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Heart FailureHeart Failure
Pathogenesis Diagnosis and Pathogenesis Diagnosis and ManagementManagement
Heart Failure (HF) DefinitionHeart Failure (HF) Definition
A complex clinical syndrome in which the heart is A complex clinical syndrome in which the heart is incapable of maintaining a cardiac output adequate incapable of maintaining a cardiac output adequate to accommodate metabolic requirements and the to accommodate metabolic requirements and the venous return.venous return.
1 World Health Statistics, World Health Organization, 1995.1 World Health Statistics, World Health Organization, 1995.
2 American Heart Association, 2002 Heart and Stroke Statistical Update.2 American Heart Association, 2002 Heart and Stroke Statistical Update.
HF Incidence and PrevalenceHF Incidence and Prevalence
• Prevalence Prevalence – Worldwide, 22 millionWorldwide, 22 million11
– United States, 5 millionUnited States, 5 million22
• Incidence Incidence – Worldwide, 2 million new cases annuallyWorldwide, 2 million new cases annually11
– United States, 500,000 new cases annuallyUnited States, 500,000 new cases annually22
• HF afflicts 10 out of every 1,000 over age 65 in HF afflicts 10 out of every 1,000 over age 65 in the U.S.the U.S.22
Prevalence of HF by Age and GenderPrevalence of HF by Age and Gender
United States: 1988-94United States: 1988-94
0
2
4
6
8
10
Percent of Population
20-24 25-34 35-44 45-54 55-64 65-74 75+
MalesFemales
Source: NHANES III (1988-94), CDC/NCHS and the American Heart AssociationSource: NHANES III (1988-94), CDC/NCHS and the American Heart Association
New York Heart Association New York Heart Association Functional ClassificationFunctional Classification
Class I:Class I: No symptoms with ordinary activityNo symptoms with ordinary activity
Class II:Class II: Slight limitation of physical activity. Comfortable at rest, Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, but ordinary physical activity results in fatigue, palpitation, dyspnea, or anginapalpitation, dyspnea, or angina
Class III:Class III: Marked limitation of physical activity. Comfortable at Marked limitation of physical activity. Comfortable at rest, but less than ordinary physical activity results in rest, but less than ordinary physical activity results in fatigue, palpitation, dyspnea, or anginal painfatigue, palpitation, dyspnea, or anginal pain
Class IV:Class IV: Unable to carry out any physical activity without Unable to carry out any physical activity without discomfort. Symptoms of cardiac insufficiency may be discomfort. Symptoms of cardiac insufficiency may be present even at restpresent even at rest
Etiology of Heart FailureEtiology of Heart Failure
What causes heart failure?What causes heart failure?• The loss of a critical quantity of functioning The loss of a critical quantity of functioning
myocardial cells after injury to the heart due to:myocardial cells after injury to the heart due to:– Ischemic Heart Disease Ischemic Heart Disease – Hypertension Hypertension – Idiopathic CardiomyopathyIdiopathic Cardiomyopathy– Infections (e.g., viral myocarditis, Chagas’ disease)Infections (e.g., viral myocarditis, Chagas’ disease)– Toxins (e.g., alcohol or cytotoxic drugs) Toxins (e.g., alcohol or cytotoxic drugs) – Valvular Disease Valvular Disease – Prolonged ArrhythmiasProlonged Arrhythmias
The Donkey Analogy The Donkey Analogy
Ventricular dysfunction limits a patient's ability to perform the Ventricular dysfunction limits a patient's ability to perform the routine activities of daily living…routine activities of daily living…
30%30%
70%70%
Diastolic DysfunctionDiastolic DysfunctionSystolic DysfunctionSystolic Dysfunction
(EF < 40%)(EF < 40%)(EF > 40 %)(EF > 40 %)
Left Ventricular DysfunctionLeft Ventricular Dysfunction
