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effect.
Restenosis and stent thrombosis are disease entities unique to patients who have previously
undergonePCI.
RestenosisisaresultofneointimalhyperplasiaandoccursmorefrequentlyinpatientswithBMS
placement,diabetics,patientswithlongareasofpriorstenting,andpatientswithstentinginsmall
arteries.
Stentthrombosisisthethromboticocclusionofapreviouslyplacedcoronarystentandpresents
as ACS or sudden cardiac death.Stent thrombosis is associatedwith a high mortalityrate and
poorprognosis.
106,107
□ Acute stent thrombosis occurs within 24 hours and is due to mechanical procedural
complicationsaswellasinadequateanticoagulationandantiplatelettherapies.
□ Subacutestentthrombosis(24hours–30days)isaconsequenceofinadequateplateletinhibition
andmechanicalstentcomplications.CessationofP2Y12inhibitortherapyduringthistimeyields
a30-to100-foldriskofstentthrombosis.
□ Late(30days–1year)stentthrombosisandverylatestent thrombosis occursprincipallywith
DESs.
□ NeoatherosclerosisisatheroscleroticplaqueuniquetopriorPCI,occursinpreviouslyplaced
stents,andcanpredisposeapatienttoanginaorplaquerupturewithsubsequentACS.
Ischemic MRisa poor prognostic indicator followingMI. Papillarymusclerupture is associated
with inferior andposterior infarcts. Theanterior papillarymuscle hasa dual bloodsupply andis
less vulnerable to rupture. The mechanism ofchronic MRafter STEMI includes papillarymuscle
dysfunctionorleaflettetheringduetoposteriorwallakinesis.
Acute MRfrom papillary muscle rupture is a severe complication of MI associated with high
mortality(seebelow).
ProgressiveMRfollowingMImaydevelopasaresultofLVchamberdilation,apicalremodeling,
orposteriorwalldyskinesis.Thesechangesleadtoleaflettetheringormitralannulardilation.
Echocardiographyisthediagnosticmodalityofchoice.
Initial treatment of MR involves aggressive afterload reduction and revascularization. Stable
patientsshouldreceiveatrialofmedicaltherapyandundergosurgeryonlyiftheyfailtoimprove.
STEMI in the setting of recent cocaine use presents a unique and challenging management
situation.
108
ST elevationcanresultfrom myocardial ischemia due to coronaryvasospasm,insitu
thrombusformation,and/or increased myocardial oxygendemand.Thecommonpathophysiologyis
excessivestimulationofα-andβ-adrenergicreceptors.Chestpainduetococaineuseusuallyoccurs
within3hoursbutmaybeseenseveraldaysfollowinguse.
Oxygen,ASA,andheparin(UFHorLMWH)shouldbeadministeredtoallpatientswithcocaineassociatedSTEMI.
Nitrates should be used preferentially to treat vasospasm. Additionally, benzodiazepines may
conferadditionalreliefbydecreasingsympathetictone.
BBsarecontraindicated;bothselectiveandnonselectiveBBsshouldbeavoided.
Phentolamine (α-adrenergic antagonist) and calcium channel blockers may reverse coronary
vasospasmandarerecommendedassecond-lineagents.
Theuseofreperfusiontherapyis controversialandshouldbereservedforthosepatientswhose
symptomspersistdespiteinitialmedicaltherapy.
□ Primary PCI is the preferred approach for the patient with persistent symptoms and ECG
changesdespite aggressive medical therapy. Itis importanttonotethatcoronaryangiography
andinterventioncarryasignificantriskofworseningvasospasm.
□ FibrinolytictherapyshouldbereservedforpatientswhoareclearlyhavingaSTEMIandwho
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cannotundergoPCI.
Complications
Myocardialdamagepredisposesthepatienttoseveralpotentialadverseconsequencesandcomplications
thatshouldbeconsideredifthepatientexperiencesnewclinicalsignsand/orsymptoms.Theseinclude
recurrentchestpain,cardiacarrhythmias,cardiogenicshock,andmechanicalcomplicationsofMI.
