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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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Drug InitialDose Target
Angiotensin-ConvertingEnzymeInhibitors
Captopril 6.25–12.5mgtid 50mgtid
Enalapril 2.5mgbid 10mgbid
Lisinopril 2.5–5.0mgdaily;canuse
bid
10–20mgbid
Ramipril 1.25–2.5mgbid 5mgbid
AngiotensinReceptorBlockers
Valsartan
a
40mgbid 160mgbid
Losartan 25mgdaily;canusebid 25–100mgdaily
Candesartan
a
2–16mgdaily 2–32mgdaily
AngiotensinReceptor–NeprilysinInhibitor
Entresto(sacubitril/valsartan) 24/26mgbid 97/103mgbid
IKfChannelInhibitor
Ivabradine 5mgbid 7.5mgbid
ThiazideDiuretics
Hydrochlorothiazide 25–50mgdaily 25–50mgdaily
Metolazone 2.5–5.0mgdailyorbid 10–20mgtotaldaily
LoopDiuretics
Bumetanide 0.5–1.0mgdailyorbid 10mgtotaldaily(maximum)
Furosemide 20–40mgdailyorbid 400mgtotaldaily
(maximum)
Torsemide 10–20mgdailyorbid 200mgtotaldaily
(maximum)
AldosteroneAntagonists
Eplerenone 25mgdaily 50mgdaily
Spironolactone 12.5–25.0mgdaily 25mgdaily
β-Blockers
Bisoprolol 1.25mgdaily 10mgdaily
Carvedilol 3.125mgbid 25–50mgbid
Metoprololsuccinate 12.5–25.0mgdaily 200mgdaily
Digoxin 0.125–0.25mgdaily 0.125–0.25mgdaily
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Hydralazine/Isosorbide
Dinitrate
37.5mg/20mgtid 75mg/40mgTID
a
ValsartanandcandesartanaretheonlyU.S.FoodandDrugAdministration–approvedangiotensinIIreceptorblockersinthe
treatmentofheartfailure.
Typically, 2–3 months of therapy is required to observe significant effects on LV function, but
reduction of cardiac arrhythmia and incidence of sudden cardiac death (SCD) may occur much
earlier.
13
β-Blockersshouldbeinstitutedata low doseandtitratedwithcarefulattentiontoblood pressure
andheartrate.SomepatientsexperiencevolumeretentionandworseningHFsymptomsthattypically
respondtotransientincreasesindiuretictherapy.
Thesurvivalbenefitofβ-blockersisproportionaltotheheartratereductionanddosageachieved.
Individualβ-blockershaveuniqueproperties,andthebeneficialeffectsofβ-blockersarenotaclass
effect.Therefore,oneofthethreeβ-blockerswithprovenbenefitonmortalityinlargeclinicaltrials
shouldbeused:
Carvedilol
14,15
Metoprololsuccinate
16
Bisoprolol
17
Angiotensin receptor–neprilysin inhibitor. Sacubitril/valsartan is a combination of the neprilysin
inhibitor(sacubitril)andARB(valsartan).
Neprilysinis aneutral endopeptidaseinvolved inthedegradationofvasoactivepeptidesincluding
the natriuretic peptides, bradykinin, and adrenomedullin. Inhibition of neprilysin increases the
availabilityofthesepeptides,whichexertfavorableeffectsinHF.
Sacubitril/valsartan was showntobesuperiortoenalapril inreducing deathandrehospitalization
amongNYHAclassII–IV patientswithHFrEFwhowerestablytolerantofACEinhibitororARB
therapy.
18
Sacubitril/valsartanisapprovedforuseinpatientswithHFrEFandNYHAclassII–IVsymptoms.
Ratesofangioedemaare increasedwith sacubitril/valsartan comparedwithACEinhibitors (0.5%
vs.0.2%)andrequirea36-hourACEinhibitorwashoutpriortoinitiation.Angioedemarateswere
comparativelyhigherinAfrican-Americans(2.4%vs.0.5%).
