About

Anjali Tiku Owens, MD, is an Associate Professor of Medicine in Cardiovascular Medicine at the Hospital of the University of Pennsylvania. She serves as an Attending Cardiologist specializing in Heart Failure and Transplantation. Dr. Owens is the Director of the Penn Familial Cardiomyopathy Program, the Hypertrophic Cardiomyopathy Clinic, and the Penn Center for Inherited Cardiovascular Disease at the University of Pennsylvania. She is also a member of the Center for Genomic Medicine Executive Committee and the Steering Committee of the Anna T. Meadows Society. Her research expertise focuses on inherited cardiomyopathy and cardiovascular genetics, with clinical expertise in familial dilated cardiomyopathy, hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, and non-compaction cardiomyopathy. Dr. Owens has contributed to the understanding of heart failure and cardiovascular genetics through her research and clinical work.

Research topics

• Biology
• Genetics
• Medicine
• Internal medicine
• Political Science
• Cardiology
• Pathology
• Endocrinology
• Bioinformatics
• Psychiatry
• Cell biology

Selected publications

• Social Determinants of Health and Clinical Outcomes in Hypertrophic Cardiomyopathy

  JAMA Cardiology · 2026-01-07

  articleOpen access

  Importance: Area-based indicators of social determinants of health (SDOH) are associated with higher risk for acquired heart disease, but their impact on conditions with a strong genetic etiology, such as hypertrophic cardiomyopathy (HCM), is not well understood. Objective: To determine the association of area-based SDOH with clinical outcomes in patients with HCM. Design, Setting, and Participants: This multicenter, prospective cohort study was conducted among US adult patients with HCM from 5 sites in the Sarcomeric Human Cardiomyopathy Registry (a multicenter prospective registry of patients with HCM) who were followed up for a median (IQR) period of 2.15 (0.15-5.82) years. Data were entered from 2015 to March 2024, and data analysis was completed from March 2024 to June 2025. Exposures: Patients' residential addresses were geocoded at the zip code level and linked to the American Communities Survey to estimate area-based (1) median household income and (2) social deprivation index (SDI), which ranges from 0 to 100, with higher scores indicating a more deprived area. Main Outcomes and Measures: Multivariate models, adjusting for age at diagnosis, body mass index, hypertension, and sex, were used to estimate the independent association of area-based median household income and SDI with heart failure (HF), ventricular arrhythmias (VA), and an overall composite outcome (VA, HF, atrial fibrillation, stroke, and death). Results: Among 4431 US adult patients with HCM, median (IQR) age at HCM diagnosis was 51.3 (38.9-61.6) years, and 1862 patients (42.0%) were female. Median (IQR) area-based household income was $80 000 ($60 000-$110 000), and median (IQR) SDI was 25 (10-55). Adjusted hazard ratios comparing the lowest income group to the highest income group were 2.07 (95% CI, 1.77-2.42; P < .001) for HF, 1.31 (95% CI, 0.97-1.78; P = .08) for VA, and 1.52 (95% CI, 1.36-1.69; P < .001) for the overall composite outcome. Adjusted hazard ratios comparing the highest SDI (ie, more deprived) group to the lowest SDI group were 1.48 (95% CI, 1.29-1.70; P < .001) for HF, 1.55 (95% CI, 1.15-2.09; P = .004) for VA, and 1.36 (95% CI, 1.22-1.50; P < .001) for the overall composite outcome. Conclusions and Relevance: In this multicenter cohort study, residing in an area with lower median household income or worse SDI were each independently associated with adverse clinical outcomes in patients with HCM. These findings suggest that despite the genetically determined nature of HCM, place of residence is associated with patient outcomes.

  PublisherOA PDFDOI

• 26-A-11567-ACC MAVACAMTEN DEMONSTRATES CLINICAL AND HEMODYNAMIC BENEFITS IN SYMPTOMATIC OBSTRUCTIVE HYPERTROPHIC CARDIOMYOPATHY WITH ONLY PROVOCABLE OUTFLOW GRADIENTS: REAL-WORLD EXPERIENCE FROM MARVEL-HCM

  Journal of the American College of Cardiology · 2026-03-27

  article
  PublisherDOI

• 26-A-11568-ACC EFFECTIVENESS AND SAFETY OF MAVACAMTEN IN A COHORT WITH HIGH BACKGROUND PREVALENCE OF ATRIAL FIBRILLATION: REAL-WORLD EXPERIENCE FROM MARVEL-HCM

