Heartfailure

2012 Focused Update

ACCF/AHA/ESC/HFA Guidelines
for the Diagnosis and Management
of Heart Failure in Adults
Update in the management of heart failure 2012

Walls have ears

Sir THOMAS LEWIS ,1933

Change before you have to
Jack Welch

Better a low dose than no dose

- Patients with acute heart failure frequently
develop chronic heart failure.
- Patients with chronic heart failure frequently
decompensate acutely.

ESC Guidelines - update

Diagnosis of heart failure 2012

New York Heart Association functional classification based on
severity of symptoms and physical activity

Symptoms and signs typical of heart failure
2012

Stages of Heart Failure

At Risk for Heart Failure:
STAGE A High risk for developing HF

STAGE B Asymptomatic LV dysfunction

Heart Failure:
STAGE C Past or current symptoms of HF

STAGE D End-stage HF

Stages of Heart Failure

• Designed to emphasize preventability of HF

• Designed to recognize the progressive
nature of LV dysfunction

Mechanisms and Models in Heart Failure

1.The "cardiorenal model" :as a problem of excessive salt and
water retention that was caused by abnormalities of renal blood
flow
2. The "hemodynamic model " :to arise largely as a result of
abnormalities of the pumping capacity of the heart and
excessive peripheral vasoconstriction
3. The ―neurohormonal hypothesis‖: a theory to explain the
mechanism of disease progression in heart failure
4. The biomechanical model :many device-based therapies that
concurrently affect LV pump performance and LV remodeling
(eg, cardiac resynchronization) are beneficial

Douglas L. Mann, MD; Michael R. Bristow; Mechanisms and Models in Heart Failure
CIRCULATION,2005

Algorithm for the diagnosis of Heart Failure or Left Ventricular Dysfunction

Suspected LV dysfunction because of signs Suspected Heart Failure because of symptoms and signs

Normal
Assess presence of cardiac disease by ECG, X-ray or
Heart failure or LV dysfunction
Natriuretic peptides ( where available)
unlikely

Tests abnormal

Normal
Imaging by Echocardiography (Nuclear angiography
Heart failure or LV dysfunction
or MRI where available)
unlikely

Tests abnormal

Additional diagnostic tests
Assess aetiology, degree, precipitating factors and
type of cardiac dysfunction Where appropriate
(e.g. coronary angiography)

Choose therapy
ESC Guidelines

Chronic Heart Failure; Drugs That Reduce
Mortality; Improve Symptoms, or Might Harm
Reduce Mortality; Must Try to Use
1. ACE inhibitors or ARBs
2. ß-Blockers
3. Spironolactone or eplerenone
4. Isosorbide-hydralazine (in some)

Improve Symptoms; Use According to Clinical Judgment
1. Diuretics
2. Digoxin (low dose)
3. Nitrates
4. Ion for anemia
5. Metabolically active agents (consider)

May be Harmful; Use Cautiously After Due Consideration
1. Inotropes and inotropic dilators
2. Antiarrhythmics, except ß-Blockers and amiodarone
3. Calcium channel blockers
4. High-dose digoxin

Drugs for the Heart, 7th, 2009

ACE-i. Mechanism of Action

VASOCONSTRICTION VASODILATATION
ALDOSTERONE PROSTAGLANDINS
VASOPRESSIN Kininogen tPA
SYMPATHETIC Kallikrein
Angiotensinogen
RENIN
Angiotensin I
BRADYKININ

A.C.E. Inhibitor Kininase II

ANGIOTENSIN II Inactive Fragments

ACE Inhibitors – In Whom and When?

Indications:
• Potentially all patients with heart failure
• First-line treatment (along with beta-blockers) in NYHA class I–IV heart failure
Contra-indications:
• History of angioedema
• Bilateral renal artery stenosis
• Significant renal dysfunction (creatinine >2.5 mg/dL or 221 µmol/L)
• Serum potassium concentration (K+ >5.0 mmol/L)
• Severe aortic stenosis
• Symptomatic or severe asymptomatic hypotension (SBP <90 mmHg)
Drug interactions to look out for:
• K+ supplements/ K+ sparing diuretics (including spironolactone)
• NSAIDs*
• AT1-receptor blockers

