About

Nipavan Chiamvimonvat is a Professor and Chair of Basic Medical Sciences at the University of Arizona College of Medicine – Phoenix. His research interests include cardiac arrhythmia disorders and cardiovascular diseases. He is involved in advancing understanding and treatment of these conditions through his work in basic medical sciences.

Research topics

• Biology
• Medicine
• Internal medicine
• Genetics
• Endocrinology
• Anatomy
• Engineering
• Neuroscience
• Electronic engineering
• Pathology
• Biophysics
• Immunology
• Materials science
• Nanotechnology
• Cell biology
• Optics
• Physics

Selected publications

• Metabolic Perturbation Exacerbates Sinoatrial Node Dysfunction in Heart Failure

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-02-10

  articleOpen access

  SUMMARY Heart failure (HF) affects approximately 6.2 million people in the United States, with a 5-year mortality exceeding 50%. Bradyarrhythmia, a known complication in HF due to sinoatrial node (SAN) dysfunction (SAND), increases the morbidity and mortality of HF patients. Insights into the mechanistic underpinnings of SAND in HF could therefore uncover vital therapeutic targets to improve clinical outcomes. The SAN cells are endowed with a dense mitochondrial network crucial for sustaining their pacemaking function on a beat-to-beat basis. We have previously demonstrated significant disruptions in the mitochondrial-sarcoplasmic reticulum connectomics, resulting in abnormal mitochondrial Ca 2+ handling and impaired mitochondrial function in HF. Here, we hypothesize that the metabolic perturbation is one of the critical mechanisms underlying SAND. To this end, we took advantage of a multi-omics approach combined with ultra-resolution imaging and functional analyses to decipher the metabolic shift that transpires in the HF SAN. Our findings revealed significant metabolic remodeling within the SAN mitochondria in HF, with a diminished reliance on fatty acid β-oxidation, enhanced utilization of ketone bodies, and heightened dependence on carbohydrate catabolism. Notably, metabolomics analyses identified the pronounced increase of glucosylceramides and ceramides as one of the mechanisms leading to mitochondrial dysfunction. We directly test this hypothesis and demonstrate that ceramides induce a dose-dependent metabolic shift from oxidative phosphorylation to glycolysis. Importantly, these alterations lead to a significant impairment in SAN automaticity in a dose-dependent manner. Collectively, the findings support the notion that ceramides are not only markers of metabolic derangement, but also active mediators of mitochondrial and metabolic dysfunction in the SAN. Overall, the study provides evidence that ceramides may be a potential therapeutic target for mitigating SAND in HF.

  PublisherOA PDFDOI

• BS-534527-003 CPNE5 IS NECESSARY FOR NORMAL SINOATRIAL NODE FUNCTION BY REGULATING CALCIUM HOMEOSTASIS

  Heart Rhythm · 2026-04-01

  article
  PublisherDOI

• Ro5‐4864, a ligand of the mitochondrial translocator protein, protects against heart failure in mice via regulation of the p62‐Keap1‐Nrf2 axis

