In Patients With Recently Diagnosed Atrial Fibrillation, Think Anticoagulation and Rhythm Control

Paulus Kirchhof

doi : 10.1161/CIRCULATIONAHA.121.055163

Circulation. 2021;144:1587–1589

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Persistent Opioid Use After Cardiac Implantable Electronic Device Procedures

Timothy M. Markman, Chase R. Brown, Lin Yang, Gustavo S. Guandalini, Matthew C. Hyman, Jeffrey S. Arkles, Pasquale Santangeli, Robert D. Schaller, Gregory E. Supple, Rajat Deo, Saman Nazarian, Sanjay Dixit, David J. Callans, Andrew E. Epstein, Francis E. Marchlinski, Peter W. Groeneveld, and David S. Frankel

doi : 10.1161/CIRCULATIONAHA.121.055524

Circulation. 2021;144:1590–1597

Prescription opioids are a major contributor to the ongoing epidemic of persistent opioid use (POU). The incidence of POU among opioid-naïve patients after cardiac implantable electronic device (CIED) procedures is unknown.

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The Opioid Epidemic: Everyone Has a Role to Play

Enas S. Kandil

doi : 10.1161/CIRCULATIONAHA.121.056230

Circulation. 2021;144:1598–1599

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Phenotypic Expression, Natural History, and Risk Stratification of Cardiomyopathy Caused by Filamin C Truncating Variants

Marta Gigli, Davide Stolfo, Sharon L. Graw, Marco Merlo, Caterina Gregorio, Suet Nee Chen, Matteo Dal Ferro, Alessia PaldinoMD, Giulia De Angelis, Francesca Brun, Jean Jirikowic, Ernesto E. Salcedo, Sylvia Turja, Diane Fatkin, Renee Johnson, J. Peter van Tintelen, Anneline S.J.M. Te Riele, Arthur A.M. Wilde, Neal K. Lakdawala, Kermshlise Picard, Daniela Miani, Daniele Muser, Giovanni Maria Severini, Hugh Calkins, Cynthia A. James, Brittney Murray, Crystal Tichnell, Victoria N. Parikh, Euan A. Ashley, Chloe Reuter, Jiangping Song, Daniel P. Judge, William J. McKenna, Matthew R.G. Taylor, Gianfranco Sinagra, and Luisa Mestroni

doi : 10.1161/CIRCULATIONAHA.121.053521

Circulation. 2021;144:1600–1611

Filamin C truncating variants (FLNCtv) cause a form of arrhythmogenic cardiomyopathy: the mode of presentation, natural history, and risk stratification of FLNCtv remain incompletely explored. We aimed to develop a risk profile for refractory heart failure and life-threatening arrhythmias in a multicenter cohort of FLNCtv carriers.

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Interferon-? Impairs Human Coronary Artery Endothelial Glucose Metabolism by Tryptophan Catabolism and Activates Fatty Acid Oxidation

Laurel Yong-Hwa Lee, William M. Oldham, Huamei He, Ruisheng Wang, Ryan Mulhern, Diane E. Handy, and Joseph Loscalzo

doi : 10.1161/CIRCULATIONAHA.121.053960

Circulation. 2021;144:1612–1628

Endothelial cells depend on glycolysis for much of their energy production. Impaired endothelial glycolysis has been associated with various vascular pathobiologies, including impaired angiogenesis and atherogenesis. IFN-? (interferon-?)–producing CD4+ and CD8+ T lymphocytes have been identified as the predominant pathological cell subsets in human atherosclerotic plaques. Although the immunologic consequences of these cells have been extensively evaluated, their IFN-?–mediated metabolic effects on endothelial cells remain unknown. The purpose of this study was to determine the metabolic consequences of the T-lymphocyte cytokine, IFN-?, on human coronary artery endothelial cells.

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Palmdelphin Regulates Nuclear Resilience to Mechanical Stress in the Endothelium

Miguel Sáinz-Jaspeado, Ross O. Smith, Oscar Plunde, Sven-Christian Pawelzik, Yi Jin, Sofia Nordling, Yindi Ding, Pontus Aspenström, Marie Hedlund, Giulia Bastianello, Flora Ascione, Qingsen Li, Cansaran Saygili Demir, Dinesh Fernando, Geoffrey Daniel, Anders Franco-Cereceda, Jeffrey Kroon, Marco Foiani, Tatiana V. Petrova, Manfred W. Kilimann, Magnus Bäck, and Lena Claesson-Welsh

doi : 10.1161/CIRCULATIONAHA.121.054182

Circulation. 2021;144:1629–1645

PALMD (palmdelphin) belongs to the family of paralemmin proteins implicated in cytoskeletal regulation. Single nucleotide polymorphisms in the PALMD locus that result in reduced expression are strong risk factors for development of calcific aortic valve stenosis and predict severity of the disease.

