XiangLiMD, PhDaTaoZhouMD, PhDabHaoMaPhDaTaoHuangPhDcXiangGaoMD, PhDdJoAnn E.MansonDrPH, MDefgLuQiMD, PhDah
doi : 10.1016/j.jacc.2021.07.023
Volume 78, Issue 12, 21 September 2021, Pages 1197-1207
Emerging evidence has linked sleep behaviors with the risk of cardiac arrhythmias. The various sleep behaviors are typically correlated; however, most of the previous studies only focused on the individual sleep behavior, without considering the overall sleep patterns.
AlanKadishMDJasonJacobsonMD
doi : 10.1016/j.jacc.2021.07.024
Volume 78, Issue 12, 21 September 2021, Pages 1208-1209
James P.HowardPhDa?Frances A.WoodMPhila?Judith A.FinegoldPhDaAlexandra N.NowbarMBBSaDavid M.ThompsonPhDaAhran D.ArnoldMBBSaChristopher A.RajkumarMBBSaSusanConnollyPhDaJaiminiCeglaPhDbChrisStridePhDcPeterSeverPhDaChristineNortonPhDdSimon A.M.ThomMDaMatthew J.Shun-ShinPhDaDarrel P.FrancisMAa
doi : 10.1016/j.jacc.2021.07.022
Volume 78, Issue 12, 21 September 2021, Pages 1210-1222
Most people who begin statins abandon them, most commonly because of side effects.
Peter P.TothMD, PhD
doi : 10.1016/j.jacc.2021.07.025
Volume 78, Issue 12, 21 September 2021, Pages 1223-1226
HironoriHaraMDabcHirokiShiomiMDdDavidvan KlaverenPhDefDavid M.KentMD, MSfEwout W.SteyerbergPhDgScotGargMD, PhDhYoshinobuOnumaMD, PhDbTakeshiKimuraMDdPatrick W.SerruysMD, PhDbi
doi : 10.1016/j.jacc.2021.07.027
Volume 78, Issue 12, 21 September 2021, Pages 1227-1238
The SYNTAX score II 2020 (SSII-2020) was derived from cross correlation and externally validated in randomized trials to predict death and major adverse cardiac and cerebrovascular events (MACE) following percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG) in patients with 3-vessel disease (3VD) and/or left main coronary artery disease (LMCAD).
John J.SquiersMDabJ. MichaelDiMaioMDa
doi : 10.1016/j.jacc.2021.07.028
Volume 78, Issue 12, 21 September 2021, Pages 1239-1241
Cian P.McCarthyMB, BCh, BAOaDhavalKolteMD, PhDaKevin F.KennedyMSaAmbarishPandeyMDbInbarRaberMDcAndrewOseranMD, MBAaRishi K.WadheraMD, MPP, MPhilcdMuthiahVaduganathanMD, MPHeJames L.JanuzziJr.MDaJason H.WasfyMD, MPhila
doi : 10.1016/j.jacc.2021.07.034
Volume 78, Issue 12, 21 September 2021, Pages 1242-1253
International Classification of Disease (ICD)-10 coding of type 1 myocardial infarction (MI) is used for reimbursement, value-based programs, and clinical research.
Andrew P.DeFilippisMD, MScaMichael E.HallMD, MScb
doi : 10.1016/j.jacc.2021.07.033
Volume 78, Issue 12, 21 September 2021, Pages 1254-1256
Aaron D.AguirreMD, PhDabcArminArbab-ZadehMD, PhDdTsunenariSoedaMD, PhDeValentinFusterMD, PhDfgIk-KyungJangMD, PhDah
doi : 10.1016/j.jacc.2021.06.050
Volume 78, Issue 12, 21 September 2021, Pages 1257-1265
Plaque rupture is the most common cause of acute coronary syndromes and sudden cardiac death. Characteristics and pathobiology of vulnerable plaques prone to plaque rupture have been studied extensively over 2 decades in humans using optical coherence tomography (OCT), an intravascular imaging technique with micron scale resolution. OCT studies have identified key features of plaque vulnerability and described the in vivo characteristics and spatial distribution of thin cap fibroatheromas as major precursors to plaque rupture. In addition, OCT data supports the evolving understanding of coronary heart disease as a panvascular process associated with inflammation. In the setting of high atherosclerotic burden, plaque ruptures often occur at multiple sites in the coronary arteries, and plaque progression and healing are dynamic processes modulated by systemic risk factors. This review details major investigations with intravascular OCT into the biology and clinical implications of plaque vulnerability and plaque rupture.
DhavalKolteMD, PhDaTaishiYonetsuMD, PhDbJong ChulYePhDcPeterLibbyMDdValentinFusterMD, PhDefIk-KyungJangMD, PhDag
doi : 10.1016/j.jacc.2021.07.030
Volume 78, Issue 12, 21 September 2021, Pages 1266-1274
Plaque erosion, a distinct histopathological and clinical entity, accounts for over 30% of acute coronary syndromes (ACS). Optical coherence tomography allows in vivo diagnosis of plaque erosion. Local flow perturbation with activation of Toll-like receptor 2 and CD8+ T cells and subsequent desquamation of endothelium and neutrophil extracellular trap formation contribute to mechanisms of plaque erosion. Compared with ACS patients with plaque rupture, those with plaque erosion are younger, have fewer traditional cardiovascular risk factors, have lower plaque burden, and are more likely to present with non–ST-segment elevation ACS. Early evidence suggests that in patients with ACS caused by plaque erosion, antithrombotic therapy without stenting may be a safe and effective option. Future randomized trials are needed to validate these findings. Clinical studies to develop noninvasive point-of-care biomarkers that distinguish plaque rupture from erosion, and to test novel therapies that target molecular pathways involved in plaque erosion are needed.
TomAdriaenssensMD, PhDa?Marc P.Allard-RatickMDb?VikasThondapuMD, PhDc?TomoyoSugiyamaMD, PhDdO. ChristopherRaffelMD, PhDePeterBarlisMD, PhDfEric K.W.PoonPhDfMakotoArakiMD, PhDbAkihiroNakajimaMDbYoshiyasuMinamiMD, PhDgMasamichiTakanoMD, PhDhOsamuKuriharaMD, PhDhValentinFusterMD, PhDijTsunekazuKakutaMD, PhDdIk-KyungJangMD, PhDbk
doi : 10.1016/j.jacc.2021.07.032
Volume 78, Issue 12, 21 September 2021, Pages 1275-1287
The development of optical coherence tomography (OCT) has revolutionized our understanding of coronary artery disease. In vivo OCT research has paralleled with advances in computational fluid dynamics, providing additional insights in the various hemodynamic factors influencing plaque growth and stability. Recent OCT studies introduced a new concept of plaque healing in relation to clinical presentation. In addition to known mechanisms of acute coronary syndromes such as plaque rupture and plaque erosion, a new classification of calcified plaque was recently reported. This review will focus on important new insights that OCT has provided in recent years into coronary plaque development, progression, and destabilization, with a focus on the role of local hemodynamics and endothelial shear stress, the layered plaque (signature of previous subclinical plaque destabilization and healing), and the calcified culprit plaque.
Harpreet S.BhatiaMDCalvinYeangMD, PhDAmosBaruchPhDXiaohongYangBSErik S.G.StroesMD, PhDSotiriosTsimikasMD
doi : 10.1016/j.jacc.2021.07.031
Volume 78, Issue 12, 21 September 2021, Pages 1288-1289
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