
Julio A. Chirinos
VerifiedUniversity of Pennsylvania · Rehabilitation Medicine
Active 1952–2026
About
Julio A. Chirinos, MD, PhD, is a Professor of Medicine (Cardiovascular Medicine) at the Hospital of the University of Pennsylvania. He serves as an Attending Physician at the Hospital of the University of Pennsylvania and is an Adjunct Faculty member at the Center for Magnetic Resonance and Optimal Imaging at the University of Pennsylvania. Dr. Chirinos is also the Co-Director of the Training Program in Cardiovascular Biology and Medicine, Clinical/Translational Science at the University of Pennsylvania Perelman School of Medicine. His research expertise includes non-invasive cardiac imaging, arterial stiffness and hemodynamics, ventricular-vascular interactions, and the cardiovascular consequences of obstructive sleep apnea. His clinical expertise encompasses echocardiography and cardiac MRI. Dr. Chirinos completed his medical education at the Catholic University of Santa Maria School of Human Medicine in 1999 and earned a PhD in Biomedical Sciences from the University of Ghent in 2012.
Research topics
- Medicine
- Computer Science
- Internal medicine
- Cardiology
- Intensive care medicine
- Pathology
- Virology
Selected publications
Mapping rare protein-coding variants on multi-organ imaging traits
Open MIND · 2026-01-01
articleMapping rare protein-coding variants on multi-organ imaging traits
UNC Libraries · 2026-02-07
articleOpen accessHypertension · 2026-05-15
articleOpen accessSenior authorBACKGROUND: Hypertension is present in 90% of individuals with heart failure with preserved ejection fraction (HFpEF) and is a major modifiable risk factor for the development of HFpEF. However, randomized controlled trial evidence for hypertension management in HFpEF is limited. METHODS: In a double-blind, randomized, crossover trial, we studied the effect of amlodipine 5 to 10 mg versus metoprolol succinate 100 to 200 mg (doses previously demonstrated to have comparable antihypertensive efficacy) for 4 weeks among adults with HFpEF and hypertension, without contraindications to initiating or withholding either drug. The primary outcome was the difference in mean home systolic BP during the final week of each treatment. RESULTS: The mean age of the 50 enrolled participants was 72±9 years, 34 (68%) were women, 33 (66%) were of Black race, mean blood pressure was 144±15/78±9 mm Hg, and 23 (46%) were receiving β-blockers before enrollment. Compared with metoprolol, systolic blood pressure was 4 (95% CI, −7 to −1; P =0.017) mm Hg lower with amlodipine. In addition, peak oxygen uptake during exercise was 1.2 (95% CI, 0.3–2.0; P =0.008) mL/min per kg higher, physical activity was 0.1 (95% CI, 0.01–0.1; P =0.019) metabolic equivalents of task/d higher, and NT-proBNP (N-terminal pro-B-type natriuretic peptide) was 200 (95% CI, −291 to −109; P <0.0001) pg/mL lower with amlodipine versus metoprolol. There was no significant difference in septal E/e′, myocardial strain, or systemic vasodilatory reserve. The frequency and severity of adverse events were similar across treatments. CONCLUSIONS: Our findings support the use of dihydropyridine calcium channel blockers as a preferred alternative to β-blockers for the management of hypertension in HFpEF. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT04434664.
Mapping rare protein-coding variants on multi-organ imaging traits
Nature Communications · 2025-12-23
articleOpen accessHuman organ structure and function are important endophenotypes for clinical outcomes. Genome-wide association studies (GWAS) have identified numerous common variants associated with phenotypes derived from magnetic resonance imaging (MRI) of the brain and body. However, the role of rare protein-coding variations affecting organ size and function is largely unknown. Here we present an exome-wide association study that evaluates 596 multi-organ MRI traits across over 50,000 individuals from the UK Biobank. We identified 107 variant-level associations and 224 gene-based burden associations (67 unique gene-trait pairs) across all MRI modalities, including PTEN with total brain volume, TTN with regional peak circumferential strain in the heart left ventricle, and TNFRSF13B with spleen volume. The singleton burden model and AlphaMissense annotations contributed 8 unique gene-trait pairs including the association between an approved drug target gene of KCNA5 and brain functional activity. The identified rare coding signals elucidate some shared genetic effects across organs, prioritize previously identified GWAS loci, and are enriched for drug targets. Overall, we demonstrate how rare variants enhance our understanding of genetic effects on human organ morphology and function and their connections to complex diseases. Here, the authors report an exome-wide association study for multi-organ imaging traits by leveraging recent bioinformatic tools such as AlphaMissense. The identified signals elucidate the genetic effects from rare variants on human organs and their connections to complex diseases
Circulation Heart Failure · 2025-05-13 · 6 citations
