TY  - CHAP
M1  - Book, Section
TI  - Chapter 31. Infective Endocarditis
A1  - Towne, Trent G.
A2  - Attridge, Rebecca L.
A2  - Miller, Monica L.
A2  - Moote, Rebecca
A2  - Ryan, Laurajo
PY  - 2013
T2  - Internal Medicine: A Guide to Clinical Therapeutics
AB  - Table  Graphic  Jump  LocationTable  31-1  Pathophysiology  (N  Engl  J  Med  2001;345:1318;  Lancet  2004;363:139;  Heart  2006;92:879;  BMJ  2006;333:334)View  Table||Download  (.pdf)Table  31-1  Pathophysiology  (N  Engl  J  Med  2001;345:1318;  Lancet  2004;363:139;  Heart  2006;92:879;  BMJ  2006;333:334)Development  of  IE  requires  simultaneous  existence  of  damage  to  endothelial  lining  of  heart  valve  &  presence  of  pathogen  capable  of  causing  IE  in  bloodstreamDamage  to  endothelial  lining  occurs  by  two  mechanisms:MechanicalTrauma,  turbulent  blood  flow,  etc.,  cause  damage  to  valvular  endotheliumResulting  damage  exposes  stromal  cells  &  extracellular  matrix  proteins  →  triggers  fibrin  &  platelet  deposition  (non-bacterial  thrombotic  endocarditis  [NBTE])Bacteria  in  bloodstream  adhere  to  the  NBTE  causing  recruitment  of  monocytes  &  subsequent  release  of  mediators  of  coagulation  cascade  &  other  factors  encouraging  growth  of  vegetationFurther  deposition  of  platelets,  fibrin,  bacteria,  &  other  proteins  &  bacterial  division  lead  to  the  maturation  of  vegetation  &  transition  of  NBTE  to  IEInflammatoryValvular  inflammation,  in  the  absence  of  mechanical  insult,  results  in  the  expression  of  proteins  on  the  endothelial  cell  surface  capable  of  binding  &  promoting  adherence  to  the  inflamed  cellsSome  microorganisms,  such  as  S.  aureus,  express  surface  fibronectin-binding  proteins;  allowing  direct  adhesion  to  inflamed  cells,  endothelial  internalization  of  bacteria,  &  endothelial  apoptosisInflammatory  events  &  apoptosis  result  in  cascade  of  events  similar  to  that  seen  in  mechanical  cases;  ultimately  results  in  formation  of  a  mature  vegetationInfective  Endocarditis:  Native  Valves  (NVES)“Classically”  seen  in  patients  with  congenital  heart  disease  &  chronic  rheumatic  heart  disease>60yoa,  degenerative  valve  &  other  cardiac  lesions  are  primary  cause  of  IE↑  frequency  of  intracardic  pacemakers  &  defibrillators  has  led  to  corresponding  increase  in  IE.  Most  frequently  caused  by  S.  aureus  (38%)  &  viridans  group  streptococci  (21%)Infective  Endocarditis:  Prosthetic  Valves  (PVES)Risk  of  PVE  ranges  from  0.3%  to  6%/patient-yearNo  significant  differences  in  infection  rates  between  mechanical  vs  bioprosthetic  valvesEarly-onset  PVE  (≤2mo  after  surgery)  dominated  by  S.  aureus  &  S.  epidermidisLate-onset  PVE  pathogen  distribution  similar  to  native  valve  diseaseProsthetic  valve  often  lengthens  treatment  duration  &  expands  therapy  requiredInfective  Endocarditis:  Intravenous  Drug  Users  (IVDUs)1–5%/y  of  IVDUs∼70%  S.  aureus>50%  involve  tricuspid  valve;  60–80%  have  no  preexisting  valvular  lesionsCure  rates  for  right-sided  (tricuspid  valve)  IE  >90%Nosocomial  Infective  Endocarditis(Int  J  Infect  Dis  2004;8:210)Acute  IE:  ≥48h  post-admission  or  directly  relating  to  hospital-based  procedure  or  admission  ≤8wk  prior  native  or  prosthetic  valves;  left-sided  valves  most  common>65%  of  patients  elderly  (>60yoa)Majority  (45–55%)  directly  attributed  to  intravascular  catheter  or  other  intravascular  deviceStaphylococci,  predominantly  S.  aureus  >75%  
SN  - 
PB  - The McGraw-Hill Companies
CY  - New York, NY
Y2  - 2024/04/17
UR  - accesspharmacy.mhmedical.com/content.aspx?aid=57292170
ER  -