Christopher Z. Lam, Aliya Gulamhusein, and Rachel M. Wald
doi : 10.1161/CIRCULATIONAHA.121.057431
Circulation. 2021;144:1977–1980
Baris Gencer, Luc Djousse, Omar T. Al-Ramady, Nancy R. Cook, JoAnn E. Manson, and Christine M. Albert
doi : 10.1161/CIRCULATIONAHA.121.055654
Circulation. 2021;144:1981–1990
Some, but not all, large-scale randomized controlled trials (RCTs) investigating the effects of marine ?-3 fatty acids supplementation on cardiovascular outcomes have reported increased risks of atrial fibrillation (AF). The potential reasons for disparate findings may be dose-related.
Michelle Samuel and Stanley Nattel
doi : 10.1161/CIRCULATIONAHA.121.057464
Circulation. 2021;144:1991–1994
Anders Sjørslev Schmidt, Kasper Glerup Lauridsen, Dorthe Svenstrup Møller, Per Dahl Christensen, Karen Kaae Dodt, Hans Rickers, Bo Løfgren, and Andi Eie Albertsen
doi : 10.1161/CIRCULATIONAHA.121.056301
Circulation. 2021;144:1995–2003
Smaller randomized studies have reported conflicting results regarding the optimal electrode position for cardioverting atrial fibrillation. However, anterior–posterior electrode positioning is widely used as a standard and believed to be superior to anterior–lateral electrode positioning. Therefore, we aimed to compare anterior–lateral and anterior–posterior electrode positioning for cardioverting atrial fibrillation in a multicenter randomized trial.
Shaohua Zhang, Yan Li, Xiuzhen Huang, Kuo Liu, Qing-Dong Wang, Alex F. Chen, Kun Sun, Kathy O. Lui, and Bin Zhou
doi : 10.1161/CIRCULATIONAHA.121.055417
Circulation. 2021;144:2004–2020
Cardiac fibrosis is a lethal outcome of excessive formation of myofibroblasts that are scar-forming cells accumulated after heart injury. It has been reported that cardiac endothelial cells (ECs) contribute to a substantial portion of myofibroblasts through endothelial to mesenchymal transition (EndoMT). Recent lineage tracing studies demonstrate that myofibroblasts are derived from the expansion of resident fibroblasts rather than from the transdifferentiation of ECs. However, it remains unknown whether ECs can transdifferentiate into myofibroblasts reversibly or EndoMT genes were just transiently activated in ECs during cardiac fibrosis.
Javier Barallobre-Barreiro, Tamás Radovits, Marika Fava, Ursula Mayr, Wen-Yu Lin, Elizaveta Ermolaeva, Diego Martínez-López, Eric L. Lindberg, Elisa Duregotti, László Daróczi, Maria Hasman, Lukas E. Schmidt, Bhawana Singh, Ruifang Lu, Ferheen Baig, Aleksandra Malgorzata Siedlar, Friederike Cuello, Norman Catibog, Konstantinos Theofilatos, Ajay M. Shah, Maria G. Crespo-Leiro, Nieves Doménech, Norbert Hübner, Béla Merkely, and Manuel Mayr
doi : 10.1161/CIRCULATIONAHA.121.055732
Circulation. 2021;144:2021–2034
Remodeling of the extracellular matrix (ECM) is a hallmark of heart failure (HF). Our previous analysis of the secretome of murine cardiac fibroblasts returned ADAMTS5 (a disintegrin and metalloproteinase with thrombospondin motifs 5) as one of the most abundant proteases. ADAMTS5 cleaves chondroitin sulfate proteoglycans such as versican. The contribution of ADAMTS5 and its substrate versican to HF is unknown.
Bridget M. Kuehn
doi : 10.1161/CIRCULATIONAHA.121.058471
Circulation. 2021;144:2035–2037
Tracy Hampton
doi : 10.1161/CIRCULATIONAHA.121.058474
Circulation. 2021;144:2038–2039
Andrés F. Miranda-Arboleda, Shireen Mohammad, and Adrian Baranchuk
doi : 10.1161/CIRCULATIONAHA.121.058181
Circulation. 2021;144:2040–2042
Masaki Nii, Ryo Inuzuka, Kei Inai, Eriko Shimada, Tokuko Shinohara, Tomomi Kogiso, Hiroshi Ono, Shinichi Ootsuki, Yoshihiko Kurita, Atsuhito Takeda, Keiichi Hirono, Kota Takei, Satoshi Yasukochi, Tadahiro Yoshikawa, Yoshiyuki Furutani, Tomohiro Shinozaki, Yutaka Matsuyama, Hideaki Senzaki, Katsutoshi Tokushige, and Toshio Nakanishi
doi : 10.1161/CIRCULATIONAHA.121.056870
Circulation. 2021;144:2043–2045
Vlad G. Zaha, Salim S. Hayek, Kevin M. Alexander, Theresa M. Beckie, W. Gregory Hundley, Lavanya Kondapalli, Bonnie Ky, Kasey J. Leger, Wouter C. Meijers, Javid J. Moslehi, Svati H. Shah, on behalf of the American Heart Association Cardio-Oncology Subcommittee of the Council on Clinical Cardiology; and Council on Genomic and Precision Medicine
doi : 10.1161/CIR.0000000000001032
Circulation. 2021;144:e551–e563
Improving cancer survival represents the most significant effect of precision medicine and personalized molecular and immunologic therapeutics. Cardiovascular health becomes henceforth a key determinant for the direction of overall outcomes after cancer. Comprehensive tissue diagnostic studies undoubtedly have been and continue to be at the core of the fight against cancer. Will a systemic approach integrating circulating blood-derived biomarkers, multimodality imaging technologies, strategic panomics, and real-time streams of digitized physiological data overcome the elusive cardiovascular tissue diagnosis in cardio-oncology? How can such a systemic approach be personalized for application in day-to-day clinical work, with diverse patient populations, cancer diagnoses, and therapies? To address such questions, this scientific statement approaches a broad definition of the biomarker concept. It summarizes the current literature on the utilization of a multitude of established cardiovascular biomarkers at the intersection with cancer. It identifies limitations and gaps of knowledge in the application of biomarkers to stratify the cardiovascular risk before cancer treatment, monitor cardiovascular health during cancer therapy, and detect latent cardiovascular damage in cancer survivors. Last, it highlights areas in biomarker discovery, validation, and clinical application for concerted efforts from funding agencies, scientists, and clinicians at the cardio-oncology nexus.
doi : 10.1161/CIR.0000000000001041
Circulation. 2021;144:e564–e593
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