articleOpen accessBACKGROUND: Exercise intolerance is a hallmark of heart failure with preserved ejection fraction (HFpEF) and is characterized by skeletal muscle (SkM) dysfunction with impaired oxidative capacity. To maintain oxidative capacity, the SkM secretes myokines such as musclin, which has been shown to potentiate NP (natriuretic peptide) signaling and induce PGC-1α (peroxisome proliferator-activated receptor-γ coactivator-1 alpha) signaling. We sought to investigate the role of musclin in SkM dysfunction in HFpEF. For this study, we selected the oxidative-predominant SkM soleus in HFpEF mice and vastus lateralis from patients with HFpEF. METHODS: Using the SAUNA model, mice underwent HFpEF induction by uninephrectomy, d-aldosterone infusion, and 1% sodium chloride drinking water for 4 weeks. Exogenous musclin was given to HFpEF mice every 2 days during the last 2 weeks of HFpEF induction. Molecular analyses were conducted on blood samples and SkM from HFpEF mice and patients with HFpEF. RESULTS: In HFpEF mice and patients with HFpEF, increased musclin expression was accompanied by decreased cyclic guanosine monophosphate levels and PGC-1α expression in SkM, suggesting impaired NP signaling. Exogenous administration of musclin in mice with HFpEF demonstrated augmented circulating musclin levels and potentiated NP signaling in SkM as shown by increased PKG1 (protein kinase G1) activity and PGC-1α expression. This was associated with a transition from type-2A to type-1 fiber (type-1 has more endurance) and increased succinate dehydrogenase activity, hindlimb blood flow, and capillary density in the soleus muscle. Exogenous musclin also mitigated cardiac hypertrophy without affecting blood pressure or diastolic function. Most importantly, HFpEF mice treated with musclin demonstrated improved functional and exercise capacity. CONCLUSIONS: Musclin mediates beneficial effects in SkM and heart with improved exercise capacity likely by improving oxidative capacity in SkM. Future studies are warranted to address the therapeutic efficacy of exogenous musclin in humans with HFpEF.
Current Hypertension Reviews · 2025-07-04 · 1 citations
articleSenior authorCorrespondingLarge artery stiffness (LAS) is widely recognized as a highly clinically relevant determinant of cardiovascular health and an independent prognostic marker. However, routine assessment of LAS has not yet been integrated into clinical practice. Arterial wall stiffness is dependent on distending pressure (i.e., mean arterial pressure), which may confound the interpretation of individual measurements. The cardio-ankle vascular index (CAVI) is an index of arterial stiffness designed to mitigate the dependence of pulse wave velocity on blood pressure. However, because CAVI incorporates pulse wave velocity measured between the heart and the ankle, it is influenced by both the stiffness of the aorta and medium-sized muscular arteries. Several observational, longitudinal studies have demonstrated that higher CAVI is associated with cardiovascular events and mortality, although most available data are derived from Asian populations. Future studies of CAVI are needed to establish its prognostic value in addition to traditionally used cardiovascular risk factors in the setting of primary prevention. This review aims to provide a brief overview of the definition, theoretical principles, practical considerations, key strengths and limitations, and the clinical utility of CAVI.
Revista de Gastroenterología de México · 2025-11-01
articleOpen accessSenior authorEl uso de la inteligencia artificial (IA) en estudios endoscópicos ha crecido en los últimos años. El presente estudio evalúa el desempeño de la IA para la detección de pólipos y adenomas en la práctica clínica diaria. Estudio transversal, se revisaron colonoscopias asistidas con inteligencia artificial (CAIA) y colonoscopias control realizadas entre enero de 2021 y mayo de 2024. Se aplicó regresión logística para la detección de adenomas, de acuerdo a sus características. Se revisaron 1251 colonoscopias. El grupo CAIA presentó mayor edad frente a la colonoscopia control (59 ± 13 vs. 56 ± 12 años; p < 0.05). No hubo diferencias entre sexo, indicación, preparación y tiempo del procedimiento. Con respecto al objetivo primario, el grupo CAIA presentó una mayor tasa de pólipos (58 vs. 52%; p < 0.05). La diferencia en la tasa de adenomas (39 vs. 33%; p > 0.05) no fue estadísticamente significativa. En el análisis de las características de los adenomas, el grupo CAIA presentó una tasa significativamente mayor de adenomas polipoides (OR: 1.28; IC 95%: 1.04-1.59), lesiones < 10 mm (OR: 1.41; IC 95%: 1.14-1.74) y lesiones localizadas en colon proximal (OR: 1.31; IC 95%: 1.05-1.65). El uso de la IA en colonoscopias incrementa, de manera no significativa, la tasa de detección de adenomas. Este aumento es significativo para la detección de adenomas polipoides, menores de 10 mm y en colon proximal. The use of artificial intelligence (AI) in endoscopic studies has grown in recent years. The present study evaluates the performance of AI in detecting polyps and adenomas in daily clinical practice. A cross-sectional study was conducted, in which AI-assisted colonoscopies (AIACs) performed between January 2021 and May 2024 were reviewed. Logistic regression was applied for adenoma detection, based on their characteristics. A total of 1,251 colonoscopies were reviewed. The patients in the AIAC group were older than the control group (59 ± 13 vs. 56 ± 12 years, P <.05). There were no differences between sex, procedure indication, bowel preparation, and procedure time. Regarding the primary aim, the AIAC group had a significantly higher polyp detection rate (58 vs. 52%; P <.05) and non-significantly higher adenoma detection rate (39 vs. 33%; P >.05), compared with the control group. In the analysis of adenoma characteristics, the identification of polypoid adenomas (OR: 1.28; 95% CI: 1.04-1.59), smaller 10 mm (OR: 1.41; 95% CI: 1.14-1.74), and located in the proximal colon (OR: 1.31; 95% CI: 1.05-1.65) was significantly higher in the AIAC group, compared with the control group. The use of AI in colonoscopies resulted in a non-significant increase in the adenoma detection rate but a significant increase in detecting polypoid adenomas smaller than 10 mm and located in the proximal colon.
