Rod Passman
doi : 10.1161/CIRCULATIONAHA.121.053170
Circulation. 2021;143:2211–2213
Atul Anand, Kuan Ken Lee, Andrew R. Chapman, Amy V. Ferry, Phil D. Adamson, Fiona E. Strachan, Colin Berry, Iain Findlay, Anne Cruikshank, Alan Reid, Paul O. Collinson, Fred S. Apple, David A. McAllister, Donogh Maguire, Keith A.A. Fox, David E. Newby, Chris Tuck, Ronald Harkess, Catriona Keerie, Christopher J. Weir, Richard A. Parker, Alasdair Gray, Anoop S.V. Shah, Nicholas L. Mills
doi : 10.1161/CIRCULATIONAHA.120.052380
Circulation. 2021;143:2214–2224
High-sensitivity cardiac troponin assays enable myocardial infarction to be ruled out earlier, but the safety and efficacy of this approach is uncertain. We investigated whether an early rule-out pathway is safe and effective for patients with suspected acute coronary syndrome.
Yader Sandoval, Allan S. Jaffe
doi : 10.1161/CIRCULATIONAHA.121.054926
Circulation. 2021;143:2225–2228
Neel M. Butala, Raj Makkar, Eric A. Secemsky, Dianne Gallup, Guillaume Marquis-Gravel, Andrzej S. Kosinski, Sreekanth Vemulapalli, Javier A. Valle, Steven M. Bradley, Tarun Chakravarty, Robert W. Yeh, David J. Cohen
doi : 10.1161/CIRCULATIONAHA.120.052874
Circulation. 2021;143:2229–2240
Stroke remains a devastating complication of transcatheter aortic valve replacement (TAVR), which has persisted despite refinements in technique and increased operator experience. While cerebral embolic protection devices (EPDs) have been developed to mitigate this risk, data regarding their impact on stroke and other outcomes after TAVR are limited.
Derrick Y. Tam, Harindra C. Wijeysundera
doi : 10.1161/CIRCULATIONAHA.121.054902
Circulation. 2021;143:2241–2243
Hidehiro Kaneko, Yuichiro Yano, Hidetaka Itoh, Kojiro Morita, Hiroyuki Kiriyama, Tatsuya Kamon, Katsuhito Fujiu, Nobuaki Michihata, Taisuke Jo, Norifumi Takeda, Hiroyuki Morita, Koichi Node, Robert M. Carey, Joao A.C. Lima, Suzanne Oparil, Hideo Yasunaga, Issei Komuro
doi : 10.1161/CIRCULATIONAHA.120.052624
Circulation. 2021;143:2244–2253
Heart failure (HF) and atrial fibrillation (AF) are growing in prevalence worldwide. Few studies have assessed to what extent stage 1 hypertension in the 2017 American College of Cardiology/American Heart Association blood pressure (BP) guidelines is associated with incident HF and AF.
Yiwei Liu, Qipeng Luo, Zhanhao Su, Junyue Xing, Jinlin Wu, Li Xiang, Yuan Huang, Haizhou Pan, Xie Wu, Xiaoling Zhang, Jun Li, Fuxia Yan, Hao Zhang
doi : 10.1161/CIRCULATIONAHA.120.051937
Circulation. 2021;143:2254–2272
Cyanotic congenital heart disease (CCHD) is a complex pathophysiological condition involving systemic chronic hypoxia (CH). Some patients with CCHD are unoperated for various reasons and remain chronically hypoxic throughout their lives, which heightens the risk of heart failure as they age. Hypoxia activates cellular metabolic adaptation to balance energy demands by accumulating hypoxia-inducible factor 1-? (HIF-1?). This study aims to determine the effect of CH on cardiac metabolism and function in patients with CCHD and its association with age. The role of HIF-1? in this process was investigated, and potential therapeutic targets were explored.
