TY  - CHAP
M1  - Book, Section
TI  - Myocarditis
A1  - Arbustini, Eloisa
A1  - Toro, Alessandro Di
A1  - Urtis, Mario
A1  - Pinney, Sean
A1  - Narula, Jagat
A2  - Fuster, Valentin
A2  - Narula, Jagat
A2  - Vaishnava, Prashant
A2  - Leon, Martin B.
A2  - Callans, David J.
A2  - Rumsfeld, John S.
A2  - Poppas, Athena
Y1  - 2022
N1  - 
T2  - Fuster and Hurst's The Heart, 15e
AB  - Chapter  SummaryThis  chapter  reviews  inflammatory  heart  diseases;  their  infectious,  autoimmune/immune-mediated,  and  toxic  etiology;  diagnostic  algorithms;  pathologic  characteristics;  clinical  manifestations;  and  management  (see  Fuster  and  Hurst’s  Central  Illustration).  The  most  common  etiology  of  infectious  myocarditis  is  viral;  immune-mediated  myocarditis  is  often  related  to  underlying  systemic  autoimmune  diseases,  and  the  most  common  toxic  causes  include  drugs.  The  term  myocarditis  is  the  key  descriptor  of  myocardial  inflammation;  it  does  not  specify  the  immune  phenotype  of  inflammatory  cells  or  the  cause.  The  diagnostic  process  involves  suspicion  based  on  clinical  presentation  of  recent  onset  of  symptoms  in  previously  healthy  individuals  with  exposure  to  infectious  or  toxic  agents,  detection  of  suggestive  imaging  abnormalities,  and  demonstration  of  the  histological  evidence  of  myocardial  inflammation  with  an  effort  to  define  etiologic  basis.  Treatment  aims  at  resolution  of  the  cause,  when  known,  and  at  the  management  of  cardiac  manifestations,  regardless  of  the  cause,  according  to  guidelines  addressing  the  clinical  phenotype.  In  most  cases,  acute  myocarditis  undergoes  spontaneous  resolution,  but  it  can  evolve  toward  chronic  inflammatory  disease  with  the  most  common  phenotype  mimicking  dilated-hypokinetic  cardiomyopathy.  Recent  reports  have  suggested  that  in  some  of  the  viral  infections,  the  viral  genome  may  be  chromosomally  incorporated  and  eventually  transmitted.  Finally,  more  eventful  outcomes  are  observed  when  inflammation  occurs  in  patients  genetically  predisposed  to  develop  dilated  cardiomyopathy.  
SN  - 
PB  - McGraw-Hill Education
CY  - New York, NY
Y2  - 2024/04/18
UR  - accesscardiology.mhmedical.com/content.aspx?aid=1202454811
ER  -