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3/4/2019
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HEART FAILURE: MANAGEMENT IN
THE ACUTE CARESETTING
ROBERT T ROGERS, ACNP-BC, AACCNORTON HEART SPECIALISTS
HEART RHYTHM CENTER
Speaker Disclosures
None
AGENDA FOR THE DAY…• 1. Overview of Heart Failure
• 2. Epidemiology
• 3. Classification
• Signs and Symptoms
• Pathophysiology
• 4. Management: Acute Care Setting
• Evaluation and workup
• Drug classes- Ace-I, Beta Blockers, Diuretics, Aldosterone Antagonists, Neprilisyin inhibitors, Corlanor
• ICD’s and biventricular pacing
• Cardiac Transplant, LVAD, etc.
Definition of Heart Failure
“Heart failure is a clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood”
ACC/AHA Guidelines 2013
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About 6.5 million adults in the United States have heart failure.1
One in 9 deaths in 2009 included heart failure as
contributing cause.1
About half of people who develop heart failure die within 5 years of diagnosis.1
Heart failure costs the nation an estimated $30.7
billion each year.3 This total includes the cost of health care services, medications to treat heart failure, and missed days
of work.
EPIDEMIOLOGY OF HF
Gheorghiade M, et al. Circulation 2005;112:3958-68
ADHERE(n=110 000)
Euro-HF(n=11 000)
OPTIMIZE-HF(n=48 612)
Demographic characteristics
Mean age, y 75 71 73
Women (%) 52 47 52
Known heart failure (%) 75 65 87
Preserved EF (%) 40 54 49
Medical history (%)
CHD 57 68 50
Hypertension 72 53 71
Diabetes 44 27 42
Atrial fibrillation 31 43 31
Renal insufficiency 30 17 30
COPD 31 ... 28
Heart Failure is Progressive
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COSTBurden of Heart Failure
• Lifetime risk > 20% for Americans >40 years of age
• 870,000 new cases diagnosed annually
• Prevalence in US: 5.7 million
ACC/AHA Guidelines 2013
Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA Guideline for the Management of Heart Failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on
Practice Guidelines. Circulation. 2013;128:e240–e327.
HF groups: ACC/AHA Guidelines
The current definition of HF based on left ventricular ejection fraction (EF):
• HF with reduced EF (HFrEF, EF ≤40%)
• HF failure with preserved EF
(HFpEF, EF ≥50%)
• HFpEF, borderline (EF 41-49%)
• HFpEF, improved (EF >40%)
ACC/AHA Guidelines 2013
Class I Asymptomatic: No limitation of physical activity. Ordinary activity does not cause sxs.
II Symptomatic with moderate exertion. Ordinary physical activity causes SOB, fatigue
IV Symptomatic at rest. Unable to carry on any activity without discomfort.
III Symptomatic with minimal exertion. Less than usual activity causes sxs
NYHA Class
5-10%
5-10%
10-25%
25-60%
1-Yr Mortality
NYHA Class and Mortality PROGNOSIS IN ADVANCED HEART FAILUREUNCHANGED IN 20 YEARS
Stevenson LW, Rose EA. Circulation 2003;108:3059
Stage D, NYHA Class IV 50% Mortality
Acute cardiogenic shock Imminent
End organ dysfunction 1 month
Inotrope-dependent 3-6 months
ACE-inhibitor intolerant 6 months
Cachexia, hyponatremia, CKD 6-12 months
Tolerating oral therapies ± 12 months
Stabilized to NYHA Class III > 24 months
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HEART FAILURE IN CONTEXTONE YEAR MORTALITY
0
10
20
30
40
50
60
70
80
90
AIDS Leukemia Lung Cancer Pancreatic Cancer End-stage HF with Optimal Medical
ManagementDiagnosis
1 Ye
ar M
orta
lity
(%)
Rose EA, et al. N Engl J Med. 2001 Nov 15;345(20):1435-43.
SYMPTOMS
CLINICAL PRESENTATION GENERALLY DIVIDED INTO TWO TYPES
CLINICAL SIGNS AND SYMPTOMS
WILL VARY BY LEFT OR RIGHT SIDED FAILURE
ACC/AHA Guidelines 2013
• Left Heart Failure: Dyspnea on exertion Dyspnea at rest Orthopnea Paroxysmal nocturnal dyspnea (PND) Fatigue, inability to exercise
• Right Heart Failure: Swelling of feet, hands Abdominal distention/fullness Right upper quadrant pain Early satiety Weight loss (cardiac cachexia)
Clinical: Symptoms of HF
ACC/AHA Guidelines 2013
• Left Heart Failure:• Rales/Crackles• Pleural effusions• CM: Displaced apical impulse• Tachycardia, LVS3, murmur of MR• Narrow pulse pressure
• Right Heart Failure:• Edema of lower extremities • Elevated JVP/+ HJR • RVS3, murmur of TR• Hepatomegaly, RUQ tenderness• Ascites• Pleural effusions
Clinical: Signs of HF
PATHOPHYSIOLOGY
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Adapted from Cohn JN. N Engl J Med. 1996;335:490–498.
Pathologicremodeling
Low ejectionfraction Death
Symptoms:DyspneaFatigueEdema
Chronicheart
failure
•Neurohormonalstimulation
•Myocardial toxicity
SuddenDeath
Pump failure
Coronary artery disease
Hypertension
Cardiomyopathy
Valvular disease
Myocardialinjury
PATHOLOGIC PROGRESSION OF CV DISEASE
Diabetes
COMPENSATORY MECHANISMS:RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM(NEUROHOMONAL MECHANISM)
Renin + Angiotensinogen
Angiotensin I
Angiotensin II
Peripheral Vasoconstriction
Afterload
Cardiac Output
Heart Failure
Cardiac Workload
Preload
Plasma Volume
Salt & Water Retention
Edema
Aldosterone Secretion
ACE
Kaliuresis
BetaStimulation
• CO• Na+
Fibrosis
NEUROHORMONAL MECHANISM
Renin
Angiotensin I
Aldosterone
Norepinephrine chronotropy, inotropy, vasoconstriction, renin secretion
sodium retention, cardiac fibrosis
Angiotensin II
ACEvasoconstriction, cardiomyocyte hypertrophy,
aldosterone and vasopressin release, thirst
Converts angiotensinogen to angiotensin I
Ejec
tion
Frac
tion
60 %
20 %Time (yrs)
Compensatory Mechanisms
SecondaryDamage
Asymptomatic Symptomatic
Mann, Circulation 1999; 100: 999-1008
ACUTE DECOMPENSATED HEART FAILURESIGNS AND SYMPTOMS
“WET”
Dyspnea, orthopnea, PND, morning cough, peripheral
edema, rales, ascites, hepatic congestion, jugular
venous distention
CARD
IAC
OU
TPU
T
PULMONARY CAPILLARY WEDGE PRESSURE
“COLD”
Nausea, early satiety, altered mental status, acidosis, worsening renal or hepatic function, reduced capillary refill,
cold skin, hypotension, narrow pulse pressure
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INPATIENT TRIAGEDECOMPENSATED HEART FAILURE
WARM AND DRYCompensated
Optimize oral therapy
Outpatient
COLD AND DRYLow Flow State
Inotropes, vasodilators, Support
ICU
COLD AND WETDecompensated
Diuretics, vasodilators, inotropes
ICU
WARM AND WETCongested
Diuretics
ED or Inpatient
Adapted from Nohria,J Cardiac Failure 2000;6:64
CARD
IAC
OU
TPU
T
PULMONARY CAPILLARY WEDGE PRESSURE
WHO’S COLD?PROPORTIONAL PULSE PRESSUREPulse Pressure
Systolic BP- Diastolic BP
Proportional Pulse PressurePulse Pressure
Systolic BP
Stevenson LW and Perloff JK. JAMA 1989;261(6):884-8
Proportional Pulse Pressure ≤ 25% predicts Cardiac Index ≤ 2.2Sensitivity 91%Specificity 83%
WHO’S WET?
