Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2804_Библиотеки_им_академика_М_И_Перельмана
.pdf
taskforceonpracticeguidelines.Circulation.2014;129:S76-S99.
81. JensenMD,RyanDH,ApovianCM,etal.2013AHA/ACC/TOSguidelineforthemanagementof
overweightandobesityinadults:areportoftheAmericanCollegeofCardiology/AmericanHeart
Associationtaskforceonpracticeguidelinesandtheobesitysociety.Circulation.2014;129:S102S138.
82. ArnettDK,BlumenthalRS,AlbertMA,etal.2019ACC/AHAGuidelineontheprimaryprevention
ofcardiovasculardisease:areportoftheAmericanCollegeofCardiology/AmericanHeart
Associationtaskforceonclinicalpracticeguidelines.Circulation.2019;140:e596-e646.
83. DasSR,EverettBM,BirtcherKK,etal.2020Expertconsensusdecisionpathwayonnovel
therapiesforcardiovascularriskreductioninpatientswithType2Diabetes:areportofthe
AmericanCollegeofCardiologysolutionsetoversightcommittee.JAmCollCardiol.
2020;76:1117-1145.
84. WiviottSD,RazI,BonacaMP,etal.Dapagliflozinandcardiovascularoutcomesintype2diabetes.
NEnglJMed.2019;380:347-357.
85. MatsushitaK,vanderVeldeM,AstorBC,etal.Associationofestimatedglomerularfiltrationrate
andalbuminuriawithall-causeandcardiovascularmortalityingeneralpopulationcohorts:a
collaborativemeta-analysis.Lancet.2010;375:2073-2081.
86. PalmerSC,NavaneethanSD,CraigJC,etal.HMGCoAreductaseinhibitors(statins)forpeople
withchronickidneydiseasenotrequiringdialysis.CochraneDatabaseSystRev.
2014;2014:CD007784.
87. ShepherdJ,BlauwGJ,MurphyMB,etal.Pravastatininelderlyindividualsatriskofvascular
disease(PROSPER):arandomisedcontrolledtrial.Lancet.2002;360:1623-1630.
88. Lloyd-JonesDM,MorrisPB,BallantyneCM,etal.2017Focusedupdateofthe2016ACCexpert
consensusdecisionpathwayontheroleofnon-statintherapiesforLDL-cholesterolloweringinthe
managementofatheroscleroticcardiovasculardiseaserisk:areportoftheAmericanCollegeof
Cardiologytaskforceonexpertconsensusdecisionpathways.JAmCollCardiol.2017;70:1785-
1822.
89. SarwarN,DaneshJ,EiriksdottirG,etal.Triglyceridesandtheriskofcoronaryheartdisease:
10,158incidentcasesamong262,525participantsin29Westernprospectivestudies.Circulation.
2007;115:450-458.
90. TiroshA,RudichA,ShochatT,etal.Changesintriglyceridelevelsandriskforcoronaryheart
diseaseinyoungmen.AnnInternMed.2007;147:377-385.
91. MillerM,StoneNJ,BallantyneC,etal.Triglyceridesandcardiovasculardisease:ascientific
statementfromtheAmericanHeartAssociation.Circulation.2011;123:2292-2333.
92. GoffDCJr,Lloyd-JonesDM,BennettG,etal.2013ACC/AHAguidelineontheassessmentof
cardiovascularrisk:areportoftheAmericanCollegeofCardiology/AmericanHeartAssociation
taskforceonpracticeguidelines.Circulation.2014;129:S49-S73.
93. vanGorselenEO,DiekmanT,HesselsJ,etal.ArtifactualmeasurementoflowserumHDLcholesterolduetoparaproteinemia.ClinResCardiol.2010;99:599-602.
94. RobinsonJG,GoldbergAC.Treatmentofadultswithfamilialhypercholesterolemiaandevidence
fortreatment:recommendationsfromtheNationalLipidassociationexpertpanelonfamilial
hypercholesterolemia.JClinLipidol.2011;5:S18-S29.