ACEinhibitorsandARBs target the compensatoryRAASactivationandattenuatevasoconstriction,
vital organhypoperfusion,hyponatremia, hypokalemia, andfluidretention.These medicationsshould
beusedassecond-linetherapyifpatientscannottolerateoraffordARNI.
ACEinhibitors
Multiple large clinical trials have clearly demonstrated that ACEinhibitors improve symptoms
andsurvivalinpatientswithLVsystolicdysfunction.
1
ACE inhibitors may also prevent the development of HF in patients with asymptomatic LV
dysfunctionandinthoseathighriskofdevelopingstructuralheartdiseaseorHFsymptoms(e.g.,
patientswithCAD,diabetesmellitus,hypertension).
NoconsensusexistsonoptimaldosingofACEinhibitorsinHF.Higherdoseshavebeenshownto
reducemorbiditywithoutimprovingoverallsurvival.
19
MostACEinhibitors are excretedbythe kidneys, necessitating carefuldose titrationinpatients
with renal insufficiency. ACE inhibitors should be used cautiously in the presence of renal
dysfunction and use should be avoided in patients with bilateral renal artery stenosis. Renal
function andpotassium levels should be monitored with dose adjustment andperiodicallywith
chronicuse.
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Ariseinserumcreatinineupto30%abovebaselinemaybeseenwheninitiatinganACEinhibitor
andshouldnotresultinreflexivediscontinuationoftherapy.
20
Additional adverse effects mayincludecough,rash, angioedema,dysgeusia, hyperkalemia, and
leukopenia.
Oralpotassiumsupplements,potassiumsaltsubstitutes,andpotassium-sparingdiureticsshouldbe
usedwithcautionduringtreatmentwithanACEinhibitor.
ACEinhibitorsarecontraindicatedinpregnancy.Enalaprilandcaptoprilmaybesafelyused
bybreastfeedingmothers.
ARBs
ARBs reducemorbidityand mortalityassociatedwith HFinpatients whoare notreceiving an
ACEinhibitor
21-23
andthereforeshouldbeinstitutedwhenACEinhibitorsarenottolerated.
In contrast to ACE inhibitors, ARBs do not increase bradykinin levels and therefore are not
associatedwithcough.
RenalprecautionsandmonitoringforARBusearesimilartoACEinhibitoruse.
UseofARBsiscontraindicatedinpatientstakingbothACEinhibitorsandaldosteroneantagonists
duetoahighriskforhyperkalemia.
ARBsarecontraindicatedinpregnancyandbreastfeeding.
MRAs attenuate aldosterone-mediated sodium retention, vascular reactivity, oxidant stress,
inflammation,andfibrosis.
MRAs are recommended for use in patients with NYHA class II–IV HF and acceptable renal
function (serumcreatinineis <2.5mg/dL inmen or <2.0 mg/dL in women, andpotassium is <5.0
mEq/L).
Spironolactone is a nonselective aldosteronereceptorantagonistthat hasbeenshownto improve
survivalanddecreasehospitalizationsinNYHAclassIII–IVpatientswithlowEF.
24
Eplerenone is a selective aldosterone receptor antagonist without the estrogenic side effects of
spironolactone.IthasprovenbeneficialinpatientswithHFfollowingMI25andinlesssymptomatic
HFpatients(NYHAclassII)withreducedEF.
26
Life-threatening hyperkalemia may occur with the use of these agents. Serum potassium must be
monitoredcloselyafterinitiation;concomitantuseofACEinhibitorsandNSAIDsandthepresence
ofrenalinsufficiencyincreasetheriskofhyperkalemia.
Gynecomastiamaydevelopin10%–20%ofmentreatedwithspironolactone;eplerenoneshouldbe
usedinthiscase.
SGLT2inhibitorspromoteosmoticdiuresisandnatriuresisandexertbeneficialpleiotropiceffectson
theheart,vasculature,andmetabolicprofile.
