Nipavan Chiamvimonvat, M.D. for UC Davis Health

Nipavan Chiamvimonvat, M.D.

Professor, Roger Tatarian Endowed Professor of Cardiovascular Medicine

Associate Chief for Research, Division of Cardiovascular Medicine

Co-Director, UC Davis Cardiovascular Research Institute (CVRI)

Staff Cardiologist at VA Medical Center



Internal Medicine

Locations and Contact

VA Northern CA Health Care System

Sacramento VA Medical Center
10535 Hospital Way
Mather, CA 95655

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Phone: 916-843-7000

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Clinical Interests

I am a physician scientist and have dedicated my career in treating patients with cardiac arrhythmia disorders with my early training in cardiac electrophysiology at the University of Calgary, Canada. Critical knowledge gaps in the treatment of cardiac arrhythmias compelled me to pursue fundamental and translational research in cardiac arrhythmias that began with my postdoctoral training at Johns Hopkins University. The combination of research and clinical practice provides me with a unique perspective in cardiac arrhythmia disorders. My experiences in patient care both drive and inform my fundamental, translational and clinical research. In addition, by bridging these two different worlds, I have the opportunities to mentor young clinicians and basic scientists to understand the importance of cross-disciplinary interactions in their work. By uniting these separate approaches, our endeavors lay the foundation for translational and clinical investigations that may someday lead to advanced new therapies.

Research/Academic Interests

Our laboratory was the first to identify several isoforms of small conductance Ca2+-activated K+ channels (SK channels) that underlie Ca2+-activated K+ current in human and mouse atrial myocytes. Even though the roles of these channels have been extensively investigated in neurons, their roles in the heart are only beginning to be recognized. We demonstrated that the channels are highly expressed in atrial compared to ventricular tissues. Null mutation of the SK2 channels results in atrial arrhythmias and AV node dysfunction. Subsequently, our findings have been supported by several different laboratories. Even more relevant to translational medicine is the finding from recent studies using genome-wide association analysis that has provided a genetic link between SK channel polymorphisms and lone atrial fibrillation (AF) in humans.

Our studies have unmasked a functional crosstalk between Cav1.3 and SK channels. We have obtained new evidence to demonstrate that the expression of several interacting proteins, -actinin2, myosin light chain 2, and filamin A, are required for the proper membrane localization of SK channels. Even more exciting is the finding that an increase in intracellular Ca2+, as seen in AF, results in an increase in membrane localization of SK channels which would be predicted to lead to a decrease in effective refractory periods, an increase in functional reentry, and the maintenance of atrial arrhythmias. Our efforts thus far have paid off. Recent studies from several laboratories have provided additional support for the importance of SK channels. Indeed, SK channels may represent a novel drug target for AF. Insights into the molecular interactions between these new classes of cardiac ion channels are likely to be highly significant clinically. Thus, our studies have provided unique insights regarding the roles of these newly described channels in the heart.

Our laboratory was the first to demonstrate beneficial effects of a novel class of soluble epoxide hydrolase (sEH) inhibitors in cardiac hypertrophy, failure and arrhythmias. This work is a collaborative effort with Dr. Hammock at UC Davis. Treatment with sEH inhibitors (sEHIs) results in the prevention of ventricular myocyte hypertrophy and electrical remodeling in pressure overload and myocardial infarction models. We further demonstrate that treatment with sEHIs prevents cardiac fibroblast (CF) proliferation and fibrosis. These results are exciting because they demonstrate broader salutary effects in cardiac remodeling (not limited to myocyte hypertrophy alone) of this novel class of compounds. sEHIs have been shown to potently block the catalytic conversion of epoxyeicosatrienoic acids (EETs) to the corresponding dihydroxyeicosatrienoic acids (DHETs). EETs are products of cytochrome P450 epoxygenases that are known to have vasodilatory as well as anti-inflammatory properties. Since atrial fibrosis has been shown to play critical roles in atrial fibrillation, we are actively testing our hypothesis that treatment with sEHIs will be beneficial in the prevention of atrial fibrillation by reducing 1) atrial fibrosis, and 2) electrical remodeling in atrial myocytes. 