• Systolic:Systolic: Impaired contractility/ejection Impaired contractility/ejection– Approximately two-thirds of heart failure patients have systolic Approximately two-thirds of heart failure patients have systolic
dysfunctiondysfunction11
• Diastolic:Diastolic: Impaired filling/relaxation Impaired filling/relaxation
1 Lilly, L. 1 Lilly, L. Pathophysiology of Heart DiseasePathophysiology of Heart Disease. Second Edition p 200. Second Edition p 200
Enlarged heartEnlarged heart
Systolic dysfunctionSystolic dysfunction
Cardiac OutputCardiac Output
• Cardiac output is the amount of blood that the Cardiac output is the amount of blood that the ventricle ejects per minuteventricle ejects per minute
Cardiac Output = HR x SVCardiac Output = HR x SV
StrokeStrokeVolumeVolume
PreloadPreload AfterloadAfterload
ContractilityContractility
Cardiac OutputCardiac Output
Heart RateHeart Rate• Synergistic LV ContractionSynergistic LV Contraction• Wall IntegrityWall Integrity• Valvular CompetenceValvular Competence
Determinants of Ventricular FunctionDeterminants of Ventricular Function
Volume Volume OverloadOverload
Pressure Pressure OverloadOverload
Loss of Loss of MyocardiumMyocardium
Impaired Impaired ContractilityContractility
LV DysfunctionLV DysfunctionEF < 40%EF < 40%
Cardiac Cardiac OutputOutput
Hypoperfusion Hypoperfusion
End Systolic Volume End Systolic Volume
End Diastolic Volume End Diastolic Volume
Pulmonary Congestion Pulmonary Congestion
Left Ventricular DysfunctionLeft Ventricular Dysfunction
Hemodynamic Basis for Hemodynamic Basis for Heart Failure SymptomsHeart Failure Symptoms
Hemodynamic Basis forHemodynamic Basis forHeart Failure SymptomsHeart Failure Symptoms
LVEDP LVEDP
Left Atrial Pressure Left Atrial Pressure
Pulmonary Capillary Pressure Pulmonary Capillary Pressure
Pulmonary CongestionPulmonary Congestion
Left Ventricular DysfunctionLeft Ventricular DysfunctionSystolic and DiastolicSystolic and Diastolic
• SymptomsSymptoms
– Dyspnea on ExertionDyspnea on Exertion
– Paroxysmal Nocturnal Paroxysmal Nocturnal DyspneaDyspnea
– TachycardiaTachycardia
– CoughCough
– HemoptysisHemoptysis
• Physical SignsPhysical Signs
– Basilar RalesBasilar Rales
– Pulmonary EdemaPulmonary Edema
– S3 GallopS3 Gallop
– Pleural EffusionPleural Effusion
– Cheyne-Stokes RespirationCheyne-Stokes Respiration
Right Ventricular FailureRight Ventricular FailureSystolic and DiastolicSystolic and Diastolic
• SymptomsSymptoms
– Abdominal PainAbdominal Pain
– AnorexiaAnorexia
– NauseaNausea
– BloatingBloating
– SwellingSwelling
• Physical SignsPhysical Signs
– Peripheral EdemaPeripheral Edema
– Jugular Venous DistentionJugular Venous Distention
– Abdominal-Jugular RefluxAbdominal-Jugular Reflux
– HepatomegalyHepatomegaly
Consequences of DecreasedConsequences of DecreasedMean Arterial PressureMean Arterial Pressure
Mean Arterial Pressure (BP)Mean Arterial Pressure (BP)==
Cardiac OutputCardiac Output
xx
Total Peripheral ResistanceTotal Peripheral Resistance
Compensatory Mechanisms Compensatory Mechanisms
Neurohormonal ActivationNeurohormonal Activation
Many different hormone systems are involved in Many different hormone systems are involved in maintaining normal cardiovascular homeostasis, maintaining normal cardiovascular homeostasis, including:including:
• Sympathetic nervous system (SNS)Sympathetic nervous system (SNS)
• Renin-angiotensin-aldosterone system (RAAS)Renin-angiotensin-aldosterone system (RAAS)
• Vasopressin (a.k.a. antidiuretic hormone, ADH)Vasopressin (a.k.a. antidiuretic hormone, ADH)
MAP = (MAP = (SV x SV x HR) x HR) x TPRTPR
Sympathetic Nervous SystemSympathetic Nervous System
ContractilityContractility TachycardiaTachycardia VasoconstrictionVasoconstriction
Compensatory Mechanisms: Compensatory Mechanisms: Sympathetic Nervous SystemSympathetic Nervous System
Decreased MAPDecreased MAP
Packer. Progr Cardiovasc Dis. 1998;39(suppl I):39-52.Packer. Progr Cardiovasc Dis. 1998;39(suppl I):39-52.