  Journal of the American College of Cardiology · 2026-03-27

  articleSenior author
  PublisherDOI

• A randomized study of digital versus genetic counselor return of actionable genetic research results to biobank participants (RESPECT3 study)

  BMC Medical Ethics · 2026-03-31

  articleOpen access

  There is consensus that research participants should be informed about plans for return of genetic research results. However, best practices for return of results in large biobank and cohort studies do not exist currently, and how best to communicate actionable genetic research results remains unclear. While having genetic counselors disclose these results may be ideal to ensure understanding, minimize distress, and optimize medical follow-up, genetic counselor (GC) workforce shortages and costs are barriers. The RESPECT3 study evaluates whether digital delivery alternatives for pre-disclosure education and return of actionable genetic research results is non-inferior to remote telehealth disclosure by a genetic counselor. The RESPECT3 Study is a hybrid type 1 effectiveness-implementation study which evaluates digital alternatives for pre-disclosure education and return of actionable research results in randomized non-inferiority trial. The return of results process in RESPECT3 uses a two-step process. In step one, participants with an actionable result and procedural controls (no actionable result) are invited to digital pre-disclosure education and provided options for opting out of results. In Step 2, those with actionable results who have not opted out are randomized to receive results via a digital disclosure intervention (digital-ROR) or with a GC. Participants include English-speaking adults who enrolled in the Penn Medicine BioBank (PMBB) and have an actionable research result according to the ACMG secondary findings list. The primary outcomes are non-inferiority of knowledge and disease specific distress (cancer and cardiovascular disease) after receipt of research results. Uptake of research results is a secondary non-inferiority outcome. Confirmatory clinical testing is covered by the study and all participants with confirmed results are referred to the appropriate clinical genetic program for clinical recommendations. The RESPECT3 study is expected to provide critical empiric data on the effectiveness of using digital alternatives for pre-disclosure education and return of genetic research results in a representative clinical population of research participants who enrolled in an institutional biobank where return of results was not the focus of the study. Equally important, our theoretically-informed process evaluation data is expected to inform modifications to identify barriers and facilitators to broader implementation. NCT04242667.

  PublisherDOI

• The Natural History of Massive Left Ventricular Hypertrophy in Pediatric Hypertrophic Cardiomyopathy: A Multiregistry Analysis

  Circulation · 2026-04-17

  article

  BACKGROUND: Massive left ventricular hypertrophy (LVH) is a risk factor for sudden cardiac death in children with hypertrophic cardiomyopathy (HCM), but little is understood about its natural history. METHODS: Patients with pediatric-onset HCM identified from 2 registries (SHaRe [Sarcomeric Human Cardiomyopathy Registry] and IPHCC [International Paediatric Hypertrophic Cardiomyopathy Consortium]) with or without massive LVH were compared. Massive LVH was defined as absolute maximal left ventricular wall thickness (MLVWT) ≥30 mm or MLVWT z score ≥+20 at &lt;18 years of age. Data from SHaRe and IPHCC include encounters from January 1960 through March 2024 and January 1970 through March 2024, respectively. Demographic, clinical, and serial MLVWT data were collected. Composite outcomes included major ventricular arrhythmia event (sudden cardiac death, aborted sudden cardiac death, or appropriate implantable cardioverter defibrillator therapy); heart failure (HF) event (left ventricular ejection fraction &lt;50%, New York Heart Association class III or IV, transplant, or HF-related death); major adverse cardiac event (stroke or any major ventricular arrhythmia or HF outcome aside from left ventricular ejection fraction &lt;50%); and HCM-related mortality (sudden cardiac death or HF-related death). Time-to-event analyses were performed using Cox proportional hazards models. RESULTS: We identified 587 patients (54 female [30%]). In 186 children with massive LVH, age at diagnosis was younger (median, 9.2 years [interquartile range, 2.1–13.1 years]) versus 13.6 years (9.7–15.5 years; P &lt;0.001) and sarcomeric genetic variants more prevalent (72% versus 61%; P =0.034), as was HCM-related mortality (unadjusted hazard ratio, 3.3 [95% CI,1.2–9.7]; P =0.026), major adverse cardiac events (hazard ratio, 2.6 [1.7–3.9]; P &lt;0.001), major ventricular arrhythmia (hazard ratio, 3.1 [1.8–5.2]; P &lt;0.001), and HF (hazard ratio, 1.9 [1.1–3.1]; P =0.013). These associations remained significant when adjusted for sex and age at HCM diagnosis. In 115 patients with massive LVH with serial MLVWT data (62%), MLVWT increased significantly from first to last measurements (median, 26 mm [interquartile range, 18–32 mm] versus 31 mm [26–35 mm]; P &lt;0.001), but there was no difference between z scores (median, +22 [interquartile range, +18 to +26] versus +23 [+20 to +28]; P =0.25). The last absolute MLVWT recorded was &gt;5 mm less than the largest recorded MLVWT in 25 patients (22%). CONCLUSIONS: In pediatric HCM, massive LVH disproportionately affects those diagnosed in early childhood with sarcomeric disease, with increased risk for adverse events. Significant MLVWT regression is seen in nearly a quarter of patients.