Stevenson LW and Perloff JK. JAMA 1989;261(6):884-8
Finding Sensitivity Specificity
JVP > 11cm 67% 74%
Edema > trace 48% 69%
Increased apical P2 37% 75%
Rales 15% 85%
Hepatomegaly 15% 92%
S3 gallop 63% 40%
Valsalva square root sign 13% 96%
Acute Heart Failure Treatment According To Hemodynamics
High Afterload Poor Contractility
Vasodilators(Nitroprusside, milrinone)
Inotropes(Dopamine, Dobutamine)
High Preload
Diuretics(Lasix, Bumex)
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MANAGEMENT OF HEART FAILURE
• 1. Diagnostic Testing
• 2. Biomarkers in the hospitalized/acute setting
• 3. Non-invasive cardiac imaging
• 4. Invasive evaluation
• 5. Treatment
Class I
Benefit >>> Risk
Procedure/ Treatment SHOULD be performed/ administered
Class IIa
Benefit >> RiskAdditional studies with focused objectives needed
IT IS REASONABLE to perform procedure/administer treatment
Class IIb
Benefit ≥ RiskAdditional studies with broad objectives needed; Additional registry data would be helpful
Procedure/Treatment MAY BE CONSIDERED
Class III
Risk ≥ BenefitNo additional studies needed
Procedure/Treatment should NOT be performed/administered SINCE IT IS NOT HELPFUL AND MAY BE HARMFUL
shouldis recommendedis indicatedis useful/effective/
beneficial
is reasonablecan be useful/effective/
beneficialis probably recommended or
indicated
may/might be consideredmay/might be reasonableusefulness/effectiveness is
unknown /unclear/uncertain or not well established
is not recommendedis not indicatedshould notis not
useful/effective/beneficialmay be harmful
Applying Classification of Recommendations and Level of Evidence
Level A
Multiple (3-5) population risk strata evaluated
General consistency of direction and magnitude of effect
Class I
• Recommen-dation that procedure or treatment is useful/ effective
• Sufficient evidence from multiple randomized trials or meta-analyses
Class IIa
• Recommen-dation in favor of treatment or procedure being useful/ effective
• Some conflicting evidence from multiple randomized trials or meta-analyses
Class IIb
• Recommen-dation’s usefulness/ efficacy less well established
• Greater conflicting evidence from multiple randomized trials or meta-analyses
Class III
• Recommen-dation that procedure or treatment not useful/effective and may be harmful
• Sufficient evidence from multiple randomized trials or meta-analyses
Applying Classification of Recommendations and Level of Evidence
Level B
Limited (2-3) population risk strata evaluated
Class I
• Recommen-dation that procedure or treatment is useful/effective
• Limited evidence from single randomized trial or non-randomized studies
Class IIa
• Recommen-dation in favor of treatment or procedure being useful/effective
• Some conflicting evidence from single randomized trial or non-randomized studies
Class IIb
• Recommen-dation’s usefulness/ efficacy less well established
• Greater conflicting evidence from single randomized trial or non-randomized studies
Class III
• Recommen-dation that procedure or treatment not useful/effective and may be harmful
• Limited evidence from single randomized trial or non-randomized studies
Applying Classification of Recommendations and Level of Evidence
Level C
Very limited (1-2) population risk strata evaluated
Class I
• Recommen-dation that procedure or treatment is useful/ effective
• Only expert opinion, case studies, or standard-of-care
Class IIa
• Recommen-dation in favor of treatment or procedure being useful/effective
• Only diverging expert opinion, case studies, or standard-of-care
Class IIb
• Recommen-dation’s usefulness/ efficacy less well established
• Only diverging expert opinion, case studies, or standard-of-care
Class III
• Recommend-ation that procedure or treatment not useful/effective and may be harmful
• Only expert opinion, case studies, or standard-of-care
Applying Classification of Recommendations and Level of Evidence DIAGNOSTIC TESTS
Initial laboratory evaluation of patients presenting with HF should include complete blood count, urinalysis, serum electrolytes (including calcium and magnesium), blood urea nitrogen, serum creatinine, glucose, fasting lipid profile, liver function tests, and thyroid-stimulating hormone.
Serial monitoring, when indicated, should include serum electrolytes and renal function.
I IIa IIb III
I IIa IIb III
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DIAGNOSTIC TESTS (CONT.)
A 12-lead ECG should be performed initially on all patients presenting with HF.
Screening for hemochromatosis or HIV is reasonable in selected patients who present with HF.
Diagnostic tests for rheumatologic diseases, amyloidosis, or pheochromocytoma are reasonable in patients presenting with HF in whom there is a clinical suspicion of these diseases.
I IIa IIb III
I IIa IIb III
I IIa IIb III
MEASUREMENT OF BNP Measurement of natriuretic peptides (B-type natriuretic peptide (BNP) or N-terminal pro-B-type natriuretic peptide (NT-proNBP) can be useful in the evaluation of patients presenting in the urgent care setting in whom the clinical diagnosis of HF is uncertain. Measurement of natriuretic peptides (BNP and NT-proBNP) can be helpful in risk stratification.
The value of serial measurements of BNP to guide therapy for patients with HF is not well established.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIIIIII
BNP (NT-proBNP) in HF
• BNP or B-type natriuretic peptide is produced mostly by cardiac ventriclesin response to stress/strain/stretch on the myocardium
• BNP has beneficial effects in heart failure: promotes vasodilation, diuresis and natriuresis
• Levels increased in patients with HF; levels correlate with wedgepressures and prognosis
• BNP < 100 pg/ml usually will r/o significant HF in acute dyspnea
BNP IS INCREASED WITH HEART FAILUREIRRESPECTIVE OF EJECTION FRACTION
Maisel AS, et al. JACC 2003;41:2010
BNP LEVELS HAVE PROGNOSTIC VALUEDIRECT CORRELATION WITH MORTALITY AND READMISSION RATE
Logeart D, et al. JACC 20042;40:976-82
HOSPITALIZED/ACUTE
Measurement of BNP or NT-proBNP is useful to support clinical judgment for the diagnosis of acutely decompensated HF, especially in the setting of uncertainty for the diagnosis.
Measurement of BNP or NT-proBNP and/or cardiac troponin is useful for establishing prognosis or disease severity in acutely decompensated HF.
I IIa IIb III
I IIa IIb III
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HOSPITALIZED/ACUTE (CONT.)
The usefulness of BNP- or NT-proBNP guided therapy for acutely decompensated HF is not well-established.
Measurement of other clinically available tests such as biomarkers of myocardial injury or fibrosis may be considered for additive risk stratification in patients with acutely decompensated HF.
I IIa IIb III
I IIa IIb III
Caveats: BNP (NT-proBNP) in HF • Patients discharged with BNP > 400-500 pg/ml at discharge
are at a higher risk for HF readmissions and mortality
• However, patients with low LVEF can have normal levels ifdiuresed well (20-25% chronic HF)
• Levels ↑ with age, especially in older women, and with renal dysfunction
•↑ in HFrEF & HFpEF (overall higher in HFrEF)•↓ ↓ in obesity • Elevated BNP also seen with RV dysfunction, PE
• Although prognostic- no definitive data to recommend titrating diuretics or meds to BNP levels- outside of structured HF programs.
CAUSES FOR ELEVATED NATRIURETIC PEPTIDE LEVELS
Cardiac Noncardiac Heart failure, including RV
syndromes Acute coronary syndrome Heart muscle disease,
including LVH Valvular heart disease
Pericardial disease Atrial fibrillation Myocarditis Cardiac surgery Cardioversion
Advancing age Anemia Renal failure Pulmonary causes: obstructive
sleep apnea, severe pneumonia, pulmonary
hypertension Critical illness Bacterial sepsis Severe burns Toxic-metabolic insults,
including cancer
chemotherapy and envenomation
NONINVASIVE CARDIAC IMAGING
Patients with suspected or new-onset HF, or those presenting with acute decompensated HF, should undergo a chest x-ray to assess heart size and pulmonary congestion, and to detect alternative cardiac, pulmonary, and other diseases that may cause or contribute to the patients’ symptoms.
A 2-dimensional echocardiogram with Doppler should be performed during initial evaluation of patients presenting with HF to assess ventricular function, size, wall thickness, wall motion, and valve function.
