Bio

Bio


Dr. Kang is an interventional cardiologist who specializes in the treatment of structural heart disease. He has expertise in complex coronary interventions, transcatheter aortic and mitral valve replacements, transcatheter mitral valve repair, left atrial appendage occlusion, PFO/septal defect closure, alcohol septal ablation, and paravalvular leak closure.

A Bay Area native, he graduated from Stanford University and obtained his medical degree at Yale University. He came back to Stanford to train in internal medicine, cardiology, and interventional cardiology before completing an advanced structural interventions fellowship at Ford Hospital.

Clinical Focus


  • Interventional Cardiology
  • Structural Interventions
  • Cardiovascular Disease

Administrative Appointments


  • Clinical Assistant Professor, Stanford School of Medicine (2020 - Present)

Education & Certifications


  • Fellowship, Henry Ford Hospital, Structural Interventions (2020)
  • Fellowship, Stanford University, Interventional Cardiology (2019)
  • Fellowship, Stanford University, Cardiovascular Medicine (2018)
  • Residency, Stanford University, Internal Medicine (2015)
  • Internship, Stanford University, Internal Medicine (2013)
  • MD, Yale School of Medicine, Medicine (2012)
  • BS, Stanford University, Biological Sciences (2006)
  • Board Certification: American Board of Internal Medicine, Interventional Cardiology (2019)
  • Board Certification: American Board of Internal Medicine, Cardiovascular Disease (2018)
  • Board Certification: National Board of Echocardiography, Adult Comprehensive Echocardiography (2018)
  • Board Certification: American Board of Internal Medicine, Internal Medicine (2015)

Teaching

Graduate and Fellowship Programs


Publications

All Publications


  • A novel noninvasive method for remote heart failure monitoring: the EuleriAn video Magnification apPLications In heart Failure studY (AMPLIFY). NPJ digital medicine Abnousi, F., Kang, G., Giacomini, J., Yeung, A., Zarafshar, S., Vesom, N., Ashley, E., Harrington, R., Yong, C. 2019; 2: 80

    Abstract

    Current remote monitoring devices for heart failure have been shown to reduce hospitalizations but are invasive and costly; accurate non-invasive options remain limited. The EuleriAn Video Magnification ApPLications In Heart Failure StudY (AMPLIFY) pilot aimed to evaluate the accuracy of a novel noninvasive method that uses Eulerian video magnification. Video recordings were performed on the neck veins of 50 patients who were scheduled for right heart catheterization at the Palo Alto VA Medical Center. The recorded jugular venous pulsations were then enhanced by applying Eulerian phase-based motion magnification. Assessment of jugular venous pressure was compared across three categories: (1) physicians who performed bedside exams, (2) physicians who reviewed both the amplified and unamplified videos, and (3) direct invasive measurement of right atrial pressure from right heart catheterization. Motion magnification reduced inaccuracy of the clinician assessment of central venous pressure compared to the gold standard of right heart catheterization (mean discrepancy of -0.80cm H2O; 95% CI -2.189 to 0.612, p=0.27) when compared to both unamplified video (-1.84cm H2O; 95% CI -3.22 to -0.46, p=0.0096) and the bedside exam (-2.90cm H2O; 95% CI -4.33 to 1.40, p=0.0002). Major categorical disagreements with right heart catheterization were significantly reduced with motion magnification (12%) when compared to unamplified video (25%) or the bedside exam (27%). This novel method of assessing jugular venous pressure improves the accuracy of the clinical exam and may enable accurate remote monitoring of heart failure patients with minimal patient risk.

    View details for DOI 10.1038/s41746-019-0159-0

    View details for PubMedID 31453375

  • Expanding transcatheter aortic valve replacement into uncharted indications. The Korean journal of internal medicine Kang, G., Kim, J. B. 2018; 33 (3): 474–82

    Abstract

    Since the first-in-man transcatheter delivery of an aortic valve prosthesis in 2002, the landscape of aortic stenosis therapeutics has shifted dramatically. While initially restricted to non-surgical cases, progressive advances in transcatheter aortic valve replacement and our understanding of its safety and efficacy have expanded its use in intermediate and possibly low surgical risk patients. In this review, we explore the past, present, and future of transcatheter aortic valve replacement.

    View details for PubMedID 29551053

  • Neprilysin Inhibitors in Cardiovascular Disease. Current cardiology reports Kang, G., Banerjee, D. 2017; 19 (2): 16-?

    Abstract

    Mortality from heart failure remains high despite advances in medical therapy over the last three decades. Angiotensin receptor-neprilysin inhibitor (ARNI) combinations are the latest addition to the heart failure medical armamentarium, which is built on the cornerstone regimen of beta blockers, angiotensin converting enzyme (ACE) inhibitors/angiotensin receptor blockers, and aldosterone antagonists. Recent trial data have shown a significant mortality benefit from ARNIs, which, as of May 2016, have now received a class I recommendation for use in patients with heart failure and reduced ejection fraction from the major American and European cardiology societies.

