Fig.11.11 ).Typicalfeaturesofcoagulativenecrosis(Chapter2)becomedetectablewithin4to12hoursofinfarction.“Wavyfibers”alsocanbepresentattheedgesofaninfarct;thesereflectthestretchingandbucklingofnoncontractiledeadfibers.Sublethalischemiacanalsoinduceintracellularmyocyte vacuolization; suchmyocytesareviablebutfrequentlycontractpoorly.
Necroticmyocardiumelicitsacuteinflammation(typicallymostprominent1to3daysafterMI),followedbyawaveofmacrophagesthatremovenecroticmyocytesandneutrophil
Table 11.2 Evolution of Morphologic Changes in Myocardial Infarction 2–8weeksGray-whitescar,progressivefromIncreasedcollagendeposition,withdecreasedbordertowardcoreofinfarctcellularity http://ebooksmedicine.net
Fig. 11.10 Acutemyocardialinfarctoftheposterolateralleftventricledemonstratedbyalackoftriphenyltetrazoliumchloridestaininginareasofnecrosis(arrow); theabsenceofstainingisduetoenzymeleakageaftercelldeath.Notetheanteriorscar(arrowhead), indicativeofremoteinfarction.Themyocardialhemorrhageattherightedgeoftheinfarct(asterisk) isduetoventricularrupture,andwastheacutecauseofdeathinthispatient(specimenisorientedwiththeposteriorwallatthetop).
fragments(mostpronounced5to10daysafterMI).Theinfarctedzoneisprogressivelyreplacedbygranulationtissue(mostprominent1to2weeksafterMI),whichinturnformstheprovisionalscaffoldinguponwhichdensecollagenousscarforms.Inmostinstances,scarringiswelladvancedbytheendofthesixthweek,buttheefficiencyofrepairdependsonthesizeoftheoriginallesionandtheabilityofthehosttissuestoheal.Healingrequiresthemigrationofinflammatorycellsandingrowthofnewvesselsfromtheinfarctmargins.Thus,anMIhealsfromitsborderstowardthecenter,andalargeinfarctmaynothealasfastorascompletelyasasmallone.Moreover,malnutrition,poorvasculature,orexogenousanti-inflammatorysteroidscanimpedeinfarctscarring(Chapter3).OnceanMIiscompletelyhealed,itisimpossibletodistinguishitsage:whetherpresentfor8weeksor10years,fibrousscarslookthesame.
The therapeutic goal in acute MI is restoration of tissue perfusion as quickly as possible (hence the adage “time is myocardium”). Such reperfusion is achieved by thrombolysis (dissolution of thrombus by tissue plasminogen activator), angioplasty, or coronary arterial bypass graft.
Fig. 11.11 Microscopicfeaturesofmyocardialinfarctionanditsrepair.(A)One-day-oldinfarctshowingcoagulativenecrosisandwavyfibers,comparedwithadjacentnormalfibers(right). Necroticcellsareseparatedbyedemafluid.(B)Denseneutrophilicinfiltrateintheareaofa2-to3-day-oldinfarct.(C)Nearlycompleteremovalofnecroticmyocytesbyphagocyticmacrophages(7to10days).(D)Granulationtissuecharacterizedbylooseconnectivetissueandabundantcapillaries.(E)Healedmyocardialinfarctconsistingofadensecollagenousscar.Afewresidualcardiacmusclecellsarepresent.(D)and(E)areMasson’strichromestain,whichstainscollagenblue.
http://ebooksmedicine.net