Recurrentchestpainmay be duetoischemia intheterritoryoftheoriginalinfarction,pericarditis,
myocardialrupture,orpulmonaryembolism.
Recurrentanginaisexperiencedby20%–30%ofpatientsafterMIwhoreceivefibrinolytictherapy
andupto10%ofpatientsintheearlytimeperiodfollowingpercutaneousrevascularization.These
symptomsmayrepresentrecurrenceofischemiaorinfarctextension.
Assessmentofthepatientmayincludeevaluationfornewmurmursorfrictionrubs,ECGtoassess
for new ischemic changes, cardiac biomarkers (troponin and CK-MB), echocardiography, and
repeatcoronaryangiographyifindicated.
Patients with recurrent chest pain should continue to receive ASA, P2Y12 inhibition,
anticoagulants,nitroglycerin,andBBtherapy.
If recurrent angina is refractory to medical treatment, urgent repeat coronary angiography and
interventionshouldbeconsidered.
Acute pericarditis occurs 24–96 hours after MI in approximately 10%–15% of patients. The
associatedchestpainis oftenpleuritic andmaybe relievedintheuprightposition.A frictionrub
maybenotedonclinicalexamination,andtheECGmayshowdiffuseST-segmentelevationandPRsegmentdepression.LeadAVRmayhavePRelevation.Treatmentisdirectedatpainmanagement.
High-doseASA(upto650mgqidmaximum)isgenerallyconsideredafirst-lineagent.NSAIDs
suchasibuprofenmaybeusedifASAisnoteffectivebutshouldbeavoidedearlyafteracuteMI.
Colchicine along with ASA may also be beneficial for recurrent symptoms and may also be
superiortoeachagentalone.
Glucocorticoids(prednisone1mg/kgdaily)maybeusefulifsymptomsaresevereandrefractory
toinitialtherapy.Steroidsshouldbeusedsparinglybecausetheymayleadtoanincreasedriskof
recurrenceofpericarditis.Useshouldalsobedeferreduntilatleast4weeksafteracuteMIdueto
theiradverseimpactoninfarcthealingandriskofventricularaneurysm.
Heparin should be avoided in the setting of pericarditis with or without pericardial effusion
becauseitmayleadtopericardialhemorrhage.
Dressler syndrome is thought to be an autoimmune process characterized by malaise, fever,
pericardial pain, leukocytosis, elevated erythrocyte sedimentation rate, and often a pericardial
effusion.Incontrasttoacutepericarditis,Dresslersyndromeoccurs1–8weeksafterMI.Treatment
isidenticaltoacutepericarditis.
Arrhythmias.CardiacrhythmabnormalitiesarecommonfollowingMIandmayincludeconduction
block, atrial arrhythmias, and ventricular arrhythmias. Arrhythmias that result in hemodynamic
compromiserequireprompt,aggressiveintervention.Ifthearrhythmiaprecipitatesrefractoryangina
orHF, urgent therapyiswarranted.For allrhythmdisturbances,exacerbatingconditionsshouldbe
addressed, including electrolyteimbalances,hypoxia, acidosis, andadverse drug effects.Referto
sectiononCardiacArrhythmiamanagementforfurtherdetails.Atropineshouldbeattemptedforall
bradyarrhythmiasinthesetting ofSTEMI. Bradycardia isa commoncomplicationofintensevagal
inputtotheAVnodeasaresultofbaroreceptoractivationinthemyocardium(alsocalledBezoldJarischreflex).
Transcutaneousand transvenouspacing. Conductionsystemdisease thatprogresses tocomplete
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heartblockorresultsinsymptomaticbradycardiacanbeeffectivelytreatedwithcardiacpacing.A
transcutaneous pacing device can be used under emergent circumstances; however, a temporary
transvenoussystemshouldbeusedforlongerdurationtherapy.
