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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2804_Библиотеки_им_академика_М_И_Перельмана
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interaction between platelets and fibrinogen,thus targeting thefinal common pathway for platelet
aggregation.
GPIIb/IIIainhibitorsplayalimitedroleinACSmanagementwiththeintroductionofmorepotent
oralantiplateletagents.
Routine use of GPIIb/IIIa antagonists on initial presentation, before angiography, in patients
undergoingtheinvasiveapproachshouldbeavoidedduetoincreasedriskofmajorbleedingand
alackofimprovementinoutcomes.
GPIIb/IIIaagentsmaybeconsideredinscenariosofworseningischemiadespiteDAPT,complex
PCI,or bridgingstrategy inpatients with anindicationforDAPT (e.g.,recentPCI)but require
surgery.
Thrombocytopenia,whichcanbesevere,isanuncommoncomplicationoftheseagentsandshould
promptdiscontinuation.
Otherconcernswithantiplateletagents
TimingofCABG
□ Duetoincreasedriskofbleeding,itiscurrentlyrecommendedthatclopidogrelbewithheldfor
atleast5dayspriortoCABG,prasugrel7daysprior,ticagrelor5daysprior,andcangrelor1–
6hoursprior.
□ CangrelororGPIIb/IIIaantagonistscanbeusedasanalternativetoclopidogrel,ticagrelor,and
prasugrel in appropriate patients with UA/NSTEMI who are known to require surgical
revascularization.
□ In general, DAPTshould notbewithheld during theinitialmanagementofACS(i.e., prior to
angiography) outofconcern for the potential need for surgical revascularization. There is a
larger risk of withholding beneficial therapy to patients in this setting than causing harm by
delayingsurgicalrevascularization.
Protonpumpinhibitors(PPIs)
□ PPIsshould be used in patients onDAPTwitha prior historyofgastrointestinal bleedingor
increased risk of bleeding (e.g., elderly, known ulcers or Helicobacter pylori infection, or
coprescribedwarfarin,steroids,orNSAIDs).
58
□ PharmacologicstudieshaveraisedconcernsaboutthepotentialofPPIstoblunttheefficacyof
clopidogrel. However, in a prospective randomized trial, no apparent cardiovascular
interactionwasnotedbetweenPPIsandclopidogrel.
59
Tripletherapy
□ ManypatientsrequiringDAPTafterPCIhaveapreexistingindicationfororalanticoagulation
(OAC),suchasatrialfibrillationorrecentvenousthromboembolism.
□ Themostrecentguidelineshavenotyetmadespecificrecommendations,butgenerallysupport
tailoring selectionoftriple therapy(DAPTplusOAC) or SAPT(singleantiplatelettherapy)
plusOACtothepatientbycomparingtheriskofbleedingtotheriskofischemicevents.
60-62
IntheAUGUSTUStrial,patientswithatrialfibrillationandrecentACSorPCItreatedwitha
P2Y12 inhibitor and apixaban, without aspirin, had fewer bleeding events and fewer
hospitalizations without significantly increased ischemic events versus regimens including
warfarin,aspirin,orboth.
63
□ Inpatientswithanaverageriskofbleedingandaverageriskofischemicevents,werecommend
triple therapy(e.g., aspirin, clopidogrel, andwarfarin) for 4 weeksfollowed by SAPT plus
OAC(e.g.,clopidogrelandwarfarin)foratleast1year.
□ In patients with either high riskofbleeding or high risk of ischemic events, we recommend
consultationwithacardiologisttotailortherapy.
Anticoagulanttherapy
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SeeTable4-13forrecommendeduseanddosinginACS.
TABLE4-13
ANTICOAGULANTMEDICATIONS
Medication Dosage Comments
Heparin
(UFH)
60units/kgIV
bolus
(maximum
dose:4000
units),12–14
units/kg/h
Heparin therapy, when used in conjunction with ASA,
has beenshownto reduce the early rate of deathor
MIbyupto60%.
64
The aPTT should be adjusted to maintain a value of
1.5–2.0timescontrol.
Enoxaparin
(LMWH)
1mg/kgSub-Q
bid
a
LMWH is at least as efficacious as UFH and may
further reduce the rate of death, MI, or recurrent
angina.