Natascha Sommer, Norbert Weissmann, Hossein-Ardeschir Ghofrani
doi : 10.1161/CIRCULATIONAHA.121.054217
Circulation. 2021;143:2273–2276
Hairuo Lin, Yingqi Zhu, Cankun Zheng, Donghong Hu, Siyuan Ma, Lin Chen, Qiancheng Wang, Zhenhuan Chen, Jiahe Xie, Yi Yan, Xiaobo Huang, Wangjun Liao, Masafumi Kitakaze, Jianping Bin, Yulin Liao
doi : 10.1161/CIRCULATIONAHA.120.047000
Circulation. 2021;143:2277–2292
Exercise can induce physiological myocardial hypertrophy (PMH), and former athletes can live 5 to 6 years longer than nonathletic controls, suggesting a benefit after regression of PMH. We previously reported that regression of pathological myocardial hypertrophy has antihypertrophic effects. Accordingly, we hypothesized that antihypertrophic memory exists even after PMH has regressed, increasing myocardial resistance to subsequent pathological hypertrophic stress.
Anand Rohatgi, Marit Westerterp, Arnold von Eckardstein, Alan Remaley, Kerry-Anne Rye
doi : 10.1161/CIRCULATIONAHA.120.044221
Circulation. 2021;143:2293–2309
Low high-density lipoprotein cholesterol (HDL-C) characterizes an atherogenic dyslipidemia that reflects adverse lifestyle choices, impaired metabolism, and increased cardiovascular risk. Low HDL-C is also associated with increased risk of inflammatory disorders, malignancy, diabetes, and other diseases. This epidemiologic evidence has not translated to raising HDL-C as a viable therapeutic target, partly because HDL-C does not reflect high-density lipoprotein (HDL) function. Mendelian randomization analyses that have found no evidence of a causal relationship between HDL-C levels and cardiovascular risk have decreased interest in increasing HDL-C levels as a therapeutic target. HDLs comprise distinct subpopulations of particles of varying size, charge, and composition that have several dynamic and context-dependent functions, especially with respect to acute and chronic inflammatory states. These functions include reverse cholesterol transport, inhibition of inflammation and oxidation, and antidiabetic properties. HDLs can be anti-inflammatory (which may protect against atherosclerosis and diabetes) and proinflammatory (which may help clear pathogens in sepsis). The molecular regulation of HDLs is complex, as evidenced by their association with multiple proteins, as well as bioactive lipids and noncoding RNAs. Clinical investigations of HDL biomarkers (HDL-C, HDL particle number, and apolipoprotein A through I) have revealed nonlinear relationships with cardiovascular outcomes, differential relationships by sex and ethnicity, and differential patterns with coronary versus noncoronary events. Novel HDL markers may also have relevance for heart failure, cancer, and diabetes. HDL function markers (namely, cholesterol efflux capacity) are associated with coronary disease, but they remain research tools. Therapeutics that manipulate aspects of HDL metabolism remain the holy grail. None has proven to be successful, but most have targeted HDL-C, not metrics of HDL function. Future therapeutic strategies should focus on optimizing HDL function in the right patients at the optimal time in their disease course. We provide a framework to help the research and clinical communities, as well as funding agencies and stakeholders, obtain insights into current thinking on these topics, and what we predict will be an exciting future for research and development on HDLs.
Tracy Hampton
doi : 10.1161/CIRCULATIONAHA.121.055402
Circulation. 2021;143:2310–2311
Dinkar Bhasin, Rahul Kumar, Anunay Gupta
doi : 10.1161/CIRCULATIONAHA.121.054890
Circulation. 2021;143:2312–2315
G. Michael Felker, Javed Butler, James L. Januzzi Jr, Akshay S. Desai, John J.V. McMurray, Scott D. Solomon
doi : 10.1161/CIRCULATIONAHA.121.054496
Circulation. 2021;143:2316–2318
Muddassir Mehmood
doi : 10.1161/CIRCULATIONAHA.120.052111
Circulation. 2021;143:e1021
Christiaan L. Meuwese, Adriaan O. Kraaijeveld, Dirk W. Donker
doi : 10.1161/CIRCULATIONAHA.120.053263
Circulation. 2021;143:e1022–e1023
Benedikt Schrage, Dirk Westermann
doi : 10.1161/CIRCULATIONAHA.121.053992
Circulation. 2021;143:e1024
doi : 10.1161/CIR.0000000000000984
Circulation. 2021;143:e1025–e1026
doi : 10.1161/CIR.0000000000000990
Circulation. 2021;143:e1027
doi : 10.1161/CIR.0000000000000995
Circulation. 2021;143:e1028
doi : 10.1161/CIR.0000000000000989
Circulation. 2021;143:e1029
doi : 10.1161/CIR.0000000000000991
Circulation. 2021;143:e1030
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