Absolute indications for temporary transvenous pacing include asystole, symptomatic
bradycardia,recurrentsinuspauses,completeheartblock,andincessantpolymorphicVT.
Temporarytransvenouspacingmayalsobewarrantedfornewtrifascicularblock,newMobitzII
block, and patients with LBBB who require a pulmonary artery catheter, given the risk of
developingcompleteheartblock.
Implantablecardioverter-defibrillators(ICDs)shouldnot routinelybeimplantedinpatientswith
reducedLV function following MI or those with VT/VF in the setting ofischemia or immediately
followingreperfusion(<48hours).
RoutineinsertionofICDsintopatientswithreducedLVfunctionimmediatelyfollowingMIdoes
notimproveoutcomes.
109-111
InpatientswithLVEF<35%lessthan40dayspostMI,considerationofawearablecardioverter
defibrillation (e.g., Zoll LifeVest) as a bridge to reevaluation for recovery of EF is
reasonable.
112,113
ICDtherapyisalsoindicatedforpatientswithrecurrentepisodesofsustainedVTorVFafter>48
hoursfollowingcoronaryreperfusion.
Cardiogenicshockisaninfrequent,butserious,complicationofMIandisdefinedashypotensionin
thesettingofinadequateventricularfunctiontomeetthemetabolicneedsoftheperipheraltissue.Risk
factors include prior MI, older age, diabetes, and anterior infarction. Organ hypoperfusion may
manifestas progressive renal failure,dyspnea, diaphoresis, or mental status changes.Hemodynamic
monitoringreveals elevatedfilling pressures(wedgepressure>20mmHg),depressedcardiacindex
(<2.5L/min/m2),andhypotension.
PatientswithcardiogenicshockinthesettingofMIhaveamortalityrateinexcessof50%.
Dobutamine and milrinone are the most frequentlyused medications for inotropic support. They
both possess vasodilatory properties (i.e., afterload reducing) and are arrhythmogenic. Milrinone
shouldbeavoidedinthesettingofrenalinsufficiency.
Dopamine can be used as both a vasopressor and inotrope but increases the risk of atrial
arrhythmiasinpatientswithshockandisnotapreferredfirst-lineagent.
Norepinephrine and phenylephrine may be required to maintain systemic BP. The use of any
vasoconstrictive agents in the setting of cardiogenic shock should prompt an evaluation for
mechanicalcirculatorysupport.
Epinephrine is a potent vasopressor and inotrope and is frequently used as an adjunct to other
medicaltherapies.TheremaybesomepreferentialbenefittoRVfunction,andthus,epinephrinemay
beusedforshocksecondarytoRVinfarctorsevereRVdysfunction.
Mechanicalcirculatory supportincludesboth temporaryanddurablesupportdevices. Temporary
supportdevicesincludeIABP,Impellacatheter,orextracorporealmembraneoxygenation(ECMO).
Temporarysupportisofferedasbridgetorecoveryorasbridgetodecisionaboutlong-termdurable
mechanicalsupportsuchasanLVassistdevice(seeChapter5,HeartFailureandCardiomyopathy).
Thechoiceoftemporarysupportdeviceisnotalwaysclearandshouldbemadebyateamfamiliar
withthemanagementofcardiogenicshock.
All patients with cardiogenic shock should undergo echocardiography to evaluate for mechanical
complicationsofMI(seethefollowingtext).
LVthrombusoccursmostofteninsettingofanteriorMIandshouldbetreatedwithanticoagulation.
Warfarin is the recommended long-term anticoagulation agent; direct oral anticoagulants (e.g.,
rivaroxaban, apixaban) have led to conflicting results regarding safety and efficacy compared to
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warfarin.
114,115
Patientsshould receive warfarinfor3–6monthsunlessotherindicationswarrant its
continueduse.YoumayrepeataTTEtoconfirmresolutionoftheLVthrombus.