65
LMWHmayincreasetherateofbleeding62andcannot
bereversedinthesettingofrefractorybleeding.
LMWHdoesnotrequiremonitoringforclinicaleffect.
Fondaparinux 2.5mgSub-Q
daily
Fondaparinux has efficacy similar to that of LMWH
withpossiblyreducedbleedingrates.
66
Bivalirudin
b
0.75mg/kgIV
bolus,1.75
mg/kg/h
When used in conjunction with ASA and clopidogrel,
bivalirudinisatleastaseffectiveasthecombinationof
ASA, UFH, clopidogrel, and GPIIb/IIIa antagonists
withdecreasedbleedingrates.67Mayincreaseriskfor
stentthrombosis.
Monitoring is required with a goal aPTT of 1.5–2.5
timescontrol.
aPTT, activated partial thromboplastin time; ASA, aspirin; GFR, glomerular filtration rate; GP, glycoprotein; LMWH, low–
molecular-weightheparin;MI,myocardialinfarction;UFH,unfractionatedheparin.
a
LMWHshouldbegivenatreduceddose(50%)inpatientswithaserumcreatinine>2mg/dLorGFR<30mL/min.
b
BivalirudinrequiresdosageadjustmentinpatientswithaGFRlessthan30mL/minorthoseonhemodialysis.
AnticoagulationaccompaniedbyDAPTisrequiredforallUA/NSTEMIpatients,whetheralongthe
earlyinvasiveorconservativepathway.
Unfractionatedheparin(UFH)worksbybindingantithrombinIII,whichcatalyzestheinactivation
ofthrombinandotherclottingfactors.
Most commonlyusedandeasilymonitored but also mostinconsistentinits anticoagulationand
metabolism.
Heparin-inducedthrombocytopenia(HIT)isaconcernwithprioruse.
Easilyreversedintheeventofaseverehemorrhagiccomplication.
AlwaysrequiresaggressivebolusdosingandanticoagulationmonitoringinthesettingofACS.
RecommendedanticoagulanttobeusedinthesettingofACS.
Low–molecular-weight heparin (LMWH) inhibits mostly factor Xa but also affects thrombin
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activity and offers an ease of administration (weight-based, twice-daily subcutaneous dose). The
riskofHITislowerbutnotabsent.
AscomparedtoUFH,LMWHhasamorepredictableanticoagulanteffect.
IthasasimilarefficacyasUFHbutisassociatedwithahigherriskofpostproceduralbleeding.
68
LMWH must be adjusted for renal dysfunction and should be avoided in patients with severe
impairments.
Enoxaparin0.3mg/kgIVshouldbeadministeredatthetimeofPCIinpatientswhohavereceived
lessthantwotherapeuticdosesorifthelastdosewasreceivedmorethan8hoursbeforePCI.
Fondaparinux is a synthetic polysaccharide that selectively inhibits factor X and can be
subcutaneouslyadministeredonadailyroutine.
Associated with an increased risk of thrombosis during PCI and should not be used without
additional antithrombin anticoagulation; as such, it is not recommended for the routine
managementofACS.
In patientsnot undergoinginvasivemanagement,fondaparinuxmaysignificantlyreducebleeding
andimproveoutcomescomparedtoLMWH.
69
Bivalirudin is a direct thrombin inhibitor given as a continuous IV infusion and requires partial
thromboplastintime(PTT)monitoringwhenusedfor>4hours.
Itdoes notcauseHITandisusedinthe treatmentofpatientswhodevelopHITorpatientswith
ACSwhohavehistoryofHIT.
Bivalirudin can be given in conjunction with ASA and clopidogrel in patients presenting with
UA/NSTEMIwhowillundergoaroutineinvasivestrategy.
Bivalirudin alone compared to UFH/LMWH + GPIIb/IIIa inhibitor was associated with less
bleeding.
70
RecentevidencehasshownthatinACSwithoutsignificantGPIIb/IIIainhibitoruse,bivalirudinis
associatedwithincreasedriskofstentthrombosisandtargetlesionrevascularization.
71
Caution should be used with routine use of bivalirudin in ACS unless there is a high risk of
bleeding.