Repeat measurement of EF and measurement of the severity of structural remodeling are useful to provide information in patients with HF who have had a significant change in clinical status; who have experienced or recovered from a clinical event; or who have received treatment, including GDMT, that might have had a significant effect on cardiac function; or who may be candidates for device therapy.
I IIa IIb III
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NONINVASIVE CARDIAC IMAGING (CONT.)
Noninvasive imaging to detect myocardial ischemia and viability is reasonable in patients presenting with de novo HF who have known CAD and no angina unless the patient is not eligible for revascularization of any kind.
Viability assessment is reasonable in select situations when planning revascularization in HF patients with CAD.
Radionuclide ventriculography or magnetic resonance imaging can be useful to assess LVEF and volume when echocardiography is inadequate.
I IIa IIb III
I IIa IIb III
I IIa IIb III
NONINVASIVE CARDIAC IMAGING (CONT.)
Magnetic resonance imaging is reasonable when assessing myocardial infiltrative processes or scar burden.
Routine repeat measurement of LV function assessment in the absence of clinical status change or treatment interventions should not be performed.
I IIa IIb III
No Benefit
I IIa IIb III
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SUMMARY RECOMMENDATIONS FOR NONINVASIVE IMAGING
Recommendation COR LOE
Patients with suspected, acute, or new-onset HF should undergo a chest x-ray
I C
A 2-dimensional echocardiogram with Doppler should be performed for initial evaluation of HF
I C
Repeat measurement of EF is useful in patients with HF who have had a significant change in clinical status or received treatment that might affect cardiac function, or for consideration of device therapy
I C
Noninvasive imaging to detect myocardial ischemia and viability is reasonable in HF and CAD
IIa C
Viability assessment is reasonable before revascularization in HF patients with CAD
IIa B
Radionuclide ventriculography or MRI can be useful to assess LVEF and volume
IIa C
MRI is reasonable when assessing myocardial infiltration or scar IIa B
Routine repeat measurement of LV function assessment should not be performed
III: No Benefit
B
INVASIVE EVALUATION
Invasive hemodynamic monitoring with a pulmonary artery catheter should be performed to guide therapy in patients who have respiratory distress or clinical evidence of impaired perfusion in whom the adequacy or excess of intra-cardiac filling pressures cannot be determined from clinical assessment.
Invasive hemodynamic monitoring can be useful for carefully selected patients with acute HF who have persistent symptoms despite empiric adjustment of standard therapies and
a. whose fluid status, perfusion, or systemic or pulmonary vascular resistance is uncertain;
b. whose systolic pressure remains low, or is associated with symptoms, despite initial therapy;
c. whose renal function is worsening with therapy;
d. who require parenteral vasoactive agents; or
e. who may need consideration for MCS or transplantation.
I IIa IIb III
I IIa IIb III
INVASIVE EVALUATION (CONT.)
When ischemia may be contributing to HF, coronary arteriography is reasonable for patients eligible for revascularization.
Endomyocardial biopsy can be useful in patients presenting with HF when a specific diagnosis is suspected that would influence therapy.
I IIa IIb III
I IIa IIb III
INVASIVE EVALUATION (CONT.)
Routine use of invasive hemodynamic monitoring is not recommended in normotensive patients with acute decompensated HF and congestion with symptomatic response to diuretics and vasodilators.
Endomyocardial biopsy should not be performed in the routine evaluation of patients with HF.
I IIa IIb III
No Benefit
I IIa IIb III
Harm
RECOMMENDATIONS FOR INVASIVE EVALUATION
Recommendation COR LOE
Monitoring with a pulmonary artery catheter should be performed in patients with respiratory distress or impaired systemic perfusion when clinical assessment is inadequate
I C
Invasive hemodynamic monitoring can be useful for carefully selected patients with acute HF with persistent symptoms and/or when hemodynamics are uncertain
IIa C
When coronary ischemia may be contributing to HF, coronary arteriography is reasonable
IIa C
Endomyocardial biopsy can be useful in patients with HF when a specific diagnosis is suspected that would influence therapy
IIa C
Routine use of invasive hemodynamic monitoring is not recommended in normotensive patients with acute HF
III: No Benefit
B
Endomyocardial biopsy should not be performed in the routine evaluation of HF
III: Harm C
INVASIVE HEMODYNAMIC MONITORING ESCAPE
ESCAPE: JAMA 2005;294:1625-1633
Shah MR et al, JAMA 2005;294(13):1664-1670
ESCAPE
META-ANALYSIS
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NON INVASIVE CVP ASSESSMENT
Management of Acute Heart Failure
THE GUIDELINESOUTPATIENT MANAGEMENT
Jessup M, Brozena S. NEJM 2003;348:2007
2013 ACCF/AHA Guideline for the Management of Heart Failure
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†Hydral-Nitrates green box: The combination of ISDN/HYD with ARNI has not been robustly tested. BP response should be carefully monitored. ‡See 2013 HF guideline. §Participation in investigational studies is also appropriate for stage C, NYHA class II and III HF.ACEI indicates angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor-blocker; ARNI, angiotensin receptor-neprilysin inhibitor; BP, blood pressure; bpm, beats
per minute; C/I, contraindication; COR, Class of Recommendation; CrCl, creatinine clearance; CRT-D, cardiac resynchronization therapy–device; Dx, diagnosis; GDMT, guideline-directed management and therapy; HF, heart failure; HFrEF, heart failure with reduced ejection fraction; ICD, implantable cardioverter-defibrillator; ISDN/HYD, isosorbide dinitrate hydral-nitrates; K+, potassium; LBBB, left bundle-branch block; LVAD, left ventricular assist device; LVEF, left ventricular ejection fraction; MI, myocardial infarction; NSR, normal sinus rhythm; and NYHA, New York Heart Association.
“OPTIMAL MEDICAL MANAGEMENT”THE NEUROHORMONAL COMPONENT
10 mg bid50 mg tid5 mg bid
20 mg qd4 mg qd
20-40 mg bid
Enalapril (Vasotec) Captopril (Capoten) Ramipril (Altace)Lisinopril (Prinivil, Zestril) Trandolapril (Mavik) Quinapril (Accupril)
Carvedilol (Coreg)Metoprolol XL/CR (Toprol XL) Bisoprolol (Zebeta)
25-50 mg bid 200 mg qd10 mg qd
ACE-inhibitor
-Blocker
PHARMACOLOGICAL THERAPY FOR MANAGEMENT OF STAGE C HFREF
Recommendations COR LOE
Diuretics
Diuretics are recommended in patients with HFrEF with fluid retention I C
ACE Inhibitors
ACE inhibitors are recommended for all patients with HFrEFI A
ARBs
ARBs are recommended in patients with HFrEF who are ACE inhibitor intolerant I A
ARBs are reasonable as alternatives to ACE inhibitor as first line therapy in HFrEF IIa A
The addition of an ARB may be considered in persistently symptomatic patients with HFrEF on GDMT IIb A
Routine combined use of an ACE inhibitor, ARB, and aldosterone antagonist is potentially harmful III: Harm C
PHARMACOLOGICAL THERAPY FOR MANAGEMENT OF STAGE C HFREF (CONT.)
Recommendations COR LOE
Beta Blockers
Use of 1 of the 3 beta blockers proven to reduce mortality is recommended for all stable patients I A
Aldosterone Antagonists
Aldosterone receptor antagonists are recommended in patients with NYHA class II-IV HF who have LVEF ≤35% I A
Aldosterone receptor antagonists are recommended in patients following an acute MI who have LVEF ≤40% with symptoms of HF or DM
I B
Inappropriate use of aldosterone receptor antagonists may be harmful III: Harm B
Hydralazine and Isosorbide Dinitrate
The combination of hydralazine and isosorbide dinitrate is recommended for African-Americans, with NYHA class III–IV HFrEF on GDMT
I A
A combination of hydralazine and isosorbide dinitrate can be useful in patients with HFrEF who cannot be given ACE inhibitors or ARBs IIa B
PHARMACOLOGIC THERAPY FOR MANAGEMENT OF STAGE C HFREF (CONT.)
