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5
HeartFailureandCardiomyopathy
BinQ.Yang,JustinC.Hartupee,JustinM.Vader
HeartFailure
GeneralPrinciples
Definition
Heartfailure(HF)isaclinicalsyndromeinwhicheitherstructuralorfunctionalabnormalitiesofthe
heartimpairitsabilitytofillwithorejectblood,resultingindyspnea,fatigue,andfluidretention.
1,2
HFis
aprogressivedisorderandisassociatedwithhighmorbidityandmortality.
Classification
HFmaybeduetoabnormalitiesinmyocardialcontraction(systolicdysfunction),relaxationandfilling
(diastolicdysfunction),orboth.
Leftventricular(LV)ejectionfraction(EF)isusedtosubdivideHFpatientsintogroupsfortherapeutic
andprognosticpurposes.3Thesegroupsare:
EF≤40%:HFwithreducedEF(HFrEF)
EF41%–49%:HFwithmildlyreducedEF(HFmrEF)
EF≥50%:HFwithpreservedEF(HFpEF)
EFwithbaseline≤40%,a≥10-pointincrease frombaselineEF,anda secondmeasurementofLVEF
>40%:HFwithimprovedEF(HFimpEF).
HF is classified in terms of natural history by American College of Cardiology/American Heart
Association(ACC/AHA) HF stageandintermsofsymptom status byNew YorkHeart Association
(NYHA)FunctionalClass(Tables5-1and5-2).
TABLE5-1
AMERICANCOLLEGEOFCARDIOLOGY/AMERICANHEARTASSOCIATION
GUIDELINESOFEVALUATIONANDMANAGEMENTOFCHRONICHEARTFAILUREIN
ADULTS
Stage Description Treatment
A Nostructuralheartdiseaseandno
symptomsbutriskfactors:CAD,
HTN,DM,cardiotoxins,familial
Lifestylemodification—diet,exercise,smoking
cessation;treathyperlipidemiaanduseACE
inhibitorforHTN
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cardiomyopathy
B AbnormalLVsystolicfunction,MI,
valvularheartdisease,butnoHF
symptoms
Lifestylemodifications,ACEinhibitor,βadrenergicblockers
C StructuralheartdiseaseandHF
symptoms
Lifestylemodifications,ACEinhibitor,βadrenergicblockers,diuretics,digoxin
D RefractoryHFsymptomstomaximal
medicalmanagement
TherapylistedunderA,B,andC,and
mechanicalassistdevice,hearttransplantation,
continuousIVinotropicinfusion,hospicecarein
selectedpatients
ACE,angiotensin-convertingenzyme;CAD,coronaryarterydisease;DM,diabetesmellitus;HF,heartfailure;HTN,hypertension;
LV,leftventricular;MI,myocardialinfarction.
AdaptedfromYancyCW,JessupM,BozkurtB,etal.2017ACC/AHA/HFSAfocusedupdateofthe2013ACCF/AHAguidelinefor
themanagementofheartfailure:areportoftheAmericanCollegeofCardiology/AmericanHeartAssociationTaskForceon
ClinicalPracticeGuidelinesandtheHeartFailureSocietyofAmerica.Circulation.2017;136(6):e137-e161.
TABLE5-2
NEWYORKHEARTASSOCIATION(NYHA)FUNCTIONALCLASSIFICATION
NYHA
Class
Symptoms
I(Mild) Nosymptomsorlimitationwhileperformingordinaryphysicalactivity(walking,
climbingstairs,etc.).
II(Mild) Mildsymptoms(mildshortnessofbreath,palpitations,fatigue,and/orangina)
andslightlimitationduringordinaryphysicalactivity.
III
(Moderate)
Markedlimitationinactivitybecauseofsymptoms,evenduringlessthanordinary
activity(walkingshortdistances[20–100m]).Comfortableonlyatrest.
IV
(Severe)
Severelimitationswithsymptomsevenwhileatrest.Mostlybedboundpatients.
