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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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Assess EF in patients with severe MR but with an inadequate assessment of EF by
echocardiography.
AssessquantitativemeasureofMRseveritywhenechocardiographyisnondiagnostic.
ViabilityassessmentmayplayaroleinconsideringtherapeuticstrategyinischemicMR.
TREATMENT
AcuteMitralRegurgitation
Whileawaitingsurgery,aggressiveafterloadreductionwithIVnitroprussideoranIABPcandiminish
theamountofMRandstabilizethepatientbypromotingforwardflowandreducingpulmonaryedema.
Thesepatientsare usuallytachycardic,butattemptstoslow downtheir heartrateshouldbe avoided
becausetheyareoftenheartratedependentforanadequateforwardCO.
ChronicMitralRegurgitation
ChronicprimaryMR
Medical therapyis reasonable inpatientswith chronic primary MRand LVEF less than 60% not
undergoingsurgery.
Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers have been
showntoreducetheregurgitantfractionandaidwithventricularremodeling.β-Blockershavealso
beenshowntoreduceseverityofMRinasymptomaticpatients.
ThereisnobenefitofvasodilatortherapyintheasymptomaticpatientwithnormalLVfunctionand
chronicsevereMR.
ChronicsecondaryMR
TreatsymptomsrelatedtoLVdysfunction.
Guideline-directedmedicaltherapy(GDMT)forLVsystolicdysfunction,includingACEinhibitors
andβ-blockers,isindicatedandhasbeenshowntoreducemortalityandtheseverityofMR.
Somepatientsmayalsoqualifyforcardiacresynchronizationtherapy,whichcanfavorablyremodel
theLVandreducetheseverityofMR.
PercutaneousIntervention
2
Transcatheteredgetoedgerepair(TEER)(i.e.,MitraClip)pinchestheleafletstogetherinanattemptto
enhance coaptation (a percutaneous treatment analogous to the surgical Alfieri stitch), creating a
double-orificevalve.
This procedure is performed via femoral venous access, and a transseptal puncture is used to
positionthedeliverysystemintheLA.
UsingfluoroscopyandTEEguidance,theclipisadvancedandattemptsaremadetograsptheleaflet
tipsoftheanteriorandposteriorMVleafletsandclipthemtogether.
Indicated for chronic severe secondaryMRwith LVEF between 20% and 50% for patients with
persistentsymptomsdespiteGDMTandappropriateanatomy(ClassIIa).
This recommendation comes from results of the COAPT trial demonstrating improvement in
survival,symptoms,andqualityoflifeinselectedpatientswithmoderatetoseveresecondaryMR
whounderwentTEERascomparedtomedicaltherapyalone.
7,8
TEERisalsoanoptionforpatientswithseverelysymptomaticwith primarysevereMRathighor
prohibitivesurgicalriskwhohavefavorableanatomy(ClassIIa).
Transcatheter mitral valve replacement is an emerging structural intervention and currently being
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investigatedinanumberofclinicaltrials.Currently,thistechnologyisonlyreservedfordegenerative
MR.
SurgicalManagement
PrimaryMR
2
SymptomaticwithchronicsevereprimaryMR(stageD)(ClassI).
Asymptomatic withchronic severe primaryMRwithEF≤60% or LV end-systolicdimension≥40
mm(stageC2;ClassI).
ChronicsevereprimaryMRundergoingcardiacsurgeryforotherindications(ClassI).
Repairisrecommendedoverreplacement(ClassI).
AsymptomaticpatientswithchronicsevereprimaryMR(stageC1)inwhomrepairishighlylikely
(>95%)andoperativemortalityislow(<1%)(ClassIIa).
SecondaryMR
2
ClassIIa:chronicseveresecondaryMRundergoingcardiacsurgeryforotherindications.
ClassIIb
SeverelysymptomaticpatientsdespiteGDMT(NYHAIII/IV)withchronicseveresecondaryMR
(stageD)andLVEF≥50%.