95. KnoppRH.Drugtreatmentoflipiddisorders.NEnglJMed.1999;341:498-511.
96. FulcherJ,O’ConnellR,VoyseyM,etal.EfficacyandsafetyofLDL-loweringtherapyamongmen
andwomen:meta-analysisofindividualdatafrom174,000participantsin27randomisedtrials.
Lancet.2015;385:1397-1405.
97. ChongPH.LackoftherapeuticinterchangeabilityofHMG-CoAreductaseinhibitors.Ann
https://t.me/med1917

Pharmacother.2002;36:1907-1917.
98. PasternakRC,SmithSCJr,Bairey-MerzCN,etal.ACC/AHA/NHLBIclinicaladvisoryontheuse
andsafetyofstatins.Circulation.2002;106:1024-1028.
99. ThompsonPD,PanzaG,ZaleskiA,etal.Statin-associatedsideeffects.JAmCollCardiol.
2016;67:2395-2410.
100. VeneroCV,ThompsonPD.Managingstatinmyopathy.EndocrinolMetabClinNorthAm.
2009;38:121-136.
101. SattarN,PreissD,MurrayHM,etal.Statinsandriskofincidentdiabetes:acollaborativemetaanalysisofrandomisedstatintrials.Lancet.2010;375:735-742.
102. CollinsR,ReithC,EmbersonJ,etal.Interpretationoftheevidencefortheefficacyandsafetyof
statintherapy.Lancet.2016;388:2532-2561.
103. KellickKA,BottorffM,TothPP,etal.Aclinician’sguidetostatindrug-druginteractions.JClin
Lipidol.2014;8:S30-S46.
104. Thelipidresearchclinicscoronaryprimarypreventiontrialresults.I.Reductioninincidenceof
coronaryheartdisease.JAMA.1984;251:351-364.
105. IllingworthDR,SteinEA,MitchelYB,etal.Comparativeeffectsoflovastatinandniacinin
primaryhypercholesterolemia.Aprospectivetrial.ArchInternMed.1994;154:1586-1595.
106. BodenWE,ProbstfieldJL,AndersonT,etal.NiacininpatientswithlowHDLcholesterollevels
receivingintensivestatintherapy.NEnglJMed.2011;365:2255-2267.
107. HPS2-THRIVECollaborativeGroup.HPS2-THRIVErandomizedplacebo-controlledtrialin25
673high-riskpatientsofERniacin/laropiprant:trialdesign,pre-specifiedmuscleandliver
outcomes,andreasonsforstoppingstudytreatment.EurHeartJ.2013;34:1279-1291.
108. DujovneCA,EttingerMP,McNeerJF,etal.Efficacyandsafetyofapotentnewselective
cholesterolabsorptioninhibitor,ezetimibe,inpatientswithprimaryhypercholesterolemia.AmJ
Cardiol.2002;90:1092-1097.
109. KnoppRH,GitterH,TruittT,etal.Effectsofezetimibe,anewcholesterolabsorptioninhibitor,
onplasmalipidsinpatientswithprimaryhypercholesterolemia.EurHeartJ.2003;24:729-741.
110. GagneC,BaysHE,WeissSR,etal.Efficacyandsafetyofezetimibeaddedtoongoingstatin
therapyfortreatmentofpatientswithprimaryhypercholesterolemia.AmJCardiol.2002;90:1084-
1091.
111. GoldbergAC,SapreA,LiuJ,etal.Efficacyandsafetyofezetimibecoadministeredwith
simvastatininpatientswithprimaryhypercholesterolemia:arandomized,double-blind,placebocontrolledtrial.MayoClinProc.2004;79:620-629.
112. BaigentC,LandrayMJ,ReithC,etal.TheeffectsofloweringLDLcholesterolwithsimvastatin
plusezetimibeinpatientswithchronickidneydisease(StudyofHeartandRenalProtection):a
randomisedplacebo-controlledtrial.Lancet.2011;377:2181-2192.
113. CannonCP,BlazingMA,GiuglianoRP,etal.Ezetimibeaddedtostatintherapyafteracute
coronarysyndromes.NEnglJMed.2015;372:2387-2397.
114. ItoMK,McGowanMP,MoriartyPM.Managementoffamilialhypercholesterolemiasinadult
patients:recommendationsfromtheNationalLipidAssociationexpertpanelonfamilial
hypercholesterolemia.JClinLipidol.2011;5:S38-S45.
