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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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StageB(progressive):patientswithprogressiveVHD(mildtomoderateseverityandasymptomatic).
StageC(asymptomaticsevere):asymptomaticpatientswhomeetcriteriaforsevereVHD.
C1:asymptomaticpatientswithacompensatedleftandrightventricle.
C2:asymptomaticpatientswithdecompensationoftheleftorrightventricle.
StageD(symptomaticsevere):patientswhohavedevelopedsymptomsasaresultofVHD.
MitralStenosis
Mitralstenosis(MS)ischaracterizedbyincompleteopeningofthemitralvalveduringdiastole,which
limitsantegradeflowandyieldsasustaineddiastolicpressuregradientbetweentheleftatrium(LA)and
theleftventricle(LV).
Etiology
RheumaticMS
Because oftheincreased useofantibiotics,the incidenceofrheumatic heartdisease as a causeof
MShasdecreased.
Two-thirds ofpatientswithrheumatic MSare female;maybeassociatedwith mitralregurgitation
(MR).
Rheumatic fever can cause fibrosis, thickening, and calcification, leading to fusion of the
commissures,leaflets,chordae,and/orpapillarymuscles.
Other causes of MS: substantial mitral annular calcification (calcific MS), systemic lupus
erythematosus (SLE), rheumatoid arthritis, congenital, oversewn or small mitral annuloplasty ring;
“functional MS” may occur with obstruction of the LA outflow because of tumor (particularly
myxoma),LAthrombus,orendocarditiswithalargevegetation.
Pathophysiology
Increased transvalvular flowor decreaseddiastolic fillingtimemay leadtoworseningsymptoms of
MS. This occurs with pregnancy, exercise, hyperthyroidism, atrial fibrillation (AF) with rapid
ventricularresponse,andfever.
MScausesincreasedpressureintheLA,whichthendilatesasacompensatorymechanism.Thiscauses
theLAtodilateandfibrose,whichthenleadstoatrialarrhythmiasandthrombusformation.
A sustained increase in pulmonary venous pressures is transmitted backward to cause pulmonary
hypertension (PH) and with time, increased pulmonary vascular resistance and right ventricular
pressureoverloadanddysfunction.
DIAGNOSIS
History
Afteraprolongedasymptomaticperiod,patientsmayreportanyofthefollowing:dyspnea,decreased
functionalcapacity,orthopnea,paroxysmalnocturnaldyspnea,fatigue,palpitations,systemicembolism,
hemoptysis,chestpain.
PhysicalExamination
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Openingsnap(OS)causedbysuddentensingofthevalveleaflets;theA2-OSintervalvariesinversely
withtheseverityofstenosis(shorterinterval=moreseverestenosis).
Mid-diastolicrumble:low-pitchedmurmurheardbestattheapexwiththebellofthestethoscope;the
severityofstenosisisrelatedtothedurationofthemurmur,notintensity.
Signsofright-sidedheartfailureandPH.
DiagnosticTesting
ECG:leftatrialenlargement(LAE),AF,rightventricularhypertrophy.
CXR:enlargedchambers,calcificationofthemitralvalveand/orannulus.
TTE
Assessvalveleafletsandsubvalvularapparatus.
Determinemitralvalvearea(MVA)andmeantransmitralgradient(severeconsideredMVA≤1.5cm
2
ormeantransmitralgradientof>5–10mmHg).
Estimatepulmonaryarterysystolicpressure(PASP)andevaluaterightventricularsizeandfunction.
Transesophagealechocardiogram(TEE):Imagingmodalityofchoiceforevaluationofanatomyand
functionalsignificance.Alsousedtoruleoutleftatrialthrombus.
Exercisestresstesting:indicatedwhensymptomsareoutofproportiontoseverityindicatedbyTTE.
Cardiac catheterization: Rarely used. Useful in cases of discordant or inconclusive data by
echocardiography.MayprovideclarificationtotheetiologyofseverePHwhenoutofproportionofthe
severityofMS.Typicallyperformedinpatientsgoingformitralvalvereplacementwithriskfactorsfor
CAD.
TREATMENT
MedicalManagement
Diuretics,β-blockers,andlow-saltdietforheartfailuresymptoms.
AFoccursin30%–40%ofpatientswithsevereMS.
Therapyismostlyaimedatratecontrolandpreventionofthromboembolism.
ClassIindicationforanticoagulationforpreventionofsystemicembolizationinpatientswithMS
regardlessofCHADS2VASCscore.
2
PercutaneousMitralBalloonCommissurotomy
Ballooninflationseparatestheleaflets,yieldinganincreasedvalvearea.