PatientswithpersistentsymptomswithchronicseveresecondaryMR(stageD)andLVEF<50%
whodonothavefavorableanatomyforTEER.
NotethatthebenefitsofsurgeryarenotwellestablishedforsecondaryMR.
AorticRegurgitation
ARmayresultfrompathologyoftheaorticvalve,theaorticroot,orboth;itisimportantthatboththe
aorticvalveandtheaorticrootareevaluatedtodeterminetheappropriatemanagementandtreatment.
ARusuallyprogresses insidiouslywitha longasymptomatic period;whenitoccursacutely, patients
areoftenverysickandmustbemanagedaggressively.
Etiology
Morecommon
Bicuspid aortic valve, rheumatic disease, calcific degeneration, infective endocarditis, idiopathic
dilatationoftheaorta,myxomatousdegeneration,systemichypertension,dissectionoftheascending
aorta,Marfansyndrome.
Lesscommon
Traumaticinjurytotheaorticvalve,collagenvasculardiseases(ankylosingspondylitis,rheumatoid
arthritis, reactive arthritis, giant cell aortitis, and Whipple disease), syphilitic aortitis, discrete
subaorticstenosis,ventricularseptaldefectwithprolapseofanaorticcusp.
AcuteAR
Infectiveendocarditis,dissectionoftheascendingaorta,trauma.
Pathophysiology
AcuteAR(Figure6-4)
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Figure 6-4 Acute aortic regurgitation.CO, cardiac output; HR, heart rate; LAP, left atrial pressure; LV, left ventricle;
LVEDP,leftventricularend-diastolicpressure;SV,strokevolume.
ChronicAR(Figure6-5)
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Figure 6-5 Chronic aortic regurgitation.CHF, congestive heart failure; CO, cardiac output; EF, ejection fraction; LV, left
ventricle;LVED,leftventricularend-diastolic;LVEDP,leftventricularend-diastolicpressure;LVH,leftventricularhypertrophy;
SV,strokevolume.
DIAGNOSIS
History
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Acute AR: patients with acute ARmay presentwith symptoms of cardiogenic shock and severe
dyspnea.OtherpresentingsymptomsmayberelatedtothecauseofacuteAR.
Chronic AR: symptoms dependonthepresence of LVdysfunction andwhether the patientis in the
compensated versus decompensated stage. Compensated patients are typically asymptomatic,
whereas those inthe decompensated stage maynotedecreased exercise tolerance, dyspnea, fatigue,
and/orangina.
PhysicalExamination
AcuteAR
Widened pulse pressure may be present, but it is often not present because forward SV (and
thereforesystolicbloodpressure)isreduced.
Mayhearbriefsoftdiastolicmurmurorsystolicflowmurmur.
Look for evidenceofaortic dissection, infective endocarditis, andcharacteristics associated with
Marfandisease.
ChronicAR
LVheave;pointofmaximalimpulseislaterallydisplaced.
Diastolic decrescendomurmur heard best at leftsternal border leaning forward at end-expiration
(severityofARcorrelateswithduration,notintensity,ofthemurmur).
Systolicflowmurmur(mostlybecauseofvolumeoverload;concomitantASmayalsobepresent).
Widenedpulse pressure (often >100 mm Hg)with a low diastolic pressure;there are numerous
eponymsforthecharacteristicsignsrelatedtoawidepulsepressure.
DiagnosticTesting
ECG:tachycardia,LVH,andLAE(morecommoninchronicAR).
CXR:pulmonaryedema,widenedmediastinum,andcardiomegaly.
TTE
Assess LV systolic function, LV dimensions at end systole and diastole, leaflet number and
morphology,assessmentoftheseverityofAR.
Lookforevidenceofendocarditisoraorticdissection,dimensionofaorticroot.
TEE
ClarifywhetherthereisabicuspidvalveifunclearonTTE.
BettersensitivityandspecificityforaorticdissectionthanTTE.