  PublisherDOI

• <i>RBM20</i> Truncating Variants and Human Cardiomyopathy

  JAMA Cardiology · 2026-04-08

  articleOpen access

  Importance: Genetic diagnosis has become increasingly important to guide clinical decision-making for patients with dilated cardiomyopathy (DCM). Pathogenic or likely pathogenic (P/LP) missense variants in the gene RBM20 cause a highly penetrant arrhythmogenic DCM, but the role of RBM20 truncating variants (RBM20tvs) is unclear. Objective: To assess the contribution of RBM20 variants to arrhythmogenic DCM. Design, Setting, and Participants: In this cohort study, participants in the genome-first UK Biobank (UKB) and All of Us populations were evaluated to assess the etiologic fraction, natural history and penetrance of RBM20 variants. Retrospective data were collected from an international cohort of patients with DCM and RBM20 variants identified at centers of excellence for genetic heart disease and compared based on time to event. Study dates are not disclosed because the institutional review board did not authorize the sharing of this information. Exposures: RBM20 variants were compared to known P/LP variants and variants of uncertain significance in RBM20 as well as titin truncating variants (TTNtvs). Main Outcomes and Measures: Major ventricular arrhythmias, end-stage heart failure, and heart failure hospitalization as measured by medical record review (retrospective cohort) and diagnostic codes (UKB). Results: Two main cohorts were studied for this project. In UK Biobank, a cohort of participants with RBM20tvs, RBM20 synonymous variants, and TTNtvs was studied. Of these 4249 participants, 1869 (44%) were male. The mean (SD) age at enrollment was 56 (8.2) years. In the RBM20 registry, of 179 patients, 105 (58.6%) were male, and the mean (SD) age at enrollment was 43.8 (19.1) years. A validation cohort from the All of Us biobank was also used. This consisted of 7002 participants, 4342 of whom (62.0%) were male, and the mean (SD) age was 52.7 (16.7) years. The etiologic fraction of RBM20 variants in arrhythmogenic DCM was 0.53 (95% CI, 0.32-0.67; P < .001). In genome-first biobanks, lifetime incidence of cardiomyopathy, heart failure, or major ventricular arrhythmia diagnosis was lower in participants with RBM20 variants than in those with TTNtvs (hazard ratio, 0.55; 95% CI, 0.36-0.84; P < .001). Patients with RBM20tvs and DCM presented to referral centers later in life than those with P/LP RBM20 and DCM (mean [SD], 53 [10] vs 34 [18] years; P < .001) and were less likely to have a family history of sudden cardiac arrest (2 of 10 [20%] vs 11 of 17 [65%]; P = .046) or cardiomyopathy (2 of 10 [20%] vs 14 of 18 [78%]; P < .001). There was no significant difference in age- and sex-adjusted incident major heart failure or arrhythmia events between patients with RBM20tv and DCM or those with P/LP RBM20 and DCM, though sex-adjusted lifetime hazard was reduced in those with RBM20tv and DCM (hazard ratio, 0.13; 95% CI, 0.03-0.56; P = .01). Conclusions and Relevance: This study found that RBM20 variants contributed to arrhythmogenic DCM phenotypes but conferred reduced lifetime disease penetrance compared to TTNtvs and milder disease severity alone than P/LP RBM20 variants. Their potential for additive interactions with other damaging variants should be considered in patients with DCM and their families.