IndicatedonlyinrheumaticMSwherethereisthickeningoftheleafletsandannulusismostlyspared.
Procedureofchoiceinexperiencedcentersinpatientswithoutcontraindications(suchasmoderateor
severeMRandleftatrialappendagethrombus).
Recommendationsforpercutaneousmitralballooncommissurotomy
2
SymptomaticpatientswithsevereMS(valvearea≤1.5cm2)(stageD)andfavorablevalveanatomy
intheabsenceofcontraindications(i.e.,LAclotormoderatetosevereMR)(ClassI)
Otherindications: Asymptomaticpatientswith severe MSandpulmonary hypertension(PASP >50
mmHg)ornewonsetAF(ClassII)
SurgicalManagement
Recommendationsformitralvalvesurgery2:SeverelysymptomaticpatientswithsevereMSwhoarenot
candidatesfororfailedpreviouspercutaneousmitralballooncommissurotomy,orwhoareundergoing
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othercardiacprocedures(ClassI).
AorticStenosis
Aorticstenosis(AS)isthemostcommoncauseofLVoutflowtractobstruction.
Othercausesofobstructionoccurabovethevalve(supravalvular)andbelowthevalve(subvalvular),
both fixed (i.e., subaortic membrane) and dynamic (i.e., hypertrophic cardiomyopathy with
obstruction).
Etiology
Calcific/degenerative
MostcommoncauseintheUS
TrileafletcalcificASusuallypresentsintheseventhtoninthdecadesoflife
Bicuspid
Occursin1%–2%ofpopulation(congenitallesion)
ASinthispopulationoccursinmuchyoungerpatients
Canbeassociatedwithaortopathies(i.e.,dissection,aneurysm)
Rheumatic
Morecommoncauseworldwide;muchlesscommonintheUS
AlmostalwaysaccompaniedbyMVdisease
Radiationinduced
Pathophysiology
ThepathophysiologyforcalcificASinvolvesboththevalveandtheventricularadaptationtothestenosis
(Figure6-1).
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Figure6-1 Pathophysiologyofaorticstenosis.CO,cardiacoutput;EF,ejectionfraction;LVEDP,leftventricular end-diastolic
pressure;LVH,leftventricularhypertrophy.
DIAGNOSIS
History
Theclassictriadofsymptomsincludesangina,syncope,andheartfailure.
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Symptoms may be masked by a progressive decline in functional capacity as patients modify their
activitiestosuittheirsymptoms.
PhysicalExamination
Harsh systolic crescendo–decrescendo murmur heard best at the right upper sternal border and
radiatingtobothcarotids;timetopeakintensitycorrelateswithseverity(laterpeak=moresevere).
DiminishedorabsentA2(softS2)suggestssevereAS.
Pulsusparvusettardus:late-peakinganddiminishedcarotidupstrokeinsevereAS.
DiagnosticTesting
ECG:LAE,leftventricularhypertrophy(LVH).
CXR:cardiomegaly,calcificationoftheaortaand/oraorticvalve.
TTE
Determinevalvemorphology(tricuspidvs.bicuspid),calculatevalveareausingcontinuityequation,
andmeasuretransvalvularmeanandpeakgradients.
SevereAS:peakjetvelocity≥4.0m/s,meangradient≥40mmHg,valvearea<1.0cm2.
TEE:usefulinselectpatientstobettervisualizevalvemorphologyanddeterminationofASseverity.
Dobutaminestressechocardiography
Useful to assess the patientwith a reduced SV(reducedor preserved ejectionfraction[EF]) and
smallcalculatedvalveareabutalow(<30–40mmHg)meantransvalvulargradient.
CanhelpdistinguishtrulysevereASfrompseudo–severeAS.
Cardiaccatheterization
HemodynamicassessmentofseverityofASinpatientsforwhomnoninvasivetestsareinconclusive
orwhenthereisdiscrepancybetweennoninvasivetestsandclinicalfindingsregardingASseverity.
Gorlin equation: used to calculate aortic valve area during invasive hemodynamic assessment;
basedonprinciplethataorticvalveareaisequaltosystolicflowacrossvalvedividedbysystolic
pressuregradienttimesaconstant.
TREATMENT
Severe symptomatic AS requires surgery or percutaneous aortic valve replacement (AVR);
currently,therearenomedicaltreatmentsproventodecreasemortalityortodelaysurgery.
Hypertensionshouldbeaddressed,anddiureticsusedforvolumeoverloadsymptoms.