115. RayKK,BaysHE,CatapanoAL,etal.SafetyandefficacyofbempedoicacidtoreduceLDL
cholesterol.NEnglJMed.2019;380:1022-1032.
116. GoldbergAC,LeiterLA,StroesESG,etal.Effectofbempedoicacidvsplaceboaddedto
maximallytoleratedstatinsonlow-densitylipoproteincholesterolinpatientsathighriskfor
cardiovasculardisease:theCLEARWisdomRandomizedClinicalTrial.JAMA.2019;322:1780-
1788.
https://t.me/med1917

117. SabatineMS,GiuglianoRP,KeechAC,etal.Evolocumabandclinicaloutcomesinpatientswith
cardiovasculardisease.NEnglJMed.2017;376:1713-1722.
118. SchwartzGG,StegPG,SzarekM,etal.Alirocumabandcardiovascularoutcomesafteracute
coronarysyndrome.NEnglJMed.2018;379:2097-2107.
119. BanerjeeP,ChanKC,TarabocchiaM,etal.FunctionalanalysisofLDLR(low-densitylipoprotein
receptor)variantsinpatientlymphocytestoassesstheeffectofevinacumabinhomozygousfamilial
hypercholesterolemiapatientswithaspectrumofLDLRactivity.ArteriosclerThrombVascBiol.
2019;39:2248-2260.
120. BrunzellJD.Clinicalpractice.Hypertriglyceridemia.NEnglJMed.2007;357:1009-1017.
121. KeechA,SimesRJ,BarterP,etal.Effectsoflong-termfenofibratetherapyoncardiovascular
eventsin9795peoplewithtype2diabetesmellitus(theFIELDstudy):randomisedcontrolledtrial.
Lancet.2005;366:1849-1861.
122. RosensonRS.Currentoverviewofstatin-inducedmyopathy.AmJMed.2004;116:408-416.
123. Alsheikh-AliAA,KuvinJT,KarasRH.Riskofadverseeventswithfibrates.AmJCardiol.
2004;94:935-938.
124. JonesPH,DavidsonMH.Reportingrateofrhabdomyolysiswithfenofibrate+statinversus
gemfibrozil+anystatin.AmJCardiol.2005;95:120-122.
125. NestelPJ,ConnorWE,ReardonMF,etal.Suppressionbydietsrichinfishoilofverylow
densitylipoproteinproductioninman.JClinInvest.1984;74:82-89.
126. HarrisWS,ConnorWE,IllingworthDR,etal.EffectsoffishoilonVLDLtriglyceridekineticsin
humans.JLipidRes.1990;31:1549-1558.
127. Kris-EthertonPM,RichterCK,BowenKJ,etal.Recentclinicaltrialsshednewlightonthe
cardiovascularbenefitsofomega-3fattyacids.MethodistDebakeyCardiovascJ.2019;15:171-
178.
128. MansonJE,CookNR,LeeIM,etal.Marinen-3fattyacidsandpreventionofcardiovascular
diseaseandcancer.NEnglJMed.2019;380:23-32.
129. BowmanL,MafhamM,WallendszusK,etal.Effectsofn-3fattyacidsupplementsinDiabetes
Mellitus.NEnglJMed.2018;379:1540-1550.
130. BhattDL,StegPG,MillerM,etal.Cardiovascularriskreductionwithicosapentethylfor
hypertriglyceridemia.NEnglJMed.2019;380:11-22.
131. AlfaddaghA,ElajamiTK,SalehM,etal.Theeffectofeicosapentaenoicanddocosahexaenoic
acidsonphysicalfunction,exercise,andjointreplacementinpatientswithcoronaryarterydisease:
asecondaryanalysisofarandomizedclinicaltrial.JClinLipidol.2018;12:937-947.e2.
132. MakiKC,McKenneyJM,ReevesMS,etal.Effectsofaddingprescriptionomega-3acidethyl
esterstosimvastatin(20mg/day)onlipidsandlipoproteinparticlesinmenandwomenwithmixed
dyslipidemia.AmJCardiol.2008;102:429-433.