Dapagliflozin and empagliflozin have been shown to decrease cardiovascular mortality and HF
hospitalizationswhenaddedtostandardtherapyinpatientswithHFrEFwithorwithoutdiabetes.
27,28
Canagliflozin has been shown to decrease the composite outcome of cardiovascular mortality,
nonfatal MI, or nonfatal stroke in patientswith type 2 diabetes andelevated cardiovascular risk.
Post-hoc analysis showed canagliflozin reduced cardiovascular mortality and HF hospitalizations
acrossarangeofsubgroups.
29
Sotagliflozin is a dualSGLT1 andSGLT2inhibitor thathasbeenshowntoreducecardiovascular
death and HF hospitalizations or urgent visits when initiated shortly before or after inpatient
dischargeinpatientswithHFanddiabetesirrespectiveofEF.
30
Currently, the U.S. Food and Drug Administration (FDA) has approved dapagliflozin and
empagliflozinfortreatmentofHFrEFindependentofdiabetes.
Diuretictherapy inconjunction with restrictionofdietarysodium andfluids oftenleads toclinical
improvementinpatientswithsymptomaticHF.Frequentassessmentofthepatient’sweightandcareful
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observationoffluidintakeandoutputareessentialduringinitiationandmaintenanceoftherapy.
Complicationsoftherapyincludehypokalemia,hyponatremia,hypomagnesemia,volumecontraction
alkalosis,intravascularvolumedepletion,andhypotension.Therefore,serumelectrolytes,BUN,and
creatininelevelsshouldbemonitoredafterinstitutionofdiuretictherapy.
Hypokalemia maybe life threateningin patientswhoare receiving digoxinor are predisposed to
ventriculararrhythmias.
Loop diuretics(furosemide,torsemide, bumetanide,ethacrynicacid)shouldbeusedinpatients
whorequiresignificantdiuresisandinthosewithmarkedlydecreasedrenalfunction.
Furosemide reduces preload acutely by causing direct venodilation when administered
intravenously,makingitusefulformanagingsevereHForacutepulmonaryedema.
Useofloopdiureticsmaybecomplicatedbyhyperuricemia,hypocalcemia,ototoxicity,rash,and
vasculitis. Furosemide, torsemide, and bumetanide are sulfa derivatives and may rarely cause
drugreactionsinsulfa-sensitivepatients;ethacrynicacidcanbeusedinsuchpatients.
Dose equivalence of oral loop diuretics is approximately 50 mg ethacrynic acid = 40 mg
furosemide=20mgtorsemide=1mgbumetanide.
Torsemideandbumetanidehave>80%oralbioavailabilityascomparedto 50%bioavailability
offurosemide. In patients requiring increased dosage of furosemide, transitionto torsemide or
bumetanideshouldbeconsidered.
Thiazidediuretics(hydrochlorothiazide,chlorthalidone)canbeusedas initialagentsinpatients
withnormalrenalfunctioninwhomonlyamilddiuresisisdesired.
Metolazone, unlike other oral thiazides, exertsits action at theproximal anddistal tubule and
maybeusefulincombinationwithaloopdiureticinpatientswithalowglomerularfiltrationrate.
Potassium-sparing diuretics (amiloride, triamterene) do notexerta potent diuretic effect when
usedalone.
Second-line therapies—In patients who have ongoing symptoms despite maximization of the four
cornerstone medications mentioned above or have intolerance/contraindications preventing use of
certainagents,additionaltherapiesmayprovidebenefit.
Vasodilatortherapyalterspreloadandafterloadtoimprovecardiacoutput.
Hydralazine acts directly on arterial smooth muscle cells to produce vasodilation and reduce
afterload. Reflex tachycardia and increased myocardial oxygen consumption may occur in the
settingofhydralazineuse,requiringcautioususeinpatientswithischemicheartdisease.
Nitrates are predominantly venodilators and help relieve symptoms of congestion. They also
reducemyocardial ischemia bydecreasing ventricular filling pressures andbydirectlydilating
coronary arteries. Nitrate therapy may precipitatehypotension,especiallyinpatients whohave
lowpreloadoraretakingphosphodiesteraseinhibitors.
