RT Book, Section
A1 Towne, Trent G.
A2 Attridge, Rebecca L.
A2 Miller, Monica L.
A2 Moote, Rebecca
A2 Ryan, Laurajo
SR Print(0)
ID 57292170
T1 Chapter 31. Infective Endocarditis
T2 Internal Medicine: A Guide to Clinical Therapeutics
YR 2013
FD 2013
PB The McGraw-Hill Companies
PP New York, NY
SN 978-0-07-174580-2
LK accesspharmacy.mhmedical.com/content.aspx?aid=57292170
RD 2024/04/20
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%