ClarifywhetherthereisendocarditiswithorwithoutrootabscessifunclearonTTE.
Bettervisualizationofaorticvalveinpatientswithaprostheticaorticvalve.
Cardiaccatheterization:assessmentofLVpressure,LVfunction,andseverityofAR(viaaorticroot
angiography) is indicated in symptomatic patients in whom the severity of AR is unclear on
noninvasiveimagingordiscordantwithclinicalfindings.
MRI/CT
Either ofthesemaybe the imagingmodalityofchoice for evaluating aortic dimensionsand/or for
evaluationofaorticdissection.
IfechocardiographyassessmentoftheseverityofARisinadequate,MRIisusefulforassessingthe
severityofAR.
TREATMENT
TheroleofmedicaltherapyinpatientswithARislimited.
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Vasodilator therapy (i.e., nifedipine, ACE inhibitor, hydralazine) is indicated to reduce systolic
bloodpressureinhypertensivepatientswithAR.
Whenendocarditisissuspectedorconfirmed,appropriateantibioticcoverageiscritical.
SurgicalManagement
AHA/ACCrecommendationsforintervention
2
SymptomaticpatientswithsevereAR(stageD)regardlessofLVsystolicfunction(ClassI).
Asymptomatic patientswith chronic severeARandLVsystolic dysfunction(EF≤55%) (stageC2;
ClassI).
PatientswithsevereAR(stageCorD)undergoingcardiacsurgeryforotherindications(ClassI).
AsymptomaticpatientswithsevereARandnormalLVsystolicfunction(EF>55%)butwithsevere
LVdilation(LVend-systolicdimension>50mm)(stageC2;ClassIIa).
Acute,severeARisalmostuniversallysymptomaticandistreatedsurgically.
If the aortic rootis dilated, itmay be repaired or replaced atthe time of AVR. For patients witha
bicuspid valve, Marfan syndrome, or a related genetically triggered aortopathy, surgeryonthe aorta
shouldbeconsideredatthetimeofAVR.
Outcome/Prognosis
Asymptomatic patients with normal LV systolic function (LVEF ≥55%): progression to symptoms
and/orLVdysfunctionapproximately6%peryear.
9
AsymptomaticpatientswithLVdysfunction(LVEF<50%):progressiontocardiacsymptoms>25%per
year.
9,10
Symptomaticpatients:mortalityrateapproximately9.4%peryear.
9
ProstheticHeartValves
The choice ofvalve prosthesis dependsonmany factors including thepatient,surgeon, cardiologist,
andclinicalscenario.
Withimprovementsinbioprostheticvalves,therecommendationforamechanicalvalveinpatients<65
yearsofageisnolongerasfirm,andbioprostheticvalveusehasincreasedinyoungerpatients.
Mechanicalvalves
Ball-and-cage(Starr–Edwards):rarely,ifever,usedtoday.
Bileaflet(i.e.,St.Jude,Carbomedics):mostcommonlyused.
Singletiltingdisk(i.e.,Björk–Shiley,MedtronicHall,Omnicarbon).
Advantages of mechanical valve: structurally stable, long-lasting, relatively hemodynamically
efficient(particularlybileaflet).
Disadvantages of mechanical valve: need for anticoagulation/risk of bleeding, risk of
thrombosis/embolismdespiteanticoagulation,severehemodynamiccompromise ifdiskthrombosis
or immobility occurs(single tilting disk),riskofendocarditis, anticoagulationissuesinwomen of
child-bearingage.
