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Left Main & Coronary Bifurcation Summit (CBS) was founded in 2006 as a think tank dedicated to the treatment of left main and coronary bifurcation lesions. CBS aims to improve cardiological care by refreshing fundamental researches, clinical trials, yearly published guidelines, emerged ideas and case-based discussion.

Association and Affiliations
- Organized by
  
  Nanjing Heart Center
  
  Asian Bifurcation Club (ABC)
  
  Nanjing First Hospital, Nanjing Medical University
- Co-organized by
  
  Chinese Society of Cardiology (CSC)
  
  Capacity Building and Continuing Education Center,National Health and Family Planning Commission (CBCEC)
  
  American Society for Cardiovascular Angiography and Interventions (SCAI)
  
  Asian Heart Society (AHS)
Contact Us
- Registration Administration of Domestic Representatives
  
  Hongjuan Peng : +86-13913895477
  
  Haimei Xu +86-13914736846
  
  cbsnj@cbsmd.cn
- Registration Administration of Overseas Representatives
  
  Ling Lin : +86 (25) 52271398
  
  +86-13951884596
  
  cbs@cbsmd.cn
- Management of Challenging Cases
  
  Yingying Zhao :+86-13815408517
  
  sub@cbsmd.cn
Address

CBS2019 Congress Secretariat, Nanjing First Hospital, Building No.9 68# Changle Road, Nanjing, China

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Recommended Paper

Management of Acute Myocardial Infarction During the COVID-19 Pandemic

COVID-19 and Thrombotic or Thromboembolic Disease: Implications for Prevention, Antithrombotic Therapy, and Follow-up

CSC Expert Consensus on Principles of Clinical Management of Patients with Severe Emergent Cardiovascular Diseases during the COVID-19 Epidemic

ACC Clinical Bulletin Focuses on Cardiac Implications of Coronavirus (COVID-19)

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HOME | SCIENTIFIC LIBRARY | Congestive Heart Failure

Congestive Heart Failure

Can We Use the Intrinsic Left Ventricular Delay (QLV) to Optimize the Pacing Configuration for Cardiac Resynchronization Therapy With a Quadripolar Left Ventricular Lead? Empagliflozin, Health Status, and Quality of Life in Patients with Heart Failure and Preserved Ejection Fraction: The EMPEROR-Preserved Trial The multiple causes and treatments of heart failure: focus on genetic and molecular mechanisms and non-pharmacological interventions Criteria for Iron Deficiency in Patients With Heart Failure When and how to use SGLT2 inhibitors in patients with HFrEF or chronic kidney disease Myeloid-Derived Growth Factor Protects Against Pressure Overload–Induced Heart Failure by Preserving Sarco/Endoplasmic Reticulum Ca2+-ATPase Expression in Cardiomyocytes A population-based study of 92 clinically recognised risk factors for heart failure: co-occurrence, prognosis and preventive potential 2021 ACC/AHA Key Data Elements and Definitions for Heart Failure: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Data Standards (Writing Committee to Develop Clinical Data Standards for Heart Failure)

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Original Research2020 Dec 11;S1550-4131(20)30658-6.

JOURNAL：Cell Metab. Article Link

The pyruvate-lactate axis modulates cardiac hypertrophy and heart failure

AA Cluntun, R Badolia, SG Drakos et al. Keywords: LVAD; MCT4; MPC; VB124; cardiac metabolism; heart failure; hypertrophy; lactate; mitochondria; pyruvate

ABSTRACT

The metabolic rewiring of cardiomyocytes is a widely accepted hallmark of heart failure (HF). These metabolic changes include a decrease in mitochondrial pyruvate oxidation and an increased export of lactate. We identify the mitochondrial pyruvate carrier (MPC) and the cellular lactate exporter monocarboxylate transporter 4 (MCT4) as pivotal nodes in this metabolic axis. We observed that cardiac assist device-induced myocardial recovery in chronic HF patients was coincident with increased myocardial expression of the MPC. Moreover, the genetic ablation of the MPC in cultured cardiomyocytes and in adult murine hearts was sufficient to induce hypertrophy and HF. Conversely, MPC overexpression attenuated drug-induced hypertrophy in a cell-autonomous manner. We also introduced a novel, highly potent MCT4 inhibitor that mitigated hypertrophy in cultured cardiomyocytes and in mice. Together, we find that alteration of the pyruvate-lactate axis is a fundamental and early feature of cardiac hypertrophy and failure.

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