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A Foot Soldier in Cardiac Metabolism: A Conversation With Heinrich Taegtmeyer, MD, DPhil
Maryjane Farr
doi : 10.1161/CIRCULATIONAHA.121.058019
Circulation. 2021;144:1659–1663
Energetic Basis for Exercise-Induced Pulmonary Congestion in Heart Failure With Preserved Ejection Fraction
Matthew K. Burrage, Moritz Hundertmark, Ladislav Valkovi?, William D. Watson, Jennifer Rayner, Nikant Sabharwal, Vanessa M. Ferreira, Stefan Neubauer, Jack J. Miller, Oliver J. Rider, and Andrew J.M. Lewis
doi : 10.1161/CIRCULATIONAHA.121.054858
Circulation. 2021;144:1664–1678
Transient pulmonary congestion during exercise is emerging as an important determinant of reduced exercise capacity in heart failure with preserved ejection fraction (HFpEF). We sought to determine whether an abnormal cardiac energetic state underpins this process.
Unmasking Nonpreserved Heart Structure, Function, and Energetics in Heart Failure With Preserved Ejection Fraction With Magnetic Resonance Imaging Coupled With Exercise
Jennifer E. Ho, Christopher Nguyen, and Gregory D. Lewis
doi : 10.1161/CIRCULATIONAHA.121.056974
Circulation. 2021;144:1679–1682
National Trends and Disparities in Hospitalization for Acute Hypertension Among Medicare Beneficiaries (1999–2019)
Yuan Lu, Yun Wang, Erica S. Spatz, Oyere Onuma, Khurram Nasir, Fatima Rodriguez, Karol E. Watson, and Harlan M. Krumholz
doi : 10.1161/CIRCULATIONAHA.121.057056
Circulation. 2021;144:1683–1693
In the past 2 decades, hypertension control in the US population has not improved and there are widening disparities. Little is known about progress in reducing hospitalizations for acute hypertension.
Loss of Mitochondrial Ca2+ Uniporter Limits Inotropic Reserve and Provides Trigger and Substrate for Arrhythmias in Barth Syndrome Cardiomyopathy
Edoardo Bertero, Alexander Nickel, Michael Kohlhaas, Mathias Hohl, Vasco Sequeira, Carolin Brune, Julia Schwemmlein, Marco Abeßer, Kai Schuh, Ilona Kutschka, Christopher Carlein, Kai Münker, Sarah Atighetchi, Andreas Müller, Andrey Kazakov, Reinhard Kappl, Karina von der Malsburg, Martin van der Laan, Anna-Florentine Schiuma, Michael Böhm, Ulrich Laufs, Markus Hoth, Peter Rehling, Michaela Kuhn, Jan Dudek, Alexander von der Malsburg, Leticia Prates Roma, and Christoph Maack
doi : 10.1161/CIRCULATIONAHA.121.053755
Circulation. 2021;144:1694–1713
Barth syndrome (BTHS) is caused by mutations of the gene encoding tafazzin, which catalyzes maturation of mitochondrial cardiolipin and often manifests with systolic dysfunction during early infancy. Beyond the first months of life, BTHS cardiomyopathy typically transitions to a phenotype of diastolic dysfunction with preserved ejection fraction, blunted contractile reserve during exercise, and arrhythmic vulnerability. Previous studies traced BTHS cardiomyopathy to mitochondrial formation of reactive oxygen species (ROS). Because mitochondrial function and ROS formation are regulated by excitation-contraction coupling, integrated analysis of mechano-energetic coupling is required to delineate the pathomechanisms of BTHS cardiomyopathy.
Altered Cardiac Energetics and Mitochondrial Dysfunction in Hypertrophic Cardiomyopathy
Sara Ranjbarvaziri, Kristina B. Kooiker, Mathew Ellenberger, Giovanni Fajardo, Mingming Zhao, Alison Schroer Vander Roest, Rahel A. Woldeyes, Tiffany T. Koyano, Robyn Fong, Ning Ma, Lei Tian, Gavin M. Traber, Frandics Chan, John Perrino, Sushma Reddy, Wah Chiu, Joseph C. Wu, Joseph Y. Woo, Kathleen M. Ruppel, James A. Spudich, Michael P. Snyder, Kévin Contrepois, and Daniel Bernstein
doi : 10.1161/CIRCULATIONAHA.121.053575
Circulation. 2021;144:1714–1731
Hypertrophic cardiomyopathy (HCM) is a complex disease partly explained by the effects of individual gene variants on sarcomeric protein biomechanics. At the cellular level, HCM mutations most commonly enhance force production, leading to higher energy demands. Despite significant advances in elucidating sarcomeric structure–function relationships, there is still much to be learned about the mechanisms that link altered cardiac energetics to HCM phenotypes. In this work, we test the hypothesis that changes in cardiac energetics represent a common pathophysiologic pathway in HCM.
Cardiovascular Benefit of Lowering Low-Density Lipoprotein Cholesterol Below 40 mg/dL
Nicholas A. Marston, Robert P. Giugliano, Jeong-Gun Park, Andrea Ruzza, Peter S. Sever, Anthony C. Keech, and Marc S. Sabatine
doi : 10.1161/CIRCULATIONAHA.121.056536
Circulation. 2021;144:1732–1734
Letter by Naeije Regarding Article, “Oxygen Pathway Limitations in Patients With Chronic Thromboembolic Pulmonary Hypertension”
Robert Naeije
doi : 10.1161/CIRCULATIONAHA.121.055607
Circulation. 2021;144:e328–e329
Response by Howden et al to Letter Regarding Article, “Oxygen Pathway Limitations in Patients With Chronic Thromboembolic Pulmonary Hypertension”
Erin J. Howden, Sergio Ruiz-Carmona, André La Gerche, Marion Delcroix, and Guido Claessen
doi : 10.1161/CIRCULATIONAHA.121.056806
Circulation. 2021;144:e330–e331
Retraction of: Abstract 03: High-Dose Intranasal Insulin During CPR Improves Neurological Outcomes in a Rat Model of Cardiac Arrest
doi : 10.1161/CIR.0000000000001036
Circulation. 2021;144:e332
Correction to: National Trends and Disparities in Hospitalization for Acute Hypertension Among Medicare Beneficiaries (1999–2019)
doi : 10.1161/CIR.0000000000001044
Circulation. 2021;144:e333