133. BarterP,GinsbergHN.Effectivenessofcombinedstatinplusomega-3fattyacidtherapyfor
mixeddyslipidemia.AmJCardiol.2008;102:1040-1045.
134. BallantyneCM,OlssonAG,CookTJ,etal.Influenceoflowhigh-densitylipoproteincholesterol
andelevatedtriglycerideoncoronaryheartdiseaseeventsandresponsetosimvastatintherapyin
4S.Circulation.2001;104:3046-3051
https://t.me/med1917

4
IschemicHeartDisease
NoahN.Williford,MarcA.Sintek
CoronaryHeartDiseaseandStableAngina
GENERALPRINCIPLES
Definition
Coronaryarterydisease (CAD)refers tothe luminal narrowingof a coronaryartery, usuallydue to
atherosclerosis.CADistheleadingcontributortoischemicheartdisease(IHD).IHDincludesangina
pectoris,myocardialinfarction(MI),andsilentmyocardialischemia.
Cardiovascular disease (CVD) includes IHD, cardiomyopathy, heart failure (HF), arrhythmia,
hypertension, cerebrovascular accident (CVA), diseases of the aorta, peripheral vascular disease
(PVD),valvularheartdisease,andcongenitalheartdisease.
Stable anginais definedas anginasymptoms or angina equivalent symptoms that are reproducedby
consistentlevelsofactivityandrelievedbyrest.
AmericanHeartAssociation/AmericanCollegeofCardiology(AHA/ACC)guidelinesprovideamore
thoroughoverviewofstableIHD.
1,2
Epidemiology
ThelifetimeriskofIHDatage40isoneintwoformenandoneinthreeforwomen.
Therearemorethan15millionAmericanswithIHD,50%ofwhomhavechronicangina.
CVDhasbecomeanimportantcauseofdeathworldwide,accountingfornearly30%ofalldeathsand
hasbecomeincreasinglysignificantindevelopingnations.
3
Etiology
CADmostcommonlyresultsfromluminalaccumulationofatheromatousplaque.
Other causes of obstructive CAD include congenital coronary anomalies, myocardial bridging,
vasculitis,andpriorradiationtherapy.
Pathophysiology
Stable angina results from progressive luminal obstruction of angiographically visible epicardial
coronaryarteriesor,lesscommonly,obstructionofthemicrovasculature,whichresultsinamismatch
betweenmyocardialoxygensupplyanddemand.
Atherosclerosis is aninflammatory process, initiatedbylipid depositioninthe arterial intima layer
followedbyrecruitmentofinflammatorycellsandproliferationofarterialsmoothmusclecellstoform
anatheroma.
https://t.me/med1917

The coronary lesionsresponsible for stable angina differ from the vulnerable plaques associated
with acute MI. The stable angina lesion is fixed and is less prone to fissuring, hence producing
symptomsthataremorepredictable.
4
Allcoronarylesionsareeccentricanddonotuniformlyaltertheinnercircumferenceoftheartery.
Epicardialcoronarylesionscausinglessthan40%luminalnarrowinggenerallydonotsignificantly
impaircoronaryflow.
Moderateangiographiclesions(40%–70% obstruction) mayinterfere withflow andare routinely
underestimatedoncoronaryangiogramsgiventheeccentricityofCAD.
RiskFactors
OfIHDevents,>90%canbeattributedtoelevationsinatleastonemajorriskfactor.
5
AssessmentoftraditionalCVDriskfactorsincludes:
Age
Bloodpressure(BP)
Bloodglucose(Note:DiabetesisconsideredanIHDriskequivalent.)
Lipidprofile(low-densitylipoprotein[LDL],high-densitylipoprotein[HDL],triglycerides);direct
LDLfornonfastingsamplesorveryhightriglycerides
Tobacco use (Note: Smoking cessation restores the risk of IHD to that of a nonsmoker within
approximately15years.)
