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Background: A pivotal clinical trial comparing the efficacy and safety of ibrutinib with zanubrutinib in patients with Waldenström macroglobulinemia (WM) did not achieve its primary endpoint of complete response or very good partial response. In addition, median progression-free survival was not reached in either treatment arm. In the absence of treatment effectiveness differentiation based on clinical trial evidence, we conducted a real-world study to assess patient characteristics, treatment patterns, and all-cause healthcare resource utilization (HRU) in patients with WM who received ibrutinib or zanubrutinib as first-line (1L) therapy. Methods: In this retrospective cohort study, we used the ConcertAI Database to collect claims data of patients with WM aged ≥18 years who initiated single-agent ibrutinib (420 mg/day) or zanubrutinib (320 mg/day) as 1L therapy on or after 9/1/2021 (index date). A 6-month washout period of guideline-recommended WM antineoplastic agents was required to confirm 1L status. Patients were excluded if they were receiving ibrutinib and zanubrutinib concurrently, died within 30 days of the index date, had a record of hematopoietic stem cell transplant, had a record of other ibrutinib indications in the 6 months before index, or were participating in a clinical trial. Baseline demographics and clinical characteristics, therapy duration (number of days between the first and last day of the medication supply), and HRU (all-cause and WM-specific) per-patient-per-month (PPPM) were assessed. Results: The study included 51 patients (ibrutinib, n=30; zanubrutinib, n=21). In both cohorts, most participants were male (ibrutinib, n=20 [67%]; zanubrutinib, n=16 [76%]), and the mean age at baseline was 73 years and 75 years, respectively. At baseline, the median Charlson Comorbidity Index was 0, and the WM-related and ibrutinib/zanubrutinib-related clinical events were similar between the two cohorts. While the zanubrutinib cohort had a higher prevalence of infections (33% vs 3%) and musculoskeletal pain (24% vs 7%) at baseline, the ibrutinib cohort had a higher prevalence of hypertension (20% vs 14%). The baseline prevalence of anemia was similar in both cohorts (ibrutinib, 27%; zanubrutinib, 29%). Mean follow-up was 6.9 months (ibrutinib) and 6.3 months (zanubrutinib). The mean ± SD duration of therapy was 152 ± 112 days (ibrutinib) and 113 ± 99 days (zanubrutinib; p=0.195). The ibrutinib cohort had a significantly lower all-cause HRU PPPM (4.53 ± 3.96 vs 8.53 ± 6.66, p=0.020) and lower WM-specific HRU PPPM (0.11 ± 0.26 vs 0.54 ± 1.14, p=0.104). Conclusions: In this real-world analysis, patients with WM treated with 1L ibrutinib had a numerically longer duration of therapy and lower all-cause and WM-specific HRU PPPM, compared to those treated with 1L zanubrutinib. Due to a small sample size and short follow-up, these findings should be interpreted cautiously.

MB and VA equal contributors AB and STO co-corresponding authors This study was initiated following evaluation of a 32 year-old woman who presented with a history of thrombocytopenia identified in childhood who subsequently developed features of myelofibrosis (MF). A bone marrow biopsy demonstrated hypercellularity in conjunction with megakaryocyte hyperplasia and marked reticulin fibrosis. Molecular testing for JAK2, CALR, and MPL mutations was negative. Given the unusual association between congenital thrombocytopenia and MF in this patient, exome sequencing was performed, revealing a heterozygous R304W mutation in the coiled coil (CC) domain of STIM1. Activating mutations in the CC and EF hand domains of STIM1 have been associated with Stormorken syndrome, a rare congenital platelet disorder associated with abnormal store operated calcium entry (SOCE). We subsequently identified a second patient with MF associated with a STIM1 activating mutation. This individual was found to have severe thrombocytopenia at birth, and exome sequencing revealed a heterozygous S88G mutation