Recommendations COR LOE
Digoxin
Digoxin can be beneficial in patients with HFrEF IIa B
Anticoagulation
Patients with chronic HF with permanent/persistent/paroxysmal AF and an additional risk factor for cardioembolic stroke should receive chronic anticoagulant therapy* I A
The selection of an anticoagulant agent should be individualized I C
Chronic anticoagulation is reasonable for patients with chronic HF who have permanent/persistent/paroxysmal AF but without an additional risk factor for cardioembolic stroke*
IIa B
Anticoagulation is not recommended in patients with chronic HFrEF without AF, prior thromboembolic event, or a cardioembolic source III: No Benefit B
Statins
Statins are not beneficial as adjunctive therapy when prescribed solely for HFIII: No Benefit A
Omega-3 Fatty Acids
Omega-3 PUFA supplementation is reasonable to use as adjunctive therapy in HFrEF or HFpEF patients IIa B
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PHARMACOLOGICAL THERAPY FOR MANAGEMENT OF STAGE C HFREF (CONT.)
Recommendations COR LOE
Other Drugs
Nutritional supplements as treatment for HF are not recommended in HFrEF III: No Benefit
B
Hormonal therapies other than to replete deficiencies are not recommended in HFrEF
III: No Benefit
C
Drugs known to adversely affect the clinical status of patients with HFrEF are potentially harmful and should be avoided or withdrawn
III: Harm B
Long-term use of an infusion of a positive inotropic drug is not recommended and may be harmful except as palliation III: Harm C
Calcium Channel Blockers
Calcium channel blocking drugs are not recommended as routine in HFrEF III: No Benefit
A
BETA BLOCKERS REDUCE MORTALITY
ACC/AHA Guidelines 2013
• Indicated for symptomatic or asymptomatic EF ≤40%.
• Use agents and target doses used in clinical trials.
• Initiate when relatively euvolemic, off IV vasoactive agents and prior to hospital d/c.
• Titrate upward every 2 to 4 weeks as long as stable.
• Most trials held titration for HR <60 or SBP <90.• Adjust other agents if dyspnea, BP, or weight
gain occur in order to titrate to target doses.
Use of Beta Blockers in HFrEF
DrugInitial Daily
Dose(s)Maximum Doses(s)
Mean Doses Achieved in Clinical Trials
Beta Blockers
Bisoprolol 1.25 mg qd 10 mg qd 8.6 mg/d
Carvedilol 3.125 mg bid 50 mg bid 37 mg/d
Carvedilol CR 10 mg qd 80 mg qd ---------
Metoprolol succinate extended release (metoprolol CR/XL)
12.5 - 25 mg qd
200 mg qd 159 mg/d
2013 ACCF/AHA Guideline for the Management of Heart Failure
Which Beta Blocker; How Much?
ACE-I REDUCES MORTALITYDrug
Initial Daily Dose(s)
Maximum Doses(s)
Mean Doses Achieved in Clinical
Trials
ACE Inhibitors
Captopril 6.25 mg 3 times 50 mg 3 times 122.7 mg/d
Enalapril 2.5 mg twice10 to 20 mg
twice16.6 mg/d
Fosinopril 5 to 10 mg once 40 mg once ---------
Lisinopril 2.5 to 5 mg once20 to 40 mg
once32.5 to 35.0 mg/d
Perindopril 2 mg once 8 to 16 mg once ---------
Quinapril 5 mg twice 20 mg twice ---------
Ramipril1.25 to 2.5 mg
once10 mg once ---------
Trandolapril 1 mg once 4 mg once ---------
2013 ACCF/AHA Guideline for the Management of Heart Failure
Which ACE I; How Much?
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ACC/AHA Guidelines 2013
• ARBs are recommended in patients with HFrEF who are ACE inhibitor-intolerant (cough +/- angioedema),unless contraindicated, to reduce morbidity and mortality.
• ARBs are reasonable to reduce morbidity and mortality as alternatives to ACE inhibitors as first-line therapy for patients with HFrEF, especially for patients already taking ARBs for other indications
• Addition of an ARB may be considered in persistently symptomatic patients with HFrEF who are already being treated with an ACE inhibitor and a beta blocker in whom an aldosterone antagonist is not indicated or tolerated.
ACE I or ARB or Both?
ACC/AHA Guidelines 2013
DrugInitial Daily
Dose(s)Maximum Doses(s)
Mean Doses Achieved in Clinical
Trials
ARBs
Candesartan 4-8 mg qd 32 mg qd 24mg/d
Losartan 25-50 mg qd 50 to 100 mg qd 129 mg/d
Valsartan 20-40 mg BID 160 mg bid 254 mg/d
Which ARB; How Much?
ALDOSTERONE ANTAGONISTS TRIALS• Aldosterone receptor antagonists [or mineralocorticoid receptor
antagonists (MRA)] are recommended in patients with NYHA class II-IV and who have LVEF of < 35%.
• Patients with NYHA class II should have a history of prior cardiovascular hospitalization or elevated plasma natriuretic peptide levels to be considered for aldosterone receptor antagonists.
• Creatinine should be < 2.5 mg/dL or less in men or < 2.0 mg/dL in women (or eGFR >30 mL/min/1.73m2) and potassium < 5.0 mEq/L.
• Careful monitoring of potassium, renal function, and diuretic dosing should be performed at initiation, within 7-10 days after initiation and followed thereafter to minimize risk of hyperkalemia and renal insufficiency.
Aldosterone Antagonists
DrugInitial Daily
Dose(s)Maximum Doses(s)
Mean Doses Achieved in
Clinical Trials
Aldosterone Antagonists
Spironolactone 12.5 to 25 mg qd 25 mg qd 26 mg/d
Eplerenone 25 mg qd 50 mg qd 42.6 mg/d
• Eplerenone is a more specific aldosterone receptor antagonist; it can be used if spironolactone causes gynecomastia or breast pain.
• It causes the same effects on potassium and renal function as spironolactone.
Aldosterone AntagonistsNITRATE/HYDRALAZINE (ISDN/HDZ) AFFECTS MORTALITY ON AFRICAN AMERICAN PATIENTS
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• HDZ/ISDN combination (BiDil) is recommended for African Americans with NYHA class III–IV HFrEF receiving optimal therapy with ACE inhibitors and beta blockers.
• HDZ/ISDN can be useful to reduce morbidity or mortality in patients with current or prior symptomatic HFrEF who cannot be given an ACE inhibitor or ARB because of drug intolerance, hypotension, or renal insufficiency, unless contraindicated.
Nitrate/Hydralazine (ISDN/HDZ)
• Digoxin can be beneficial in patients with HFrEFand sinus rhythm to decrease hospitalizations for HF: consider adding if on other therapy and still symptomatic
• Digoxin can be used in HF patients with atrial fibrillation to help rate control
• **Dose: 0.125 -0.25 mg qd depending on renal function (levels not for dosing but for toxicity)
• **Interaction with amiodarone, which ↑ Digoxin levels
Digoxin
New Agent:Neprilysin as a Therapeutic Target
Inactive fragments
Neprilysin
Natriuretic peptides AdrenomedullinBradykininSubstance P(angiotensin II)
• Neprilysin breaks down endogenous vasoactive peptides, including the natriuretic peptides
• Inhibition of neprilysin potentiates the action of those peptides
• Because angiotensin II is also a substrate for neprilysin, neprilysin inhibitors must be co-administered with a RAAS blocker
• The combination of a neprilysin inhibitor and an ACEI is associated with unacceptably high rates of angioedema
Corti R et al. Circulation. 2001;104:1856-1862.
Sacubitril/Valsartan (Entresto): Angiotensin Receptor–Neprilysin Inhibitor (ARNI)
ANGIOTENSIN RECEPTOR NEPRILYSIN INHIBITOR (ARNI)
ARNIEntresto (Combintion of Sacubitril and Valsartan)
• Sacubitril: Prodrug that inhibits neprilysin leading to increased levels of natriuretic peptides
• Valsartan: Angiotensin II receptor blocker
Side Effects
Angioedema, hypotension, impaired renal function, and hyperkalemia.
• Should not be administered concomitantly with ACE inhibitors or within 36 hours of the last dose of an ACEI.