6
Familyhistory of premature CAD: Defined as first-degree male relative with IHD before age55
yearsorfemalerelativebeforeage65years
Measures forobesity,particularlycentralobesity;bodymassindexgoalisbetween18.5 and24.9
kg/m2;waistcircumferencegoalis<40informenand<35inforwomen
As of 2013, AHA/ACC guidelines recommend assessing 10-year atherosclerotic cardiovascular
disease(ASCVD)riskforpatientsaged40–79 years usingnewrace andage-specific pooledcohort
equations.
7
The ASCVD risk calculator is available online (http://tools.cardiosource.org/ASCVD-Risk-
Estimator/).
If there remains uncertainty about lower risk estimates, high-sensitivity C-reactive protein (≥2
mg/dL),coronaryarterycalciumscore(≥300Agatstonunitsor≥75thpercentile),orankle-brachial
index(<0.9)maybeobtainedtoreviseriskestimatesupward.
Traditionalriskfactorsnotedaboveshouldbeassessedinpatientsyoungerthan40yearsandevery
4–6 years after 40;10-yearASCVDriskshouldbe calculated every 4–6 years in patients 40–79
yearsofage.
LifetimeriskcanbeassessedusingtheASCVDriskcalculatorandmaybehelpfulinthesettingof
counselingpatientsaboutlifestylemodifications.
Prevention
Primaryprevention:SeeChapter3,PreventiveCardiology.
ClinicalPresentation
HISTORY
Typical angina has three features: (1) substernal chest discomfort with a characteristic qualityand
durationthatis(2)provokedbystressorexertionand(3)relievedbyrestornitroglycerin.
https://t.me/med1917

Atypicalanginahastwoofthesethreecharacteristics.
Noncardiacchestpainmeetsoneornoneofthesecharacteristics.
Chronicstable anginais reproduciblyprecipitatedina predictable manner byexertion or emotional
stressandrelievedwithin5–10minutesbysublingualnitroglycerinorrest.
The severity of angina may be quantified using the Canadian Cardiovascular Society (CCS)
classificationsystem(Table4-1).
TABLE4-1
CANADIANCARDIOVASCULARSOCIETY(CCS)CLASSIFICATIONSYSTEM
Class Definition
CCS1Anginawithstrenuousorprolongedactivity
CCS2Anginawithmoderateactivity(walkinggreaterthantwolevelblocksoroneflightof
stairs)
CCS3Anginawithmildactivity(walkinglessthantwolevelblocksoroneflightofstairs)
CCS4Anginathatoccurswithanyactivityoratrest
Anginalsymptomsmayincludetypicalchestdiscomfortoranginalequivalents.
DatafromSangareddiV,AnandC,GnanaveluG,etal.CanadianCardiovascularSocietyclassificationofeffortangina:an
angiographiccorrelation.CoronArteryDis.2004;15(2):111-114.
Associatedsymptomsmayincludedyspnea,diaphoresis,nausea,vomiting,dizziness,jawpain,andleft
armpain.
Female patients and those with diabetes or chronic kidney disease may have minimal or atypical
symptomsthatserveasanginalequivalents.Suchsymptomsincludedyspnea(mostcommon),epigastric
pain,andnausea.
The clinician’s assessment of the pretest probability of IHD is the important driver for further
diagnostictesting inpatientswithoutknownCADandis largelyascertainedfromtheclinicalhistory
(Table4-2).Patientswithalowpretestprobability(<5%)ofCADareunlikelytobenefitfromfurther
diagnostictestingaimedatdetectingCAD.
TABLE4-2
PRETESTPROBABILITYOFCORONARYARTERYDISEASEBYAGE,GENDER,AND
SYMPTOMS
Age(y) Asymptomatic Nonanginal
ChestPain
Atypical/Probable
AnginaPectoris
Typical/Definite
AnginaPectoris
Gender Women Men Women Men Women Men Women Men
30–39 <5 <5 2 4 12 34 26 76
40–49 <5 <10 3 13 22 51 55 87
https://t.me/med1917

50–59 <5 <10 7 20 31 65 73 93
60–69 <5 <5 14 27 51 72 86 94
Verylow<5% Low<10% Intermediate10%–80% High>80%
DatafromGibbonsRJ,BaladyGJ,BrickerJT,etal.(CommitteeMembers).ACC/AHA2002guidelineupdateforexercisetesting–
summaryarticle:areportoftheAmericanCollegeofCardiology/AmericanHeartAssociationTaskForceonPracticeGuidelines
(CommitteetoUpdatethe1997ExerciseTestingGuidelines).Circulation.2002;106(14):1883-1892.