*avoid unless essential
McMurray J, Cohen-Solal A, Dietz R, Eichhorn E, Erhardt L,
Hobbs R, Maggioni A, Pina I, Soler-Soler J, Swedberg K

ESC Guidelines - update

Practical Recommendations for Heart Failure Treatment:
Putting Guidelines into Practice

— ACE INHIBITORS —

ACE Inhibitors – How to Use
• Start with a low dose
• Double dose at not less than two weekly intervals
• Aim for target dose or, failing that, the highest tolerated dose
• Remember some ACE inhibitor is better than no ACE inhibitor
• Monitor blood chemistry (urea, creatinine, K+) and blood pressure
• When to stop up-titration/down-titration – see PROBLEM SOLVING




ACE Inhibitors – Advice to Patient
• Explain expected benefits (see WHY?)
• Treatment is given to improve symptoms, to prevent worsening of heart failure and to
increase survival
• Symptoms improve within a few weeks to a few months
• Advise patients to report principal adverse effects
(i.e. dizziness/symptomatic hypotension, cough)




ACE Inhibitors – Problem Solving
Cough:
• Cough is common in patients with heart failure, many of whom have smoking-related lung
disease
• Cough is also a symptom of pulmonary oedema, which should be excluded if a new or
worsening cough develops
• ACE inhibitor-induced cough rarely requires treatment discontinuation
• If a very troublesome cough develops (e.g. one stopping the patient sleeping) and can be
proven to be due to ACE inhibition (i.e. it recurs after ACE inhibitor withdrawal and
rechallenge), substitution with an AT1-receptor blocker can be considered




ACE Inhibitors – Problem Solving (continued)
Worsening renal function:
• Some increase in urea (blood urea nitrogen), creatinine and K+ is to be expected after
initiation; if the increase is small and asymptomatic no action is necessary
• An increase in creatinine of up to 50% above baseline, or 3 mg/dL (266 µmol/L), whichever is
the smaller, is acceptable
• An increase in K+ 6.0 mmol/L is acceptable
• If urea, creatinine or K+ rise excessively, consider stopping concomitant nephrotoxic drugs
(e.g. NSAIDs), other K+ supplements/ K+ retaining agents (triamterene, amiloride) and, if no
signs of congestion, reducing the dose of diuretic
• If greater rises in creatinine or K+ than those outlined above persist, despite adjustment of
concomitant medications, halve the dose of ACE inhibitor and recheck blood chemistry; if
there is still an unsatisfactory response, specialist advice should be sought




ACE Inhibitors – Problem Solving (continued)
Worsening renal function (cont.):
• If K+ rises to >6.0 mmol/L, or creatinine increases by >100% or to above 4 mg/dL (354
µmol/L), the dose of ACE inhibitor should be stopped and specialist advice sought
• Blood chemistry should be monitored serially until K+ and creatinine have plateaued

NOTE: it is very rarely necessary to stop an ACE inhibitor and clinical deterioration is likely if
treatment is withdrawn; ideally, specialist advice should be sought before treatment
discontinuation


Role of Angiotensin II in Vascular Disease
Blocking the RAAS with ACE inhibitors and ARBs

Chung, Unger., Am J Hypertens 1999;12:150S–156S

Renin-Angiotensin Mechanism
Beta-blocker
ACEI
ARB

renal juxtaglomerular

BRAUNWALD'S HEART DISEASE

Benefits of RAAS Blockade for
Renal Protection
 Haemodynamic effects
 Reduction in systemic BP
 Reduction in glomerular capillary pressure
 Reduction in proteinuria

Angiotensin II

 Non-haemodynamic effects
 Stimulation of extracellular matrix degradation
 Inhibition of macrophage/monocyte infiltration

Potential Mechanisms whereby Angiotensin II
Receptor Blockers (ARBs) Interact with Peroxisome
Proliferator-activated Receptor Gamma (PPAR )
Angiotensin II

ARB
AT2
AT1

ARB
L RA
p300
Anti-diabetic
PPAR RxR
Anti-hypertensive
Anti-inflammatory
PPRE Gene

5’ 3’
Acta Diabetologia (2005) 42:S26-S32

Morbidity and Mortality along the
Cardiovascular Continuum

Remodeling Ventricular
Dilation

Myocardial Congestive
Infarction Heart Failure
CAPRICORN
Atherosclerosis ISIS 1 MERIT-HF End-Stage
and LVH BHAT CIBIS Heart Disease
TIMI-II and Death

Risk Factors MAPHY COPERNICUS
Diabetes
UKPDS Death
Hypertension

Adapted from Dzau V, Braunwald E. Am Heart J. 1991;121:1244-1263.