Epidemiology
IntheUnitedStates,over6.5millionadultsover20yearsofagearelivingwithHFandthisnumberis
expectedtoexceed8millionby2030.
4
Approximately1millionnewcasesofHFarediagnosedeachyear.
HFaccountsforapproximately1millionhospitalizationsperyear.
Estimated1-and5-yearmortalityratesare22%and42.3%,respectively.
5
Etiology
SeeTable5-3.
TABLE5-3
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HEARTFAILUREETIOLOGY
IschemicCardiomyopathy Nonischemic
Cardiomyopathy
Severe angiographic coronary artery disease, post–
myocardial infarction, or evidence of hibernating
myocardium
Other risk factors include tobacco use, hypertension,
diabetes,andobesity
Ischemic cardiomyopathy is the most common cause of
heartfailure
Idiopathic
Familial
Myocarditis (infectious or
autoimmune)
Infiltrative (amyloidosis,
sarcoidosis,
hemochromatosis)
Peripartum
Valvularheartdisease
Toxin-induced (e.g., alcohol,
amphetamine,
chemotherapy)
Tachycardia-induced
High-output(peripheralshunt,
chronicanemia)
Generalized myopathy (e.g.,
musculardystrophy)
Pathophysiology
HFbeginswithaninitialinsultleadingtomyocardialinjury.
Regardlessofetiology,themyocardialinjuryleadstoapathologicremodeling,whichmanifestsasan
increaseinLVvolume(dilatation)and/ormass(hypertrophy).
Compensatory adaptations initially maintain cardiac output; specifically, there is activation of the
renin–angiotensin–aldosteronesystem(RAAS)andvasopressin(antidiuretichormone),whichleadsto
increased sodium retention and peripheral vasoconstriction. Thesympathetic nervoussystem is also
activated (Figure 5-1), with increased levels of circulating catecholamines, resulting in increased
myocardial contractility. Over time,these neurohormonal pathways result in direct cellular toxicity,
fibrosis,arrhythmias,andpumpfailure.
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Figure5-1 Activationofthesympatheticnervoussystem.ACE,angiotensin-convertingenzyme;ARB,angiotensinIIreceptor
blocker;SGLT2i,sodium–glucosecotransporter2inhibitor.
Diagnosis
ClinicalPresentation
History
Afflictedpatientsmostcommonlypresentwiththefollowingsymptoms:
Dyspnea(onexertionand/oratrest)
Fatigue
Exerciseintolerance
Orthopnea,paroxysmalnocturnaldyspnea
Bendopnea(dyspneawhenleaningforward)
Systemicorpulmonaryvenouscongestion(lowerextremityswellingorcough/wheezing)
Presyncope,palpitations,andanginamayalsobepresent
Otherpossible presentationsincludeincidentaldetection ofasymptomaticcardiomegalyorsymptoms
related to coexisting arrhythmia, conduction disturbance, thromboembolic complications, or sudden
death.
ClinicalmanifestationsofHFvarydependingontheseverityandrapidityofcardiacdecompensation,
underlyingetiology,age,andcomorbiditiesofthepatient.
Extremedecompensationmaypresentascardiogenicshock(resultingfrombothlowarterialandhigh
venous pressures), characterized by hypoperfusion of vital organs, renal failure (decreased urine
output),mentalstatuschanges(confusionandlethargy),or“shockliver”(elevatedliverfunctiontests).
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PhysicalExamination
ThegoalofthephysicalexaminationinHFis toestimateintracardiacpressures, cardiac output,and
end-organperfusion.
Elevated right-sided pressures result in lower extremity edema, jugular venous distension (JVD),
abdominojugularreflux,pleuralandpericardialeffusions,hepaticcongestion,andascites.
JVDisthemostspecificandreliablephysical examinationindicator ofright-sided volume overload
and is representative of left-sided filling pressures except in cases of disproportionate right heart
dysfunction(e.g.,pulmonaryhypertension,severetricuspidregurgitation,andpericardialdisease).