2016 ACC/AHA Update on New Pharmacological therapy for Heart Failure1. McMurray JJ et al. N Engl J Med. 2014;371:993-1004
PARADIGM-HF: CV Death or HF Hospitalization (Primary Endpoint)
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NEW DRUG: IVABRADINE (CORLANOR)• Hyperpolarization-activated cyclic nucleotide-gated (HCN)
channel blocker.
• Reduces diastolic depolarization slope in the SA node, thereby decreasing heart rate via direct sinus node inhibition without direct effects on myocardial contractility and intracardiacconduction
• Indicated to reduce the risk of HF hospitalization in patients with stable, symptomatic chronic HF with LVEF ≤35%, who are in sinus rhythm with resting heart rate ≥70 bpm and either are on maximally tolerated doses of beta-blockers or have a contraindication to beta-blocker use
2016 ACC/AHA Update on New Pharmacological therapy for Heart Failure
SHIFT Trial Primary Composite Endpoint: CV Death or Hospitalization for Worsening HF
Swedberg K et al. Lancet. 2010;376:875-885.
Medications & DevicesEffects on Mortality
↓ Symptoms ↓ Hospitalizations ↓ Mortality
Diuretics √ √ (?) ?
ACE I /ARBs √ √ √
Beta-Blockers √ √ √Aldosterone Antagonists √ √ √
Digitalis √ √ X
Nitrates/Hydralazine √ √ √
Neprilysin Inhibitor √ √ √
Ivabradine √ √ X
AICD (Defibrillators) X X √
CRT (BiV pacemakers) √ √ √
Medical Therapy for Stage C HFrEF: Magnitude of Benefit in RCTs
RR ↓ Mortality
NNT to ↓ mortality(standardized 36
months)
RR↓ HF Hospital.
ACE I / ARB 17% 26 31%
Beta-Blockers 34% 9 41%
Aldosterone Antagonists 30% 6 35%
Nitrates/Hydralazine 43% 7 33%
A NOTE ABOUT HEART FAILURE WITH PRESERVED EF:SYSTOLIC VS DIASTOLIC
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HFPEF CLINICAL TRIALS• Trials have not shown
significant mortality or morbidity benefit with use of ACEI/ARB specifically in HFpEF
• No trials showing definite benefit of Beta blockers, sildenafil
• TOPCAT trial: Randomized-double blind trial of spironolactone (15-45 mg) vs. placebo in HFpEF patients (LVEF >45%) with • Prior HF hospitalization or• BNP > 100 pg/ml
HFpEF
TREATMENT OF HFPEFRecommendations COR LOE
Systolic and diastolic blood pressure should be controlled according to published clinical practice guidelines I B
Diuretics should be used for relief of symptoms due to volume overload
I C
Coronary revascularization for patients with CAD in whom angina or demonstrable myocardial ischemia is present despite GDMT
IIaC
Management of AF according to published clinical practice guidelines for HFpEF to improve symptomatic HF
IIa C
Use of beta-blocking agents, ACE inhibitors, and ARBs for hypertension in HFpEF IIa C
ARBs might be considered to decrease hospitalizations in HFpEF
IIb B
Nutritional supplementation is not recommended in HFpEF
III: No Benefit
C
? Spironolactone in select pts
Stage DRefractory HF
Marked HF symptoms at restRecurrent hospitalizations despite GDMT
Maintenance of GDMT During Hospitalization
The Hospitalized Patient
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MAINTENANCE OF GDMT DURING HOSPITALIZATION
In patients with HFrEF experiencing a symptomatic exacerbation of HF requiring hospitalization during chronic maintenance treatment with GDMT, it is recommended that GDMT be continued in the absence of hemodynamic instability or contraindications.
Initiation of beta-blocker therapy is recommended after optimization of volume status and successful discontinuation of intravenous diuretics, vasodilators, and inotropic agents. Beta-blocker therapy should be initiated at a low dose and only in stable patients. Caution should be used when initiating beta blockers in patients who have required inotropes during their hospital course.
I IIa IIb III
I IIa IIb III
Diuretics in Hospitalized Patients
The Hospitalized Patient DIURETICS IN HOSPITALIZED PATIENTS
Patients with HF admitted with evidence of significant fluid overload should be promptly treated with intravenous loop diuretics to reduce morbidity.
If patients are already receiving loop diuretic therapy, the initial intravenous dose should equal or exceed their chronic oral daily dose and should be given as either intermittent boluses or continuous infusion. Urine output and signs and symptoms of congestion should be serially assessed, and the diuretic dose should be adjusted accordingly to relieve symptoms, reduce volume excess, and avoid hypotension.
I IIa IIb III
I IIa IIb III
DIURETICS IN HOSPITALIZED PATIENTS (CONT.)
The effect of HF treatment should be monitored with careful measurement of fluid intake and output, vital signs, body weight that is determined at the same time each day, and clinical signs and symptoms of systemic perfusion and congestion. Daily serum electrolytes, urea nitrogen, and creatinine concentrations should be measured during the use of intravenous diuretics or active titration of HF medications.
When diuresis is inadequate to relieve symptoms, it is reasonable to intensify the diuretic regimen using either:
a. higher doses of intravenous loop diuretics.b. addition of a second (e.g., thiazide) diuretic.
I IIa IIb III
I IIa IIb III
DIURETICS IN HOSPITALIZED PATIENTS (CONT.)
Low-dose dopamine infusion may be considered in addition to loop diuretic therapy to improve diuresis and better preserve renal function and renal blood flow.
I IIa IIb III
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Commonly Used Diuretics
Sodi
um E
xcre
tion
Rate
Maximal Response
Threshold
Loop Diuretic Dose
How Much Diuretic Should I Give? …Enough
CEILING DOSES OF LOOP DIURETICS
FUROSEMIDE BUMETANIDE TORSEMIDE
IV po IV po IV po
Renal Insufficiencymoderate 80 80 2-3 2-3 20-50 20-50
severe 200 240 8-10 8-10 50-100 50-100
Cirrhosis (normal GFR) 40 80-160 1 1 10-20 10-20
CHF (normal GFR) 40-80 160-240 2-3 2-3 20-50 20-50
Adapted from Brater C. New Engl J Med 1999
WHAT TO DO WHEN THE CREATININE RISESHINT: IT’S ALWAYS “PRE-RENAL”
Check volume status Orthostatics, skin turgor, mucous membranes
Check blood pressure (especially at peak onset of vasodilators)
Restrict sodium intake (and water if hyponatremic)
Check for intrinsic renal problems U/A with sediment
Consider vasodilators or inotropes
Consider ultrafiltration
Parenteral Therapy in Hospitalized HF
The Hospitalized Patient PARENTERAL THERAPY IN HOSPITALIZED HF
If symptomatic hypotension is absent, intravenous nitroglycerin, nitroprusside or nesiritide may be considered an adjuvant to diuretic therapy for relief of dyspnea in patients admitted with acutely decompensated HF.
I IIa IIb III
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Renal Replacement Therapy
The Hospitalized Patient RENAL REPLACEMENT THERAPY
Ultrafiltration may be considered for patients with obvious volume overload to alleviate congestive symptoms and fluid weight.
Ultrafiltration may be considered for patients with refractory congestion not responding to medical therapy.
I IIa IIb III
I IIa IIb III
VASODILATOR THERAPY
In patients with evidence of severely symptomatic fluid overload in the absence of systemic hypotension, vasodilators such as intravenous nitroglycerin, nitroprusside or neseritide can be beneficial when added to diuretics and/or in those who do not respond to diuretics alone.
I IIa IIb III
VASODILATOR THERAPYNIPRIDE: A CHALLENGE
Mullens W et al. J Am Coll Cardiol 2008;52:200–7
MO
RTAL
ITY
NIPRIDE
NO NIPRIDE
Retrospective anaylsis (n = 175)ADHF with Cardiac Index < 2.0
RR = 0.54
Kass DA. Nature Medicine 2009; (15): 24 – 25
INOTROPES Dobutamine
Milrinone
INOTROPES…ARE NOT “PRESSORS”
Felker GM, O’Connor CM. Am Heart J 2001;142:393-401Felker GM, O’Connor CM. Am Heart J 2001;142:393-401
DRUG SV HR SVR BPDobutamine +++ ++ +/- +/-
Milrinone +++ + (SVT) - -Dopamine* + ++ ++ ++
*assuming moderate dose (2 – 5 mcg/kg/min)
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INFUSION OF POSITIVE INOTROPIC DRUGSIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
Routine intermittent infusions of vasoactive and positive inotropic agents are not recommended for patients with refractory end-stage HF.