A combinationof hydralazine and isosorbide dinitrate (starting dose: 37.5/20 mg threetimes
daily), when added to β-blockers and ACEi/ARB, was shown to reduce mortality inAfrican-
Americanpatients.
31
IntheabsenceofACEi/ARBs,MRAs,andβ-blockers,thecombinationofnitratesandhydralazine
improvessurvivalinpatientswithHFrEF32andshouldthereforebeconsideredforuseinHFrEF
patientsunabletotolerateRAASblockade.
Vericiguatisasolubleguanylatecyclasestimulatorthatincreasescyclicguanosinemonophosphate,
leadingtovasodilationandimprovedendothelialfunction.
Vericiguat was shown to reduce cardiovascular death and HF hospitalization in patients with
HFrEF and worsening symptoms or recent decompensation.33 It is indicated for use in this
populationasanadditiontobackgroundtherapywithACE/ARB/ARNI,MRAs,andβ-blockers.
IvabradineisaninhibitoroftheIKfchannelinvolvedingenerating“pacemaker”currentsincardiac
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tissue.
IvabradinewasshowntoreduceHFhospitalizationandHFdeathinoutpatientswithHFrEFand
is indicated for the reduction of HF hospitalization in patients with EF <35%, stable HF
symptoms,andsinusrhythmwitharestingheartrate≥70bpmwhoarealreadytakingβ-blockers
atthehighesttolerateddose.
34
Digitalis glycosides (digoxin) increase myocardial contractility and may attenuate the
neurohormonalactivationassociatedwithHF.
Digoxin has been shown to decrease rates of HF hospitalizations without improving overall
mortality.
35
Digoxin has a narrow therapeutic index, and serum levels should be followed closely,
particularlyinpatientswithunstablerenalfunction.
The usual daily dose is 0.125–0.25 mg and should be decreased in patients with renal
insufficiency.
Womenandpatientswithhigherserumdigoxinlevels(1.2–2.0ng/mL)haveanincreasedmortality
risk.
36,37
Discontinuationofdigoxininpatientswhoarestable ona regimenofdigoxin,diuretics, andan
ACEinhibitormayresultinclinicaldeterioration.
38
Drug interactions with digoxin are common andmay lead to toxicity. Agents that may increase
levels include erythromycin, tetracycline, quinidine, verapamil, flecainide, and amiodarone.
Electrolyte abnormalities (particularly hypokalemia), hypoxemia, hypothyroidism, renal
insufficiency,andvolumedepletionmayalsoexacerbatetoxicity.
Digoxin isnotdialyzable, andtoxicityisonlytreatablebythe administrationofdigoxinimmune
Fab.
Therapieswithunprovenbenefit
α-Adrenergic receptor antagonists have not been shown to improve survival in HF, and
hypertensivepatientstreatedwithdoxazosinasfirst-linetherapyareatincreasedriskofdeveloping
HF.
CalciumchannelblockershavenofavorableeffectsonmortalityinHFrEF.
Dihydropyridinecalcium channel blockers such as amlodipinemaybe usedinhypertensive HF
patientsalreadyonmaximalguideline-directedmedicaltherapy (GDMT);however,theseagents
donotimprovemortality.
39,40
NondihydropyridinecalciumchannelblockersshouldbeavoidedinHFrEFbecausetheirnegative
inotropiceffectsmaypotentiateworseningHF.
SympathomimeticagentsarereservedforthetreatmentofsevereHF.Beneficialandadverseeffects
aremediatedbystimulationofmyocardialβ-adrenergicreceptors.Themostimportantadverseeffects
are related toarrhythmias andexacerbationofmyocardial ischemia. Patientswithrefractorychronic
HFmaybenefitsymptomaticallyfromcontinuousambulatoryadministrationofparenteralinotropesas
palliative therapyor as a bridge to mechanical ventricular supportor cardiac transplantation. Risks
includelife-threateningarrhythmiasorcatheter-relatedinfections.