Mechanicalcomplications
Aneurysm. After MI, the affected area of the myocardium may undergo infarct expansion and
thinning, forming an aneurysm. The wall motion may become dyskinetic, making the endocardial
surfacesusceptibletomuralthrombusformation.
LV aneurysm is suggested by persistent ST elevation on the ECG and may be diagnosed by
imagingstudiesincludingventriculography,echocardiography,andMRI.
Anticoagulationiswarrantedtolowertheriskofembolicevents,especiallyifamuralthrombus
ispresent.
SurgicalinterventionmaybeappropriateiftheaneurysmresultsinHForventriculararrhythmias
thatarenotsatisfactorilymanagedwithmedicaltherapy.
Ventricular pseudoaneurysm. Incomplete rupture of the myocardial free wall can result in
formationofaventricularpseudoaneurysm.Inthiscase,bloodescapesthroughthemyocardialwall
andiscontainedwithinthevisceralpericardium.Inthepost-CABGpatient,hemorrhagefromfrank
ventricular rupture may be contained within the fibrotic pericardial space producing a
pseudoaneurysm.
Echocardiography (TTE with contrast or TEE) is the preferred diagnostic test to assess for a
pseudoaneurysm,oftenallowingdifferentiationfromatrueaneurysm.
Prompt surgical intervention for pseudoaneurysms is advised because of the high incidence of
myocardialrupture.
Freewallrupture representsa rare butcatastrophic complicationofSTEMI inthemodernearlyreperfusion era. Rupture typicallyoccurs withinthefirstweek after MI andpresentswith sudden
hemodynamic collapse. This complication can occur after anterior or inferior MI and is more
commonlyseeninhypertensivewomenwiththeirfirstlargetransmuralMI,inpatientsreceivinglate
therapywithfibrinolytics,andpatientsgivenNSAIDsorglucocorticoids.
Echocardiography may identify patients with particularly thinned ventricular walls at risk for
rupture.
Despiteoptimalintervention,mortalityoffreewallruptureremains>90%.
Papillarymusclerupture(pleasealsorefertoearlierMRsection)isararecomplicationafterMI
andisassociatedwith abruptclinicaldeterioration.Theposteriormedialpapillarymuscle ismost
commonlyaffectedduetoitsisolatedvascularsupply,butanterolateralpapillarymusclerupturehas
beenreported.Ofnote,papillarymusclerupturemaybeseeninthesettingofarelativelysmallacute
MIorevenNSTEMI.
The diagnostic test of choice is echocardiography with Doppler imaging and/or TEE because
physicalexamrevealsamurmurinonly 50%ofcases.
Initialmedicaltherapyshouldincludeaggressiveafterloadreduction.PatientswithrefractoryHF
andthose with hemodynamic instability may require inotropic support with dobutamine and/or
IABP.Surgicalrepairisindicatedinthemajorityofpatients.
VentricularseptalruptureismostcommonlyassociatedwithanteriorMIoccurring3–5daysafter
MI.Theperforationmayfollowadirectcoursebetweentheventriclesoraserpiginousroutethrough
theseptalwall.
DiagnosiscanbemadebyechocardiographywithDopplerimagingandoftenrequiresTEE.
Diagnosisshould be suspectedinthepostinfarctpatientwhodevelopsHFsymptoms andanew
holosystolicmurmur.
Stabilization with afterload reduction, inotropic support, and/or IABP may be necessary for
hemodynamicallyunstablepatientsuntildefinitivetherapywithsurgicalrepaircanbeperformed.
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Inhemodynamicallystablepatients,surgeryisbestdeferredforatleastaweektoimprovepatient
outcome.Leftuntreated,mortalityapproaches90%.
Percutaneousdeviceclosureinthecardiaccatheterization laboratorycanbeperformedinselect
patientswithanunacceptablesurgicalrisk.
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