JVD is best visualized with oblique light and the patient at 45 degrees. Venous pulsations are
differentiated from carotid pulsation by their biphasic nature, respiratory variability, and
compressibility.
Abdominojugularrefluxsuggestsanimpairedabilityoftherightventricletohandleaugmentedpreload
andmaybeduetoconstrictionorpulmonaryhypertensioninadditiontomyocardialdisease.
Elevatedleft-sidedpressuresmayresultinpulmonaryrales,butralesareabsentinthemajorityofHF
patientswithelevatedleft-sidedfillingpressures.
Inthesettingofsystolicdysfunction,athird(S3)orfourth(S4)heartsoundaswellastheholosystolic
murmurs of tricuspid or mitral regurgitation (MR) may be present; carotid upstrokes may also be
diminished.
Low cardiac output is suggested by a proportional pulse pressure (pulse pressure/diastolic blood
pressure)≤25%,diminishedcarotidupstroke,andcoolextremities.
DiagnosticTesting
Laboratories
Initial laboratory studies should include complete blood count, basic metabolic panel, magnesium,
liverfunctiontests,lipidprofile,andthyroidfunctiontests.
B-type natriuretic peptide (BNP) and the biologically inactive cleavage product N-terminal
prohormoneBNP(NT-proBNP)arereleasedbymyocytesinresponsetostretch,volumeoverload,and
increased filling pressures. Natriurietic peptides serve as a natural compensatory mechanism to
enhancenatriuresis.
Elevated BNP/NT-proBNP is present in patients with asymptomatic LV dysfunction as well as
symptomaticHF.
BNP/NT-proBNPlevelshavebeenshowntocorrelatewithHFseverityandtopredictsurvival.6A
serumBNP>400pg/mLisconsistentwithHF;however,specificityisreducedinpatientswithrenal
dysfunctionandlevels maybelow inthesetting ofobesity.AserumBNPlevel <100pg/mLhasa
goodnegativepredictivevaluetoexcludeHFinpatientspresentingwithdyspnea.7Age-specificcut
points have also been identified; for example, NT-proBNP levels of 450, 900, and 1800 pg/mL
optimallyidentifiedacuteHFforpatientsage<50,50–75,and>75,respectively.
8
Additional laboratorytestingina patientwithnew-onsetHFwithoutcoronaryarterydisease (CAD)
mayincludediagnostictestsforHIV,hepatitis,andhemochromatosis.Whenclinicallysuspected,serum
tests for rheumatologic diseases (antinuclear antibody, antineutrophil cytoplasmic antibody, etc.),
amyloidosis (serum protein electrophoresis, urine protein electrophoresis), or pheochromocytoma
(catecholamines)shouldbeconsidered.
Electrocardiography
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AnECGshouldbeperformedtolookforevidenceofischemia(ST-Twaveabnormalities),hypertrophy
(increasedvoltage),infiltration(reducedvoltage),previousmyocardialinfarction(MI)(Qwaves),
conductionblock(PRinterval),interventricularconductiondelays(prolongedQRS),andarrhythmias
(supraventricularandventricular).
Imaging
Chestradiographyshouldbeperformedtoevaluatethepresenceofpulmonaryedemaorcardiomegaly
andrule outother etiologies of dyspnea(e.g.,pneumonia, pneumothorax).Althoughchestradiograph
findings ofcephalizationandinterstitial edemaare highlyspecific for identifying patientspresenting
with acute HF (specificity of 98% and 99%, respectively), they have limited sensitivity (41% and
27%,respectively).
9
Anechocardiogramshouldbeperformedtoassessrightventricular(RV)andLVsystolicanddiastolic
function,valvularstructureandfunction,andchambersizeandtoexcludecardiactamponade.
LV function may also be evaluated using radionuclide ventriculography (i.e., multigated acquisition
[MUGA]scan)orcardiaccatheterizationwithventriculographyandinvasivehemodynamics.