Opie 2008

Positively
inotropic
Tachycardia
Dromotropic

AC : adenyl cyclase ; Gs : stimulatory protein G; PKA ; protein kinase A ; P :
phosphorylate
PDE : phosphodiesterase ; Ach : acetylcholine LH. Drug for the Heart. Elsevier Saunders 2009, 7th ed p.3
Opie

Cardiac effects of beta-blockers

Interacting drugs

Nodal depression by

Negative
chronotropic

Negative
dromotropic

Anti-
arrhythmic

Negative
inotropic

Anti-ischemic

Opie LH. Drug for the Heart. Elsevier Saunders 2009


— BETA BLOCKERS —

Beta Blockers – In Whom and When?
Cautions/seek specialist advice:
• Severe (NYHA Class IV) heart failure
• Current or recent (<4 weeks) exacerbation of heart failure (e.g. hospital admission with
worsening heart failure)
• Heart block or heart rate <60 beats/min
• Persisting signs of congestion – raised jugular venous pressure, ascites, marked
peripheral oedema
Drug interactions to look out for:
• verapamil/diltiazem (should be discontinued)
• amiodarone



Beta Blockers – How to Use
• Start with a low dose
• Double dose at not less than two-weekly intervals
• Aim for target dose or, failing that, the highest tolerated dose
• Remember some beta-blocker is better than no beta-blocker
• Monitor HR, BP, clinical status (symptoms, signs – especially signs of congestion, and body
weight)
• Check blood chemistry 1–2 weeks after initiation and 1–2 weeks after final dose titration
• A specialist heart failure nurse may assist with patient education, follow-up (in
person/by telephone) and dose up-titration
• When to down-titrate/stop up-titration – see PROBLEM SOLVING

Heart Failure: A Firm Indication for beta Blockade – Titration and Doses of Drugs

Beta Blockers First Dose 3rd Week 5th-6th Week Final Dose

Carvedilol 3.125 6.25 2 12.5 2 25 2

Metoprolol SR 25 50 100 200

Bisoprolol 1.25 3.75 5.0 10.0

Nebivolol 1.25 2.5 5.0 10




Beta Blockers – Which and What Dose?

Starting dose Target dose
 bisoprolol 1.25 mg od 10 mg od
 carvedilol 3.125 mg bd 25–50 mg bd
 metoprolol CR/XL 12.5–25 mg od 200 mg od

od = once daily; bd = twice daily



Beta Blockers – Problem Solving
Worsening symptoms/signs (e.g. increasing dyspnoea,
fatigue, oedema, weight gain):
• If increasing congestion, double the dose of diuretic and/or halve the dose of beta-blocker (if
increasing diuretic does not work)
• If marked fatigue (and/or bradycardia – see below), halve the dose of beta-blocker (rarely
necessary)
• Review patient in 1–2 weeks; if not improved, seek specialist advice
• If serious deterioration, halve the dose of beta-blocker or stop this treatment (rarely
necessary); seek specialist advice



Beta Blockers – Problem Solving (continued)
Low heart rate:
• If <50 beats/min and worsening symptoms – halve the dose of beta-blocker or, if
severe deterioration, stop beta-blocker (rarely necessary)
• Review need for other heart-rate slowing drugs (e.g. digoxin, amiodarone, diltiazem)
• Arrange ECG to exclude heart block
• Seek specialist advice



Beta Blockers – Problem Solving (continued)
Asymptomatic low blood pressure:
• Does not usually require any change in therapy
Symptomatic hypotension:
• If dizziness, light-headedness and/or confusion and a low blood pressure occur, reconsider
need for nitrates, calcium channel blockers and other vasodilators
• If no signs/symptoms of congestion, consider reducing diuretic dose
• If these measures do not solve problem, seek specialist advice