CNS sympathetic outflowCNS sympathetic outflow
Disease progressionDisease progression
Cardiac sympatheticCardiac sympatheticactivityactivity
11--receptorsreceptors
22--receptorsreceptors
11--receptorsreceptors
VasoconstrictionVasoconstrictionSodium retentionSodium retention
Myocardial toxicityMyocardial toxicityIncreased arrhythmiasIncreased arrhythmias
SympatheticSympatheticactivity to kidneysactivity to kidneys
+ peripheral vasculature+ peripheral vasculature
ActivationActivationof RASof RAS11-- 11--
Sympathetic Activation in Heart FailureSympathetic Activation in Heart Failure
VasoconstrictionVasoconstriction
Oxidative StressOxidative Stress
Cell GrowthCell Growth ProteinuriaProteinuria
LV remodelingLV remodeling
Vascular remodelingVascular remodeling
AngiotensinogenAngiotensinogen
Angiotensin IAngiotensin I
Angiotensin IIAngiotensin II
AT I receptorAT I receptor
ReninRenin
AngiotensinAngiotensinConvertingConverting
EnzymeEnzyme
Compensatory Mechanisms: Compensatory Mechanisms: Renin-Angiotensin-Aldosterone (RAAS)Renin-Angiotensin-Aldosterone (RAAS)
MAP = (MAP = (SV x SV x HR) x HR) x TPRTPR
Renin-Angiotensin-AldosteroneRenin-Angiotensin-Aldosterone(( renal perfusion) renal perfusion)
Salt-water retentionSalt-water retentionThirstThirst
SympatheticSympatheticaugmentationaugmentation VasoconstrictionVasoconstriction
Compensatory Mechanisms: Compensatory Mechanisms: Renin-Angiotensin-Aldosterone (RAAS)Renin-Angiotensin-Aldosterone (RAAS)
Decreased systemic blood pressureDecreased systemic blood pressure
Central baroreceptorsCentral baroreceptors
Stimulation of hypothalamus, which producesStimulation of hypothalamus, which producesvasopressin for release by pituitary glandvasopressin for release by pituitary gland
Release of vasopressin by pituitary glandRelease of vasopressin by pituitary glandVasoconstrictionVasoconstriction
Increased systemic blood pressureIncreased systemic blood pressure
--
Compensatory Mechanisms: Compensatory Mechanisms: Neurohormonal Activation – VasopressinNeurohormonal Activation – Vasopressin
Compensatory Neurohormonal Stimulation: Compensatory Neurohormonal Stimulation: Summary Summary
Decreased Cardiac OutputDecreased Cardiac Output
SympatheticSympatheticnervous systemnervous system
Renin-angiotensinRenin-angiotensinsystemsystem
Antidiuretic hormoneAntidiuretic hormone(vasopressin)(vasopressin)
HeartHeartraterate
ContractilityContractility VasoconstrictionVasoconstriction Circulating volumeCirculating volume
AnteriolarAnteriolar
MaintainMaintainbloodblood
pressurepressure
CardiacCardiacoutputoutput
StrokeStrokevolumevolume
++--++
VenousVenous
Venous return Venous return to heartto heart
(( preload)preload)
Peripheral edemaPeripheral edemaand pulmonaryand pulmonary
congestioncongestion
Other NeurohormonesOther Neurohormones
• Natriuretic Peptides: Three known typesNatriuretic Peptides: Three known types– Atrial Natriuretic Peptide (ANP)Atrial Natriuretic Peptide (ANP)
• Predominantly found in the atriaPredominantly found in the atria
• Diuretic and vasodilatory propertiesDiuretic and vasodilatory properties
– Brain Natriuretic Peptide (hBNP) Brain Natriuretic Peptide (hBNP) • Predominantly found in the cardiac ventricles Predominantly found in the cardiac ventricles
• Diuretic and vasodilatory propertiesDiuretic and vasodilatory properties
– C-type Natriuretic Peptide (CNP)C-type Natriuretic Peptide (CNP)• Predominantly found in the central nervous systemPredominantly found in the central nervous system
• Limited natriuretic and vasodilatory propertiesLimited natriuretic and vasodilatory properties
Hemodynamic Hemodynamic (balanced vasodilation)(balanced vasodilation)
•• veinsveins•• arteriesarteries•• coronary arteriescoronary arteries
NeurohormonalNeurohormonalaldosteronealdosteronenorepinephrinenorepinephrine
RenalRenaldiuresis & natriuresisdiuresis & natriuresis
DR I
MKRG
S SS
SGLG
FC CS SG
SGQVM
K V L RR
H
KPS
Pharmacological Actions of hBNPPharmacological Actions of hBNP