in the EF hand of STIM1. A bone marrow biopsy obtained at 6 months of age revealed atypical megakaryocytes and grade 1-2 MF. A repeat biopsy at age 2 showed persistence of stable MF. The unusual finding of MF in these two patients suggested the possibility of altered calcium signaling as a shared mechanism driving congenital platelet disorders such as Stormorken syndrome and myeloproliferative neoplasms (MPNs) including MF. In support of this notion, we identified elevated STIM1 expression in MF vs normal megakaryocyte progenitors, as well as in platelets from patients with essential thrombocythemia (ET) vs healthy controls. Additionally, we found that STIM1 expression was significantly elevated in CD34+ hematopoietic stem/progenitor cells (HSPCs) from both ET and MF patients vs healthy controls. Notably, STIM1 expression was increased in both JAK2 and CALR-mutant MF patients. Collectively, these findings provide evidence of aberrant STIM1 expression in MPN patient cells. To determine the functional role of STIM1 in MPN disease development, colony assays and patient-derived xenograft (PDX) experiments were performed with MF patient CD34+ cells subjected to CRISPR ablation of STIM1. Strikingly discordant results were observed with JAK2 vs CALR-mutant patient samples. Abrogation of STIM1 in CALR-mutant CD34+ cells led to decreased colony formation, and NSGS mice engrafted in parallel with STIM1-targeted cells exhibited decreased human CD45+ cell engraftment in conjunction with prolonged survival. These findings suggest an important role for STIM1 in CALR-mutant MPN disease phenotypes. In contrast, targeting of STIM1 in JAK2-mutant CD34+ cells led to increased colony formation and exacerbated disease phenotypes in vivo as manifested by enhanced human CD45+ cell engraftment, worsened splenomegaly, and early lethality. Similar results were obtained in experiments utilizing pharmacologic inhibitors of SOCE activity. Taken together, these findings indicate that the consequences of aberrant STIM1 activity may be context-dependent relating to specific MPN driver mutations. To expand these observations, we identified a separate cohort of 9 family members in Italy with Stormorken syndrome and confirmed STIM1 EF hand mutations. In ex vivo megakaryocytic differentiation assays, cells from affected individuals exhibited a defect in proplatelet formation. These observations were corroborated by initial analyses of a newly generated Stim1 R304W conditional knock-in mouse which recapitulated the characteristic thrombocytopenia found in patients with Stormorken syndrome. In summary, this study represents the first demonstration of MF development in patients with Stormorken syndrome, thereby uncovering a previously unrecognized hallmark of altered calcium signaling via aberrant STIM1 activation underlying Stormorken syndrome and MPNs. Our findings suggest distinct mechanisms relating to the interaction between JAK2 vs CALR mutation and altered STIM1 activity. Further studies of these relationships may have important ramifications for potential therapeutic approaches targeting these pathways.

Background: Waldenström Macroglobulinemia (WM) is an indolent lymphoma with heterogeneous outcomes. The recently developed, Revised International Prognostic Scoring System for WM (rIPSS-WM) did not examine the prognostic impact of MYD88L265P, a somatic alteration present in most patients with WM. Moreover, rIPSS-WM could only be partially validated in an external cohort. Here, we report the performance of rIPSS-WM and propose a refined prognostic model with external validation. Methods: We reviewed medical records of treatment-naïve patients with active WM consecutively seen at Mayo Clinic, Rochester (MCR) between 01/01/1996 and 12/31/2017. We applied the rIPSS-WM model in patients with data available for all required parameters, including age, serum beta-2 microglobulin (β2M), serum lactate dehydrogenase (LDH) and serum albumin at diagnosis to assess the prognostic utility of this model. We then identified the dichotomized