NOTE: Beta-blockers should not be stopped suddenly unless absolutely necessary (there is a
risk of a ‘rebound’ increase in myocardial ischaemia/infarction and arrhythmias); ideally
specialist advice should be sought before treatment discontinuation

Aldosterone Inhibitors

Spironolactone ALDOSTERONE
Competitive antagonist of the -
aldosterone receptor
(myocardium, arterial walls, kidney)

• Retention Na+ • Collagen
Edema deposition
• Retention H2O

Fibrosis
• Excretion K+ - myocardium
Arrhythmias
• Excretion Mg2+ - vessels

The Renin-Angiotensin-Aldosterone System

Weber K. N Engl J Med 2001;345:1689-1697

The Renin-Angiotensin-Aldosterone (RAA) System

Kidneys Adrenal cortex
Liver secretes secrete secretes
angiotensinogen renin aldosterone

Angiotensin
converting
Blood Renin enzyme
(ACE)

Angiotensinogen Angiotensin I Angiotensin II Aldosterone

NA+ retention
Growth Vascular H2O retention
factor Sympathetic
smooth muscle K+ excretion
stimulation activation
constriction Mg+ excretion

Điều hòa ngược trong bài tiết
Aldosterone
Afferent Arteriole Angiotensinogen
Glomerulus
Renin
_
_ A-I
“Short
Volume Loop” Converting
Enzyme
Efferent Arteriole A-II
Na
reabsorption

K excretion
Cortical
Collecting _
Adrenal
Duct
K

Extraadrenal Production of Aldosterone by Endothelial and
Vascular Smooth-Muscle Cells in an Intramyocardial
Coronary Artery

Weber K. N Engl J Med 2001;345:1689-1697

Heart Failure
Angiotensinogen
Renin
Angiotensin I
ACE ACEI reduces
Angiotensin II levels
Angiotensin II

ACTH K+
Elevated
Other ALDOSTERONE Na+

Verospirone & Eplerenone blocks
Aldosterone at receptors

Pathologic Fluid retention Hypokalemia,
LVH/myocardial And edema Hypomagnesemia,
fibrosis arrhythmias

Morbidity
Mortality

Role of Aldosterone in CV Disease

Angiotensin II–K+ –ACTH- Norepinephrine – Serotonin – Endothelin-NO

Aldosterone

Kidneys Brain Blood Vessels Heart
+SNS
Na+ reabsorption Blood Cytokine Activation
K+ excretion Pressure Vascular Inflammation Cardiac Hypertrophy
Endothelial Dysfunction Myocardial fibrosis

Hypertension Vascular Injury LV Hypertrophy

Ventricular Remodeling
End-stage renal disease, MI, HF, Arrhythmias

Aldosterone in Heart Failure
Aldosterone

 K+  Mg++  Arterial compliance
 LV
 Fibrosis  Baroreceptor function
 Na+
mass  Norepinephrine uptake
&  Norepinephrine
Uptake  Endothelial function
fibrosis  PAI-1
 Heart rate
variability

 Ischemic
 Edema  Remodeling  Arrhythmia
Events

Progression of HF Sudden cardiac death

Aldosterone Antagonists
 Non-diuretic doses
 RALES trial
 Spironolactone
 Class III-IV

 EPHESUS trial
 Eplerenone
 Low EF after MI

Randomized Aldactone
Evaluation Study (RALES)
1.00

0.95

0.90

0.85

0.80

0.75

Probability 0.70
Spironolactone
of Survival
0.65

0.60
p< 0.001
0.55 Placebo
0.50

0.45

0.00
0 3 6 9 12 15 18 21 24 27 30 33 36
Months

Pitt et al. N Engl J Med. 1999;341(10):709-717.