Anti-ischemictherapy(pleasealsorefertoTreatmentsectionofstableangina)
Nitroglycerin
Treatmentcanbeinitiatedatthetimeofpresentationwithsublingualnitroglycerin.NOTE:40%
ofpatientswithchestpainnotduetoCADwillgetreliefwithnitroglycerin62(seeTable4-9).
Patients with ongoing ischemic symptoms or those who require additional agents to control
significanthypertensioncanbetreatedwithIVnitroglycerinuntilpainrelief,hypertensioncontrol,
orbothareachieved.
Rule out right ventricular (RV) infarct prior to administration of nitrates because this can
precipitateprofoundhypotension.
β-Adrenergicblockers(BBs)(pleasealsorefertotheTreatmentsectionforstableangina)
Oraltherapyshouldbestartedearlyintheabsenceofcontraindications.
TreatmentwithanIV preparationshould be reservedfortreatmentofarrhythmia, ongoing chest
pain,oradvancedhypertensionratherthanroutineuse.
Routine use of IV BBs is associated with increased risk of cardiogenic shock and should be
avoided.
Contraindications to BB therapy include advanced AV block, active bronchospasm,
decompensatedHF,cardiogenicshock,hypotension,andbradycardia.
Morphine2–4mgIVmaybeusedasanadjuncttoBB,nitrates,andcalciumchannelblockers.Care
mustbeusednottomaskfurtherclinicalevaluationbyheavyuseofnarcoticmedications.
Adjunctivemedicaltherapy
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ACEinhibitors(refer toTreatmentsectionforstable angina)are effective antihypertensive agents
andhavebeenshowntoreducemortalityinpatientswith CAD and LVsystolicdysfunction.ACE
inhibitors should be used inpatients with LV dysfunction (EF < 40%), hypertension, or diabetes
presentingwithACS.ARBsareappropriateinpatientswhocannottolerateACEinhibitors.
Aldosteroneantagonistsshouldbeadded,iftherearenocontraindications(potassium>5mEq/L
or creatinine clearance [CrCl] < 30 mL/min), after initiation of ACE inhibitors to patients with
diabetesoranLVEF<40%.
3-Hydroxy-3-methylglutaryl–coenzymeA(HMG-CoA)reductaseinhibitors(statins)arepotent
lipid-lowering agents that reduce theincidence ofischemia, MI, anddeath in patients withCAD.
High-intensity statinsshould be routinelyadministered within24 hours of presentation inpatients
presentingwithACS.Alipidprofileshouldbeobtainedinallpatients.
Aggressive statin therapy reduces the risk of recurrent ischemia, MI, and death in patients
presentingwithACS.
62
A reduction in adverse CVD outcomes following early initiation of a high-dose statin with
achievementofanLDL<70mg/dLcanbeseenasearlyas30daysfollowinginitialpresentation
withACS.72AggressiveLDLloweringalsoreducestheincidenceofperiproceduralMIfollowing
PCI.
67,73
NSAIDsareassociatedwithanincreasedriskofdeath, MI,myocardialrupture,hypertension,and
HF in large meta-analyses.74 Adverse outcomes have been observed for both nonselective and
selectivecyclooxygenase-2(COX-2)agents.NSAIDsshouldbediscontinuedinpatientspresenting
withUA/NSTEMI.
BloodglucoseshouldnotbetightlycontrolledindiabeticpatientswhohavesufferedACSbecause
itmayincreasemortality.Goalis<180mg/dLwhileavoidinghypoglycemiaatallcosts.
Revascularization
PCI
Pleasesee“Revascularization”sectionunderStableAnginaforinvasivemanagementstrategies.
CABG
The indications for PCI versus CABG in patients with UA/NSTEMI are similar to those for
individuals with chronic stable angina (please see “Revascularization” section under Stable
Angina).
The urgency of revascularization should weigh heavily in the decision for CABG; patients in
cardiogenic shock may benefit from PCI andmechanical supportcompared toemergency cardiac
surgery.
NSTEMIinthesettingofcriticalleftmainCADshouldprompturgentsurgicalrevascularizationand
consideration of intra-aortic balloon pump (IABP) for stabilization prior to the induction of
anesthesia.