clinical and laboratory parameters prognostic for overall survival (OS) by univariate analyses (UVA) in our cohort. The significant parameters were analyzed to independently predict OS in a multivariable analysis (MVA) and to create a prognostic model, which was subsequently validated in an independent multi-institutional cohort. Results: We identified 889 patients with active WM at MCR, with a median follow-up of 8.2 [95% confidence interval (CI): 7.5-9] years. The estimated median OS for this cohort was 10.6 (95%CI: 9.7-11.4) years. Patients with available data in this cohort for the validation of rIPSS-WM (n=241) were risk stratified into very low (n=46), low (n=64), intermediate (n=58), high (n=46) and very-high risk groups (n=27) per rIPSS-WM, with the respective 5-year OS rates of 96%, 76%, 72%, 77% and 32%, demonstrating overlapping survival curves for the low, intermediate and the high-risk groups. Because rIPSS-WM could not be validated, we used the data from the MCR cohort and identified age at diagnosis of active WM, LDH >upper limit of normal (ULN), β2M >3µg/mL and albumin <3.5g/dL as statistically significant prognostic markers for OS on UVA. Notably, the presence of MYD88 L265P did not impact OS [median 11.4 years (95%CI: 10.1-not reached (NR) for MYD88 L265P genotype (n=231) versus 10 years (95% CI: 8.1-NR) for MYD88 WT genotype (n=65); p=0.33]. On MVA, LDH >ULN (HR 2.34), serum albumin <3.5 g/dL (HR 1.5) and age groups 65-75 years (HR 1.4) and >75 years (HR 2.6) were independently prognostic. Based on comparable HRs, we assigned a score of 1 point each to serum albumin <3.5 g/dL and age group 66-75 years and similarly, 2 points each for age >75 years and serum LDH >ULN per their impact on OS. Patients with the composite scores of 0, 1 and 2 were categorized as low risk, low- intermediate risk and intermediate risk, respectively. Due to similar OS for the scores of 3 to 5, these were combined to form the high-risk group of our proposed model: Modified Staging System for WM (MSS-WM). The median OS was 14.6 years [95%CI: 9.1 years-NR] for low-risk (score 0, n=71, 21%), 11.2 years (95% CI: 9.1-15.2 years) for low-intermediate risk (score 1, n=110, 32%), 8.1 years (95% CI: 6.4-12.2) for intermediate risk (score 2, n=81, 24%) and 5.5 years (95 % CI: 3.9-11 years) for the high-risk group (score ≥3, n=79, 23%); p<0.0001. In this derivation cohort, the 5-year OS rate was 93%, 82%, 69% and 55% and 10-year OS rate was 60%, 53%, 45% and 30% for the low, low-intermediate, intermediate, and high-risk cohort, respectively ( Figure 1A). We also validated MSS-WM using competing risk analysis (p=0.001) and in the cohort of rituximab treated patients (p<0.0001). We then used data from an independent series of 335 treatment-naïve symptomatic patients from academic institutions (n=5) across the US and Europe for external validation of the MSS-WM model. The median follow-up for the validation cohort was 6.3 years (95% CI: 5.5-7.2 years). The 5-year OS was 93%, 90%, 75% and 57% and the estimated 10-year OS was 91%, 80%, 64% and 35% for the low risk (n= 86, 26%), low-intermediate (n=107, 32%), intermediate (n=86, 26%) and high-risk (n=59, 18%) cohorts, respectively (p<0.0001, Figure 1B). Conclusions: Our proposed model, MSS-WM, is a simple, clinically useful, externally validated model that reliably risk stratifies previously untreated patients with active WM into four groups that have distinct outcomes based on the composite scores derived from the patients' age, serum albumin and serum LDH at diagnosis.

