Fig.11.19B );thesearecollectionsoflymphocytes(primarilyTcells),scatteredplasmacells,andplumpactivatedmacrophagescalledAnitschkow cells associatedwithzonesoffibrinoidnecrosis.TheAnitschkowcellshaveabundantcytoplasmandnucleiwithchromatinthatiscentrallycondensedintoaslender,wavyribbon(so-called“caterpillarcells”).Duringacuterheumaticfever,Aschoffbodiescanbefoundinanyofthethreelayersoftheheart—pericardium,myocardium,orendocardium(includingvalves).Hence,rheumaticfeverissaidtocausepancarditis,withthefollowingsalientfeatures:
Thepericardiummayexhibitafibrinousexudate,whichgenerallyresolveswithoutsequelae.
Themyocardialinvolvement—myocarditis—takestheformofscatteredAschoffbodieswithintheinterstitialconnectivetissue.
Fig.11.19A )forming1-to2-mmvegetations—verrucae—thatcauselittledisturbanceincardiacfunction.
Chronic rheumatic heart disease ischaracterizedbyorganizationofacuteinflammationandsubsequentscarring.Aschoffbodiesarereplacedbyfibrousscarsothattheselesionsarerarelyseeninchronicdisease.Mostcharacteristically,valvecuspsandleafletsbecomepermanentlythickenedandretracted.Classically,themitralvalvesexhibitleaflet thickening, commissural fusion and shortening,and thickening and fusion of the chordae tendineae (
Fig.11.19CtoE ).Fibrousbridgingacrossthevalvularcommissuresandcalcificationcreate“fishmouth”or“buttonhole”stenoses(
Fig.11.19C ).Microscopicexaminationshowsneovascularization(visiblyevidentin
Fig.
11.19D )anddiffusefibrosisthatobliteratesthenormalleafletarchitecture.
Themostimportantfunctionalconsequenceofrheumaticheartdiseaseisvalvular stenosis and regurgitation; stenosistendstopredominate.Themitralvalvealoneisinvolvedin70%ofcases,andcombinedmitralandaorticdiseaseinseeninanother25%;thetricuspidvalveislessfrequently(andlessseverely)involved;andthepulmonicvalvealmostalwaysescapesinjury.Withtightmitralstenosis,theleftatriumprogressivelydilatesowingtopressureoverload,precipitatingatrialfibrillation.Thecombinationofdilationandfibrillationisafertilesubstrateforthrombosis,andformationoflargemuralthrombiiscommon.Long-standingpassivevenouscongestiongivesrisetopulmonaryvascularandparenchymalchangestypicalofleft-sidedheartfailure.Intime,thisleadstorightventricularhypertrophyandfailure.Withpuremitralstenosis,theleftventriclegenerallyisnormal.
Acute rheumatic fever occurs most often in children; the principal clinical manifestation is carditis. Nevertheless, http://ebooksmedicine.net