Bioprostheticvalves
Porcineaorticvalvetissue(i.e.,Hancock,Carpentier-Edwards)
Bovinepericardialtissue(i.e.,Carpentier-EdwardsPerimount)
Advantagesofbioprostheticvalve: noneedfor anticoagulation,low thromboembolismrisk,low
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riskofcatastrophicvalvefailure
Disadvantages of bioprosthetic valve: structural valve deterioration, riskofendocarditis, still a
small risk (approximately 0.04%–0.34% per year in meta-analysis) of thromboembolism without
anticoagulation
11
Homograft(cadaveric):rarelyused;mostcommonlyusedtoreplacethepulmonicvalve
TREATMENT
Anticoagulation with a vitamin K antagonist (VKA) and international normalized ratio (INR)
monitoringisrecommendedinpatientswithamechanicalprostheticvalve(ClassI).
2
Goal INR of 2.5 is recommended in patients with a mechanical AVR and no risk factors for
thromboembolism.GoalINR3.0inpatientswithamechanical AVRandadditionalriskfactorsfor
thromboembolic events (AF, previous thromboembolism, LV dysfunction, or hypercoagulable
conditions)oranoldergenerationmechanicalAVR(suchasball-in-cage)(ClassI).
GoalINR3.0inpatientswithamechanicalMVreplacement(ClassI).
Aspirin in addition to VKA therapy for mechanical prosthetic valves is no longer routinely
recommendedintheabsenceofotherindicationsforaspirintherapy.
Aspirin 75–100 mg dailyis reasonable in all patients witha bioprosthetic aortic or mitral valve
(ClassIIa).
Anticoagulanttherapywithoraldirectthrombininhibitorsoranti-Xaagentsshouldnotbeused
inpatientswithmechanicalvalveprostheses(ClassIII).
Bridgingtherapyforprostheticvalves2:
Continuation of VKA anticoagulation with a therapeutic INR is recommended in patients with
mechanical heart valves undergoing minor procedures (i.e., dental extractions) where bleedingis
easilycontrolled(ClassI).
Temporary interruption of VKA anticoagulation, without bridging agents while the INR is
subtherapeutic,isrecommendedinpatientswithbileafletmechanicalAVRandnootherriskfactors
forthrombosiswhoareundergoinginvasiveorsurgicalprocedures(ClassI).
Bridging anticoagulation is reasonable for patients who are undergoing invasive procedures and
have mechanical AVR with thromboembolic riskfactors, an older generation mechanical AVR, or
mechanicalMVR(ClassIIa).
InfectiveEndocarditisinNativeorProstheticValves
Patientsatriskorwithsuspectedendocarditisshouldreceiveantibiotictherapyaftertwosetsofblood
cultures(ClassI).
2
These patients should be evaluated for need and timing of surgery: early surgery is recommended
(Class I) for those with valve dysfunction causing heart failure, resistant organisms (fungi,
staphylococcus),heartblock/abscess,persistentinfection.
Surgeryisalsorecommendedforrelapsingprostheticvalveendocarditis(ClassI).
2
Those with large mobile vegetations of the native valve and recurrent emboli canbe evaluated for
earlysurgery(ClassII).
2
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ManagementofPregnantPatientswithProstheticHeart
Valves(Figure6-6)
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Figure 6-6 Anticoagulation management in pregnant patients with prosthetic valves.INR, international normalized ratio;
LMWH,lowmolecular weightheparin.(ModifiedfromNishimuraRA,OttoCM,BonowRO,et al.2014AHA/ACC guideline
for the management of patients with valvular heart disease: executive summary. A report of the American College of
Cardiology/AmericanHeartAssociationtaskforceonpractice guidelines. JAmCollCardiol. 2014;63:2438-2488.Copyright©
2014AmericanHeartAssociation,Inc.,andtheAmericanCollegeofCardiologyFoundation.Withpermission.)
REFERENCES
1. ImazioM,BobbioM,CecchiE,etal.Colchicineinadditiontoconventionaltherapyforacute
pericarditis.Circulation.2005;112:2012-2016.
2. OttoCM,NishimuraRA,BonowRO,etal.2020ACC/AHAguidelineforthemanagementof
patientswithvalvularheartdisease:areportoftheAmericanCollegeofCardiology/American
HeartAssociationJointCommitteeonclinicalpracticeguidelines.Circulation.2021;143:e72e227.