Background: Data on the clinical activity of venetoclax (ven) in lymphoplasmacytic lymphoma (LPL) are primarily limited to a phase 2 trial of ven monotherapy for a 2-year duration in 32 patients (pts) with relapsed/refractory IgM LPL who received a median of 2 prior treatments (tx), including 16 pts with prior BTK inhibitors (BTKi) (Castillo et al, JCO 2021). Overall response rate (ORR) was 84% and median progression-free survival (PFS) was 30 months (mos). We report the clinical activity of ven and prognostic factors associated with outcomes in a larger cohort. Methods: We included pts with LPL treated with ven alone at 9 US centers. The primary outcome was ORR, which included minor response (MR), partial response (PR), very good PR (VGPR), and complete response (CR) per IWWM-7. Secondary outcomes included PFS, overall survival (OS), safety of ven, and predictors of ORR, PFS, and OS. Results: Sixty-two pts were included. Twenty pts (32%) received ven on a clinical trial. At ven initiation, median age was 65 years (range 38 - 87) , 61% were male, serum monoclonal (M) protein was IgM in 50 pts (91%) (IgG/IgA in 3 (5%), absent in 2 (4%), missing n=7), median hemoglobin (Hb) was 10.4 g/dL (range 5.7-16.4), and median serum IgM was 2580 mg/dL (range 5-9300). Mutations of MYD88 and CXCR4 were present in 52 (95%; missing n = 7) and 19 (38%; missing n = 12) pts, respectively. Median lines of tx (LOT) before ven was 3 (range 1-11, 58% ≥3) including antiCD20 monoclonal antibody n=54 (87%), BTKi n=48 (77%), proteasome inhibitor n=40 (65%), and bendamustine n=31 (50%). Pts who received ven on a clinical trial were less heavily pretreated (median prior LOT = 1.5, 20% ≥3) compared with pts treated off trial (median prior LOT = 4, 76% ≥3). ORR to prior BTKi was 71% (CR 4%, VGPR 10%, PR 35%, MR 21%) (missing n=5), with a median duration of tx of 14 mos (range 0.5-119). BTKi was stopped due to progressive disease (PD) in 60% and toxicity in 40%. ORR to most recent tx before ven was 58% (CR 3%, VGPR 8%, PR 32%, MR 15%); 21% SD, 7% PD, and 15% missing. BTKi was the most frequently used tx immediately before ven (48%). Six pts (10%) required plasmapheresis up to 30 days before starting ven. Median time from diagnosis to ven initiation was 5.9 years (range 0.3-23). Ven starting dose was 200 mg in 33 pts (55%), 20 mg in 11 (18%), and 100 mg in 10 (17%) (other n=6, missing n=2). Ten pts (17%) were admitted for ven tx initiation. Maximum ven dose was 400 mg in 16 (27%) and 800 mg in 38 pts (63%) (other n=6, missing n=2). ORR to ven (missing n=3) was 73% (95% confidence interval [CI] 63-86%) (CR 2%, VGPR 21%, PR 44%, MR 7%); 23% were refractory (SD 13%, PD 10%). Median time to best response was 4 mos (range 0.5-30). Median time to peak Hb was 5 mos (range 0.1-24) and to nadir serum M protein level was 8 mos (range 0.5-34). With a median follow-up of 21.9 mos (range 2.3-70.4), the median and 3-year PFS were 30.4 mos (95% CI 11.0-38.6) and 40% (95% CI 25-54%), respectively (Figure). Median and 3-year OS were not reached (NR) (95% CI NR-NR) and 83% (95% CI 70-91%), respectively. Lymphoma was the most common cause of death (n=8/11, 73%). In univariable analyses (UVA), tx with ven on a clinical trial was associated with higher ORR (90% vs 64%; odds ratio = 8.67, 95% CI 1.04-72.16, p=.046) and superior PFS (median 39 mos (95% CI, 28.4-NR) vs 11 mos (95% CI 6.4-NR), p=.028) without a significant difference in OS. Other factors evaluated in UVA to assess association with ORR, PFS and OS were age at ven start, response to last prior tx, prior tx with BTKi, and CXCR4 mutation status. Of these, receipt of prior tx with BTKi was associated with inferior PFS (HR=2.7, 95% CI 1.1-6.5, p=.024), whereas age >65 years at ven start (HR=8.6, 95% 1.1-67.8, p=0.042) and receipt of ≥3 prior tx (HR=12.0, 95% 1.5-95.9, p=.019) were associated with inferior OS. Four pts (7%) developed laboratory tumor lysis syndrome (TLS) including 2 (3%) with clinical TLS. TLS occurred at the 400 or 800 mg dose in 3 pts (missing n=1). Ven dose interruptions and/or reductions occurred in 39%. Three pts (5%) had febrile neutropenia. Ven was stopped due to PD in 21 pts (34%), planned tx completion in 15 (24%) (median tx duration = 25 mos, range 24-28), toxicity 6 (10%), and other 4 (6%); 16 pts (26%) remain on ven. Median duration of tx for those who stopped ven was 12 mos (range 1-33). Conclusion: Ven is an effective tx option for pts with relapsed or refractory LPL. Compared with the phase 2 study, ORR and PFS were lower in this cohort of more heavily pretreated pts.