Scientific Reports · 2025-11-10
articleOpen accessThis study examines the association of aortic geometric traits with flow characteristics and disease outcomes in 3204 patients from the Penn Medicine Biobank (PMBB). Using an nnU-Net, the thoracic aorta was segmented from CT scans to measure traits such as diameter and length. A one-dimensional reduced-order Navier-Stokes model (ROM) simulated aortic pulse pressure under various physiological conditions. Phenome-wide association studies (PheWAS) were conducted to link aortic traits to diseases using electronic health records (EHR). Significant associations were identified between aortic pulse pressure and conditions like aortic aneurysms, heart valve disorders, hypertension, and obesity. Notably, pulse pressure-but not aortic diameter-was also linked to diseases such as diabetes mellitus, wheezing, and chronic airway obstruction. The ROM-simulated pulse pressure showed not only previously recognized associations with diseases such as aortic aneurysm and hypertension, but also associations with conditions affecting organs outside the aorta. ROM hemodynamic simulations can be applied to thoracic images at the scale of thousands of patients. The ROM-simulated pulse pressure showed not only previously recognized associations with diseases including aortic aneurysm and hypertension, but also other diseases outside the aorta.
Mayo Clinic Proceedings · 2025-07-01
editorialOpen accessSenior authorJournal of the American Heart Association · 2025-08-12
articleOpen accessSenior authorCorrespondingBackground Large‐artery stiffness (LAS) significantly contributes to cardiovascular morbidity and death and is characterized by increased pulse pressure (PP). The biology underlying large‐artery stiffness in humans remains incompletely understood. Methods and Results We investigated associations between PP and circulating levels of 2941 proteins among 53 016 UK Biobank participants. Analyses were adjusted for age, sex, mean arterial pressure, body mass index and stroke volume. Interaction analyses assessed the effect modification by sex on these relationships. We evaluated causal associations between plasma protein levels and PP, using inverse variance–weighted Mendelian randomization as the main analysis and Bayesian colocalization as a sensitivity analysis. A 5% false discovery rate threshold was used to account for multiple comparisons. Measured levels of 871 proteins were significantly associated with PP when adjusting for age, sex, mean arterial pressure, and body mass index, and 61 remained significantly associated after further adjusting for stroke volume. Top associations included NPPB (natriuretic peptide B), thrombospondin‐2, paraoxonase‐2, and sclerostin. Genetic analyses indicated that genetically predicted levels for 16 proteins were significantly associated with PP after false discovery rate correction, including fibroblast growth factor 5 (β IVW per SD change in protein levels=0.47 [95% CI, 0.34–0.61]), NPPB (β IVW =−1.40 [95% CI, −1.85 to −0.95]), insulin‐like growth factor binding 3 (β IVW =−1.143 [95% CI, −1.57 to −0.71]), and furin (β IVW , 1.31 [95% CI, 0.88–1.73]). Conclusions Using complementary epidemiological approaches to triangulate findings, our study identifies novel proteins with a putative causal effect on PP. Notably, our findings identify NPPB with high statistical confidence. This may have potentially impactful implications given the current availability of Food and Drug Administration–approved medications to boost NPPB effects.
Frequent coauthors
- 578 shared
Raymond R. Townsend
- 557 shared
Patrick Segers
Ghent University Hospital
- 464 shared
Payman Zamani
University of Pennsylvania Health System
- 303 shared
David R. Jacobs
University of Minnesota
- 301 shared
Daniel Duprez
University of Minnesota
- 299 shared
João A.C. Lima
Johns Hopkins Medicine
- 294 shared
Richard A. Kronmal
University of Washington
- 273 shared
Scott Lilly
The Ohio State University
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