Abraham WT and Schrier RW, 1994Abraham WT and Schrier RW, 1994
Produced by a thin lining of cells within the arteries and veins Produced by a thin lining of cells within the arteries and veins called the endotheliumcalled the endothelium
Endothelium-derived relaxing factors (EDRF) – Vasodilators:Endothelium-derived relaxing factors (EDRF) – Vasodilators:• Nitric Oxide (NO)Nitric Oxide (NO)• BradykininBradykinin• ProstacyclinProstacyclin
Endothelium-derived constricting factors (EDCF) – Endothelium-derived constricting factors (EDCF) – Vasoconstrictors:Vasoconstrictors:
• Endothelin IEndothelin I
Endothelium-Derived Vasoactive SubstancesEndothelium-Derived Vasoactive Substances
LV DysfunctionLV Dysfunction
Decreased cardiac outputDecreased cardiac outputand and
Decreased blood pressureDecreased blood pressure
Frank-Starling MechanismFrank-Starling MechanismRemodelingRemodeling
Neurohormonal activationNeurohormonal activation
Increased cardiac output (via increasedIncreased cardiac output (via increasedcontractility and heart rate)contractility and heart rate)
Increased blood pressure (via vasoconstrictionIncreased blood pressure (via vasoconstriction and increased blood volume) and increased blood volume)
Increased cardiac workloadIncreased cardiac workload(increased preload and afterload)(increased preload and afterload)
Vicious Cycle of Heart FailureVicious Cycle of Heart Failure
Initially Adaptive, Deleterious if SustainedInitially Adaptive, Deleterious if Sustained
ResponseResponseShort-Term Short-Term EffectsEffects
Long-Term EffectsLong-Term Effects
Salt and Water RetentionSalt and Water Retention Augments PreloadAugments Preload Pulmonary Congestion, Pulmonary Congestion, AnasarcaAnasarca
VasoconstrictionVasoconstriction Maintains BP for perfusion Maintains BP for perfusion of vital organsof vital organs
Exacerbates pump Exacerbates pump dysfunction (excessive dysfunction (excessive afterload), increases afterload), increases cardiac energy cardiac energy expenditureexpenditure
Sympathetic StimulationSympathetic Stimulation Increases HR and ejectionIncreases HR and ejection Increases energy Increases energy expenditureexpenditure
Neurohormonal Responses to ImpairedNeurohormonal Responses to ImpairedCardiac PerformanceCardiac Performance
Jaski, B, MD: Jaski, B, MD: Basics of Heart Failure: A Problem Solving ApproachBasics of Heart Failure: A Problem Solving Approach
Assessing Heart FailureAssessing Heart Failure
• Patient HistoryPatient History
• Physical ExaminationPhysical Examination
• Laboratory and Diagnostic TestsLaboratory and Diagnostic Tests
Diagnostic Evaluation of Diagnostic Evaluation of New Onset Heart FailureNew Onset Heart Failure
• Determine the type of cardiac dysfunction Determine the type of cardiac dysfunction (systolic vs. diastolic)(systolic vs. diastolic)
• Determine EtiologyDetermine Etiology
• Define prognosisDefine prognosis
• Guide therapyGuide therapy
Diagnostic Evaluation of Diagnostic Evaluation of New Onset Heart FailureNew Onset Heart Failure
Initial Work-up:Initial Work-up:
• ECGECG
• Chest x-rayChest x-ray
• Blood workBlood work
• Echocardiography Echocardiography
M-Mode EchoM-Mode Echo 2D Echo2D Echo
RARALALA
RVRVLVLV
SeptumSeptum
LV cavityLV cavity
LV WallLV Wall
Diagnostic Evaluation of Diagnostic Evaluation of New Onset Heart FailureNew Onset Heart Failure
The Vicious Cycle of The Vicious Cycle of Heart Failure ManagementHeart Failure Management
Chronic HFChronic HF
MD’s OfficeMD’s Office
Emergency Emergency RoomRoom
HospitalizationHospitalization
SOBSOB
WeightWeight
PO LasixPO LasixIV Lasix IV Lasix or Admitor Admit
Diurese & Diurese & HomeHome
General MeasuresGeneral Measures
Lifestyle Modifications:Lifestyle Modifications:
• Weight reductionWeight reduction
• Discontinue smokingDiscontinue smoking
• Avoid alcohol and other Avoid alcohol and other cardiotoxic substancescardiotoxic substances
• ExerciseExercise