DifferentialDiagnosis
A wide range ofdisorders maymanifestwithchestdiscomfortandmay include both cardiovascular
andnoncardiovascularetiologies(Table4-3).
TABLE4-3
DIFFERENTIALDIAGNOSISOFCHESTPAINEXCLUDINGEPICARDIAL
ATHEROSCLEROSIS
Diagnosis Comments
Cardiovascular
Aorticstenosis Anginalepisodescanoccurwithsevereaorticstenosis.
HCM Subendocardialischemiamayoccurwithexerciseand/orexertion.
Prinzmetal
angina
Coronaryvasospasmthatmaybeelicitedbyexertionoremotionalstress.
Pericarditis Pleuriticchestpainassociatedwithpericardialinflammationfrominfectious
orautoimmunedisease.
Aortic
dissection
Maymimicanginalpainand/orinvolvethecoronaryarteries.
Cocaineuse Resultsincoronaryvasospasmand/orthrombusformation.
Other
Anemia MarkedanemiacanresultinamyocardialO2supply–demandmismatch.
Thyrotoxicosis IncreaseinmyocardialdemandmayresultinanO2supply–demand
mismatch.
Esophageal
disease
GERDandesophagealspasmcanmimicangina(responsivetoNTG).
Biliarycolic Gallstonescanusuallybevisualizedonabdominalsonography.
Respiratory
diseases
Pneumoniawithpleuriticpain,pulmonaryembolism,pulmonaryhypertension.
Musculoskeletal Costochondritis,cervicalradiculopathy.
https://t.me/med1917

GERD,gastroesophagealrefluxdisease;HCM,hypertrophiccardiomyopathy;NTG,nitroglycerin.
A careful history focused on cardiac risk factors, physical exam, and initial laboratory evaluation
usuallynarrowsthedifferentialdiagnosis.
InpatientswithestablishedIHD,alwayslookforexacerbatingfactorsthatcontributetoischemia.
Any process that reduces myocardial oxygen supply or increases demand can cause or exacerbate
angina(Table4-4).
TABLE4-4
CONDITIONSTHATMAYPROVOKEOREXACERBATEISCHEMIA/ANGINA
INDEPENDENTOFWORSENINGATHEROSCLEROSIS
IncreasedOxygenDemand DecreasedOxygenSupply
Noncardiac
Hyperthermia
Hyperthyroidism
Sympathomimetic toxicity (i.e.,
cocaineuse)
Hypertension
Anxiety
Anemia
Sicklecelldisease
Hypoxemia
Pneumonia
Asthmaexacerbation
Chronicobstructivepulmonarydisease
Pulmonaryhypertension
Pulmonaryfibrosis
Obstructivesleepapnea
Pulmonaryembolus
Sympathomimetic toxicity (i.e., cocaine use,
pheochromocytoma)
Hyperviscosity
Polycythemia
Leukemia
Thrombocytosis
Hypergammaglobulinemia
Cardiac
Hypertrophiccardiomyopathy
Aorticstenosis
Dilatedcardiomyopathy
Tachycardia
Ventricular
Supraventricular
Aorticstenosis
Elevatedleftventricularend-diastolicpressure
Hypertrophiccardiomyopathy
Microvasculardisease
https://t.me/med1917

ModifiedfromFihnSD,GardinJM,AbramsJ,etal.2012ACCF/AHA/ACP/AATS/PCNA/SCAI/STSGuidelineforthediagnosisand
managementofpatientswithstableischemicheartdisease:areportoftheAmericanCollegeofCardiologyFoundation/American
HeartAssociationTaskForceonPracticeGuidelines,andtheAmericanCollegeofPhysicians,AmericanAssociationfor
ThoracicSurgery,PreventiveCardiovascularNursesAssociation,SocietyforCardiovascularAngiographyandInterventions,and
SocietyofThoracicSurgeons.JAmCollCardiol.2012;60(24):e44-e164.Copyright©2012AmericanCollegeofCardiology
FoundationandtheAmericanHeartAssociation,Inc.Withpermission.
