Dr. Longoria is a board-certified, fellowship-trained cardiothoracic surgeon. He is a clinical associate professor in the Department of Cardiothoracic Surgery at Stanford University School of Medicine.

Deeply accomplished in all facets of complex adult cardiothoracic procedures, Dr. Longoria is a high-volume surgeon with more than 20 years of experience and an exceptionally low mortality and complication rate.

Dr. Longoria’s surgical experience includes complex mitral valve and tricuspid valve repair, coronary artery bypass grafting, adult congenital repair, as well as procedures for high risk VAD patients. He performs cardiac transplantation, carotid endarterectomy, and implantation of all FDA-approved mechanical circulatory support devices. Additionally, he performs catheter-based valvular procedures (such as transcatheter aortic valve replacement, or TAVR) and open and video-assisted thoracoscopic surgery (VATS) for pulmonary surgical procedures.

He has an applied interest in atrial fibrillation (AFib) and is a nationally recognized expert in the minimally invasive surgical treatment of Atrial Fibrillation (AFib). Dr. Longoria was issued a method patent from the U.S. Patent and Trademark Office for developing the TTMaze (Totally Thoracoscopic) procedure that is central to the Dual Epicardial Endocardial Persistent (DEEP) AFib clinical trial.

Before joining Stanford, Dr. Longoria was the surgical director of cardiac ablation at a prominent AFib center certified by the Society of Chest Pain Centers. He holds patents for a synthetic chord used to connect tissue and for specialized methods he developed to treat cardiac arrhythmias.

At Stanford, Dr. Longoria brings a commitment to patientcentric, personalized care. He is committed to making the experience of surgery as pleasant as possible for his patients. He is also excited for the opportunity to conduct translational research that utilizes the most advanced technology available, in collaboration with colleagues from other disciplines.

For his outcomes and high patient satisfaction ratings, Dr. Longoria has earned awards and recognition, including being named a Top Doctor of Sacramento by his peers for the last five years in a row. He has also been an honoree of the President’s Award for patient satisfaction by the Sutter Independent Physicians.

Dr. Longoria has published articles on genetic variants associated with atrial fibrillation, thoracoscopic left atrial appendage clipping, radiofrequency ablation, and other topics. His work has appeared in the Journal of Thoracic and Cardiovascular Surgery, Annals of Thoracic Surgery, Journal of the American College of Cardiology, Journal of Cardiovascular Electrophysiology, and elsewhere.

He has made numerous presentations on atrial fibrillation surgery and other topics at conferences including the Annual Meeting of the American Association of Thoracic Surgery, Society of Thoracic Surgeons, and International Society for Heart and Lung Transplantation.

Dr. Longoria is a Fellow of the American College of Surgeons and American College of Cardiology. He is a member of the Society of Thoracic Surgeons, Western Thoracic Surgical Association, the International Society for Minimally Invasive Cardiothoracic Surgery, and the Heart Rhythm Society.

Clinical Focus

  • Cardiac Surgery
  • Minimally Invasive Atrial Fibrillation Surgery
  • Thoracic and Cardiac Surgery

Academic Appointments

Professional Education

  • Board Certification: American Board of Thoracic Surgery, Thoracic and Cardiac Surgery (2001)
  • Residency: UC Davis Health Dept of Surgery (1997) CA
  • Residency: Beth Israel Deaconess Medical Center (1999) MA
  • Medical Education: University of Illinois College of Medicine Office of the Registrar (1990) IL

All Publications

  • Leiomyosarcoma of the inferior vena cava: a case report. Journal of surgical case reports Graves, A. n., Longoria, J. n., Graves, G. n., Ianiro, C. n. 2020; 2020 (11): rjaa479


    Leiomyosarcoma (LMS) of the inferior vena cava (IVC) is an extremely rare malignancy with <400 cases reported. We present a 42-year-old woman with a 3-day history of vague and non-specific abdominal pain. Examination revealed mild tenderness to the epigastrium and right upper quadrant with no other findings. Abdominal ultrasound was performed, which revealed a large hypoechoic mass overlying the IVC. Abdominal computed tomography (CT) was performed which revealed an 8.9 × 7.9 × 9 cm multilobulated lesion encasing the IVC. A CT-guided biopsy was performed which revealed a primary LMS of the IVC. Surgical en bloc excision was performed with an end-to-end Dacron graft for IVC reconstruction. Histopathology confirmed LMS of the vessel wall with negative surgical margins.