3. LeonMB,SmithCR,MackM,etal.Transcatheteraortic-valveimplantationforaorticstenosisin
patientswhoCannotundergosurgery.NEnglJMed.2010;363:1597-1607.
4. LeonMB,SmithCR,MackMJ,etal.Transcatheterorsurgicalaortic-valvereplacementin
intermediate-riskpatients.NEnglJMed.2016;374:1609-1620.
5. SmithCR,LeonMB,MackMJ,etal.Transcatheterversussurgicalaortic-valvereplacementin
high-riskpatients.NEnglJMed.2011;364:2187-2198.
6. ReardonMJ,MieghemNMV,PopmaJJ,etal.Surgicalortranscatheteraortic-valvereplacementin
intermediate-riskpatients.NEnglJMed.2017;376:1321-1331.
7. StoneGW,LindenfeldJ,AbrahamWT,etal.Transcathetermitral-valverepairinpatientswith
heartfailure.NEnglJMed.2018;379:2307-2318.
8. MackMJ,AbrahamWT,LindenfeldJ,etal.CardiovascularoutcomesassessmentoftheMitraClip
inpatientswithheartfailureandsecondarymitralregurgitation:Designandrationaleofthe
COAPTtrial.AmHeartJ.2018;205:1-11.
9. DujardinKS,Enriquez-SaranoM,SchaffHV,BaileyKR,SewardJB,TajikAJ.Mortalityand
morbidityofaorticregurgitationinclinicalpractice.Circulation.1999;99:1851-1857.
10. MaurerG.Aorticregurgitation.Heart.2006;92:994.
11. PuriR,AuffretV,Rodés-CabauJ.Bioprostheticvalvethrombosis.JAmCollCardiol.
2017;69:2193-2211.
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7
CardiacArrhythmias
SandeepS.Sodhi,DanielH.Cooper,MitchellN.Faddis
Tachyarrhythmias
ApproachtoTachyarrhythmias
GENERALPRINCIPLES
Tachyarrhythmiasareencounteredinbothinpatientandoutpatientsettings.
Recognitionandstepwiseanalysisoftheserhythmsfacilitateappropriatemanagement.
Clinicaldecision-makingisguidedbypatientsymptomsandsignsofhemodynamicstability.
Definition
Cardiacrhythmswhoseventricularrateexceeds100beatsperminute(bpm).
Classification
BroadlyclassifiedintothefollowingbasedonthewidthoftheQRScomplexontheECG:
Narrow-complex tachyarrhythmia (QRS <120 ms): Arrhythmia originates within the atria
(supraventriculartachycardia[SVT])andrapidlyactivatestheventriclesviaHis–Purkinjesystem.
Wide-complex tachyarrhythmia (WCT) (QRS ≥120 ms): Arrhythmia originates withinthe ventricles
anddoes notdependon the His–Purkinje system (ventricular tachycardia [VT]) or originatesin the
atriaandtravelstotheventricleseitherviaanabnormalHis–Purkinjesystem(SVTwithaberrancy)or
throughanaccessorypathway.
Etiology
Mechanismdividedintodisordersofimpulseconductionandimpulseformation
Disorders of impulse conduction: Reentry is the most common mechanism of tachyarrhythmias.
Reentrantmechanismcanoccurwhen differentialrefractoryperiods andconductionvelocitiesallow
for propagation of an activation wavefront in a unidirectional manner around a zone of scar or
refractorycardiactissue.Reentryoftheactivationwavefrontaroundamyocardialcircuitsustainsthe
arrhythmia(e.g.,VT).
Disordersofimpulseformation:Enhancedautomaticity(e.g.,acceleratedjunctionalandaccelerated
idioventricularrhythm)andtriggeredactivity(e.g.,longQTsyndrome[LQTS]anddigitalistoxicity)
areother,lesscommonmechanismsoftachyarrhythmias.
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