  The Journal of Physiology · 2026-04-04

  articleOpen access

  Abstract The 18‐kDa mitochondrial translocator protein (TSPO) has been shown to modulate mitochondrial function and the cardiac response to pressure overload. We have previously shown that conditional knockout of TSPO limited the development of heart failure in the murine model of transverse aortic constriction (TAC). In this study, we hypothesized that similar protection could be achieved by a ligand of TSPO, Ro5‐4864 (Ro5), in an in‐vivo model of pressure‐overload induced heart failure. To test this hypothesis, C57/BL6J mice had TAC or sham surgery, with daily 0.1 mg/kg Ro5 or saline intra‐peritoneal injection for 8 weeks, with echocardiographic measurement of left ventricular (LV) size and function. Cardiac tissue protein expression was then analyzed by LC/MS. Markers of inflammation were quantified via western blot. Isolated murine cardiomyocytes were co‐treated with 25 µM H 2 O 2 and 2.5 µg Ro5 to investigate oxidative stress. The results of these experiments showed that Ro5‐4864 significantly prevented the TAC‐induced decline in LV function, as well as the associated increases in natriuretic peptide A and collagen alpha‐1 (XII) expression observed in saline‐treated animals. Ro5‐4864 also reduced oxidative stress and activated the Nrf2 pathway, likely due to decreased p62 accumulation secondary to enhanced mitophagy and restoration of autophagic flux. These in vivo findings were supported by complementary in vitro experiments in cardiomyocytes, where Ro5 attenuated oxidative stress induced by exogenous H 2 O 2 . In conclusion, these results indicate that Ro5‐4864 mitigates the development of pressure overload induced heart failure in mice, suggesting that pharmacologic modulation of the TSPO represents a promising therapeutic strategy for the prevention or treatment of heart failure. image Key points This study employed Ro5‐4864, a ligand of the mitochondrial translocator protein (TSPO), to test the hypothesis that pharmacologic inhibition of TSPO could limit the development of heart failure in a murine model of transverse aortic constriction (TAC). Ro5‐4864 preserved left ventricular function after TAC and limited the biochemical markers of heart failure and fibrosis. Proteomic analysis showed a significant effect of Ro5 on markers of immune activation, oxidative stress and inflammation. Ro5‐4864 increased the expression of Nrf2, a transcription factor that induces cytoprotective proteins such as NQO1 and SOD2, coupled with regulators of Nrf2 such as p62 and Keap1. These data establish a foundation for further development of anti‐inflammatory interventions in heart failure.

  PublisherDOI

• B-type natriuretic peptide changes and left ventricular remodeling dynamics in heart failure with reduced ejection fraction

  Frontiers in Cardiovascular Medicine · 2026-01-08 · 1 citations

  articleOpen access

  Background B-type natriuretic peptide (BNP) is an important biomarker in heart failure with reduced ejection fraction (HFrEF). We aimed to explore changes in BNP and their relationship with long-term dynamics of left ventricular (LV) geometry. Methods This was a single-center retrospective cohort. Inclusion criteria included LV ejection fraction (LVEF) < 40% measured by echocardiography, BNP ≥100 pg/mL at baseline, and a subsequent BNP measure within a year. Percent BNP change from baseline was computed and divided into tertiles. Percent change tertiles represented decreasing (min—max, −63.3 to −10.4), minimal changes (−10.4 to 2.8), and rising BNP levels (2.9 to 12.6). The study endpoint included LV internal dimension at end-systole (LVIDs), LV internal dimension at end-diastole (LVIDd), and LVEF. The secondary endpoint consisted of all-cause mortality. Results A total of 887 patients were included. Baseline characteristics, including age, sex, blood pressure, atrial fibrillation, baseline BNP, and LVEF, varied among tertiles ( p < 0.05). When comparing to the rising BNP tertile, the decreasing BNP tertile showed decreased trends of LVIDs ( p = 0.001), LVIDd ( p = 0.006); and increased trends of LVEF ( p = 0.008). All-cause mortality was higher in the rising BNP tertile ( p < 0.05) compared to the decreasing tertile. Conclusion In a real-world routine HFrEF cohort, this study demonstrates the time-dependent relationship between BNP changes, LV remodeling dynamics, and survival outcomes. Findings contribute to the literature supporting BNP as a dynamic marker for LV remodeling.