    View details for DOI 10.1093/jscr/rjaa479

    View details for PubMedID 33274043

    View details for PubMedCentralID PMC7694595

  • Thoracoscopic Left Atrial Appendage Clipping: A Multicenter Cohort Analysis. JACC. Clinical electrophysiology van Laar, C., Verberkmoes, N. J., van Es, H. W., Lewalter, T., Dunnington, G., Stark, S., Longoria, J., Hofman, F. H., Pierce, C. M., Kotecha, D., van Putte, B. P. 2018; 4 (7): 893–901


    OBJECTIVES: This study sought to document the closure rate, safety, and stroke rate after thoracoscopic left atrial appendage (LAA) clipping.BACKGROUND: The LAA is the main source of stroke in patients with atrial fibrillation, and thoracoscopic clipping may provide a durable and safe closure technique.METHODS: The investigators studied consecutive patients undergoing clipping as part of a thoracoscopic maze procedure in 4 referral centers (the Netherlands and the United States) from 2012 to 2016. Completeness of LAA closure was assessed by either computed tomography (n= 100) or transesophageal echocardiography (n= 122). The primary outcome was complete LAA closure (absence of residual LAA flow and pouch<10 mm). The secondary outcomes were 30-day complications; the composite of ischemic stroke, hemorrhagic stroke, or transient ischemic attack; and all-cause mortality.RESULTS: A total of 222 patients were included, with a mean age of 66 ± 9 years, and 68.5% were male. The mean CHA2DS2-VASc (congestive heart failure, hypertension, age≥75 years, diabetes mellitus, prior stroke or transient ischemic attack or thromboembolism, vascular disease, age 65 to 74 years, sex category [female]) score was 2.3 ± 1.0. Complete LAA closure was achieved in 95.0% of patients. There were no intraoperative or clip-related complications, and the overall 30-day freedom from any complication rate was 96.4%. The freedom from cerebrovascular events after surgery was 99.1% after median follow-up of 20 months (interquartile range: 14 to 25 months; 369 patient-years of follow-up), and overall survival was 98.6%. The observed rate of cerebrovascular events after LAA clipping was low (0.5per 100 patient-years).CONCLUSIONS: LAA clipping during thoracoscopic ablation is a feasible and safe technique for closure of the LAA in patients with atrial fibrillation. The lower than expected rate of cerebrovascular events after deployment was likely multifactorial, including not only LAA closure, but also the effect of oral anticoagulation and rhythm control.

    View details for DOI 10.1016/j.jacep.2018.03.009

    View details for PubMedID 30025689

  • Protecting the right phrenic nerve during catheter ablation: Techniques and anatomical considerations. HeartRhythm case reports Stark, S., Roberts, D. K., Tadros, T., Longoria, J., Krishnan, S. C. 2017; 3 (4): 199–204

    View details for DOI 10.1016/j.hrcr.2016.08.012

    View details for PubMedID 28491802

  • Atrial Fibrillation Associated Genetic Variants and Left Atrial Histology: Evaluation for Molecular Sub-Phenotypes JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY Roberts, J. D., Yang, J., Gladstone, R. A., Longoria, J., Whitman, I. R., Dewland, T. A., Miller, C., Robles, A., Poon, A., Seiler, B., Laframboise, W. A., Olgin, J. E., Kwok, P., Marcus, G. M. 2016; 27 (11): 1264–70


    Genome wide association studies have identified several single nucleotide polymorphisms (SNPs) associated with atrial fibrillation (AF), but the mechanisms underlying these relationships have not yet been elucidated. Inflammation and fibrosis have been posited as important mechanisms responsible for AF. We sought to investigate the impact of SNP carrier status on inflammation and fibrosis in left atrial appendage tissue.Carrier status of 10 AF-associated SNPs was evaluated on DNA extracted from left atrial appendage tissue in 176 individuals (120 with AF). The presence of inflammation was evaluated through visual quantification of leukocyte infiltration following hematoxylin and eosin staining, while fibrosis was quantified using picrosirius red with fast green staining. Unadjusted and adjusted linear and logistic regression models were utilized to evaluate for an association between SNP carrier status and inflammation and fibrosis. On adjusted logistic regression analysis, the rs7164883 SNP (intronic within HCN4) was associated with a reduced odds of inflammation (odds ratio: 0.42; 95% CI: 0.22-0.81, P = 0.01), and was not associated with fibrosis on adjusted linear regression analysis (β-coefficient: -0.31; 95% CI: -1.03-0.40, P = 0.40). None of the remaining SNPs exhibited significant associations with left atrial inflammation or fibrosis.Among 10 AF-associated SNPs, a single genetic variant was associated with reduced left atrial inflammation, while no histologic differences were observed in the remaining 9. The known AF-associated SNPs do not appear to predispose to the development of pro-inflammatory or pro-fibrotic AF sub-phenotypes.