DiagnosticTesting
Generaldiagnostictesting
A resting ECGcanbe helpful in determining the presence of prior infarcts or conductionsystem
diseaseandmayalertthecliniciantothepossibilityofCADinpatientswithchestpain.
Atransthoracicechocardiogram(TTE)canbeusefulindeterminingpresenceofleftventricular(LV)
dysfunctionorvalvularheartdiseasethatmayaffectthemanagementanddiagnosisofIHD.TTEcan
alsobeusedtoassessforrestingwallmotionabnormalitiesthatmaybetheresultofpriorMI.
Evidenceofvascular diseaseor prior MI onthe diagnostic testingmodalities notedabove should
raisethepretestprobabilityofIHDinpatientspresentingwithchestpain.
Stresstestingoverview
Allstress testingrequires (1)acardiovascularstressand(2) a wayofevaluatingcardiac changes
consistentwithischemia. Thelatteris alwaysdonewith continuousECG;however,itcanbedone
eitherwithorwithoutanimagingmodality.
Many stress testing modalities provide not only detection of ischemia/CAD but also prognostic
informationbasedontheburdenofischemia.
Table 4-5 provides an overview of the sensitivity and specificity for each stress and imaging
modalityalongwithadvantagesanddisadvantagesforthecliniciantoconsider.
TABLE4-5
DIAGNOSTICACCURACYOFCOMMONSTRESSTESTINGMODALITIESINPATIENTS
WITHOUTKNOWNISCHEMICHEARTDISEASE
TestType Sensitivity Specificity Advantages Disadvantages
ECG
Exercise 61% 70%–77%
Easytoperform
Inexpensive
Less diagnostic
accuracy,
especially in
women
No viability
assessment
Pharmacologic — —
Echocardiography
Exercise 70%–85% 77%–89%
Gather other important
information on diastolic
function, valvular
disorders, and
pulmonarypressures
Limited by
imagequality
Diagnostic
accuracy
reduced with
Pharmacologic
(dobutamine)
85%–90% 79%–90%
https://t.me/med1917

Can assess viability with
pharmacologicstress
resting wall
motion
abnormalities
NuclearPerfusionImaging
Exercise 82%–88% 70%–88%
More sensitive for small
areasofischemia/infarct
Very accurate ejection
fractionassessment
Easy to compare to
priorstudies
Significant
radiation
May
underestimate
severe
balanced
ischemia
No other valve
or other
structural
information
Viability may
require
separate
testing
Pharmacologic
(adenosine,
regadenoson,or
dobutamine)
82%–91% 75%–90%
CardiacMRI
Exercise — —
Excellent assessment of
viability
Anatomic detail of heart
and great vessels
superb
Expensive
Requires
closedMRI
Exercise option
not typically
available
Pharmacologic
a
91% 81%
Alldiagnosticaccuraciesunadjustedforreferralbias.
1,2
a
Vasodilatorstressonly;dobutaminehassensitivityof83%andspecificityof86%.
Stresstestingindications
SeetheACCF2013MultimodalityAppropriateUseCriteriafortheDetectionandRiskAssessment
ofStableIschemicHeartDisease10foracomprehensivelistoftheindicationsforstresstesting.
Thefollowingaresomeofthemorecommonindications:
PatientswithoutknownCAD:
□ Patientswithanginalsymptomswhoareintermediaterisk
□ Asymptomaticintermediate-riskpatientswhoplanonbeginningavigorousexerciseprogramor
workinginahigh-riskoccupation(e.g.,airlinepilot)
□ Atypical symptoms in patients with a high risk of IHD (i.e., diabetes or vascular disease
patients)
PatientswithknownCAD:
□ Post-MIriskstratification(seesectiononST-segmentelevationMI)
□ Preoperativeriskassessmentifitwillchangemanagementpriortosurgery
□ Recurrentanginalsymptomsdespitemedicaltherapyorrevascularization
https://t.me/med1917
Соседние файлы в папке Библиотека им академика М.И. Перельмана