SevereASwithdecompensatedHForshock:Severaloptionsmayhelpbridgethepatienttodefinitive
surgeryorpercutaneousprocedure:intra-aorticballoonpump(IABP)(contraindicatedinpatientswith
moderatetosevereaorticregurgitation[AR]),sodiumnitroprusside,balloonaorticvalvuloplasty.
AHA/ACCguidelineindicationsforsurgicalorpercutaneousAVR
2
SymptomaticpatientswithsevereAS(ClassI).
AsymptomaticpatientswithsevereASandanLVEF<50%(StageC2)(ClassI).
AsymptomaticpatientswithsevereASundergoingcardiacsurgeryforotherindications(ClassI).
Class IIB indicationsinclude: Asymptomatic patientswith decreased exercise tolerance bystress
testing,asymptomaticpatientswith verysevereAS(aorticvelocity>5m/s),asymptomaticpatients
withelevatedBNP,orincreaseinaorticvelocity≥0.3m/speryearonserialexaminations.
DecisionformechanicalversusbioprostheticAVRinvolvesshareddecision-makingwiththepatient
regarding risks of anticoagulant therapy and expected longevity of new valve. In general, it is
reasonable to recommend a mechanical prosthesis in patients <50 years of age who do not have a
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contraindicationtoanticoagulationduetotheimproveddurabilityofthistypeofvalve.Alternatively,it
is reasonable to recommenda bioprosthetic valve over a mechanical valve inpatients whoare >65
yearsofage(ClassIIa).
2
Transcatheter aortic valve implantation (TAVI) is an option for patients who are considering
bioprostheticAVR.
Requires evaluation by a team of cardiologists and cardiac surgeons. TAVI procedure uses
fluoroscopic and echocardiographic guidance to place a stented bioprosthetic valve within the
stenotic valve. This can be performed via a transfemoral, transaortic, subclavian, transcaval, or
transapicalapproach.
To date, clinical trials have demonstrated that in patients at prohibitive risk for surgery, TAVI
reduces mortality compared with medical therapy3; for high-risk patients and intermediate-risk
patients,TAVIandsurgicalvalvereplacementhavesimilaroutcomes.
4-6
ACC/AHAguidelinesfordecisionforsurgicalaorticvalvereplacement(SAVR)versusTAVI
2
ClassIindicationforTAVIinpatientswhoareatprohibitiveriskforsurgeryifexpectedsurvival
is>12monthswithanacceptablequalityoflife.
SAVR is recommended for patients with severe AS who are <65 years of age or have life
expectancyof>20years(ClassI).
Inpatientswhoare65–80yearsofage,eitherSAVRortransfemoralTAVIareoptions(ClassI).
ForsymptomaticpatientswithsevereASwhoare>80yearsofageorforyoungerpatientswitha
lifeexpectancy<10years,transfemoralTAVIisrecommendedinpreferencetoSAVR(ClassI).
OngoingstudiesareassessingtheroleofTAVIinexpandedpatientpopulations.
Prognosis
AS is a progressive disease typically characterized byan asymptomatic phase until the valve area
reachesaminimumthreshold,generally<1.0cm2.Intheabsenceofsymptoms,patientswithAShavea
goodprognosiswithariskofsuddendeathestimatedtobeapproximately1%peryear.
Once patients experience symptoms, their average survival is 2–3 years with a highrisk ofsudden
death.
MitralRegurgitation
PreventionofMRisdependentontheintegratedandproperfunctionoftheMV(annulusandleaflets),
subvalvular apparatus(chordae tendineae andpapillarymuscles), LA,andLV;abnormal function or
sizeofanyoneofthesecomponentscanleadtoMR.
PrimaryMRreferstoMRcausedprimarilybylesionstothevalveleafletsand/orchordaetendineae
(i.e.,myxomatousdegeneration,endocarditis,rheumatic).
SecondaryMR,or functional MR,referstoMRcausedprimarilybyventriculardysfunctionusually
withaccompanyingannulardilatation(i.e.,dilatedcardiomyopathyandischemicMR).
It is critical to define the mechanism of MR andthe time course (acute vs. chronic) because these
significantlyimpactclinicalmanagement.
Etiology
PrimaryMR
Degenerative(overlapwithMVprolapsesyndrome)
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Usuallyoccurs as a primary condition (Barlow disease or fibroelastic deficiency) but hasalso
been associated with heritable diseases affecting the connective tissue including Marfan
syndrome,Ehlers–Danlossyndrome,osteogenesisimperfecta,etc.
Occursin1.0%–2.5%ofthepopulationinafemale-to-maleratioof2:1.
