About

Eric Adler is the Professor and Chair of the Department of Classics at the University of Maryland. He received his Ph.D. in classical studies from Duke University and has previously taught at Rice University, the University of Minnesota, and Connecticut College. His scholarly interests include Roman historiography, Latin prose, the history of classical scholarship, and the history of the humanities. Adler is the author of three monographs: 'The Battle of the Classics: How a Nineteenth-Century Debate Can Save the Humanities Today,' 'Classics, the Culture Wars, and Beyond,' and 'Valorizing the Barbarians: Enemy Speeches in Roman Historiography.' He also edited 'Humanistic Letters: The Irving Babbitt – Paul Elmer More Correspondence,' which publishes the extant letters of two leading figures of the New Humanism movement, along with a comprehensive introduction. Currently, he is working on a biography of Irving Babbitt. Adler's work often explores the influence of classical scholarship on modern cultural and political debates, and he has contributed to various academic journals and popular outlets, engaging with topics related to classical studies, humanism, and the humanities.

Research topics

• Medicine
• Internal medicine
• Intensive care medicine
• Cardiology
• Pediatrics
• Radiology
• Pathology

Selected publications

• AAV-TNNI3 rescues an experimental murine Tnni3 mutation resulting in thin filament mediated DCM

  Journal of Molecular and Cellular Cardiology · 2026-01-04

  articleOpen accessSenior author

  Cardiac thin filament mutations in TNNI3 are associated with up to 3 % of hypertrophic (HCM) cardiomyopathy cases and contribute to severe restrictive (RCM) and dilated (DCM) cardiomyopathy caseloads. As such, thin filament cardiomyopathy mediated by TNNI3 mutations is an orphan disease with unmet therapeutic need. Gene therapy is one approach to addressing orphan disease but has been restricted to the repletion of protein deficiency. Based on the best available knowledge, TNNI3 gene therapy has never been applied in the context of a functional mutant protein. Described here is the viral gene therapy rescue at a 4-month endpoint of an experimental murine Tnni3 mutation resulting in slow-onset dilated cardiomyopathy (DCM) with cardiac failure at 12-18 months. Mutant mice treated with AAV encoding wild-type (WT) human TNNI3 at 1.0E+14 vg/kG prevented the onset of DCM pathology. This work describes the first adeno-associated virus (AAV) gene therapy replacement of functional mutated Tnni3 protein. The results suggest a broader application of gene therapy for gene replacement.

  PublisherDOI

• Withdrawal of aspirin in patients with left ventricular assist device treated with vitamin K antagonists: impact of anticoagulation quality in the randomized ARIES-HM3 trial

  European Heart Journal · 2025-11-07 · 5 citations

  articleOpen access

  BACKGROUND AND AIMS: Left ventricular assist devices (LVADs), including the HeartMate 3 (HM3), have improved outcomes in patients with advanced heart failure. Use of vitamin K antagonists (VKA) is mandated to reduce the risk of thrombotic events, but there is heterogeneity in management. Time in therapeutic range (TTR) is a crucial metric for assessing the quality of VKA management. The ARIES-HM3 trial demonstrated that aspirin can be safely omitted from the antithrombotic regimen, resulting in reduced bleeding without increased thrombosis. This pre-specified trial analysis explores the relationship of quality of VKA management assessed by TTR with haemocompatibility-related outcomes. METHODS: ARIES-HM3 was an international, randomized, double-blind, placebo-controlled study of aspirin (100 mg/day) or placebo (1:1) with VKA therapy in patients with de-novo HM3 placement. Participants were stratified into low TTR or high TTR groups based on median levels (n = 554). Primary endpoint success and secondary endpoint rates were stratified based on TTR groups. Bleeding rates at 12 months were estimated using an Andersen-Gill model with TTR as a single continuous variable, and multivariable regression analysis was performed. RESULTS: The percentage of patients with a TTR above or below the median of 56 was similar between the aspirin and placebo groups. More participants achieved primary endpoint success with TTR ≥56% (77% vs 66.9%, P = .01). Higher TTR was associated with lower bleeding rates at 12 months (26.4 vs 49.2 events per 100 participant-years; rate ratio 1.84, 95% confidence interval [CI] 1.37-2.53) without stroke increase (3.2 vs 2.8 events per 100 participant-years; rate ratio 0.88 [95% CI: 0.30-2.53]). No interaction was observed between the assigned treatment group and TTR. Modelling demonstrated a constant decrease in bleeding as a function of increasing TTR. Female sex and Black race were independent predictors of low TTR (odds ratio: 1.70 [95% CI: 1.12-2.57]; 1.62 [95% CI: 1.11-2.35], respectively), with more frequent INRs below the therapeutic range. Multivariable modelling identified age ≥65 years, aspirin use, TTR <56%, and blood urea nitrogen ≥30 mg/dL as predictors of non-surgical bleeding. CONCLUSIONS: The quality of VKA management as measured by TTR correlates with the occurrence of non-surgical bleeding in patients with the HM3 LVAD, with a lower TTR associated with an increased bleeding risk. These data provide new clinical direction to define a benchmark TTR to achieve further mitigation of residual risk of bleeding and enhance haemocompatibility with the HM3 LVAD.

