TY  - CHAP
M1  - Book, Section
TI  - Inflammation and Atherosclerosis
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
Y1  - 2022
N1  - 
T2  - Fuster and Hurst's The Heart, 15e
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.  
SN  - 
PB  - McGraw-Hill Education
CY  - New York, NY
Y2  - 2022/05/20
UR  - accesscardiology.mhmedical.com/content.aspx?aid=1191371087
ER  -