Myxomatous proliferation andcartilage formation can occur inthe leaflets, chordae tendineae,
and/orannulus.
Rheumatic
MaybeisolatedMRorcombinedMR/MS.
Causedbythickeningand/orcalcificationoftheleafletsandchords.
Infectiveendocarditis:usuallycausedbydestructionoftheleaflettissue(i.e.,perforation).
SecondaryMR
Dilatedcardiomyopathy
Annulardilatationfromventricularenlargement.
Papillary muscle displacement because of ventricular enlargement and remodeling prevents
adequateleafletcoaptation.
Ischemic
Mechanism of MR usually involves one or both of the following: (1) annular dilatation from
ventricular enlargement; (2) local LV remodeling withpapillary muscle displacement(boththe
dilatationoftheventricleandtheakinesis/dyskinesisofthewalltowhichthepapillarymuscleis
attachedcanpreventadequateleafletcoaptation).
MRmaydevelopacutelyfrompapillarymusclerupture(seebelow).
OthercausesofMR
Congenital, infiltrative diseases (i.e., amyloid), SLE (Libman–Sacks endocarditis), hypertrophic
obstructivecardiomyopathy,mitralannularcalcification,paravalvularprostheticleak,drug toxicity
(e.g.,Fen-phen).
AcutecausesofMR
Ruptured papillary muscle or ruptured chordae tendineae, usually in setting of acute MI. The
posteromedialpapillarymuscleismorelikelytorupturethantheanterolateralpapillarymuscle;the
anterolateral muscle has dual blood supply from both the left anterior descending artery and left
circumflexartery.
Infectiveendocarditis.
Pathophysiology
AcuteMR(Figure6-2)
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Figure6-2 Acutemitralregurgitation.CO,cardiacoutput;EF,ejectionfraction;HR,heartrate;LA,leftatrium;LAP,left
atrialpressure;LV,leftventricle;LVEDP,leftventricularend-diastolicpressure;SV,strokevolume.
ChronicMR(Figure6-3)
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Figure6-3 Chronicmitralregurgitation.CO,cardiacoutput;EF,ejectionfraction;LA,leftatrium;LAP,leftatrialpressure;LV,
leftventricle;LVEDP,leftventricularend-diastolic pressure;MR,mitralregurgitation;PH,pulmonaryhypertension;SV,stroke
volume.
DIAGNOSIS
History
AcuteMR:mostprominentsymptomisrelativelyrapidonsetofsignificantshortnessofbreath,which
mayleadquicklytorespiratoryfailure.
ChronicMR
SymptomswilldependontheetiologyofMRandtimingofpresentation.
In primary MR (usually degenerative MR) that has gradually progressed, the patient may be
asymptomatic evenwhen the MR is severe. As compensatorymechanisms fail, patients may note
dyspneaonexertion(maybe becauseofPHand/orpulmonaryedema),palpitations(from anatrial
arrhythmia),fatigue,andvolumeoverload.
PhysicalExamination
AcuteMR
Tachypneawithrespiratorydistress,tachycardia,hypotension.
Systolicmurmur,usuallyattheapex(maynotbeholosystolicandmaybeabsent).
ChronicMR
Apicalholosystolicmurmurthatradiatestotheaxilla.
InMVprolapse,thereisamidsystolicclickheardbeforethemurmur.
S2maybewidelysplitbecauseofanearlyA2.
Othersignsofheartfailure(lowerextremityedema,increasedJVP,rales,etc.).
DiagnosticTesting
ECG:LAE,LVH,AF.
CXR:enlargedLA,pulmonaryedema,enlargedpulmonaryarteries,andcardiomegaly.
TTE: assess etiologyof MR, LA size andLV dimensions (dilated in chronic severe MR), EF (LV
dysfunctionispresentifEF≤55%),qualitativeandquantitativemeasuresofMRseverity.
TEE
Providesbettervisualizationofthevalvetohelpdefineanatomy,presenceofendocarditis(valvular
vegetations),andfeasibilityofrepair.
May help determine severity of MR when TTE is nondiagnostic, particularlyin the setting ofan
eccentricjet.
Rightheartcatheterization
Better characterize PH in patients with chronic severe MR and determine LA filling pressure in
patientswithunclearsymptoms.
Giant“V”wavesonpulmonarycapillarywedgepressuretracingmaysuggestsevereMR.
Leftheartcatheterization
MayinfluencetherapeuticstrategyinischemicMR.
EvaluationofCADinpatientswithriskfactorsundergoingMVsurgery.
MRI/nucleartesting
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