Dr. Sandoval is a board-certified cardiologist and a clinical assistant professor in the Division of Cardiovascular Medicine at Stanford University School of Medicine. He completed his residency at the University of Texas at Austin, where he continued on as chief resident before going on to complete his fellowship in cardiovascular disease at the Medical University of South Carolina. Prior to his residency, he completed a research fellowship at Massachusetts General Hospital (MGH).

His clinical interests include preventive cardiology and management of heart failure. He is particularly focused on treating patients with the complex clinical syndrome of heart failure with preserved ejection fraction (HFpEF).

His interest in preventive cardiology grew through his participation in clinics for the uninsured and underinsured during his training. These experiences fostered his passion for understanding and addressing health care disparities. He is deeply committed to providing exceptional patient care with a personalized approach to treatment and improving the lives of his patients.

He is a member of the American College of Cardiology.

Clinical Focus

  • Cardiovascular Disease

Academic Appointments

Honors & Awards

  • Member, American College of Cardiology (ACC)

Professional Education

  • Board Certification: National Board of Echocardiography, Adult Echocardiography (2022)
  • Board Certification: American Board of Internal Medicine, Cardiovascular Disease (2021)
  • Board Certification: American Board of Internal Medicine, Internal Medicine (2017)
  • Fellowship: Medical University of South Carolina Cardiology Fellowship (2021) SC
  • Residency: University of Texas at Austin Internal Medicine Residency Program (2018) TX
  • Medical Education: Universidad Internacional del Ecuador School of Medicine (2011) Ecuador

All Publications

  • Coronary sinus biomarker sampling compared to peripheral venous blood for predicting outcomes in patients with severe heart failure undergoing cardiac resynchronization therapy: the BIOCRT study. Heart rhythm Truong, Q. A., Januzzi, J. L., Szymonifka, J., Thai, W. E., Wai, B., Lavender, Z., Sharma, U., Sandoval, R. M., Grunau, Z. S., Basnet, S., Babatunde, A., Ajijola, O. A., Min, J. K., Singh, J. P. 2014; 11 (12): 2167-75


    A significant minority of patients receiving cardiac resynchronization therapy (CRT) remain nonresponsive to this intervention.This study aimed to determine whether coronary sinus (CS) or baseline peripheral venous (PV) levels of established and emerging heart failure (HF) biomarkers are predictive of CRT outcomes.In 73 patients (aged 68 ± 12 years; 83% men; ejection fraction 27% ± 7%) with CS and PV blood samples drawn simultaneously at the time of CRT device implantation, we measured amino-terminal pro-B-type natriuretic peptide (NT-proBNP), galectin-3 (gal-3), and soluble ST2 (sST2) levels. NT-proBNP concentrations >2000 pg/mL, gal-3 concentrations >25.9 ng/mL, and sST2 concentrations >35 ng/mL were considered positive on the basis of established PV cut points for identifying "high-risk" individuals with HF. CRT response was adjudicated by the HF Clinical Composite Score. A major adverse cardiovascular event (MACE) was defined as the composite end point of death, cardiac transplant, left ventricular assist device, and HF hospitalization at 2 years.NT-proBNP concentrations were 20% higher in the CS than in the periphery, while gal-3 and sST2 concentrations were 10% higher in the periphery than in the CS (all P < .001). There were 45% CRT nonresponders at 6 months and 16 (22%) patients with MACE. Triple-positive CS values yielded the highest specificity of 95% for predicting CRT nonresponse. Consistently, CS strategies identified patients at higher risk of developing MACE, with >11-fold adjusted increase for triple-positive CS patients compared to triple-negative patients (all P ≤ .04). PV strategies were not predictive of MACE.Our findings suggest that CS sampling of HF biomarkers may be better than PV sampling for predicting CRT outcomes. Larger studies are needed to confirm our findings.

    View details for DOI 10.1016/j.hrthm.2014.07.007

    View details for PubMedID 25014756

    View details for PubMedCentralID PMC4254015