  PublisherOA PDFDOI

• Regulation of cardiac pacemaking activities in health and disease

  The Journal of Physiology · 2026-04-29 · 1 citations

  articleSenior author

  Abstract The human heart beats 60–80 times a minute, which can amount to more than 3 billion heartbeats in one's lifetime. Each heartbeat is initiated by the sinoatrial node (SAN), a highly complex structure consisting of specialized cells that spontaneously fire action potentials (APs), propagating throughout the heart. Its automaticity is orchestrated by ion channels and transporters that contribute to the membrane and Ca 2+ clocks, collectively known as the ‘coupled clock’. Their activity is tightly regulated by autonomic and hormonal signalling pathways, most prominently β‐adrenergic receptor (β‐AR) signalling, which increases heart rate via activation of adenylyl cyclase (AC) and subsequent production of 3′,5′‐cyclic adenosine monophosphate (cAMP). In contrast, parasympathetic signalling through muscarinic M 2 receptors reduces cAMP levels and activates inwardly rectifying K + currents, thereby slowing pacemaker activity. The current topical review discusses recent literature encompassing the mechanisms of SAN regulation in health and disease, including cardiac arrhythmia syndrome such as catecholaminergic polymorphic ventricular arrhythmia, autoimmune cardiac ion channelopathies, and SAN dysfunction in heart failure (HF). SAN dysfunction in HF frequently manifests as bradyarrhythmia, a complication that significantly increases the morbidity and mortality of HF patients and confers an increased risk of sudden cardiac death. Recent studies support the previously unrecognized roles of mitochondrial–sarcoplasmic reticulum connectomics in SAN dysfunction commonly seen with HF. In addition, the roles of distinct AC isoforms that are preferentially expressed and compartmentalized in the SAN to serve a specialized function will be discussed. Finally, the review will consider recent advances in the development of biological pacemakers. image

  PublisherDOI

• Phosphoinositide Depletion and Compensatory Phospho-Signaling in Angiotensin II-Induced Heart Disease

  Circulation Research · 2026-03-20 · 1 citations

  articleOpen access

  BACKGROUND: Contractile dysfunction, hypertrophy, and cell death during heart failure are linked to altered Ca 2+ handling and elevated levels of the hormone AngII (angiotensin II), which signals through G q (Guanine nucleotide-binding protein alpha subunit q)-coupled AT 1 Rs (AngII type 1 receptors), initiating hydrolysis of phosphatidylinositol (4,5)-bisphosphate. Chronic elevation of AngII contributes to cardiac pathology, but the mechanisms linking sustained AngII signaling to heart dysfunction remain incompletely understood. Here, we demonstrate that chronic AngII exposure profoundly disrupts cardiac phosphoinositide homeostasis, triggering a cascade of cellular adaptations that ultimately impair cardiac function. METHODS: Mice received 1-week infusions of AngII, bisperoxovanadium (1,10 phenanthroline), both, or saline via osmotic minipumps. We used mass spectrometry, super-resolution microscopy, electrophysiology, confocal imaging, immunoblot, echocardiography, and histology to assess phosphoinositide levels, L-type voltage-gated calcium channel Ca V 1.2 localization, Ca 2+ handling, protein phosphorylation, cardiac function, and fibrosis. RESULTS: Chronic AngII infusion caused widespread phosphoinositide imbalance, reducing phosphatidylinositol, phosphatidylinositol phosphate, phosphatidylinositol bisphosphate, and phosphatidylinositol (3,4,5)-trisphosphate levels. Ca V 1.2 channels were partially redistributed from t-tubules to endosomal compartments. Despite reduced sarcolemmal channel expression, Ca 2+ currents and transients were maintained through enhanced PKA (protein kinase A)–mediated and CaMKII (Ca 2+ /calmodulin-dependent protein kinase II)–mediated phosphorylation of Ca 2+ -handling proteins. However, this compensation proved insufficient as cardiac function progressively declined, marked by pathological hypertrophy, t-tubule disruption, and diastolic dysfunction. PTEN (phosphatase and tensin homolog) inhibition preserved Akt signaling and protected against cardiac dysfunction and fibrosis without preventing cellular remodeling or altered calcium handling. CONCLUSIONS: These findings reveal a complex interplay between phosphoinositide signaling, ion channel trafficking, and compensatory phospho-regulation in AngII-induced cardiac pathology. We establish phosphatidylinositol (3,4,5)-trisphosphate depletion as a critical link between chronic AngII signaling and cardiac dysfunction. The dissociation between persistent cellular remodeling and preserved organ function with PTEN inhibition reveals that cardioprotection occurs primarily through reduced fibrosis. PTEN inhibition, thus, emerges as a promising therapeutic strategy for heart failure associated with pathological renin-angiotensin system activation, with potential to complement existing therapies by targeting antifibrotic responses.