Use of parenteral inotropes in normotensive patients with acute decompensated HF without evidence of decreased organ perfusion is not recommended.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIII
OPTIME-CHF: Cuffe, Califf, Adams KF et al. JAMA 2002; 287(12):1541
OPTIME-CHF (RCT n = 951)ADHF not requiring inotropeMilrinone (500 mcg/kg/min) vs. Placebo
DIGOXIN: THE ONLY “INOTROPE” WITH DATADIG TRIAL
N Engl J Med 1997;336:525-33
Total mortality
HF Mortalityp=NS
p=0.06
DIGOXIN: THE ONLY “INOTROPE” WITH DATADIG TRIAL
N Engl J Med 1997;336:525-33
RR 0.75p < 0.001D
eath
or H
F H
ospi
taliz
atio
n
Time (Months)
DIGOXIN
PLACEBO
INOTROPES
• Indicated in the presence of acute or chronic hemodynamic compromise with end organ dysfunction.
• Bridge to mechanical circulatory support (MCS)
• Bridge to transplant
• Palliative
INOTROPES IN ADVANCED HF
• Milrinone and Dobutamine are two commonly used inotropes approved for HF use in the US.
• Both increase cardiac output by increasing the intracellular level of cyclic adenosine monophosphate (cAMP)
• Dobutamine increases cAMP indirectly through adrenergic agonism.
• Milrinone, a phosphodiesterase inhibitor, directly blocks cAMPbreakdown
DOBUTAMINE
• Sympathomimetic amine, which acts on beta-1, beta-2, and alpha-1 adrenergic receptors.
• Strong inotropic effect and relatively weak chronotropic effect
• No significant change in BP due to its alpha-1 agonist activity causing vasoconstriction, that balances the beta-2 vasodilatory effect.
• The use is problematic in patients who take beta blockers due to its adrenergic properties
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MILRINONE
• Milrinone inhibits phosphodiesterase 3 (PDE3), which prevents the degradation of cAMP and ultimately leads to an increase in protein kinase A (PKA).
• It is an inodilator, both increasing cardiac contractility and reducing afterloadwith a consequent reduction in left ventricular filling pressures.
• PKA increases contractility of the left ventricle and cardiac output through cAMP dependent-PKA
MILRINONE
• Less myocardial oxygen consumption with milrinone when compared to dobutamine.
• Can be used in patients on beta blockers, because its effects are not dependent on beta adrenoreceptors.
• Milrinone not only acts as a systemic but also a pulmonary vasodilator.
• It is the preferred agent in patients with pulmonary hypertension and HF.
SIMILARITIES
• Most of the hemodynamic effects of dobutamine and milrinoneare similar.
• Increase cardiac output
• Cause peripheral vasodilation
• Decrease pulmonary capillary wedge pressure
DIFFERENCESDobutamine Milrinone
Greater increase in heart rate More hypotension
Greater increase in myocardial oxygen consumption
Greater reduction in left and right heart filling pressures
Greater proarrhythmic effect, including ventricular tachycardia
Greater reduction in MAP and PAP
Effects are attenuated in patients who receive beta blockers
Greater hemodynamic effects in general when the patient is on beta blockers
Less expensive: US $380± $533 (for a course of in-hospital inotrope therapy)
Expensive: US $16,270± $1,334 (for a course of in-hospital inotrope therapy)
Longer duration of action after discontinuation, especially in the presence of renal dysfunction
MORTALITY ON INOTROPIC SUPPORT
Rogers JG, Butler J, Lansman SL, et al. 2007;50(8):741-47
PARENTERAL THERAPY IN HOSPITALIZED HF
If symptomatic hypotension is absent, intravenous nitroglycerin, nitroprusside or nesiritide may be considered an adjuvant to diuretic therapy for relief of dyspnea in patients admitted with acutely decompensated HF.
I IIa IIb III
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ADVANCED HEART FAILURE• Limited treatment option
- Heart transplantation
- Mechanical circulatory support (MCS)
- Long-term inotropic therapy
- Palliative care
ADVANCED HF THERAPIES
• Mechanical Circulatory support • ECMO
• LVAD
VENTRICULAR ASSIST DEVICES
Consideration of an left ventricular assist device as permanent or “destination” therapy is reasonable in highly selected patients with refractory end-stage HF and an estimated 1-year mortality over 50% with medical therapy.
III IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIII IIaIIaIIa IIbIIbIIb IIIIIIIIIIIaIIaIIa IIbIIbIIb IIIIIIIII
Jarv
ik20
00
Hea
rtM
ate
II
CARDIAC TRANSPLANTATION
• Ideal treatment for advanced HF• Provides increased longevity and symptomatic
relief• Approximately 3,000 people are on waiting list
at any given time• In 2015, there was only 2804 donors in US
United Network for Organ Sharing [UNOS] (2017)
LISTING CRITERIA FOR HEART
TRANSPLANTATION
• Cardiopulmonary exercise testing: VO2 max <14ml/kg/min if patients intolerant to BB; <12ml/kg/min in the presence f BB; or <50% of predicted VO2 in young patients (50yrs) and women.
• Acceptable pulmonary artery pressure
• Age <70
• Diabetes well controlled
• Absence on neoplasm
• Psychosocial support
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CONTRAINDICATION
• Noncompliance with medical regimen
• Active substance abuse
• Severe symptomatic cerebrovascular disease
• Severe organ dysfunction (lung, kidney, liver, coagulopathy)
• Active infection
• Active mental illness
• Inadequate social support
• Fixed, severe pulmonary hypertension
• Morbid obesity (BMI > 35 kg/m2)
• Age > 70 years
• Recent or uncured malignancy
DEFIBRILLATORS REDUCE MORTALITY
Implantable Cardiac Defibrillators (ICD)
• Sustained ventricular tachycardia is associated with sudden cardiac death in HF.
• About one-third of mortality in HF is due to sudden cardiac death.
• ICDs for primary prevention have been shown to improve survival in selected patients with HF
Indications for ICD Therapy• ICD therapy is recommended for primary prevention of
SCD in selected patients with HFrEF at least 40 days post-MI with LVEF ≤35%, and NYHA class II or III symptoms on chronic GDMT, who are expected to live ≥1 year
• ICD therapy is recommended for primary prevention of SCD in selected patients with HFrEF at least 40 days post-MI with LVEF ≤30%, and NYHA class I symptoms while receiving GDMT, who are expected to live ≥1 year
• ** ICDs do not improve symptoms; most patients should be on GDMT; should have an expected life-expectancy of at least 1 year
2013 ACCF/AHA Guideline for the Management of Heart Failure
ICD Therapy and Heart Failure
ICD THERAPY IS RECOMMENDED FOR SECONDARY PREVENTION
OF SCD IN PATIENTS WHO SURVIVED VF OR HEMODYNAMICALLY
UNSTABLE VT, OR VT WITH SYNCOPE AND WHO HAVE AN LVEF LESS
THAN OR EQUAL TO 40%, WHO ARE RECEIVING CHRONIC OPTIMAL
MEDICAL THERAPY, AND WHO HAVE A REASONABLE EXPECTATION OF
SURVIVAL WITH A GOOD FUNCTIONAL STATUS FOR MORE THAN 1 YEAR.
ICD THERAPY IS RECOMMENDED FOR PRIMARY PREVENTION TO
REDUCE TOTAL MORTALITY BY A REDUCTION IN SCD IN PATIENTS WITH
LV DYSFUNCTION DUE TO PRIOR MI WHO ARE AT LEAST 40 DAYS POST-
MI, HAVE AN LVEF LESS THAN OR EQUAL TO 30% TO 40%, ARE NYHAFUNCTIONAL CLASS II OR III RECEIVING CHRONIC OPTIMAL MEDICALTHERAPY, AND WHO HAVE REASONABLE EXPECTATION OF SURVIVALWITH A GOOD FUNCTIONAL STATUS FOR MORE
THAN 1 YEAR.
