diagnosis of HCC, 60.14% (53,895) were White, 13.67% (12250) were Black, 15.64% (14015) were Hispanic, 6.48% (5805) were Asian/Pacific Islander, 0.8% (720) were Native American, while 3.27% (2930) belonged to other ethnicities. There were significant racial differences in comorbidities with hypertension being most prevalent in Black patients (42.53%), diabetes mellitus in Native American patients (45.14%) and dyslipidemia in Asian/Pacific Islander patients (32.39%). When compared to White patients, ACIHM was the significantly higher in Black patients with adjusted odds ratio (aOR) of 1.305 (95% CI 1.123-1.517, p=0.001), Asian/Pacific Islander patients with aOR 1.271 (95% CI 1.024-1.578, p=0.03) and Other races patients with aOR 1.578 (95% CI 1.2-2.076, p=0.001). AF was significantly lower in all races when compared to White patients. CVA was significantly higher in Black patients with aOR 1.654 (95% CI 1.329-2.059, p<0.001) compared to White patients. SCD was significantly higher in Asian/Pacific Islander patients with aOR 2.22 (95% CI 1.364-3.612, p=0.001) when compared to White patients. https://docs.google.com/document/d/1wM_b0jmNjChKEfpyj5SL6HmSKEhDo0N3X5H76jC-w0I/edit?usp=sharing Conclusions: In patients with HCC, Asian/Pacific Islander patients had higher ACIHM and SCD while Black patients had higher ACIHM and CVA as compared to White patients. This study highlights the importance for development of healthcare strategies stratified by race which may aid to mitigate the higher risk of MACCE in certain races. Further research involving possible genetic influences and social determinants of health contributing to poorer outcomes in people of color becomes imperative.