Article in Journal of the American Heart Association, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
26 authors.
Sruthi SelvakumarDepartment of Internal Medicine University of South Florida Morsani College of Medicine Tampa FL USA.
Sanath ShettySection of Cardio-Oncology Moffitt Cancer Center and Research Institute Tampa FL USA.
Alexis Behne SharmaMorsani College of Medicine University of South Florida Tampa FL USA.ORCID 0009-0003-7523-6886
Fatima Tuz ZahraDepartment of Malignant Hematology Moffitt Cancer Center and Research Institute Tampa FL USA.ORCID 0000-0001-5989-1117
Elicia WangMorsani College of Medicine University of South Florida Tampa FL USA.
Himara KoelmeyerDepartment of Internal Medicine University of South Florida Morsani College of Medicine Tampa FL USA.
Joe CarverDivision of Cardiovascular Medicine, Thalheimer Center for Cardio-Oncology University of Pennsylvania Philadelphia PA USA.
Michael G FradleyDivision of Cardiovascular Medicine, Thalheimer Center for Cardio-Oncology University of Pennsylvania Philadelphia PA USA.ORCID 0000-0001-8352-8975
Wonyoung JungDivision of Cardiovascular Medicine, Thalheimer Center for Cardio-Oncology University of Pennsylvania Philadelphia PA USA.ORCID 0000-0003-4749-4637
Bonnie KyDivision of Cardiovascular Medicine, Thalheimer Center for Cardio-Oncology University of Pennsylvania Philadelphia PA USA.ORCID 0000-0002-6628-9981
Benedicte LefebvreDivision of Cardiovascular Medicine, Thalheimer Center for Cardio-Oncology University of Pennsylvania Philadelphia PA USA.
Marielle Scherrer-CrosbieDivision of Cardiovascular Medicine, Thalheimer Center for Cardio-Oncology University of Pennsylvania Philadelphia PA USA.ORCID 0000-0001-6375-9266
Nicholas S WilcoxDivision of Cardiovascular Medicine, Thalheimer Center for Cardio-Oncology University of Pennsylvania Philadelphia PA USA.ORCID 0000-0002-3693-7650
Kai Yi WuDivision of Cardiovascular Medicine, Thalheimer Center for Cardio-Oncology University of Pennsylvania Philadelphia PA USA.
Onyee ChanDepartment of Malignant Hematology Moffitt Cancer Center and Research Institute Tampa FL USA.ORCID 0000-0003-2872-1961
Zhuoer XieDepartment of Malignant Hematology Moffitt Cancer Center and Research Institute Tampa FL USA.
Andrew T KuykendallDepartment of Malignant Hematology Moffitt Cancer Center and Research Institute Tampa FL USA.
David A SallmanDepartment of Malignant Hematology Moffitt Cancer Center and Research Institute Tampa FL USA.ORCID 0000-0003-0504-8233
Eric PadronDepartment of Malignant Hematology Moffitt Cancer Center and Research Institute Tampa FL USA.ORCID 0000-0002-4707-7916
Mohammed AlomarDepartment of Malignant Hematology Moffitt Cancer Center and Research Institute Tampa FL USA.ORCID 0000-0002-4713-7245
John L ClevelandDepartment of Tumor Microenvironment and Metastasis Moffitt Cancer Center and Research Institute Tampa FL USA.ORCID 0000-0002-7561-9065
Qianxing MoDepartment of Biostatistics and Bioinformatics Moffitt Cancer Center and Research Institute Tampa FL USA.ORCID 0000-0002-0021-7694
Rami KomrokjiDepartment of Malignant Hematology Moffitt Cancer Center and Research Institute Tampa FL USA.ORCID 0000-0002-1876-5269
Jeffrey E LancetDepartment of Malignant Hematology Moffitt Cancer Center and Research Institute Tampa FL USA.ORCID 0000-0002-7751-7310
Seongseok Yun *Department of Malignant Hematology Moffitt Cancer Center and Research Institute Tampa FL USA.ORCID 0000-0001-7343-1635
Dae Hyun Lee *Section of Cardio-Oncology Moffitt Cancer Center and Research Institute Tampa FL USA.ORCID 0000-0001-8141-0404
Funding
TRANSLATIONAL RESEARCHP30CA076292 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI Christine O'Connell · 1998 to 2026
$93.5M
MENTORING IN PATIENT-ORIENTED RESEARCH IN DEEP PHENOTYPING IN CARDIO-ONCOLOGYK24HL167127 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI Bonnie Ky · 2023 to 2026
backgroundVenetoclax, a potent B-cell leukemia/lymphoma-2 inhibitor, is an antineoplastic agent used in various hematologic malignancies, including acute myeloid leukemia (AML). The aim of the study is to evaluate the incidence, risk factors, and outcomes of major adverse cardiac events (MACEs) among patients with newly diagnosed AML receiving venetoclax-based therapy.
methodsWe conducted a retrospective, single-center cohort study of 214 patients with newly diagnosed AML treated with venetoclax. MACE was defined as a composite of new-onset heart failure, heart failure exacerbation requiring hospitalization, myocardial infarction/coronary revascularization, or stroke/transient ischemic attack during active venetoclax-based therapy. The Fine-Gray subdistribution hazard model determined the association between baseline clinical characteristics and MACEs, with noncardiovascular death as a competing risk. A Cox proportional hazard model determined the association between time-dependent MACEs and overall survival.
resultsAmong 214 patients (mean age, 71.5 years; 41% women), MACEs occurred in 14 (6.5%) patients. Patients with non-de novo (secondary /treatment-related) AML had a higher incidence of MACEs compared with de novo AML (85.7% versus 14.3%; subdistribution hazard ratio [HR], 7.1 [95% CI, 1.5-33];
conclusionsIn conclusion, MACE is a clinically significant event that occurs in 6.5% of patients with AML treated with venetoclax and is a higher-risk event for patients with secondary AML or treatment-related AML.
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.
Cardiovascular Adverse Events During Venetoclax-Based Treatment in Acute Myeloid Leukemia. · full record | OpenQuestion