Monitoring/Follow-Up
ThehighestrateofprogressiontoMIordevelopmentofrecurrentMIisinthefirst2monthsafter
presentationwiththeindexepisode.Beyondthattime,mostpatientshaveaclinicalcoursesimilarto
thosewithchronicstableangina.
Patientsshouldbedischargedondualantiplatelet,BB,andstatintherapy.
MostpatientsshouldbedischargedonACEinhibitors.
Patientsshouldbeevaluatedfortheneedofaldosteroneantagonists.
Screenforlifestressorsanddepression.Referfordepressiontreatmentasneeded.
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Smokingcessationandriskfactormodificationshouldbestressed.
Referraltocardiacrehabilitationshouldalsobepursued.
ST-SegmentElevationMyocardialInfarction
GENERALPRINCIPLES
Definition
STEMIisdefinedasaclinicalsyndromeofmyocardialischemiainassociationwithpersistentECG
STelevations(see“DiagnosticTesting”section).
STEMIisamedicalemergency.
Compared toUA/NSTEMI,STEMIis associatedwith a higher in-hospitaland30-daymorbidityand
mortality.Leftuntreated,themortalityrateofSTEMIcanexceed30%,andthepresenceofmechanical
complications (papillary muscle rupture, ventricular septal defect [VSD], and free wall rupture)
increasesthemortalityrateto90%.
Ventricularfibrillation(VF)accountsforapproximately50%ofmortalityandoftenoccurswithinthe
firsthourfromsymptomonset.
Keys to treatment of STEMI include rapid recognition and diagnosis, coordinated mobilization of
healthcareresources,andpromptreperfusiontherapy.
Mortalityisdirectlyrelatedtototalischemiatime.
AHA/ACCguidelinesprovideamorethoroughoverviewofSTEMI.
75
Epidemiology
STEMI accounts for approximately 25%–30% of ACS cases annually, and the incidence has been
declining.
Over the lastseveral decades, therehasbeena dramatic improvement inshort-termmortalitytothe
currentrateof6%–10%.
Approximately 30% of STEMI presentations occur in women, but outcomes and complications
continuetobeworsecomparedwithmalecounterparts.
Pathophysiology
STEMI is caused by acute, total occlusion of an epicardial coronary artery, most often due to
atheroscleroticplaquerupture/erosionandsubsequentthrombusformation.
As compared to NSTEMI/UA, thrombotic occlusion is complete such that there is total transmural
ischemia/infarctinthedistributionofthelarge,occludedartery.
DIAGNOSIS
ClinicalPresentation
HISTORY
Severetearingchestpainorfocalneurologicdeficitsshouldraiseconcernforaorticdissection.Aortic
dissection can mimic ACS; in addition, dissections of the ascending aorta may involve the right
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coronaryarteryandcauseSTelevationsontheECG.
STEMImayhaveanatypicalpresentationparticularlyinfemale,elderly,andpostoperativepatients,as
well as those with diabetes and chronic or end-stage kidney disease. Such patients may experience
atypicalornochestpainandmayinsteadpresentwithconfusion,dyspnea,unexplainedhypotension,or
HF.
STEMI should always be considered as an etiology when any patient is hemodynamically
compromised(i.e.,postoperative,delirium,orshock).
Theinitialhistorybytheclinicianshouldalwaysincludeaninquiryaboutpriorcardiacproceduresor
surgery.PriorPCIorCABGcanhaveprofoundimplicationsforacuterevascularizationmanagement.
Theclinicianshouldassessforabsoluteandrelativecontraindicationstothrombolytictherapy(seethe
following text) and potential issues complicating primary PCI (IV contrast allergy, PVD/peripheral
revascularization,renaldysfunction,centralnervoussystemdisease,pregnancy,bleedingdiathesis,or
severecomorbidity).
Inquire about recent cocaine use. In this setting, aggressive medical therapy with nitroglycerin,
coronary vasodilators, and benzodiazepines should be administered before reperfusion therapy is
considered.
PHYSICALEXAMINATION
Physicalexaminationshouldbedirectedatidentifyinghemodynamicinstability,pulmonarycongestion,
mechanicalcomplicationsofMI,andothercausesofacutechestdiscomfort.