  PublisherDOI

• Deep Learning Echocardiographic Trajectories of Heart Failure With Preserved Ejection Fraction

  JACC Advances · 2026-03-18

  articleOpen access

  BACKGROUND: Heart failure with preserved ejection fraction (HFpEF) is a dynamic chronic disease. Specific disease trajectories remain unclear. OBJECTIVES: This study aims to investigate cardiac structure and function trajectories measured by echocardiography and their relationship with clinical outcomes. METHODS: This was a retrospective cohort from a single center of HFpEF patients with follow-up echocardiogram at ≥ 1 year. Seven longitudinal echocardiographic variables of cardiac geometry and function were utilized to identify trajectory. Longitudinal phenomapping analysis was conducted with machine and deep learning longitudinal clustering. The primary outcome was all-cause mortality, while the secondary outcome consisted of changes in B-type natriuretic peptide levels overtime. A panel of longitudinal laboratory biomarkers was used for exploratory outcomes. RESULTS: In total, 1,626 HFpEF cases were included; training and validation sets were randomly derived. Echocardiographic trajectories were identified: Echo-Trajectory #1, a stable remodeling trajectory; Echo-Trajectory #2, an increased remodeling course; and Echo-Trajectory #3, decreased remodeling trajectory with right ventricular dysfunction. Baseline clinical characteristics varied significantly among Echo-Trajectories by sex, age, blood pressure, obesity, comorbidities, and left ventricular mass index (P < 0.05). Compared to Echo-Trajectories #2 and #3, Trajectory #1 had a better all-cause mortality outcome (P < 0.001). Similarly, Echo-Trajectory #1 presented favorable trajectories of natriuretic peptides, sodium, and renal function (P < 0.05). CONCLUSIONS: Longitudinal phenomapping resulted in echocardiographic trajectories of cardiac structure and function with different clinical, laboratory, and survival characteristics. HFpEF is a dynamic condition, and longitudinal phenomapping may improve trajectory characterization and guide treatment strategies.

  PublisherDOI

• BPS2026 - PIP2 activates SK channels by a similar mechanism across all known isoforms

  Biophysical Journal · 2026-02-01

  article
  PublisherDOI

• PO-04-253 A NEURAL CONTROLLED DIFFERENTIAL EQUATION AND GRAPH FUSION FRAMEWORK FOR AFIB OUTCOME PREDICTION

  Heart Rhythm · 2026-04-01

  articleOpen access
  PublisherOA PDFDOI

• BPS2026 – De novo design of ion channel modulators using deep learning for therapeutic applications

  Biophysical Journal · 2026-02-01

  article
  PublisherDOI

Recent grants

• NIH Grant R13HL139086

  NIH · $30k · 2019

• NIH Grant I01BX000576

  NIH · 2020

• Metabolomics study in patients post myocardial infarction

  NIH · 2017–2023

• NIH Grant R01HL075274

  NIH · $1.5M · 2009

• Decoding the enigma of cardiac amplification

  NIH · $2.2M · 2017–2023

Frequent coauthors

• Valeriy Timofeyev

  University of California, Davis

  162 shared

• Padmini Sirish

  University of California, Davis

  108 shared

• Phung N. Thai

  University of California, Davis

  102 shared

• Ebenezer N. Yamoah

  University of Nevada, Reno

  96 shared

• Xiao-Dong Zhang

  76 shared

• Anil Singapuri

  University of California, Davis

  68 shared

• Ling Lü

  Nanjing Normal University

  66 shared

• Lu Ren

  Second Xiangya Hospital of Central South University

  65 shared

Education

• Doctor of Medicine

  University of Toronto

  1984