Medical Considerations:Medical Considerations:• Treat HTN, hyperlipidemia, Treat HTN, hyperlipidemia,
diabetes, arrhythmiasdiabetes, arrhythmias
• Coronary revascularizationCoronary revascularization
• AnticoagulationAnticoagulation
• ImmunizationImmunization
• Sodium restrictionSodium restriction
• Daily weightsDaily weights
• Close outpatient monitoringClose outpatient monitoring
Pharmacologic ManagementPharmacologic Management
DigoxinDigoxin
• Enhances inotropy of cardiac muscleEnhances inotropy of cardiac muscle
• Reduces activation of SNS and RAASReduces activation of SNS and RAAS
• Controlled trials have shown long-term digoxin therapy:Controlled trials have shown long-term digoxin therapy:– Reduces symptomsReduces symptoms– Increases exercise toleranceIncreases exercise tolerance– Improves hemodynamicsImproves hemodynamics– Decreases risk of HF progressionDecreases risk of HF progression– Reduces hospitalization rates for decompensated HFReduces hospitalization rates for decompensated HF– Does not improve survivalDoes not improve survival
Digitalis CompoundsDigitalis Compounds
Like the carrot placed in front of the donkeyLike the carrot placed in front of the donkey
Pharmacologic ManagementPharmacologic Management
DiureticsDiuretics
• Used to relieve fluid retentionUsed to relieve fluid retention
• Improve exercise toleranceImprove exercise tolerance
• Facilitate the use of other drugs indicated for heart failure Facilitate the use of other drugs indicated for heart failure
• Patients can be taught to adjust their diuretic dose based on Patients can be taught to adjust their diuretic dose based on changes in body weightchanges in body weight
• Electrolyte depletion a frequent complicationElectrolyte depletion a frequent complication
• Should never be used alone to treat heart failureShould never be used alone to treat heart failure
• Higher doses of diuretics are associated with increased Higher doses of diuretics are associated with increased mortalitymortality
Pharmacologic ManagementPharmacologic Management
ACE Inhibitors ACE Inhibitors
• Blocks the conversion of angiotensin I to angiotensin II; Blocks the conversion of angiotensin I to angiotensin II; prevents functional deteriorationprevents functional deterioration
• Recommended for all heart failure patientsRecommended for all heart failure patients
• Relieves symptoms and improves exercise toleranceRelieves symptoms and improves exercise tolerance
• Reduces risk of death and decreases disease progressionReduces risk of death and decreases disease progression
• Benefits may not be apparent for 1-2 months after initiationBenefits may not be apparent for 1-2 months after initiation
Diuretics, ACE InhibitorsDiuretics, ACE Inhibitors
Reduce the number of sacks on the wagonReduce the number of sacks on the wagon
Pharmacologic ManagementPharmacologic Management
Beta-BlockersBeta-Blockers
• Cardioprotective effects due to blockade of excessive SNS Cardioprotective effects due to blockade of excessive SNS stimulation stimulation
• In the short-term, beta blocker decreases myocardial In the short-term, beta blocker decreases myocardial contractility; increase in EF after 1-3 months of usecontractility; increase in EF after 1-3 months of use
• Long-term, placebo-controlled trials have shown symptomatic Long-term, placebo-controlled trials have shown symptomatic improvement in patients treated with certain beta-blockersimprovement in patients treated with certain beta-blockers11
• When combined with conventional HF therapy, beta-blockers When combined with conventional HF therapy, beta-blockers reduce the combined risk of morbidity and mortality, or reduce the combined risk of morbidity and mortality, or disease progressiondisease progression11
1 Hunt, SA, et al ACC/AHA Guidelines for the Evaluation and Management 1 Hunt, SA, et al ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult, 2001 p. 20.of Chronic Heart Failure in the Adult, 2001 p. 20.