Cardiovascular Medicine

Center/Program Affiliation

Cardiovascular Services

Undergraduate School

Biology, University of Toronto, Toronto, Ontario, Canada 1980

Medical School

M.D., University of Toronto, Toronto, Ontario, Canada 1984


Internal Medicine, University of Toronto, Toronto, Ontario, Canada 1984-1985


Internal Medicine, University of Toronto, Toronto, Ontario, Canada 1985-1987


Clinical Cardiac Electrophysiology, University of Calgary, Calgary, Alberta, Canada 1989-1991


Cardiology, University of Western Ontario, Toronto, Ontario, Canada 1987-1989

Career Achievement Award, Department of Internal Medicine, UC Davis, 2017

Dean’s Excellence in Mentoring Award, UC Davis, 2011

Medical Research Council of Canada Research Fellowship, 1993, 1994, 1995, 1996, 1997

Runner up for the 1996 Young Investigator Award from North American Society for Pacing and Electrophysiology (NASPE), 1996

Heart and Stroke Foundation of Canada Research Fellowship, 1991, 1992, 1993

To view a detailed list of  Dr. Chiamvimonvat's publications, please click here.

Ledford HA, Ren L, Thai PN, Park S, Timofeyev V, Sirish P, Xu W, Emigh AM, Priest JR, Perez MV, Ashley EA, Yarov-Yarovoy V, Yamoah EN, Zhang XD, Chiamvimonvat N. Disruption of protein quality control of the human ether-à-go-go related gene K+ channel results in profound long QT syndrome. Heart Rhythm. 2022 Feb;19(2):281-292. doi:10.1016/j.hrthm.2021.10.005. Epub 2021 Oct 9. PMID:34634443.

Lyu Y, Thai PN, Ren L, Timofeyev V, Jian Z, Park S, Ginsburg KS, Overton J, Bossuyt J, Bers DM, Yamoah EN, Chen-Izu Y, Chiamvimonvat N, Zhang XD. Beat-to-beat dynamic regulation of intracellular pH in cardiomyocytes. iScience. 2021 Dec 13;25(1):103624. doi:10.1016/j.isci.2021.103624. PMID:35005560.

Smithers RL, Kao HKJ, Zeigler S, Yechikov S, Nolta JA, Chan JW, Chiamvimonvat N, Lieu DK. Making Heads or Tails of the Large Mammalian Sinoatrial Node Micro-Organization. Circ Arrhythm Electrophysiol. 2021 Dec;14(12):e010465. doi:10.1161/CIRCEP.121.010465. Epub 2021 Nov 19. PMID:34794338.

Thai PN, Miller CV, King MT, Schaefer S, Veech RL, Chiamvimonvat N, Bers DM, Dedkova EN. Ketone Ester D-β-Hydroxybutyrate-(R)-1,3 Butanediol Prevents Decline in Cardiac Function in Type 2 Diabetic Mice. J Am Heart Assoc. 2021 Oct 5;10(19):e020729. doi:10.1161/JAHA.120.020729. Epub 2021 Sep 29. PMID:34583524.

Zhang XD, Thai PN, Ren L, Perez Flores MC, Ledford HA, Park S, Lee JH, Sihn CR, Chang CW, Chen WC, Timofeyev V, Zuo J, Chan JW, Yamoah EN, Chiamvimonvat N. Prestin amplifies cardiac motor functions. Cell Rep. 2021 May 4;35(5):109097. doi:10.1016/j.celrep.2021.109097. PMID:33951436.

Ren L, Yu S, Xu W, Overton JL, Chiamvimonvat N, Thai PN. Lack of association of antihypertensive drugs with the risk and severity of COVID-19: A meta-analysis. J Cardiol. 2021 May;77(5):482-491. doi:10.1016/j.jjcc.2020.10.015. Epub 2020 Nov 2. PMID:33168337.

Shimkunas R, Hegyi B, Jian Z, Shaw JA, Kazemi-Lari MA, Mitra D, Leach JK, Li X, Jaradeh M, Balardi N, Chen YJ, Escobar AL, Baker AJ, Bossuyt J, Banyasz T, Chiamvimonvat N, Lam KS, Bers DM, Izu LT, Chen-Izu Y. Mechanical Load Regulates Excitation-Ca2+ Signaling-Contraction in Cardiomyocyte. Circ Res. 2021 Mar 19;128(6):772-774. doi:10.1161/CIRCRESAHA.120.318570. Epub 2021 Feb 19. PMID:33601939.

Yechikov S, Kao HKJ, Chang CW, Pretto D, Zhang XD, Sun YH, Smithers R, Sirish P, Nolta JA, Chan JW, Chiamvimonvat N, Lieu DK. NODAL inhibition promotes differentiation of pacemaker-like cardiomyocytes from human induced pluripotent stem cells. Stem Cell Res. 2020 Dec;49:102043. doi:10.1016/j.scr.2020.102043. Epub 2020 Oct 12. PMID:33128951.

Campbell KT, Silva EA. Biomaterial Based Strategies for Engineering New Lymphatic Vasculature. Adv Healthc Mater. 2020 Sep;9(18):e2000895. doi:10.1002/adhm.202000895. Epub 2020 Jul 30. PMID:32734721.