Clinical Focus

  • Cardiac Electrophysiology
  • Clinical Cardiac Electrophysiology

Academic Appointments

Honors & Awards

  • F32 Ruth L. Kirschstein National Research Service Award, NIH (07/2009-06/2011)
  • Postdoctoral Fellowship Award (deferred), American Heart Association, Western States Affiliate (07/2009-06/2011)
  • Outstanding Clinical Fellow - Cardiovascular Medicine, Stanford University Medical Center (2009)
  • Chief Fellow - Cardiovascular Medicine, Stanford University Medical Center (2009-2010)

Professional Education

  • Fellowship:Stanford University (2010) CA
  • Residency:Stanford University Hospital -Clinical Excellence Research Center (2006) CA
  • Board Certification: Clinical Cardiac Electrophysiology, American Board of Internal Medicine (2013)
  • Fellowship:Stanford University (2012) CA
  • Board Certification: Cardiovascular Disease, American Board of Internal Medicine (2011)
  • Fellowship, Stanford University Hospital, Cardiovascular Medicine (2010)
  • Board Certification: Internal Medicine, American Board of Internal Medicine (2006)
  • Medical Education:New York University - School Of Medicine (2003) NY
  • BA, Harvard University (Cognitive Neuroscience), MA (1998)

Research & Scholarship

Clinical Trials

  • Attain Performa(TM) Quadripolar Lead Study Recruiting

    The purpose of the study is to evaluate the safety and efficacy of the Medtronic Attain Performa Quadripolar Leads (Model 4298, 4398, and 4598) during and post the implant procedure. This study will also assess the interactions of the Attain Performa leads with the entire Medtronic CRT-D system.

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Journal Articles

  • Pacemaker Therapy in Atrial Fibrillation Journal of Cardiology and Vascular Medicine Park, S., Wang, P. J., Zei, P. C., Hsia, H. H., Turakhia, M., Perez, M. V., Al-Ahmad, A. 2013; 1: 1-7
  • Hemodynamic Monitoring A Practical Approach to Cardiovascular Medicine Shirley Park & Euan Ashley, Reza Ardehali, Paul J. Wang, Marco Perez (eds, ) 2011: Chapter 26
  • Optical Control of Cardiomyocyte Depolarization and Inhibition Utilizing Channelrhodopsin-2 (ChR2) and a Third Generation Halorhodopsin (eNpHR3.0) Circulation Shirley Park, Ragu Vijaykumar, Paul G. Yock, Paul J. Wang, Karl Deisseroth 2010; 122 (21): A14882
  • Two Hsp70 family members expressed in atherosclerotic lesions PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Han, Z. H., Truong, Q. A., Park, S., Breslow, J. L. 2003; 100 (3): 1256-1261


    Gene expression profiling was carried out comparing Con A elicited peritoneal macrophages from C57BL6 and FVBN wild-type and apolipoprotein (apo)E knockout mice. An EST, was expressed at higher levels in C57BL6 compared with FVBN mice. mapped to an atherosclerosis susceptibility locus on chromosome 19 revealed in an intercross between atherosclerosis-susceptible C57BL6 and atherosclerosis-resistant FVBN apoE knockout mice. A combination of database search and Northern analysis confirmed that corresponded to 3'-UTR of a hitherto predicted gene, named HspA12A. Blasting the National Center for Biotechnology Information database revealed a closely related homologue, HspA12B. HspA12A and -B have very close human homologues. TaqMan analysis confirmed the increased HspA12A expression (2.6-fold) in elicited peritoneal macrophages from C57BL6 compared with FVBN mice. TaqMan analysis also revealed increased HspA12A and HspA12B expression (87- and 6-fold, respectively) in lesional versus nonlesional portions of the thoracic aorta from C57BL6 apoE knockout mice on a chow diet. In situ hybridization confirmed that both genes were expressed within lesions but not within nonlesional aortic tissue. Blasting of HspA12A and HspA12B against the National Center for Biotechnology Information database (NR) revealed a hit with the Conserved Domain database for Hsp70 (pfam00012.5, Hsp70). Both genes appear to contain an atypical Hsp70 ATPase domain. The BLAST search also revealed that both genes were more similar to primitive eukaryote and prokaryote than mammalian Hsp70s, making these two genes distant members of the mammalian Hsp70 family. In summary, we describe two genes that code for a subfamily of Hsp70 proteins that may be involved in atherosclerosis susceptibility.

    View details for DOI 10.1073/pnas.252764399

    View details for Web of Science ID 000180838100088

    View details for PubMedID 12552099

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