Cardiac Resynchronization Pacing: Consequences of a Prolonged QRS
Delayed Ventricular ActivationDelayed lateral wall contractionDisorganized ventricular contractionDecreased pumping efficiency
Reduction in diastolic filling times
Prolongation of the duration of mitral regurgitation
Sinus node
AVnode
Conduction block
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• Intraventricular Activation • Organized ventricular activation
sequence• Coordinated septal and freewall
contraction• Improved pumping efficiency
Mechanism: Ventricular Resynchronization
Sinus node
AVnode
Stimulation therapy
Conduction block
Cardiac Resynchonization Rx (CRT)
• LVEF < 35%• Greatest benefit in patients with sxtic HF
with LBBB + QRS > 150 msec already on GDMT and in sinus rhythm
• Can consider in patients with symptomatic HF with LBBB and QRS 120-149 msec
• Can consider in symptomatic HF with non-LBBB and QRS > 150 msec
• Can be considered in atrial fibrillation if ventricular pacing is needed and rate control will allow nearly 100% ventricular pacing with CRT
2013 ACCF/AHA Guideline for the Management of Heart Failure
Inpatient and Transitions of Care
The Hospitalized Patient INPATIENT AND TRANSITIONS OF CARE
The use of performance improvement systems and/or evidence-based systems of care is recommended in the hospital and early postdischarge outpatient setting to identify appropriate HF patients for GDMT, provide clinicians with useful reminders to advance GDMT, and to assess the clinical response.
I IIa IIb III
INPATIENT AND TRANSITIONS OF CARE
Throughout the hospitalization as appropriate, before hospital discharge, at the first postdischarge visit, and in subsequent follow-up visits, the following should be addressed:
a. initiation of GDMT if not previously established and not contraindicated; b. precipitant causes of HF, barriers to optimal care transitions, and limitations in postdischarge support; c. assessment of volume status and supine/upright hypotension with adjustment of HF therapy, as appropriate; d. titration and optimization of chronic oral HF therapy; e. assessment of renal function and electrolytes, where appropriate; f. assessment and management of comorbid conditions; g. reinforcement of HF education, self-care, emergency plans, and need for adherence; andh. consideration for palliative care or hospice care in selected patients.
I IIa IIb III
INPATIENT AND TRANSITIONS OF CARE
Multidisciplinary HF disease-management programs are recommended for patients at high risk for hospital readmission, to facilitate the implementation of GDMT, to address different barriers to behavioral change, and to reduce the risk of subsequent rehospitalization for HF.
Scheduling an early follow-up visit (within 7 to 14 days) and early telephone follow-up (within 3 days) of hospital discharge is reasonable.
Use of clinical risk prediction tools and/or biomarkers to identify patients at higher risk for postdischarge clinical events is reasonable.
I IIa IIb III
I IIa IIb III
I IIa IIb III
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THERAPIES IN THE HOSPITALIZED HF PATIENT
Recommendation COR LOE
HF patients hospitalized with fluid overload should be treated with intravenous diuretics
I B
HF patients receiving loop diuretic therapy, should receive an initial parenteral dose greater than or equal to their chronic oral daily dose, then should be serially adjusted
I B
HFrEF patients requiring HF hospitalization on GDMT should continue GDMT unless hemodynamic instability or contraindications
I B
Initiation of beta-blocker therapy at a low dose is recommended after optimization of volume status and discontinuation of intravenous agents
I B
Thrombosis/thromboembolism prophylaxis is recommended for patients hospitalized with HF
I B
Serum electrolytes, urea nitrogen, and creatinine should be measured during the titration of HF medications, including diuretics
I C
THERAPIES IN THE HOSPITALIZED HF PATIENT (CONT.)
Recommendation COR LOE
When diuresis is inadequate, it is reasonable toa) Give higher doses of intravenous loop diuretics; or b) add a second diuretic (e.g., thiazide)
IIa
B
B
Low-dose dopamine infusion may be considered with loop diuretics to improve diuresis
IIb B
Ultrafiltration may be considered for patients with obvious volume overload
IIb B
Ultrafiltration may be considered for patients with refractory congestion IIb C
Intravenous nitroglycerin, nitroprusside or nesiritide may be considered an adjuvant to diuretic therapy for stable patients with HF
IIb B
In patients hospitalized with volume overload and severe hyponatremia, vasopressin antagonists may be considered
IIb B
HOSPITAL DISCHARGE
Recommendation or Indication COR LOE
Performance improvement systems in the hospital and early postdischarge outpatient setting
to identify HF for GDMTI B
Before hospital discharge, at the first postdischarge visit, and in subsequent follow-up visits,
the following should be addressed:
a) initiation of GDMT if not done or contraindicated;
b) causes of HF, barriers to care, and limitations in support;
c) assessment of volume status and blood pressure with adjustment of HF therapy;
d) optimization of chronic oral HF therapy;
e) renal function and electrolytes;
f) management of comorbid conditions;
g) HF education, self-care, emergency plans, and adherence; and
h) palliative or hospice care.
I B
Multidisciplinary HF disease-management programs for patients at high risk for hospital readmission are recommended
I B
A follow-up visit within 7 to 14 days and/or a telephone follow-up within 3 days of hospital
discharge is reasonableIIa B
Use of clinical risk-prediction tools and/or biomarkers to identify higher-risk patients is
reasonableIIa B
Surgical/Percutaneous/ Transcatheter Interventional
Treatments of HF
Guideline for HF
SURGICAL/PERCUTANEOUS/TRANSCATHETER INTERVENTIONAL
TREATMENT OF HFCoronary artery revascularization via CABG or percutaneous intervention is indicated for patients (HFpEF and HFrEF) on GDMT with angina and suitable coronary anatomy, especially for a left main stenosis (>50%) or left main equivalent disease.
CABG to improve survival is reasonable in patients with mild to moderate LV systolic dysfunction (EF 35% to 50%) and significant (≥70% diameter stenosis) multivessel CAD or proximal LAD coronary artery stenosis when viable myocardium is present in the region of intended revascularization.
I IIa IIb III
I IIa IIb III
SURGICAL/PERCUTANEOUS/TRANSCATHETER INTERVENTIONAL TREATMENT OF HF (CONT.)
CABG or medical therapy is reasonable to improve morbidity and cardiovascular mortality for patients with severe LV dysfunction (EF <35%), HF, and significant CAD.
Surgical aortic valve replacement is reasonable for patients with critical aortic stenosis and a predicted surgical mortality of no greater than 10%.
Transcatheter aortic valve replacement after careful candidate consideration is reasonable for patients with critical aortic stenosis who are deemed inoperable.
I IIa IIb III
I IIa IIb III
I IIa IIb III
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SURGICAL/PERCUTANEOUS/TRANSCATHETER INTERVENTIONAL TREATMENT OF HF (CONT.)
CABG may be considered with the intent of improving survival in patients with ischemic heart disease with severe LV systolic dysfunction (EF <35%), and operable coronary anatomy whether or not viable myocardium is present.
Transcatheter mitral valve repair or mitral valve surgery for functional mitral insufficiency is of uncertain benefit and should only be considered after careful candidate selection and with a background of GDMT.
Surgical reverse remodeling or LV aneurysmectomy may be considered in carefully selected patients with HFrEF for specific indications including intractable HF and ventricular arrhythmias.
