L
Lan S. Chen
Researcher at Indiana University
Publications - 53
Citations - 3206
Lan S. Chen is an academic researcher from Indiana University. The author has contributed to research in topics: Stellate ganglion & Atrial fibrillation. The author has an hindex of 24, co-authored 53 publications receiving 2769 citations. Previous affiliations of Lan S. Chen include The Catholic University of America & University of California, Los Angeles.
Papers
More filters
Journal ArticleDOI
Role of the Autonomic Nervous System in Atrial Fibrillation: Pathophysiology and Therapy
TL;DR: In this article, the authors focus on the relationship between the autonomic nervous system and the pathophysiology of atrial fibrillation and the potential benefit and limitations of neuromodulation in the management of this arrhythmia.
Journal ArticleDOI
Nerve sprouting and sudden cardiac death.
Ji Min Cao,Lan S. Chen,Bruce H. KenKnight,Toshihiko Ohara,Moon Hyoung Lee,Jerome Tsai,William W. Lai,Hrayr S. Karagueuzian,Paul L. Wolf,Michael C. Fishbein,Peng Sheng Chen +10 more
TL;DR: It is concluded that chronic myocardial infarction results in sympathetic nerve sprouting and creates a high-yield model of spontaneous VT, VF, and SCD in chronic MI.
Role of the Autonomic Nervous System in Atrial Fibrillation: Pathophysiology and Therapy
TL;DR: It is concluded that autonomic nerve activity plays an important role in the initiation and maintenance of AF, and modulating autonomic nervous function may contribute to AF control.
Journal ArticleDOI
Mechanisms of Cardiac Nerve Sprouting After Myocardial Infarction in Dogs
Shengmei Zhou,Lan S. Chen,Yasushi Miyauchi,Mizuho Miyauchi,Saibal Kar,Simon Kangavari,Michael C. Fishbein,Behrooz G. Sharifi,Peng Sheng Chen +8 more
TL;DR: A rapid and persistent upregulation of NGF and GAP43 expression at the infarcted site underlies the mechanisms of cardiac nerve sprouting after myocardial infarction.
Journal ArticleDOI
Histopathological substrate for chronic atrial fibrillation in humans
TL;DR: HCN4-/PAS-positive cardiomyocytes and CD117/c-kit-positive ICLC scattered among abundant inflammatory infiltrate, fibrous tissue, and sympathetic nerve structures in the atria and at the PV-LA junctions might be a substrate for the maintenance of chronic AF.