ß-Blockersß-Blockers
Limit the donkey’s speed, thus saving energyLimit the donkey’s speed, thus saving energy
Pharmacologic ManagementPharmacologic Management
Aldosterone AntagonistsAldosterone Antagonists
• Generally well-toleratedGenerally well-tolerated
• Shown to reduce heart failure-related morbidity and Shown to reduce heart failure-related morbidity and mortality mortality
• Generally reserved for patients with NYHA Class III-IV HFGenerally reserved for patients with NYHA Class III-IV HF
• Side effects include hyperkalemia and gynecomastia. Side effects include hyperkalemia and gynecomastia. Potassium and creatinine levels should be closely Potassium and creatinine levels should be closely monitoredmonitored
Pharmacologic ManagementPharmacologic Management
Angiotensin Receptor Blockers (ARBs)Angiotensin Receptor Blockers (ARBs)
• Block ATBlock AT11 receptors, which bind circulating angiotensin II receptors, which bind circulating angiotensin II
• Examples: valsartan, candesartan, losartanExamples: valsartan, candesartan, losartan
• Should not be considered equivalent or superior to ACE Should not be considered equivalent or superior to ACE inhibitorsinhibitors
• In clinical practice, ARBs should be used to treat patients In clinical practice, ARBs should be used to treat patients who are ACE intolerant due to intractable cough or who who are ACE intolerant due to intractable cough or who develop angioedemadevelop angioedema
Proven Outcomes for HF TherapiesProven Outcomes for HF Therapies
• Improve SurvivalImprove Survival– ACE inhibitorACE inhibitor
– ARBARB– Beta blockerBeta blocker
– Aldosterone receptor Aldosterone receptor antagonistantagonist
– Hydralazine/long-acting Hydralazine/long-acting nitratesnitrates
• Reduce HospitalizationReduce Hospitalization– ACE inhibitorACE inhibitor– ARBARB
– Beta blockerBeta blocker
– Aldosterone receptor Aldosterone receptor antagonistantagonist
– Hydralazine/long-acting Hydralazine/long-acting nitratesnitrates
– DigoxinDigoxin
Cardiac Resynchronization TherapyCardiac Resynchronization Therapy
Increase the donkeyIncrease the donkey’s’s (heart) efficiency (heart) efficiency
Patient IndicationsPatient Indications
CRT device:CRT device:– Moderate to severe HF (NYHA Class III/IV) patients Moderate to severe HF (NYHA Class III/IV) patients
– Symptomatic despite optimal, medical therapySymptomatic despite optimal, medical therapy
– QRS QRS 130 msec 130 msec
– LVEF LVEF 35% 35%
CRT plus ICD:CRT plus ICD:– Same as above with ICD indicationSame as above with ICD indication
Cardiac Resynchronization TherapyCardiac Resynchronization Therapy
Cardiac Resynchronization Therapy: Cardiac Resynchronization Therapy: Creating Realistic Patient ExpectationsCreating Realistic Patient Expectations
• Approximately two-third of patients should Approximately two-third of patients should experience improvement (responders vs. experience improvement (responders vs. non-responders)non-responders)11
– Some patients may not experience immediate Some patients may not experience immediate improvementimprovement
Note: CRT is adjunctive and is not intended to replace medical therapy. Note: CRT is adjunctive and is not intended to replace medical therapy. Patients will continue to be followed by HF Specialist and Physician Patients will continue to be followed by HF Specialist and Physician managing implantable devices.managing implantable devices.
1 Abraham, WT, et. Al. Cardiac Resynchronization in Chronic Heart Failure. 1 Abraham, WT, et. Al. Cardiac Resynchronization in Chronic Heart Failure. N Engl J MedN Engl J Med 2002;346:1845-53 2002;346:1845-53
SummarySummary
• Heart failure is a chronic, progressive disease that is Heart failure is a chronic, progressive disease that is generally not curable, but treatablegenerally not curable, but treatable
• Most recent guidelines promote lifestyle modifications and Most recent guidelines promote lifestyle modifications and medical management with ACE inhibitors, beta blockers, medical management with ACE inhibitors, beta blockers, digoxin, and diuretics digoxin, and diuretics
• It is estimated 15% of all heart failure patients may be It is estimated 15% of all heart failure patients may be candidates for cardiac resynchronization therapy (see later candidates for cardiac resynchronization therapy (see later section for details)section for details)
• Close follow-up of the heart failure patient is essential, with Close follow-up of the heart failure patient is essential, with necessary adjustments in medical managementnecessary adjustments in medical management