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Inflammation and Immune Response in Arrhythmogenic Cardiomyopathy: State-of-the-Art Review

Babken Asatryan, Angeliki Asimaki, Andrew P. Landstrom, Mohammed Y. Khanji, Katja E. Odening, Leslie T. Cooper, Francis E. Marchlinski, Anna R. Gelzer, Christopher Semsarian, Tobias Reichlin, Anjali T. Owens, and C. Anwar A. Chahal

doi : 10.1161/CIRCULATIONAHA.121.055890

Circulation. 2021;144:1646–1655

Arrhythmogenic cardiomyopathy (ACM) is a primary disease of the myocardium, predominantly caused by genetic defects in proteins of the cardiac intercalated disc, particularly, desmosomes. Transmission is mostly autosomal dominant with incomplete penetrance. ACM also has wide phenotype variability, ranging from premature ventricular contractions to sudden cardiac death and heart failure. Among other drivers and modulators of phenotype, inflammation in response to viral infection and immune triggers have been postulated to be an aggravator of cardiac myocyte damage and necrosis. This theory is supported by multiple pieces of evidence, including the presence of inflammatory infiltrates in more than two-thirds of ACM hearts, detection of different cardiotropic viruses in sporadic cases of ACM, the fact that patients with ACM often fulfill the histological criteria of active myocarditis, and the abundance of anti–desmoglein-2, antiheart, and anti-intercalated disk autoantibodies in patients with arrhythmogenic right ventricular cardiomyopathy. In keeping with the frequent familial occurrence of ACM, it has been proposed that, in addition to genetic predisposition to progressive myocardial damage, a heritable susceptibility to viral infections and immune reactions may explain familial clustering of ACM. Moreover, considerable in vitro and in vivo evidence implicates activated inflammatory signaling in ACM. Although the role of inflammation/immune response in ACM is not entirely clear, inflammation as a driver of phenotype and a potential target for mechanism-based therapy warrants further research. This review discusses the present evidence supporting the role of inflammatory and immune responses in ACM pathogenesis and proposes opportunities for translational and clinical investigation.

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Association Between Sarcomeric Variants in Hypertrophic Cardiomyopathy and Myocardial Oxygenation: Insights From a Novel Oxygen-Sensitive Cardiovascular Magnetic Resonance Approach

Betty Raman, Elizabeth M. Tunnicliffe, Kenneth Chan, Rina Ariga, Moritz Hundertmark, Eric O. Ohuma, Sanjay Sivalokanathan, Yi Jie Gifford Tan, Masliza Mahmod, Aaron T. Hess, Theodoros D. Karamitsos, Joseph Selvanayagam, Michael Jerosch-Herold, Hugh Watkins, and Stefan Neubauer

doi : 10.1161/CIRCULATIONAHA.121.054015

Circulation. 2021;144:1656–1658

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Letter by Lai et al Regarding Article, “Cardiovascular Risk Factor Trajectories Since Childhood and Cognitive Performance in Midlife: The Cardiovascular Risk in Young Finns Study”

Yuhui Lai, Xiaodong Zhuang, and Xinxue Liao

doi : 10.1161/CIRCULATIONAHA.121.055853

Circulation. 2021;144:e307

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Response by Hakala et al to Letter Regarding Article, “Cardiovascular Risk Factor Trajectories Since Childhood and Cognitive Performance in Midlife: The Cardiovascular Risk in Young Finns Study”

Juuso O. Hakala, Olli T. Raitakari, and Suvi P. Rovio

doi : 10.1161/CIRCULATIONAHA.121.056807

Circulation. 2021;144:e308–e309

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Systems of Care for ST-Segment–Elevation Myocardial Infarction: A Policy Statement From the American Heart Association

Alice K. Jacobs, Murtuza J. Ali, Patricia J. Best, Mark C. Bieniarz, Vincent J. Bufalino, William J. French, Timothy D. Henry, Lori Hollowell, Edward C. Jauch, Michael C. Kurz, Michael Levy, Puja Patel, Travis Spier, R. Harper Stone, Katie L. Tataris, Randal J. Thomas, Jessica K. Zègre-Hemsey, on behalf of the American Heart Association Advocacy Coordinating Committee

doi : 10.1161/CIR.0000000000001025

Circulation. 2021;144:e310–e327

The introduction of Mission: Lifeline significantly increased timely access to percutaneous coronary intervention for patients with ST-segment–elevation myocardial infarction (STEMI). In the years since, morbidity and mortality rates have declined, and research has led to significant developments that have broadened our concept of the STEMI system of care. However, significant barriers and opportunities remain. From community education to 9-1-1 activation and emergency medical services triage and from emergency department and interfacility transfer protocols to postacute care, each critical juncture presents unique challenges for the optimal care of patients with STEMI. This policy statement sets forth recommendations for how the ideal STEMI system of care should be designed and implemented to ensure that patients with STEMI receive the best evidence-based care at each stage in their illness.

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