  PublisherOA PDFDOI

• Antihypertensive Dosing During Mavacamten Therapy for Obstructive Hypertrophic Cardiomyopathy

  Journal of Cardiac Failure - Intersections · 2026-01-02

  articleOpen accessSenior author
  PublisherOA PDFDOI

• Long-Term Real-World Outcomes of Mavacamten in Symptomatic Obstructive Hypertrophic Cardiomyopathy up to 108 Weeks

  Journal of Clinical Medicine · 2025-11-18 · 3 citations

  articleOpen accessSenior authorCorresponding

  Background/Objectives: Mavacamten is a first-in-class cardiac myosin inhibitor approved for the treatment of symptomatic obstructive hypertrophic cardiomyopathy (HCM). Long-term data regarding its real-world safety and effectiveness are limited. We aimed to describe the real-world experience of mavacamten in a large obstructive HCM cohort at a high-volume HCM center in the United States. Methods: Adult patients initiated on mavacamten between 29 April 2022 and 19 January 2025 at a single HCM center (n = 163) were retrospectively identified. Clinical effectiveness and safety data were collected through 108 weeks of treatment. Results: Rapid and sustained reductions in resting (baseline mean 53.0 ± 36.7 mm Hg to 10.0 ± 11.0 mm Hg) and Valsalva left ventricular outflow tract gradients (baseline mean 79.7 ± 33.2 mm Hg to 16.6 ± 15.4 mm Hg) were observed during treatment throughout the study period along with substantial improvements in New York Heart Association (NYHA) class (75% with &gt;1 NYHA class improvement by Week 12). Mean maximal left ventricular wall thickness significantly decreased (β = 0.01 mm per week). Ten patients (6.1%) required temporary drug interruption due to decrement in left ventricular ejection fraction, and mavacamten was discontinued in six patients (3.7%). Doses of background beta blocker and nondihydropyridine calcium channel blocker were significantly reduced during the study period (p &lt; 0.001). Conclusions: In this large single-center real-world experience of mavacamten therapy, mavacamten was highly effective and maintained an acceptable safety profile, comparable to the clinical trial long-term extension experience.

  PublisherOA PDFDOI

• Abstract 4365842: Chronic Aficamten Treatment Results in Sustained Favorable Cardiac Remodeling in Patients with Symptomatic Obstructive Hypertrophic Cardiomyopathy: Insights From the FOREST-HCM Trial

  Circulation · 2025-11-03

  article

  Background: Aficamten treatment over 24 weeks in SEQUOIA-HCM (NCT05186818) improved left ventricular (LV) outflow tract gradients (LVOT-G), showed evidence of favorable cardiac remodeling, and improved measures of LV diastolic function in patients with obstructive hypertrophic cardiomyopathy (oHCM). Whether longer-term treatment over 48 weeks results in further cardiac remodeling is unknown. Research Question: This study evaluates the effect of chronic treatment with aficamten on echocardiographic measures of cardiac structure and function in FOREST-HCM (NCT04848506), an open-label extension study that enrolled patients who completed a parent study with aficamten. Methods: Serial echocardiograms were performed in patients receiving open-label aficamten (5–20 mg daily) titrated to relieve LVOT obstruction (Valsalva LVOT &lt;30 mmHg) while maintaining LV ejection fraction (LVEF) 50%. Results: As of August 31, 2024, 169 patients (mean±SD age 60±13 years; 45.6% female, 95.6% White, 2.4% Black, 1.2% Asian) completed 48 weeks of follow-up. Aficamten treatment resulted in sustained improvement in Valsalva and resting LVOT-G, LV wall thickness, left atrial volume index, and lateral and septal E/e' ( Figure 1 ). LVEF decreased mildly (-7±8%) and remained stable within a normal range between weeks 24 and 48. After 48 weeks, 74 patients demonstrated improvement in the total number of normal LV diastolic function measures ( Figure 2 ). Conclusion: Treatment with aficamten for 48 weeks in patients with oHCM resulted in significant improvement in important measures of cardiac structure and function, with continued benefit after 24 weeks and no meaningful adverse effects on LV systolic function, indicating sustained and favorable long-term cardiac remodeling.

  PublisherDOI

• Hypertension in Patients With Obstructive Hypertrophic Cardiomyopathy Treated With Mavacamten

  JACC Heart Failure · 2025-10-01

  articleOpen accessSenior author
  PublisherOA PDFDOI

Frequent coauthors

• Iacopo Olivotto

  Istituti di Ricovero e Cura a Carattere Scientifico

  139 shared

• Roberto Barriales‐Villa

  Instituto de Salud Carlos III

  118 shared

• Scott D. Solomon

  Harvard University

  108 shared

• Ahmad Masri

  Oregon Health & Science University

  99 shared

• Lubna Choudhury

  Northwestern University

  97 shared

• Pablo García‐Pavía

  Hospital Universitario Puerta de Hierro Majadahonda

  94 shared

• Martin S. Maron

  Morristown Medical Center

  91 shared

• Caroline Coats

  87 shared

Awards & honors

• Infectious Hemoptysis with No Signs of Infection (Society of…