Subendocardial infarctions are MIs limited to the inner third of the myocardium; these infarcts typically do not exhibit ST segment elevations or Q waves on the ECG tracing (so-called “non–ST-segment elevated MIs” or “NSTEMIs”), although they can have ST-segment depressions or T wave abnormalities. As mentioned earlier, the subendocardial region is most vulnerable to hypoperfusion and hypoxia. Thus, in the setting of http://ebooksmedicine.net severe coronary artery disease, transient decreases in oxygen delivery (as from hypotension, anemia, or pneumonia) or increases in oxygen demand (as with tachycardia or hypertension) can cause subendocardial ischemic injury. This pattern also can occur when an occlusive thrombus lyses before a full-thickness infarction can develop.
• Microscopic infarcts occur in the setting of small-vessel occlusions and may not show any diagnostic ECG changes. These can occur in the setting of vasculitis, embolization of valve vegetations or mural thrombi, or vessel spasm due to elevated catecholamines, as may occur in extreme emotional stress, with certain tumors (e.g., pheochromocytoma), or as a consequence of cocaine use.
MORPHOLOGYNearlyalltransmuralinfarcts(involving50%ormoreoftheventriclethickness)affectatleastaportionoftheleftventricleand/orinterventricularseptum.Roughly15%to30%ofMIsthatinvolvetheposteriororposteroseptalwallalsoextendintotherightventricle.Isolatedrightventricleinfarctsoccurinonly1%to3%ofcases.Evenintransmuralinfarcts,anarrowrim(approximately0.1mm)ofviablesubendocardialmyocardiumispreservedbydiffusionofoxygenandnutrientsfromtheventricularlumen.
ThegrossandmicroscopicappearanceofanMIdependsontheageoftheinjury.Areasofdamageprogressthroughahighlycharacteristicsequenceofmorphologicchangesfromcoagulativenecrosis,toacuteandthenchronicinflammation,tofibrosis(
Table11.2 ).Myocardialnecrosisproceedsinvariablytoscarformationwithoutanysignificantregeneration;studieslookingatwhethertissuestemcellscanbeusedtoregeneratefunctionalmyocardiumareongoingbuthaveyettobearfruit.
Grossand/ormicroscopicrecognitionofveryrecentmyocardialinfarctscanbechallenging,particularlywhendeathoccurswithinafewhours.Myocardial infarcts less than 12 hours old usually are not grossly apparent. However,infarctsmorethan3hoursoldcanbevisualizedbyexposingmyocardiumtovitalstains,suchastriphenyltetrazoliumchloride,asubstrateforlactatedehydrogenase.Becausethisenzymeisdepletedintheareaofischemicnecrosis(itleaksoutofthedamagedcells),theinfarctedareaisunstained(pale),whileoldscarsappearwhiteandglistening(
Fig.11.10 ).By 12 to 24 hours after MI, an infarct usually can be grossly identified by a red-blue discoloration caused by stagnated, trapped blood. Thereafter,infarctsbecomeprogressivelybetterdelineatedassoft,yellow-tanareas;by10to14days,infarctsarerimmedbyhyperemic(highlyvascularized)granulationtissue.Overthesucceedingweeks,theinfarctedtissueevolvestoafibrousscar.
Table11.2