Dobutamine (see Table 5-5) is a synthetic analog of dopamine with predominantly β1-
adrenoreceptoractivity.Itincreasescardiacoutput,lowerscardiacfillingpressures,andgenerally
has a neutral effect on systemic blood pressure. Dobutamine tolerance has been described, and
several studies have demonstrated increased mortality in patients treated with continuous
dobutamine. Dobutamine has no significant role in the treatment of HF resulting from diastolic
dysfunctionorahigh-outputstate.
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TABLE5-5
INOTROPIC/SYMPATHOMIMETICAGENTS
A
Drug Dose Mechanism Effects/Side
Effects
Dopamine 1–3μg/kg/min Dopaminergic
receptors
Splanchnic
vasodilation
2–8μg/kg/min β1-Receptor
agonist
+Inotropic
7–10μg/kg/min α-Receptor
agonist
↑SVR
Dobutamine 2.5–15.0μg/kg/min β1->β2->α-
receptor
agonist
+Inotropic,↓
SVR,
tachycardia
Epinephrine 0.05–1μg/kg/min;titratetodesiredmeanarterial
pressure.Mayadjustdoseevery10–15minby
0.05–0.2μg/kg/mintoachievedesiredblood
pressuregoal
β1>α1
Lowdoses=
β
Highdoses=
α
+Inotropic,↑
SVR
Milrinone
b
50-μg/kgbolusIVover10min,0.375–0.75
μg/kg/min
↑cAMP +Inotropic,↓
SVR
cAMP,cyclicadenosinemonophosphate;SVR,systemicvascularresistance;↑,increased;↓,decreased.
a
Increasedriskofatrialandventriculartachyarrhythmias.
b
Needsdoseadjustmentforcreatinineclearance.
Phosphodiesterase inhibitors increase myocardial contractility and produce vasodilation by
increasing intracellular cyclic adenosine monophosphate. Milrinone is indicated for treatment of
refractory HF. Hypotension may develop in patients who receive vasodilator therapy or have
intravascular volume contraction,or both. Milrinone may improve hemodynamics inpatients who
are treated concurrently with dobutamine or dopamine. Data suggest that in-hospital short-term
milrinone administration in addition to standard medical therapy does not reduce the length of
hospitalizationorthe60-daymortalityorrehospitalizationratewhencomparedwithplacebo.
41
Oralinotropes
Omecamtivmecarbilbindscardiacmyosinanddirectlyaugmentscardiacsarcomerefunction.Use
ofomecamtiv mecarbil in addition to guidelinemedical therapyinpatients withNYHA II-IV HF
resultedinlowerratesofthecompositeoutcomeofHFeventsorcardiovasculardeath.42Thisagent
isnotyetFDAapproved.
ChronicMedicalTherapyWithPreservedEjectionFraction(Figure5-3)
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Figure5-3 Chronicmedicaltherapiesforheartfailurewithpreservedejectionfraction(HFpEF).ACEi,angiotensin-converting
enzyme inhibitor;Afib, atrial fibrillation;ARB,angiotensinIIreceptorblocker; ARNI,angiotensin receptor–neprilysininhibitor;
CAD,coronaryarterydisease;LVEF,leftventricular ejectionfraction;OSA,obstructivesleepapnea;SGLT2i,sodium–glucose
cotransporter2inhibitor.
NopharmacotherapyhasbeendefinitivelyshowntoimprovemortalityinHFpEF.
The use of ACE inhibitors, ARBs, spironolactone, and β-blockers is reasonable and may be
associatedwithasmallreductioninHFhospitalizationrates.
Sacubitril/valsartan did not reduce cardiovascular mortality or HF hospitalizations compared to
valsartaninpatientswithHFpEFandEF>45%.However,sacubitril/valsartandidhaveabeneficial
effect in patients who had less than normal LVEF. Therefore, FDA has approved
sacubitril/valsartanforuse inallpatients withHFpEF, withbenefitmost likelyinpatientswith
lessthannormalLVsystolicfunction.