    View details for DOI 10.1007/s11886-017-0827-0

    View details for PubMedID 28185171

  • Pulmonary artery pulsatility index predicts right ventricular failure after left ventricular assist device implantation. journal of heart and lung transplantation Kang, G., Ha, R., Banerjee, D. 2016; 35 (1): 67-73

    Abstract

    Right ventricular failure (RVF) is a major cause of morbidity and mortality after left ventricular assist device (LVAD) implantation. The pulmonary artery pulsatility index (PAPi) is a novel hemodynamic index that predicts RVF in the setting of myocardial infarction, although it has not been shown to predict RVF after LVAD implantation.We performed a retrospective, single-center analysis to examine the utility of the PAPi in predicting RVF and RV assist device (RVAD) implantation in 85 continuous-flow LVAD recipients. We performed a multivariate logistic regression analysis incorporating previously identified predictors of RVF after LVAD placement, including clinical and echocardiographic variables, to determine the independent effect of PAPi in predicting RVF or RVAD after LVAD placement.In this cohort, the mean PAPi was 3.4 with a standard deviation of 2.9. RVF occurred in 33% of patients, and 11% required a RVAD. Multivariate analysis, adjusting for age, blood urea nitrogen (BUN), and Interagency Registry for Mechanically Assisted Circulatory Support profile, revealed that higher PAPi was independently associated with a reduced risk of RVAD placement (odds ratio [OR], 0.30; 95% confidence interval [CI], 0.07-0.89). This relationship did not change significantly when echocardiographic measures were added to the analysis. Stratifying the analysis by the presence of inotropes during catheterization revealed that PAPi was more predictive of RVAD requirement when measured on inotropes (OR, 0.21; 95% CI, 0.02-0.97) than without (OR, 0.49; 95% CI, 0.01-1.94). Furthermore, time from catheterization to LVAD did not significantly affect the predictive value of the PAPi (maximum time, 6 months). Receiver operating characteristic curve analysis revealed that optimal sensitivity and specificity were achieved using a PAPi threshold of 2.0.In LVAD recipients, the PAPi is an independent predictor of RVF and the need for RVAD support after LVAD implantation. This index appears more predictive in patients receiving inotropes and was not affected by time from catheterization to LVAD in our cohort.

    View details for DOI 10.1016/j.healun.2015.06.009

    View details for PubMedID 26212656

  • In vivo cardiac reprogramming contributes to zebrafish heart regeneration NATURE Zhang, R., Han, P., Yang, H., Ouyang, K., Lee, D., Lin, Y., Ocorr, K., Kang, G., Chen, J., Stainier, D. Y., Yelon, D., Chi, N. C. 2013; 498 (7455): 497-?

    Abstract

    Despite current treatment regimens, heart failure remains the leading cause of morbidity and mortality in the developed world due to the limited capacity of adult mammalian ventricular cardiomyocytes to divide and replace ventricular myocardium lost from ischaemia-induced infarct. Hence there is great interest to identify potential cellular sources and strategies to generate new ventricular myocardium. Past studies have shown that fish and amphibians and early postnatal mammalian ventricular cardiomyocytes can proliferate to help regenerate injured ventricles; however, recent studies have suggested that additional endogenous cellular sources may contribute to this overall ventricular regeneration. Here we have developed, in the zebrafish (Danio rerio), a combination of fluorescent reporter transgenes, genetic fate-mapping strategies and a ventricle-specific genetic ablation system to discover that differentiated atrial cardiomyocytes can transdifferentiate into ventricular cardiomyocytes to contribute to zebrafish cardiac ventricular regeneration. Using in vivo time-lapse and confocal imaging, we monitored the dynamic cellular events during atrial-to-ventricular cardiomyocyte transdifferentiation to define intermediate cardiac reprogramming stages. We observed that Notch signalling becomes activated in the atrial endocardium following ventricular ablation, and discovered that inhibiting Notch signalling blocked the atrial-to-ventricular transdifferentiation and cardiac regeneration. Overall, these studies not only provide evidence for the plasticity of cardiac lineages during myocardial injury, but more importantly reveal an abundant new potential cardiac resident cellular source for cardiac ventricular regeneration.