    View details for DOI 10.1111/jce.13083

    View details for Web of Science ID 000387393800002

    View details for PubMedID 27574037

  • Targeted Deep Sequencing Reveals No Definitive Evidence for Somatic Mosaicism in Atrial Fibrillation CIRCULATION-CARDIOVASCULAR GENETICS Roberts, J. D., Longoria, J., Poon, A., Gollob, M. H., Dewland, T. A., Kwok, P., Olgin, J. E., Deo, R. C., Marcus, G. M. 2015; 8 (1): 50–U100


    Studies of ≤15 atrial fibrillation (AF) patients have identified atrial-specific mutations within connexin genes, suggesting that somatic mutations may account for sporadic cases of the arrhythmia. We sought to identify atrial somatic mutations among patients with and without AF using targeted deep next-generation sequencing of 560 genes, including genetic culprits implicated in AF, the Mendelian cardiomyopathies and channelopathies, and all ion channels within the genome.Targeted gene capture and next-generation sequencing were performed on DNA from lymphocytes and left atrial appendages of 34 patients (25 with AF). Twenty AF patients had undergone cardiac surgery exclusively for pulmonary vein isolation and 17 had no structural heart disease. Sequence alignment and variant calling were performed for each atrial-lymphocyte pair using the Burrows-Wheeler Aligner, the Genome Analysis Toolkit, and MuTect packages. Next-generation sequencing yielded a median 265-fold coverage depth (interquartile range, 64-369). Comparison of the 3 million base pairs from each atrial-lymphocyte pair revealed a single potential somatic missense mutation in 3 AF patients and 2 in a single control (12 versus 11%; P=1). All potential discordant variants had low allelic fractions (range, 2.3%-7.3%) and none were detected with conventional sequencing.Using high-depth next-generation sequencing and state-of-the art somatic mutation calling approaches, no pathogenic atrial somatic mutations could be confirmed among 25 AF patients in a comprehensive cardiac arrhythmia genetic panel. These findings indicate that atrial-specific mutations are rare and that somatic mosaicism is unlikely to exert a prominent role in AF pathogenesis.

    View details for DOI 10.1161/CIRCGENETICS.114.000650

    View details for Web of Science ID 000349873200008

    View details for PubMedID 25406240

    View details for PubMedCentralID PMC4334693

  • Telomere Length and the Risk of Atrial Fibrillation Insights Into the Role of Biological Versus Chronological Aging CIRCULATION-ARRHYTHMIA AND ELECTROPHYSIOLOGY Roberts, J. D., Dewland, T. A., Longoria, J., Fitzpatrick, A. L., Ziv, E., Hu, D., Lin, J., Glidden, D. V., Psaty, B. M., Burchard, E. G., Blackburn, E. H., Olgin, J. E., Heckbert, S. R., Marcus, G. M. 2014; 7 (6): 1026–32


    Advanced age is the most important risk factor for atrial fibrillation (AF); however, the mechanism remains unknown. Telomeres, regions of DNA that shorten with cell division, are considered reliable markers of biological aging. We sought to examine the association between leukocyte telomere length (LTL) and incident AF in a large population-based cohort using direct LTL measurements and genetic data. To further explore our findings, we compared atrial cell telomere length and LTL in cardiac surgery patients.Mean LTL and the TERT rs2736100 single nucleotide polymorphism were assessed as predictors of incident AF in the Cardiovascular Health Study (CHS). Among the surgical patients, within subject comparison of atrial cell telomere length versus LTL was assessed. Among 1639 CHS participants, we observed no relationship between mean LTL and incident AF before and after adjustment for potential confounders (adjusted hazard ratio, 1.09; 95% confidence interval: 0.92-1.29; P=0.299); chronologic age remained strongly associated with AF in the same model. No association was observed between the TERT rs2736100 single nucleotide polymorphism and incident AF (adjusted hazard ratio: 0.95; 95% confidence interval: 0.88-1.04; P=0.265). In 35 cardiac surgery patients (26 with AF), atrial cell telomere length was longer than LTL (1.19 ± 0.20 versus 1.02 ± 0.25 [T/S ratio], P<0.001), a finding that remained consistent within the AF subgroup.Our study revealed no evidence of an association between LTL and incident AF and no evidence of relative atrial cell telomere shortening in AF. Chronological aging independent of biological markers of aging is the primary risk factor for AF.

    View details for DOI 10.1161/CIRCEP.114.001781

    View details for Web of Science ID 000346360100008

    View details for PubMedID 25381796

    View details for PubMedCentralID PMC4294941