Cardiac MRI may be useful in assessing ventricular function and evaluating the presence of
intracardiacshunting,valvularheartdisease,infiltrativecardiomyopathy,myocarditis,and/orprevious
MI.
Cardiac positron emission tomography (PET) may be useful in the diagnosis and surveillance of
cardiacsarcoidosis.
Bone scintigraphy (99m technetium-labeled pyrophosphate scan) should be considered if there is
clinical suspicion for transthyretin (TTR) amyloidosis once immunoglobulin light chain (AL)
amyloidosishasbeenruledout.
DiagnosticProcedures
Coronaryangiographyshouldbeperformedinpatientswithanginaorevidenceofischemia,unlessthe
patientisnotacandidateforrevascularization.
Stressnuclearimagingorechocardiographymaybeanacceptablealternativeforassessingischemiain
patients presenting with HF who have known CAD and no angina, unless they are ineligible for
revascularization.
Right heartcatheterizationwith placementofa pulmonary artery catheter may help guide therapy in
patientswithhypotensionandevidenceofshock.
Cardiopulmonaryexercise testing withmeasurement of peakoxygenconsumption(VO2) is useful in
assessingfunctionalcapacityandinidentifyingcandidatesforhearttransplantation.
10
Endomyocardialbiopsyshouldbeconsideredwhenseekingaspecificdiagnosisthatwouldinfluence
therapy, specifically in patients with rapidly progressive and unexplained cardiomyopathy; those in
whom active myocarditis, especially giant cell myocarditis, is considered; and those with possible
infiltrativeprocessessuchascardiacamyloidosisandsarcoidosis.
11
TreatmentofHeartFailure
Pharmacotherapy
Ingeneral,pharmacologictherapyinchronicHFisaimedatblockingtheneurohormonalpathwaysthat
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contribute to cardiac remodeling and the progression of HF resulting in reduced symptoms,
hospitalizations,andmortality.
The cornerstone of medical therapy for HF includes β-adrenergic blockade, neprilysin and RAAS
inhibition,anddiuretictherapytoimprovesymptomsofvolumeoverload.
Pharmacotherapy is determined by the presence of a preserved or reduced LVEF. Several
pharmacotherapiesforHFrEFhavebeendemonstratedtoreducedeathandhospitalizationandimprove
qualityoflifeinHF.Nopharmacotherapyhasbeenunequivocallydemonstratedtoimprovemortalityin
patientswithHFpEF.
ChronicMedicalTherapywithReducedEjectionFraction(Figure5-2)
Figure5-2 Chronicmedicaltherapies forheartfailure withreduced ejectionfraction(HFrEF).ACEi,angiotensin-converting
enzymeinhibitor;ARB,angiotensinIIreceptorblocker;ARNI,angiotensinreceptor–neprilysininhibitor;bpm,beatsperminute;
HR,heart rate; LVEF,left ventricular ejectionfraction; NSR,normalsinus rhythm; SGLT2i, sodium–glucose cotransporter 2
inhibitor.
First-line therapies—all patients with HFrEF should be placed on a β-blocker, angiotensin
receptor–neprilysin inhibitor (ARNI) (or angiotensin-converting enzyme [ACE] inhibitor or
angiotensin II receptor blocker [ARB]), mineralocorticoid receptor antagonist (MRA), and
sodium-glucosecotransporter2(SGLT2)inhibitor.
β-Adrenergicreceptorantagonists(β-blockers)(Table5-4).β-Blockersareacriticalcomponentof
HFtherapyandworkbyblockingtheeffectsofchronicadrenergicstimulationontheheart.
Largerandomizedtrials havedocumented the beneficial effects ofβ-blockers onfunctionalstatus,
diseaseprogression,andsurvivalinpatientswithNYHAclassII–IVsymptoms.
12
TABLE5-4
DRUGSCOMMONLYUSEDFORTREATMENTOFHEARTFAILURE
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