43,44
SpironolactonereducedHFhospitalizationinpatientswithHFpEFinalargerandomizedtrial,but
mortalitywasnotreduced.
45
SGLT2inhibitors have themost extensive data for improved outcomes in HFpEF. Empagliflozin
reducedthe composite outcome of HF hospitalizations andcardiac death inpatients with HFpEF,
independent of diabetes, driven by decrease in HF hospitalizations.46 In a prespecified, pooled
analysis from two placebo-controlled trials of type 2 diabetics with HF, sotagliflozin reduced
cardiovascular death and HF hospitalizations or urgent visits, irrespective of EF.
30,47
SGLT2
inhibitorsshouldbeconsideredinallpatientswithHFpEF.
Control of blood pressure, treatment of atrial fibrillation (AF), and treatment of coronary disease
through pharmacotherapy and/or revascularization in accordance with practice guidelines is
recommended.
AntiarrhythmicTherapy
Suppression of asymptomatic ventricular premature beats or nonsustained ventricular tachycardia
(NSVT) using antiarrhythmicdrugs inpatientswith HFdoes not improvesurvival andmayincrease
mortalityasaresultoftheproarrhythmiceffectsofthedrugs.
48
For patients with AF as a suspected cause of new-onset HF, a rhythm control strategy should be
pursued. For patients with preexisting HF who develop AF, despite evidence suggesting improved
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symptomstatus inpatientstreatedwith rhythm control,the use ofantiarrhythmic drugtherapyforthe
maintenanceofsinusrhythmhasnotbeenshowntoimprovemortality.
49
AgentsrecommendedforthemaintenanceofsinusrhythminHFwithreducedLVEFincludedofetilide
andamiodarone.SotalolmayalsobeconsideredinpatientswithmildlydepressedLVEF.Theseagents
require close monitoring oftheQTinterval. In patientswith severe LVsystolic dysfunctionandHF,
dronedaroneshouldnotbeused.
50
CatheterablationforAFinpatientswithHFascomparedwithmedicaltherapywasassociatedwitha
lower rate of mortality in one randomized trial, but guideline consensus for use has not been
formalized.
51
AnticoagulantandAntiplateletTherapy
AlthoughpatientswithHFareatrelativelygreaterriskforthromboembolicevents,theabsoluteriskis
modest,and routine anticoagulation is not recommended in HF patients inthe absenceof AF, prior
thromboembolism,oracardioembolicsource.
In patients with AF, use of the CHADS2 or CHA2DS2-VASc risk score is recommended for
determiningwhentouseanticoagulanttherapies.
Thedirectoralanticoagulantsdabigatran,rivaroxaban,andapixabanhavebeenshowntobeeffective
inHFpatientswithnonvalvularAF.
There areinsufficientdatatosupportthe routineuseofaspirininpatientswith HFwhodo nothave
coronarydiseaseoratherosclerosis.
NonpharmacologicTherapiesforHeartFailure
Coronary revascularization reduces ischemia and may improve systolic function in patients with
CADandHF.
Surgical or percutaneous revascularization is recommended inHF patients with anginaandsuitable
anatomy(classIrecommendation)andmaybeconsideredinpatientswithoutanginawhohavesuitable
anatomy, whether in the presence of viable myocardium (class IIa recommendation) or nonviable
myocardium(classIIbrecommendation).
1
Inalarge,randomizedtrialofHFpatientswithCADandLVEF<35%comparingmedicaltherapyto
medical therapy plus coronary artery bypass graft surgery (CABG), there was no difference in the
primary outcome ofdeathfrom anycauseat5years. Atlongerfollow-upintervalsofupto10years,
the rates ofdeath from anycause and death from cardiovascular causes were significantlylower in
patients whounderwent CABGin addition to medical therapythan those receiving medical therapy
alone.