  PublisherOA PDFDOI

• Patient Perspectives on Genetic Testing in Transthyretin Amyloid Cardiomyopathy: Framing the Conversation to Improve Implementation

  Journal of Cardiac Failure - Intersections · 2025-08-05 · 2 citations

  articleOpen access
  PublisherOA PDFDOI

• Hypertrophic cardiomyopathy

  Nature Reviews Disease Primers · 2025-08-14 · 10 citations

  article
  PublisherDOI

• Recurrent Atrial Myxoma in a Patient With Carney Complex 26 Years After Heart Transplantation

  JACC Case Reports · 2025-07-01

  articleOpen accessSenior author

  BACKGROUND: Carney complex, a familial syndrome caused by germline PRKA1A mutation, predisposes to recurrent cardiac myxomas. In refractory cases, orthotopic heart transplantation (OHT) can be considered for assumed curative treatment of recurrent myxoma. CASE SUMMARY: We present a case of recurrent cardiac myxoma arising from residual native right atrial tissue in a woman with Carney complex 26 years after OHT for recurrent myxoma. DISCUSSION: To our knowledge, this represents the first reported case of recurrent cardiac myxoma after OHT in a patient with Carney complex. Surgical ablation of remaining atrial tissue during OHT for myxoma may reduce the risk of recurrence, and lifelong surveillance after myxoma resection in Carney complex may be indicated. TAKE-HOME MESSAGE: This case highlights a rare genetic syndrome that can cause recurrent cardiac myxomas. If OHT is performed in the context of Carney complex, attention to surgical and surveillance strategies to prevent and detect recurrence is key.

  PublisherDOI

• Abstract 4370053: Unique Insights into the Pathobiology of TNNI3 Cardiomyopathy using Novel Murine and Porcine Models of Disease

  Circulation · 2025-11-03

  articleSenior author

  Background: Cardiac troponin I (cTnI, encoded by TNNI3 ) inhibits contraction by preventing actin-myosin interaction. Pathogenic TNNI3 variants can cause cardiomyopathy, but no targeted therapies exist. We identified a family with restrictive cardiomyopathy carrying the cTnI A157V variant. Previously, we generated a homozygous mouse model (cTnI A158V, murine equivalent) that showed impaired cardiac relaxation on invasive hemodynamics but had normal lifespan and no cardiac hypertrophy or fibrosis. Aims: It is known that murine models of cardiomyopathies often exhibit milder phenotypes than humans, limiting their translational utility. Hence, to better model human disease, we generated a homozygous cTnI A158V pig model using CRISPR-Cas9. We aimed to characterize phenotypic and molecular differences between the mouse and pig models to gain insight into disease mechanisms. Methods: Heart tissue was collected from wild-type (WT) and homozygous A158V mice (9-10 months) and from WT and homozygous A158V pigs (2 months). Bulk RNA sequencing (RNA-seq) was performed on RNA extracted from A158V pig hearts (n=5) and compared to publicly available data from age-matched WT pigs (n=10) supplemented by one in-house WT control. Protein lysates were analyzed by Western blot. Isolated myofibrils were measured using the fast solution switching method. Results: A158V pigs had 100% mortality by 2 months (n=7), with gross hypertrophy and fibrosis. Myofibril studies showed significant prolongation of the linear relaxation phase in both A158V pigs (p&lt;0.01) and mice (p&lt;0.01) compared to respective WTs, with no significant differences in active tension in both models. Both models showed reduced phosphorylation of cTnI at serine 23/24, reaching significance in pigs (p=0.046) but not in mice (p=0.064). Unsupervised clustering of bulk-RNAseq data separated A158V from WT, with genotype explaining 44% and 53% of transcriptional variation in mice and pigs, respectively. Gene set enrichment analysis revealed significant upregulation of inflammatory pathways in A158V pigs only. Conclusions: Both A158V mouse and pig models recapitulate impaired cardiac relaxation seen in affected patients as shown by myofibril studies. However, the pig model more closely mirrors the human phenotype, including early mortality, hypertrophy, and fibrosis. Inflammatory pathway upregulation was observed only in A158V pigs, suggesting that inflammation may play a role in the severity or progression of disease.