TheidentificationofanewsystolicmurmurmaysuggestthepresenceofischemicMRoraVSD.
Alimitedneurologicexamtodetectbaselinecognitiveandmotordeficitsandavascularexamination
(lower extremity pulses and bruits) will aid in determiningcandidacyand planning for reperfusion
treatment.
CardiogenicshockduetorightventricularMI(RVMI)maybeclinicallysuspectedbythepresenceof
hypotension,elevatedjugularvenouspressure,andabsenceofpulmonarycongestion.
BilateralarmBPsshouldbeobtainedtoassessforthepresenceofaorticdissection.
DiagnosticTesting
ELECTROCARDIOGRAPHY
TheECGisparamounttothediagnosisofSTEMIandshouldbeobtainedwithin10minutesof
presentation.IfthediagnosisofSTEMIisindoubt,serialECGsmayhelpelucidatethediagnosis.Classic
findingsincludethefollowing:
PeakeduprightTwavesarethefirstECGmanifestationofmyocardialinjury.
STelevationscorrelatewiththeterritoryofinjuredmyocardium(Table4-14).
TABLE4-14
ELECTROCARDIOGRAM-BASEDANATOMICDISTRIBUTION
STElevation MyocardialTerritory CoronaryArtery
V1–V6orLBBB Anteriorandseptalwalls ProximalLADorleftmain
V1–V
2
Septum ProximalLADorseptalbranch
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V2–V
4
Anteriorwall LAD
V5–V
6
Lateralwall LCX
II,III,aVF Inferiorwall RCAorLCX
I,aVL Highlateralwall DiagonalorproximalLCX
LAD,leftanteriordescendingartery;LBBB,leftbundlebranchblock;LCX,leftcircumflexartery;RCA,rightcoronaryartery.
DiagnosticECGcriteriaforSTEMI
76
When ST elevations reach threshold values in two or more anatomically contiguous leads, a
diagnosisofSTEMIcanbemade.
Inmen>40yearsofage,thresholdvalueforabnormalST-segmentelevationattheJpointis≥2mm
inleads V2 andV3 and >1 mm in all other leads. In men < 40 years of age,threshold value for
abnormalST-segmentelevationattheJpointinleadsV2andV3is>2.5mm.
Inwomen,thethresholdvalueofabnormalST-segmentelevationattheJpointis>1.5mminleads
V2andV3and>1mminallotherleads.
Inright-sidedleads(V3RandV4R),thethresholdforabnormalSTelevationattheJpointis0.5mm,
exceptinmales<30yearsinwhomitis1mm.Right-sidedleadsshouldbeobtainedinallpatients
with evidence of inferior wall ischemia to rule out RV ischemia. RV infarction can occur with
proximalrightcoronaryartery(RCA)lesions.
Inposteriorleads(V7,V8,andV9),thethresholdforabnormalSTelevationattheJpointis0.5mm.
All patients with ST-segment depression inleads V1–V3, inferior wall ST elevation, or tall R
waves in V1–V3 should have posterior leads placed inorder to diagnose a posterior wall MI.
Posterior STEMIs are usually due to occlusion of the circumflex artery and are often
misdiagnosedasUA/NSTEMI.RwavesinV1orV2representQwavesoftheposteriorterritory.
Ischemiaofthecircumflexarterymayalsobeelectrocardiographicallysilent.
The presence of reciprocal ST-segment depression opposite of the infarct territory increases the
specificityforacuteMI.
NewLBBBsuggestsalargeanteriorwallMIwithaworseprognosis.
ECGcriteriaforSTEMIinpatientswithpreexistingLBBBorRVpacingcanbefoundinTable4-15.
Abovecriteriadonotapply.
TABLE4-15
CRITERIAFORST-SEGMENTELEVATIONFORPRIORLBBBORRV-PACEDRHYTHM
ECGChange
ST-segmentelevation>1mminthepresenceofapositiveQRScomplex(concordantwith
theQRS)
ST-segmentelevation>5mminthepresenceofanegativeQRScomplex(disconcordant
withtheQRS)
ST-segmentdepression>1mminV1–V
3
LBBB,leftbundlebranchblock;RV,rightventricular.