    View details for DOI 10.1038/nature12322

    View details for Web of Science ID 000320929400055

    View details for PubMedID 23783515

  • Plasma BIN1 correlates with heart failure and predicts arrhythmia in patients with arrhythmogenic right ventricular cardiomyopathy HEART RHYTHM Hong, T., Cogswell, R., James, C. A., Kang, G., Pullinger, C. R., Malloy, M. J., Kane, J. P., Wojciak, J., Calkins, H., Scheinman, M. M., Tseng, Z. H., Ganz, P., De Marco, T., Judge, D. P., Shaw, R. M. 2012; 9 (6): 961-967

    Abstract

    Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a disorder involving diseased cardiac muscle. Bridging integrator 1 (BIN1) is a membrane-associated protein important to cardiomyocyte homeostasis and is downregulated in cardiomyopathy. We hypothesized that BIN1 could be released into the circulation and that blood-available BIN1 can provide useful data on the cardiac status of patients whose hearts are failing secondary to ARVC.To determine whether plasma BIN1 levels can be used to measure disease severity in patients with ARVC.We performed a retrospective cohort study of 24 patients with ARVC. Plasma BIN1 levels were assessed for their ability to correlate with cardiac functional status and predict ventricular arrhythmias.Mean plasma BIN1 levels were decreased in patients with ARVC with heart failure (15 ± 7 vs 60 ± 17 in patients without heart failure, P <.05; the plasma BIN1 level was 60 ± 10 in non-ARVC normal controls). BIN1 levels correlated inversely with number of previous ventricular arrhythmia (R = -.47; P <.05), and low BIN1 levels correctly classified patients with advanced heart failure or ventricular arrhythmia (receiver operator curve area under the curve of 0.88 ± 0.07). Low BIN1 levels also predicted future ventricular arrhythmias (receiver operator curve area under the curve of 0.89 ± 0.09). In a stratified analysis, BIN1 levels could predict future arrhythmias in patients without severe heart failure (n = 20) with an accuracy of 82%. In the 7 patients with ARVC with serial blood samples, all of whom had evidence of disease progression during follow-up, plasma BIN1 levels decreased significantly (a decrease of 63%; P <.05).Plasma BIN1 level seems to correlate with cardiac functional status and the presence or absence of sustained ventricular arrhythmias in a small cohort of patients with ARVC and can predict future ventricular arrhythmias.

    View details for DOI 10.1016/j.hrthm.2012.01.024

    View details for Web of Science ID 000304242900025

    View details for PubMedID 22300662

  • Foxn4 directly regulates tbx2b expression and atrioventricular canal formation GENES & DEVELOPMENT Chi, N. C., Shaw, R. M., De Val, S., Kang, G., Jan, L. Y., Black, B. L., Stainier, D. Y. 2008; 22 (6): 734-739

    Abstract

    Cardiac chamber formation represents an essential evolutionary milestone that allows for the heart to receive (atrium) and pump (ventricle) blood throughout a closed circulatory system. Here, we reveal a novel transcriptional pathway between foxn4 and tbx genes that facilitates this evolutionary event. We show that the zebrafish gene slipjig, which encodes Foxn4, regulates the formation of the atrioventricular (AV) canal to divide the heart. sli/foxn4 is expressed in the AV canal, and its encoded product binds to a highly conserved tbx2 enhancer domain that contains Foxn4- and T-box-binding sites, both necessary to regulate tbx2b expression in the AV canal.

    View details for DOI 10.1101/gad.1629408

    View details for Web of Science ID 000254083400007

    View details for PubMedID 18347092

  • Angiogenic role of LYVE-1-positive macrophages in adipose tissue CIRCULATION RESEARCH Cho, C., Koh, Y. J., Han, J., Sung, H., Lee, H. J., Morisada, T., Schwendener, R. A., Brekken, R. A., Kang, G., Oike, Y., Choi, T., Suda, T., Yoo, O., Koh, G. Y. 2007; 100 (4): E47-E57

    Abstract

    Here we report the discovery of a characteristic dense vascular network (DVN) in the tip portion of epididymal adipose tissue in adult mice. The DVN is formed by angiogenesis rather than by vasculogenesis, and has functional blood circulation. This DVN and its subsequent branching may provide a new functional route for adipogenesis. The recruitment, infiltration, and accumulation of bone marrow-derived LYVE-1(+) macrophages in the tip region are crucial for the formation of the DVN. Matrix metalloproteinases (MMPs) and the VEGF-VEGFR2 system are responsible not only for the formation of the DVN, but also for the recruitment and infiltration of LYVE-1(+) macrophages into the epididymal adipose tissue tip region. SDF-1, but not the MCP-1-CCR2 system, is a critical factor in recruitment and ongoing retention of macrophages in this area. We also demonstrate that the tip region of epididymal adipose tissue is highly hypoxic, and thus provides a microenvironment conducive to the high expression and enhanced activities of VEGF, VEGFR2, MMPs, and SDF-1 in autocrine and paracrine manners, to create an ideal niche for the recruitment, retention, and angiogenic action of macrophages. These findings shed light on the complex interplay between macrophage infiltration, angiogenesis, and adipogenesis in the tip region of adult epididymal adipose tissue, and provide novel insight into the regulation of alternative outgrowth of adipose tissue.

    View details for DOI 10.1161/01.RES.0000259564.92792.93

    View details for Web of Science ID 000244571600020

    View details for PubMedID 17272806

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