Background: In patients with Waldenström macroglobulinemia (WM), continuous once-daily ibrutinib-based therapy has been associated with long-term progression-free survival. In addition, patients who continued ibrutinib-based treatment had better survival outcomes than those who discontinued treatment within the first few years. Evidence based on a single-center retrospective study suggests that dose reduction (DR) can be used to effectively manage ibrutinib-related adverse events (AEs) and avoid early treatment discontinuation. However, real-world data on outcomes in patients with WM after ibrutinib DR are limited. In this real-world study, we analyzed short-term (1-year follow-up) dosing patterns and time to treatment discontinuation (TTD) in patients with WM, with and without DR, who were receiving first-line (1L) ibrutinib. Methods: Medicare Fee-for-Service closed-claim medical or pharmacy records were used to identify patients diagnosed with WM who initiated 1L single-agent ibrutinib (420 mg/day) from January 2014 to December 2020. Observed patients were enrolled in Medicare ≥12 months before and after ibrutinib initiation and had post-initiation AEs (both prevalent and incident AEs with DR recommendation from the US Prescribing Information), as identified via ICD-9 or ICD-10 codes. Ibrutinib DR was defined as a reduction of the starting dose following the first AE within the 1-year follow-up period. Patients without a DR were defined as those who had received ibrutinib 420 mg per day during the 1-year follow-up period. Patients with a DR in the absence of AEs and patients with a DR prior to any AE were excluded from the analysis. Demographics, clinical characteristics, time to first AE, and TTD were analyzed among cohorts with and without DR. TTD was defined and evaluated as the time from first observed AE after ibrutinib initiation to the earliest occurrence of (1) a gap of >120 days between the end of 1L therapy and the follow-up period, (2) initiation of a next line of therapy, or (3) death. TTD was analyzed using Kaplan-Meier methodology, log rank test, and a Cox proportional hazards model adjusted for baseline and time-varying covariates. Results: We identified 404 patients (DR, n = 58 [14%]; no DR, 346 [86%]). Overall, 249 patients (62%) were men, 267 patients (66%) had hypertension, 55 patients (14%) had atrial fibrillation, and 114 patients (28%) had other cardiovascular conditions at baseline. The mean ± SD age at baseline was 77 ± 8 years. In both cohorts, the median Charlson Comorbidity Index was 4.0. Among the 404 patients, mean ± SD time from ibrutinib initiation to first AE was 28 ± 44 days. Mean ± SD time between first AE and DR was 137 ± 102 days. Mean TTD was 8.3 months (DR) and 6.2 (no DR) ( P = 0.018; Figure). At 6 and 12 months of follow-up, fewer patients with DR discontinued treatment compared with patients without DR (6 months: 24% vs 46%, P = 0.002; 12 months: 36% vs 50%, P = 0.064). After controlling for baseline and time-varying demographic and clinical characteristics, patients with DR were not significantly more likely to discontinue treatment compared with patients without DR (hazard ratio [95% CI], DR vs no DR: 1.24 [0.86-1.78]). Conclusion: These short-term (1-year follow-up) findings suggest TTD was not impacted by DR of ibrutinib following AEs. Thus, ibrutinib DR can be an effective strategy to manage AEs while maintaining clinical efficacy. Of note, causal association between AE and subsequent DR cannot be inferred from the claims database due to the cross-sectional nature of this study.

(1) Background: Telemetry units allow the continuous monitoring of vital signs and ECG of patients. Such physiological indicators work as the digital signatures and biomarkers of disease that can aid in detecting abnormalities that appear before cardiac arrests (CAs). This review aims to identify the vital sign abnormalities measured by telemetry systems that most accurately predict CAs. (2) Methods: We conducted a systematic review using PubMed, Embase, Web of Science, and MEDLINE to search studies evaluating telemetry-detected vital signs that preceded in-hospital CAs (IHCAs). (3) Results and Discussion: Out of 45 studies, 9 met the eligibility criteria. Seven studies were case series, and 2 were case controls. Four studies evaluated ECG parameters, and 5 evaluated other physiological indicators such as blood pressure, heart rate, respiratory rate, oxygen saturation, and temperature. Vital sign changes were highly frequent among participants and reached statistical significance compared to control subjects. There was no single vital sign change pattern found in all patients. ECG alarm thresholds may be adjustable to reduce alarm fatigue. Our review was limited by the significant dissimilarities of the studies on methodology and objectives. (4) Conclusions: Evidence confirms that changes in vital signs have the potential for predicting IHCAs. There is no consensus on how to best analyze these digital biomarkers. More rigorous and larger-scale prospective studies are needed to determine the predictive value of telemetry-detected vital signs for IHCAs.

