RT Book, Section
A1 Siddiqi, Hasan K.
A1 Ridker, Paul M
A2 Fuster, Valentin
A2 Narula, Jagat
A2 Vaishnava, Prashant
A2 Leon, Martin B.
A2 Callans, David J.
A2 Rumsfeld, John
A2 Poppas, Athena
SR Print(0)
ID 1191371087
T1 Inflammation and Atherosclerosis
T2 Fuster and Hurst's The Heart, 15e
YR 2022
FD 2022
PB McGraw-Hill Education
PP New York, NY
SN 9781264257560
LK accesscardiology.mhmedical.com/content.aspx?aid=1191371087
RD 2022/05/20
AB Chapter  SummaryThis  chapter  discusses  the  role  of  inflammation  in  the  development  of  atherosclerotic  disease,  with  lessons  from  basic  science  and  clinical  studies  informing  future  strategies  for  prevention  and  treatment.  Historically  considered  a  disease  driven  by  dyslipidemia,  the  central  role  of  inflammation  in  atherosclerosis  has  been  elucidated  in  recent  years  with  the  concept  of  residual  inflammatory  risk  as  an  important  contributor  to  atherosclerotic  disease.  Various  stimuli  and  insults  converge  on  the  immune  system  leading  to  activation  of  multiple  immune  effectors,  including  the  innate  and  adaptive  immune  system,  that  have  key  roles  in  the  development  of  atherosclerosis  (see  Fuster  and  Hurst’s  Central  Illustration).  The  use  of  biomarkers  and  inflammatory  intermediaries  including  C-reactive  protein  (CRP),  interleukin  (IL)-1,  and  IL-6  for  risk  stratification  and  mechanistic  elucidation  is  of  key  interest.  Recent  therapies  targeting  inflammatory  pathways,  including  the  NLRP3  inflammasome  and  IL-1  pathway,  have  shown  promise  in  reducing  this  residual  inflammatory  risk  for  atherosclerosis  in  high-risk  populations,  with  positive  results  seen  in  multiple  large  clinical  trials.  In  addition,  public  health  efforts  to  improve  nutrition,  reduce  obesity,  and  combat  environmental  pollution  will  play  a  role  in  reducing  the  inflammatory  contribution  to  atherosclerosis.