  PublisherDOI

• Correction to: Randomized Study Comparing a Novel Intranasal Formulation of Bumetanide to Oral and Intravenous Formulations

  Circulation · 2025-03-10 · 2 citations

  erratumSenior author
  PublisherDOI

• Deep learning enables fully automated cineCT-based assessment of regional right ventricular function

  medRxiv · 2025-09-30

  preprintOpen access

  Abstract Background Right ventricular (RV) function is a key factor in the diagnosis and prognosis of heart disease. However, current advanced CT-based assessments rely on semi-automated segmentation of the RV blood pool and manual delineation of the RV free and septal wall boundaries. Both of these steps are time-consuming and prone to inter- and intra-observer variability. Methods We developed and evaluated a fully automated pipeline consisting of two deep learning methods to automate volumetric and regional strain analysis of the RV from contrast-enhanced, ECG-gated cineCT images. The Right Heart Blood Segmenter (RHBS) is a 3D high resolution configuration of nnU-Net to define the endocardial boundary, while the Right Ventricular Wall Labeler (RVWL) is a 3D point cloud-based deep learning method to label the free and septal walls. We trained our models using a diverse cohort of patients with different RV phenotypes and tested in an independent cohort of patients with aortic stenosis undergoing TAVR. Results Our approach demonstrated high accuracy in both cross-validation and independent validation cohorts. RHBS and RVWL both yielded Dice scores of 0.96, and accurate volumetry metrics. RVWL achieved high Dice scores (&gt;0.90) and high accuracy (&gt;93%) for wall labeling. The combination of RHBS and RVWL provided accurate assessment of free and septal wall regional strain, with a median cosine similarity value of 0.97 in the independent cohort. Conclusions A fully automated 3D cineCT-based RV regional strain analysis pipeline has the potential to significantly enhance the efficiency and reproducibility of RV function assessment, enabling the evaluation of large cohorts and multi-center studies. Key Points RV endocardial segmentation of contrast enhanced CT scans can be utilized to perform volumetry, and when paired with labeling of free and septal walls, regional evaluation of surface strain. However, this has previously been performed using time-intensive semi-automated segmentation methods and manually labeling free wall and septal wall regions.. Here, we describe an automated, deep learning-based approach which uses two separate DL models to define the endocardial boundary (in 3D) and then label the free and septal walls on the endocardial surface. Our approach facilitates rapid and automatic advanced phenotyping of patients. This reduces prior limitations of potential interobserver variability and challenges associated with evaluating large cohorts.

  PublisherOA PDFDOI

• STUDY DESIGN AND RATIONALE OF SUNRISE-FA, A PHASE 1/2 STUDY OF THE SAFETY AND EFFICACY OF LX2006 GENE THERAPY IN PARTICIPANTS WITH CARDIOMYOPATHY ASSOCIATED WITH FRIEDREICH’S ATAXIA

  Journal of the American College of Cardiology · 2025-03-29

  articleOpen accessSenior author
  PublisherDOI

• Developing therapeutics for rare cardiovascular diseases

  American Heart Journal · 2025-09-13

  articleOpen access
  PublisherOA PDFDOI

Recent grants

• Induced Pluripotent Stem Cells for the Study of Long QT Syndrome

  NIH · $672k · 2011–2016

Frequent coauthors

• Enrico Ammirati

  Società Italiana di Reumatologia

  96 shared

• Victor Pretorius

  UC San Diego Health System

  79 shared

• Luciano Potena

  University of Bologna

  76 shared

• Paolo G. Camici

  Vita-Salute San Raffaele University

  75 shared

• Andrea Garascia

  75 shared

• Antonio Cannatà

  British Heart Foundation

  75 shared

• Piero Gentile

  Società Italiana di Reumatologia

  74 shared

• Gianfranco Sinagra

  Azienda Sanitaria Universitaria Integrata di Trieste

  74 shared