Abstract Background A decrease in antimicrobial stewardship activities has been observed in our hospital since the beginning of the pandemic. The study aim was to evaluate the impact of decrease in antimicrobial stewardship activities in Klebsiella pneumoniae and Escherichia coli acquired multidrug-resistance. Methods The quarterly percentage of broad-spectrum antibiotic prescriptions evaluated by antimicrobial stewardship team (AMST), the quarterly consumption of broad-spectrum antimicrobials and the quarterly proportion of multidrug-resistant K. pneumoniae and E. coli were assessed between October 2016 and December 2022, with 2 periods of time, before the pandemic (October 2016-March 2020) and after the pandemic (April 2020-December 2022).Time series analysis was performed with ARIMA models to evaluate the association between decrease in AMST activities with multidrug-resistance in K. pneumoniae or E. coli. Correlation between broad-spectrum antibiotic prescriptions reviewed by AMST with broad-spectrum antimicrobials consumption and proportion of multidrug-resistance in K. pneumoniae or E. coli in urine cultures was assessed using the Pearson correlation coefficient. Results Percentage of broad-spectrum antimicrobials evaluated by AMST was 77% in first period and 29% in second period. The mean of broad-spectrum antibiotics consumption in first period was 13.02 DDD/100 bed-days and 15.35 DDD/100 bed-days in second period. Decrease of AMST activities was associated with an 37% increase in multidrug-resistant K. pneumoniae in second period compared with first period (p=0.02). No differences were found in E. coli. Correlation between percentage of AMST-reviewed broad-spectrum antibiotics with consumption of these antibiotics was good (correlation coefficient -0,7; p< 0,01). Correlation between ASMT-reviewed broad-spectrum antibiotics and multidrug-resistant K. pneumoniae was moderate (correlation coefficient -0.44; p=0,02). No correlation between ASMT-reviewed broad-spectrum antibiotics and multidrug-resistant E. coli (correlation coefficient 0,09; p=0,6) was found. Conclusion Decrease in antimicrobial stewardship activities was associated with high isolation of multidrug-resistant K. pneumoniae in urine cultures. Disclosures All Authors: No reported disclosures

Key Points AKI survivors experience gaps in care that contribute to worse outcomes, experience, and cost. Challenges to optimal care include issues with information transfer, education, collaborative care, and use of digital health tools. Research is needed to study these challenges and inform optimal use of diagnostic and therapeutic interventions to promote recovery AKI affects one in five hospitalized patients and is associated with poor short-term and long-term clinical and patient-centered outcomes. Among those who survive to discharge, significant gaps in documentation, education, communication, and follow-up have been observed. The American Society of Nephrology established the AKINow taskforce to address these gaps and improve AKI care. The AKINow Recovery workgroup convened two focus groups, one each focused on dialysis-independent and dialysis-requiring AKI, to summarize the key considerations, challenges, and opportunities in the care of AKI survivors. This article highlights the discussion surrounding care of AKI survivors discharged without the need for dialysis. On May 3, 2022, 48 patients and multidisciplinary clinicians from diverse settings were gathered virtually. The agenda included a patient testimonial, plenary sessions, facilitated small group discussions, and debriefing. Core challenges and opportunities for AKI care identified were in the domains of transitions of care, education, collaborative care delivery, diagnostic and therapeutic interventions, and digital health applications. Integrated multispecialty care delivery was identified as one of the greatest challenges to AKI survivor care. Adequate templates for communication and documentation; education of patients, care partners, and clinicians about AKI; and a well-coordinated multidisciplinary posthospital follow-up plan form the basis for a successful care transition at hospital discharge. The AKINow Recovery workgroup concluded that advancements in evidence-based, patient-centered care of AKI survivors are needed to improve health outcomes, care quality, and patient and provider experience. Tools are being developed by the AKINow Recovery workgroup for use at the hospital discharge to facilitate care continuity.

Abstract Background Impella is an advanced ventricular assist device frequently used as a bridge to heart transplantation. The association of Impella with increased rates of gout flares has not been studied. Our primary aim is to determine the rates of gout flares in patients on Impella support. Methodology A retrospective study was conducted between January 2017 and September 2022 involving all patients who underwent heart transplantation. The cohort was divided into groups based on Impella support for statistical analysis. In patients receiving Impella support, outcome measures were compared based on the development of gout flares. Results 213 patients were analyzed, with 19.71% supported by Impella. Impella and non-Impella groups had similar age, race, and BMI, but more males were in the Impella group. Gout and chronic kidney disease were more prevalent in Impella-supported patients, while coronary artery disease was less common. The incidence of gout flare was significantly higher in Impella patients (31% vs. 5.3%). The Impella group had an adjusted odds ratio for in-hospital gout flare of 8.069 (95% CI = 2.13–35.08, P = 0.003). Impella-supported patients with gout flares had longer intensive care unit and hospital stays but no difference in mortality or other outcomes. Conclusion Our study is the first to identify the potential association between Impella support and increased rates of gout flares in hospitalized patients. Future studies are required to confirm this association and further elucidate the biological pathways. It is imperative to consider introducing appropriate measures to prevent and promptly manage gout flares in Impella-supported patients.