Bertram Pitt, Deepak L. Bhatt
doi : 10.1161/CIRCULATIONAHA.121.054442
Circulation. 2021;144:4–6
Elizabeth Jordan, Laiken Peterson, Tomohiko Ai, Babken Asatryan, Lucas Bronicki, Emily Brown, Rudy Celeghin, Matthew Edwards, Judy Fan, Jodie Ingles, Cynthia A. James, Olga Jarinova, Renee Johnson, Daniel P. Judge, Najim Lahrouchi, Ronald H. Lekanne Deprez, R. Thomas Lumbers, Francesco Mazzarotto, Argelia Medeiros Domingo, Rebecca L. Miller, Ana Morales, Brittney Murray, Stacey Peters, Kalliopi Pilichou, Alexandros Protonotarios, Christopher Semsarian, Palak Shah, Petros Syrris, Courtney Thaxton, J. Peter van Tintelen, Roddy Walsh, Jessica Wang, James Ware, Ray E. Hershberger
doi : 10.1161/CIRCULATIONAHA.120.053033
Circulation. 2021;144:7–19
Each of the cardiomyopathies, classically categorized as hypertrophic cardiomyopathy, dilated cardiomyopathy (DCM), and arrhythmogenic right ventricular cardiomyopathy, has a signature genetic theme. Hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy are largely understood as genetic diseases of sarcomere or desmosome proteins, respectively. In contrast, >250 genes spanning >10 gene ontologies have been implicated in DCM, representing a complex and diverse genetic architecture. To clarify this, a systematic curation of evidence to establish the relationship of genes with DCM was conducted.
Anjali Tiku Owens, Sharlene M. Day
doi : 10.1161/CIRCULATIONAHA.121.054961
Circulation. 2021;144:20–22
Adrian Wells, David Reeves, Lora Capobianco, Calvin Heal, Linda Davies, Anthony Heagerty, Patrick Doherty, Peter Fisher
doi : 10.1161/CIRCULATIONAHA.120.052428
Circulation. 2021;144:23–33
Depression and anxiety in cardiovascular disease are significant, contributing to poor prognosis. Unfortunately, current psychological treatments offer mixed, usually small improvements in these symptoms. The present trial tested for the first time the effects of group metacognitive therapy (MCT; 6 sessions) on anxiety and depressive symptoms when delivered alongside cardiac rehabilitation (CR).
Yuxuan Luo, Nan Jiang, Herman I. May, Xiang Luo, Anwarul Ferdous, Gabriele G. Schiattarella, Guihao Chen, Qinfeng Li, Chao Li, Beverly A. Rothermel, Dingsheng Jiang, Sergio Lavandero, Thomas G. Gillette, Joseph A. Hill
doi : 10.1161/CIRCULATIONAHA.120.052384
Circulation. 2021;144:34–51
Cardiac hypertrophy is an independent risk factor for heart failure, a leading cause of morbidity and mortality globally. The calcineurin/NFAT (nuclear factor of activated T cells) pathway and the MAPK (mitogen-activated protein kinase)/Erk (extracellular signal-regulated kinase) pathway contribute to the pathogenesis of cardiac hypertrophy as an interdependent network of signaling cascades. How these pathways interact remains unclear and few direct targets responsible for the prohypertrophic role of NFAT have been described.
Malik Bisserier, Prabhu Mathiyalagan, Shihong Zhang, Firas Elmastour, Peter Dorfmüller, Marc Humbert, Gregory David, Sima Tarzami, Thomas Weber, Frederic Perros, Yassine Sassi, Susmita Sahoo, Lahouaria Hadri
doi : 10.1161/CIRCULATIONAHA.120.047978
Circulation. 2021;144:52–73
Epigenetic mechanisms are critical in the pathogenesis of pulmonary arterial hypertension (PAH). Previous studies have suggested that hypermethylation of the BMPR2 (bone morphogenetic protein receptor type 2) promoter is associated with BMPR2 downregulation and progression of PAH. Here, we investigated for the first time the role of SIN3a (switch-independent 3a), a transcriptional regulator, in the epigenetic mechanisms underlying hypermethylation of BMPR2 in the pathogenesis of PAH.
Adam J. Nelson, Neha J. Pagidipati, Vanita R. Aroda, Matthew A. Cavender, Jennifer B. Green, Renato D. Lopes, Hussein Al-Khalidi, Tanya Gaynor, Lisa A. Kaltenbach, Julienne K. Kirk, Ildiko Lingvay, Melissa L. Magwire, Emily C. O’Brien, Jonathan Pak, Rodica Pop-Busui, Caroline R. Richardson, Monica Reed, Cagri Senyucel, Laura Webb, Darren K. McGuire, Christopher B. Granger
doi : 10.1161/CIRCULATIONAHA.121.053766
Circulation. 2021;144:74–84
Multiple sodium glucose cotransporter-2 inhibitors (SGLT-2i) and glucagon-like peptide-1 receptor agonists (GLP-1RA) have been shown to impart significant cardiovascular and kidney benefits, but are underused in clinical practice. Both SGLT-2i and GLP-1RA were first studied as glucose-lowering drugs, which may have impeded uptake by cardiologists in the wake of proven cardiovascular efficacy. Their significant effect on cardiovascular and kidney outcomes, which are largely independent of glucose-lowering effects, must drive a broader use of these drugs. Cardiologists are 3 times more likely than endocrinologists to see patients with both type 2 diabetes and cardiovascular disease, thus they are ideally positioned to share responsibility for SGLT-2i and GLP-1RA treatment with primary care providers. In order to increase adoption, SGLT-2i and GLP-1RA must be reframed as primarily cardiovascular and kidney disease risk-reducing agents with a side effect of glucose-lowering. Coordinated and multifaceted interventions engaging clinicians, patients, payers, professional societies, and health systems must be implemented to incentivize the adoption of these medications as part of routine cardiovascular and kidney care. Greater use of SGLT-2i and GLP-1RA will improve outcomes for patients with type 2 diabetes at high risk for cardiovascular and kidney disease.
Sami Viskin, Ibrahim Marai, Raphael Rosso
doi : 10.1161/CIRCULATIONAHA.121.054991
Circulation. 2021;144:85–89
Hokyou Lee, Yuichiro Yano, So Mi Jemma Cho, Hyeok-Hee Lee, Dong-Wook Kim, Donald M. Lloyd-Jones, Hyeon Chang Kim
doi : 10.1161/CIRCULATIONAHA.121.054212
Circulation. 2021;144:90–92
Jeffrey Willett, Stephan Achenbach, Fausto J. Pinto, Athena Poppas, Mitchell S.V. Elkind
doi : 10.1161/CIRCULATIONAHA.121.054369
Circulation. 2021;144:e1–e5
Yuping Li, Guangyu Lu
doi : 10.1161/CIRCULATIONAHA.121.054075
Circulation. 2021;144:e6–e7
Nicholas S. Hendren, James A. de Lemos, Justin L. Grodin
doi : 10.1161/CIRCULATIONAHA.121.054556
Circulation. 2021;144:e8–e9
doi : 10.1161/CIR.0000000000000997
Circulation. 2021;144:e10
doi : 10.1161/CIR.0000000000000998
Circulation. 2021;144:e11
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