52,53
Cardiac resynchronization therapy (CRT) or biventricular pacing (see Chapter 7, Cardiac
Arrhythmias)canimprovequalityoflifeandreducetheriskofdeathincertainpatientswithanEFof
≤35%, NYHA class II–IV HF, and conduction abnormalities (left bundle branch block[LBBB] and
atrioventriculardelay).
54,55
CRTcanalsobeuseful(classIIArecommendation)inthefollowingsituations:
LVEF ≤35%, sinus rhythm, a non-LBBB pattern with a QRS ≥150 ms, and NYHA class
III/ambulatoryclassIVsymptomsonGDMT.
LVEF≤35%,sinus rhythm,LBBBwithaQRS120–149ms,andNYHAclassII,III,orambulatory
IVsymptomsonGDMT.
AFandLVEF≤35%onGDMTifthepatientrequiresventricularpacingandatrioventricularnodal
ablationorratecontrolallowsnear100%ventricularpacingwithCRT.
Patients on GDMT who have LVEF ≤35% and are undergoing new or replacement device
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implantationwithanticipatedfrequentventricularpacing(>40%ofthetime).
FactorsmoststronglyfavoringresponsetoCRTincludefemalesex,QRSduration≥150ms,LBBB,
bodymassindex<30kg/m2,nonischemiccardiomyopathy,andasmallleftatrium.
56
Implantable cardioverter-defibrillator (ICD) placement for primary prevention of SCD is
recommendedforselectedHFpatientswithapersistentlyreducedLVEF≤35%.
SCDoccurssixtoninetimesmoreofteninpatientswithHFcomparedwiththegeneralpopulation
andistheleadingcauseofdeathinambulatoryHFpatients.
Multiple large, randomized trials have demonstrated a survival benefit of 1%–1.5% per year in
patientswithbothischemicandnonischemiccardiomyopathy.
Patients should receive at least 3–6 months of optimal GDMT prior to reassessment of EF and
implantationofanICD.
FollowinganacuteMIorrevascularization,LVEFshouldbeassessedafter40daysofGDMTprior
toICDimplantation.
ICDtherapyshouldbereservedforpatientsexpectedtootherwiselive>1yearwithgoodfunctional
capacity. ICD therapy should not be used in end-stage HF patients who are not candidates for
transplantationordurablemechanicalcirculatorysupport(MCS).
CardioMEMS™ is an implantable hemodynamic monitoring system delivered into the pulmonary
artery that can be used to monitor a patient’s ambulatory pulmonary artery pressures and allow
cliniciansto adjustmedications accordingly. It has been shown to reducehospitalizationinpatients
withNYHAclassIIIHF,irrespectiveofLVEF.
57
SurgicalManagement
Surgicalornonsurgicalreplacementorrepair ofthe mitralvalve inthe setting ofareducedLVEF
andsevereMRisdiscussedelsewhere(seeChapter6,PericardialandValvularHeartDisease).
In select patients who are on maximallytolerated medical therapywith symptomatic moderate to
severeMR,MitraclipTMresultedinlowermortalityandHFhospitalizations.
58
Leftventricularassistdevices(LVADs)aresurgicallyimplantedpumpsthatdrawbloodfromtheleft
ventricle,energizeflowthroughamotorunit,anddelivertheenergizedbloodtotheaorta,resultingin
augmentedcardiac output andlower intracardiac fillingpressures. Thesedevices may be temporary
(CentriMag, percutaneous LVADs) or durable (HeartWare, HeartMate II, HeartMate III). Due to
clinicalinferiority,HeartWareandHeartMateIIarenolongermanufactured.HeartMate3istheonly
durableLVADcommerciallyavailableintheUnitedStates.
TemporaryMCSisindicatedforpatientswithsevereHFaftercardiacsurgeryorindividualswith
intractablecardiogenicshockafteracuteMI.
DurableMCSisindicatedasa“bridgetotransplantation”forpatientsawaitinghearttransplantation
oras“destination”therapyforselectpatientsineligiblefortransplantwithrefractoryend-stageHF
andHF-relatedlifeexpectancywiththerapyof<2years.