Sgarbossa’s (GUSTO) criteria: Am J Cardiol. 1996;77:423; N Engl J Med. 1996;334:481; Pacing Clin Electrophysiol.
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2001;24:1289.
ECG changes that mimic MI. ST-segment elevation and Q waves may result from numerous
etiologies otherthan acuteMI, including prior MI with aneurysm formation,aortic dissection,LV
hypertrophy,pericarditis,myocarditis,pulmonaryembolism,ortheymaybeanormalfinding(Table
4-16).ItiscriticaltoobtainpriorECGstoclarifythediagnosis.
TABLE4-16
DIFFERENTIAL DIAGNOSIS OF ST-SEGMENT ELEVATION ON ECG EXCLUDING
STEMI
CardiacEtiologies OtherEtiologies
PriorMIwithaneurysmformation
Aorticdissectionwithcoronaryinvolvement
Pericarditis
Myocarditis
LVhypertrophyoraorticstenosis(withstrain)
a
Hypertrophiccardiomyopathy
Coronaryvasospasm(cocaine,Prinzmetalangina)
Earlyrepolarization(normalvariant)
Brugadasyndrome
Pulmonaryembolism
Hyperkalemia
LV,leftventricular;MI,myocardialinfarction;ST-segmentelevationmyocardialinfarction.
a
Strainmayoccurinnumeroussettingsincludingsystemichypertension,hypotension,tachycardia,exercise,andsepsis.
Qwaves.DevelopmentofnewpathologicQwavesisconsidereddiagnosticfortransmuralMIbut
mayoccurinpatientswithprolongedischemiaorpoorcollateralsupply.ThepresenceofQwaves
onlyis notanindicationforacute reperfusiontherapy; however,itis veryhelpfultohave anold
ECGtocomparetoinordertodeterminechronicity.Diagnosticcriteriaincludethefollowing:
InleadsV2andV3,apathologicQwaveis≥0.02secondoraQScomplexinV2orV3.Anisolated
QwaveinleadV1orleadIIIisnormal.
InleadsotherthanV1throughV3,presenceofaQwave≥0.03secondand≥0.1mVdeeporaQS
complexinanytwocontiguousleadssuggestspriorMI.
R wave ≥0.04 second in V1 and V2 and R/S ratio ≥1 with a positive T wave suggest prior
posteriorMI(intheabsenceofRVhypertrophyorrightbundlebranchblock[RBBB]).
LABORATORIESANDIMAGING
STEMI diagnosis and initiation of treatment are done in a patient who reports prolonged chest
discomfort or anginal equivalent with qualifying ECG findings. Attempting to wait for results of
cardiacbiomarkerswilladdunnecessarydelay.
Blood samples should be sent for cardiac biomarkers (troponin), complete blood cell count,
coagulation studies (aPTT, prothrombintime [PT], international normalized ratio [INR]), creatinine,
electrolytes including magnesium, and type and screen. A lipid profile should be obtained in all
patientswithSTEMIforsecondaryprevention(notehowever,thatlipidlevelsmaybefalselylowered
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duringtheacutephaseofMI).
Initialcardiacbiomarkers(includingtroponinassays)maybenormal,dependingonthetimeinrelation
tosymptomonset.
The risk of subsequent cardiac death is directly proportional to the increase in cardiac-specific
troponins.Measuringbiomarkersuntilthepeaklevelhasbeenattainedcanbeusedtodetermineinfarct
size.
Routineuseof cardiac noninvasive imaging is notrecommendedforthe initial diagnosis ofSTEMI.
When the diagnosis is in question, a TTE can be performed to document regional wall motion
abnormalities. Ifnotadequately evaluatedbyTTE,a transesophageal echocardiogram (TEE) canbe
obtainedtoassessforacutecomplicationsofMIandpresenceofaorticdissection.
Aportablechestradiographisusefultoassessforpulmonaryedemaandevaluateforothercausesof
chestpainincludingaorticdissection.Importantly,anormalmediastinalwidthdoesnotexcludeaortic
dissection,especiallyifclinicallysuspected.
TREATMENT
Prompt treatment should be initiatedas soonas the diagnosis is suspected, as mortalityandrisk of
subsequentHFaredirectlyrelatedtoischemiatime(Figure4-4).
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