I IIa IIb III
I IIa IIb III
I IIa IIb III
SURGICAL/PERCUTANEOUS/TRANSCATHETER INTERVENTIONAL TREATMENT OF HF
Recommendation COR LOE
CABG or percutaneous intervention is indicated for HF patients on GDMT with angina
and suitable coronary anatomy especially, significant left main stenosis or left main
equivalent disease
I C
CABG to improve survival is reasonable in patients with mild to moderate LV systolic
dysfunction and significant multivessel CAD or proximal LAD stenosis when viable
myocardium is present
IIa B
CABG or medical therapy is reasonable to improve morbidity and mortality for patients
with severe LV dysfunction (EF <35%), HF and significant CAD IIa B
Surgical aortic valve replacement is reasonable for patients with critical aortic stenosis
and a predicted surgical mortality of no greater than 10%IIa B
Transcatheter aortic valve replacement is reasonable for patients with critical aortic
stenosis who are deemed inoperable IIa B
CABG may be considered in patients with ischemic heart disease, severe LV systolic
dysfunction and suitable coronary anatomy whether or not viable myocardium is presentIIb B
Transcatheter mitral valve repair or mitral valve surgery for functional mitral insufficiency
is of uncertain benefit IIb B
Surgical reverse remodeling or LV aneurysmectomy may be considered in HFrEF for
specific indications including intractable HF and ventricular arrhythmias IIb B
COORDINATING CARE FOR PATIENTS WITH CHRONIC HF
Effective systems of care coordination with special attention to care transitions should be deployed for every patient with chronic HF that facilitate and ensure effective care that is designed to achieve GDMT and prevent hospitalization.
Every patient with HF should have a clear, detailed and evidence-based plan of care that ensures the achievement of GDMT goals, effective management of comorbid conditions, timely follow-up with the healthcare team, appropriate dietary and physical activities, and compliance with Secondary Prevention Guidelines for cardiovascular disease. This plan of care should be updated regularly and made readily available to all members of each patient’s healthcare team.
Palliative and supportive care is effective for patients with symptomatic advanced HF to improve quality of life.
I IIa IIb III
I IIa IIb III
I IIa IIb III DISCHARGE
RECONCILING AND ADJUSTING MEDICATIONSOPTIMIZE-HF AND B-CONVINCED: DON’T STOP THE B-BLOCKERS
In patients with reduced ejection fraction experiencing a symptomatic exacerbation of HF requiring hospitalization during chronic maintenance treatment with oral therapies known to improve outcomes, particularly ACE inhibitors or ARBs and beta-blocker therapy, it is recommended that these therapies be continued in most patients in the absence of hemodynamic instability or contraindications.
OPTIMIZE-HF substudy: Fonarow GC et al. JACC 2008; 52(3) 190-199
WITHDRAWN
NOT TREATED
CONTINUED
NEWLY STARTED
MO
RTAL
ITY
DAYS SINCE DISCHARGEHR death = 2.3
OPTIMIZE-HF (n = 5791)1. Admitted with HF2. Pre-specified follow-upDeath or hospitalization
CAN WE WAIT TO START THE BETA-BLOCKERS?IMPACT - HF
Galtis WA, et al. JACC 2004;43:1534
Free
dom
from
Dea
th a
nd R
ehos
pita
lizat
ion
Days Since Randomization
Pre-discharge
Post-discharge
157 158
159 160
161 162
3/4/2019
28
ACE-INHIBITOR OR BETA-BLOCKER FIRST?CIBIS-III
(Willenheimer R, et al. Circulation 2005;112:2426-2435)
ACE-INHIBITOR OR BETA-BLOCKER FIRST?CIBIS-III
Willenheimer R, et al. Circulation 2005;112:2426-2435
Bisoprolol first
Enalapril first
(HR 0.94 (077-1.16), p= 0.0.019 for non-inferiority
Even
t-fr
ee S
urvi
val
Time (months)
REFERRAL FOR REFRACTORY END-STAGE HF
Referral for cardiac transplantation in potentially eligible patients is recommended for patients with refractory end-stage HF.
Referral of patients with refractory end-stage HF to an HF program with expertise in the management of refractory HF is useful.
Quality Metrics/Performance Measures
Guideline for HF
QUALITY METRICS/PERFORMANCE
MEASURESPerformance measures based on professionally developed clinical practice guidelines should be used with the goal of improving quality of care for HF.
Participation in quality improvement programs and patient registries based on nationally endorsed, clinical practice guideline-based quality and performance measures may be beneficial in improving quality of HF care.
I IIa IIb III
I IIa IIb III
ACCF/AHA/AMA-PCPI 2011 HF PERFORMANCE MEASUREMENT SET
Measure Description* Care
Setting
Level of
Measurement
1. LVEF
assessment
Percentage of patients aged ≥18 y with a diagnosis of HF for whom the
quantitative or qualitative results of a recent or prior (any time in the
past) LVEF assessment is documented within a 12 mo period
Outpatient Individual
practitioner
2. LVEF
assessment
Percentage of patients aged ≥18 y with a principal discharge diagnosis
of HF with documentation in the hospital record of the results of an
LVEF assessment that was performed either before arrival or during
hospitalization, OR documentation in the hospital record that LVEF
assessment is planned for after discharge
Inpatient Individual
practitioner
Facility
3. Symptom
and activity
assessment
Percentage of patient visits for those patients aged ≥18 y with a
diagnosis of HF with quantitative results of an evaluation of both
current level of activity and clinical symptoms documented
Outpatien
t
Individual
practitioner
*Please refer to the complete measures for comprehensive information, including measure exception.
Adapted from Bonow et al. J Am Coll Cardiol. 2012;59:1812-32.
163 164
165 166
167 168
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29
ACCF/AHA/AMA-PCPI 2011 HF PERFORMANCE MEASUREMENT SET (CONT.)
Measure Description* Care
Setting
Level of
Measurement
4. Symptom
management†
Percentage of patient visits for those patients aged ≥18 y with a
diagnosis of HF and with quantitative results of an evaluation of both
level of activity AND clinical symptoms documented in which patient
symptoms have improved or remained consistent with treatment goals
since last assessment OR patient symptoms have demonstrated
clinically important deterioration since last assessment with a
documented plan of care
Outpatient Individual
practitioner
5. Patient self-care education†‡
Percentage of patients aged ≥18 y with a diagnosis of HF who were provided with self-care education on ≥3 elements of education during
≥1 visits within a 12 mo period
Outpatient Individual practitioner
6. Beta-blocker
therapy for LVSD (outpatient and
inpatient setting)
Percentage of patients aged ≥18 y with a diagnosis of HF with a
current or prior LVEF <40% who were prescribed beta-blocker therapy with bisoprolol, carvedilol, or sustained release metoprolol
succinate either within a 12 mo period when seen in the outpatient
setting or at hospital discharge
Inpatient
and Outpatient
Individual
practitioner Facility
*Please refer to the complete measures for comprehensive information, including measure exception. †Test measure designated for use in internal quality improvement programs only. These measures are not appropriate for any other purpose, e.g., pay for performance, physician ranking or public reporting programs.‡New measure.
Adapted from Bonow et al. J Am Coll Cardiol. 2012;59:1812-32.
ACCF/AHA/AMA-PCPI 2011 HF PERFORMANCE MEASUREMENT SET (CONT.)
Measure Description* Care Setting Level of
Measurement
7. ACE Inhibitor or
ARB Therapy for
LVSD (outpatient and
inpatient setting)
Percentage of patients aged ≥18 y with a diagnosis of HF with a
current or prior LVEF <40% who were prescribed ACE inhibitor or
ARB therapy either within a 12 mo period when seen in the outpatient
setting or at hospital discharge
Inpatient
and
Outpatient
Individual
practitioner
Facility
8. Counseling
regarding ICD
implantation for
patients with LVSD on
combination medical
therapy†‡
Percentage of patients aged ≥18 y with a diagnosis of HF with current
LVEF ≤35% despite ACE inhibitor/ARB and beta-blocker therapy for
at least 3 mo who were counseled regarding ICD implantation as a
treatment option for the prophylaxis of sudden death
Outpatient Individual
practitioner
9. Post-discharge
appointment for heart
failure patients
Percentage of patients, regardless of age, discharged from an inpatient
facility to ambulatory care or home health care with a principal
discharge diagnosis of HF for whom a follow-up appointment was
scheduled and documented including location, date and time for a
follow-up office visit, or home health visit (as specified)
Inpatient Facility
*Please refer to the complete measures for comprehensive information, including measure exception. †Test measure designated for use in internal quality improvement programs only. These measures are not appropriate for any other purpose, e.g., pay for performance, physician ranking or public reporting programs.‡New measure.
Adapted from Bonow et al. J Am Coll Cardiol. 2012;59:1812-32.
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169 170
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