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3/4/2019 1 HEART FAILURE: MANAGEMENT IN THE ACUTE CARE SETTING ROBERT T ROGERS, ACNP-BC, AACC NORTON 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 1 2 3 4 5 6

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Page 1: 115-Acute Heart Failure [Autosaved] · ^ À v } v >t U Z } X ] µ o ] } v î ì ì ï V í ì ô W ï ì ñ õ ^ P U Ez, o /s ñ ì 9 D } o ] Ç µ ] } P v ] Z } l / u u ] v v v }

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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

1 2

3 4

5 6

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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

7 8

9 10

11 12

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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

13 14

15 16

17 18

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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

19 20

21 22

23 24

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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

25 26

27 28

29 30

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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)

31 32

33 34

35 36

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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

37 38

39 40

41 42

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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

43 44

45 46

47 48

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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

I IIa IIb III

I IIa IIb III

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

49 50

51 52

53 54

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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

55 56

57 58

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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

61 62

63 64

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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

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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.

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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.

QUESTIONS?

• Also, feel free to email me questions to

[email protected]

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