59
Complications of durable LVADs include RV dysfunction, gastrointestinal bleeding, driveline
infections,aorticinsufficiency,pumpthrombosis,hemolysis,andstrokes.Newermagneticlevitation
technologyofferslessriskofpumpthrombosisanddisablingstroke.
60,61
ThedecisiontoinstituteMCSmustbe madeinconsultation with a HFcardiologist anda cardiac
surgeonwhohaveexperiencewiththistechnology.
Cardiac transplantation is an option for selected patients with severe end-stage HF refractory to
aggressivemedicaltherapyandforwhomnootherconventionaltreatmentoptionsareavailable.
Approximately3700transplantswereperformedintheUnitedStatesin2020andthenumberofheart
transplantshasbeenslowlyincreasing.
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Candidates considered for transplantation should generally be <65 years old (although selected
older patientsmayalso benefit), haveadvancedHF(NYHA class IV),havea strongpsychosocial
supportsystem,haveexhaustedallothertherapeuticoptions,andbefreeofirreversibleextracardiac
organ dysfunction that would limit functional recovery or predispose them to posttransplant
complications.
62
Survival rates afterhearttransplantareapproximately90%,75%, and50%at1, 5, and10 years,
respectively. Annual statistics can be found on the United Network for Organ Sharing website
(www.unos.org).
Posttransplant complications may include acute or chronic rejection, typical and atypical
infections, and adverse effects of immunosuppressive agents. Surgical complications and acute
rejectionarethemajorcausesofdeathinthefirstposttransplantyear.Cardiacallograftvasculopathy
andmalignancyaretheleadingcausesofdeathafterthefirstposttransplantyear.
Lifestyle/RiskModification
Dietarycounselingforsodiumandfluidrestrictionshouldbeprovided.Dailyintakeofapproximately
2gofsodiumperdayformostpatientsandfluidrestriction<1.5L/dforpatientswith hyponatremia
(serumsodium<130mEq/L)arereasonable.
Smokingcessationshouldbestronglyencouraged.
AbstinencefromalcoholisrecommendedinsymptomaticHFpatientswithlowEF.
Exercise training is recommended in stable HF patients as an adjunct to pharmacologic treatment.
ExercisetraininginpatientswithHFhasbeenshowntoimproveexercisecapacity(peakVO2maxas
well as 6-minute walk time), improve quality of life, and decrease neurohormonal activation.
Treatment programs should be individualized and include a warm-up period, 20–30 minutes of
exerciseatthedesiredintensity,andacool-downperiod.
WeightlossshouldberecommendedinobeseHFpatients.
SpecialConsiderations
MinimizationofmedicationswithdeleteriouseffectsinHFshouldbeemphasized.
Negative inotropes (e.g., verapamil, diltiazem) should be avoided in patients with impaired
ventricular contractility, as should over-the-counter β stimulants (e.g., compounds containing
ephedra,pseudoephedrinehydrochloride).
NSAIDs,whichantagonizetheeffectofACEinhibitors anddiuretictherapy, shouldbeavoided if
possible.
Administration of supplementaloxygen mayrelieve dyspnea, improve oxygen delivery, reduce the
workofbreathing,andlimitpulmonaryvasoconstrictioninpatientswithhypoxemiabutisnotroutinely
recommendedinpatientswithoutmeasurablehypoxemia.
Sleepapneahasaprevalencerateashighas50%intheHFpopulation.Treatmentofobstructivesleep
apneawith nocturnal positive airwaypressureimproves symptoms andEF.63 However,treatment of
central sleep apnea with adaptive servo-ventilation in patients with HFrEF was associated with
increasedmortality.
64
Dialysisor ultrafiltration may be beneficial in patientswith severe HF and renal dysfunction who
cannotrespondadequatelytofluidandsodiumrestrictionanddiuretics.65Ultrafiltrationisnotsuperior
toascaleddiureticregimeninpatientswithacuteHFandcardiorenalsyndromeandisassociatedwith
higher rate of adverse events.66 Other mechanical methods of fluid removal such as therapeutic
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