EPHESUS
 Total deaths
 478 eplerenone
 554 placebo

 CV deaths
 407 eplerenone
 483 placebo


— SPIRONOLACTONE—

Spironolactone – In Whom and When?
Indications:
• Potentially all patients with symptomatically moderately severe or severe heart
failure
• Second-line therapy (after ACE inhibitors and beta-blockers) in patients with NYHA
class III–IV heart failure
Cautions/seek specialist advice:
• Significant renal dysfunction (creatinine >221 µmol/L or 2.5 mg/dL)
• Significant hyperkalaemia (K+ >5.0 mmol/L)



Spironolactone – How to Use
• Start at 25 mg once daily
• Check blood chemistry at 1, 4, 8 and 12 weeks; 6, 9 and 12 months; 6
monthly thereafter
• If K+ rises to between 5.5 and 6.0 mmol/L, or creatinine rises to 2.5 mg/dL (221
µmol/L), reduce dose to 25 mg on alternate days and monitor blood chemistry closely

• If K+ rises to >6.0 mmol/L, or creatinine to >4.0 mg/dL (354 µmol/L), stop spironolactone and
seek specialist advice



Spironolactone – Advice to Patient
• Explain expected benefits (see WHY?)
• Treatment is given to improve symptoms, prevent worsening of heart failure and to
increase survival
• Symptom improvement occurs within a few weeks to a few months of starting treatment

• Avoid NSAIDs not prescribed by a physician (self-purchased ‗over the counter‘ treatment,
e.g. ibuprofen)
• Temporarily stop spironolactone if diarrhoea and/or vomiting occur and contact physician



Spironolactone – Problem Solving
Worsening renal function/hyperkalaemia:
• See HOW TO USE section
• Major concern is hyperkalaemia (K+ >6.0 mmol/L) though this was uncommon in RALES; a
high-normal K+ may be desirable in heart failure patients, especially if taking digoxin

• It is important to avoid other K+ retaining drugs (e.g. K+ sparing diuretics) and nephrotoxic
agents (e.g. NSAIDs)
• Some ‗low salt‘ substitutes have a high K+ content
• Male patients may develop breast discomfort and/or gynaecomastia

Diuretics

Thiazides
Inhibit active exchange of Cl-Na
Cortex in the cortical diluting segment of the
ascending loop of Henle

K-sparing
Inhibit reabsorption of Na in the
distal convoluted and collecting tubule

Loop diuretics
Medulla Inhibit exchange of Cl-Na-K in
the thick segment of the ascending
loop of Henle

Loop of Henle
Collecting tubule

Diuretic Therapy
Renal Reabsorption of Na (
Hypomagnesemia
and Mg)
Hyponatremi Saluresis &
a Diuresis
Plasma Volume

Cardiac Renal Blood
PRA
Output Flow

Postural GFR Distal Ca++ Aldosterone
hypotension Reabsorption
Pre-renal Proximal
Kaliuresis
Azotemia Reabsorption
Hyper-
(?)
CLUric acid CLcalcium Hypokalemia
cholesterole
mia
Hyperuricemia Hypercalcemia
Glucose Tolerence
Kaplan’s Clinical Hypertension ,
2006

Thiazides, Loop Diuretics. Adverse Effects
• K+, Mg+ (15 - 60%) (sudden death ???)
• Na+
• Stimulation of neurohormonal activity
• Hyperuricemia (15 - 40%)
• Hypotension. Ototoxicity. Gastrointestinal.
Alkalosis. Metabolic
Sharpe N. Heart failure. Martin Dunitz 2000;43
Kubo SH , et al. Am J Cardiol 1987;60:1322
MRFIT, JAMA 1982;248:1465
Pool Wilson. Heart failure. Churchill Livinston 1997;635

Diuretic Resistance

• Neurohormonal activation
• Rebound Na+ uptake after volume loss
• Hypertrophy of distal nephron
• Reduced tubular secretion (renal failure, NSAIDs)
• Decreased renal perfusion (low output)
• Altered absortion of diuretic
• Noncompliance with drugs
Brater NEJM 1998;339:387
Kramer et al. Am J Med 1999;106:90

Managing Resistance to Diuretics
• Restrict Na+/H2O intake (Monitor Natremia)
• Increase dose (individual dose, frequency, i.v.)
• Combine: furosemide + thiazide / spiro / metolazone
• Dopamine (increase cardiac output)
• Reduce dose of ACE-i
• Ultrafiltration

Motwani et al Circulation 1992;86:439

Vasodilators
VENOUS Venous
Nitrates Vasodilatation
Molsidomine

MIXED
Calcium antagonists
-adrenergic Blockers
ACE-I, ARBs
K+ channel activators
Nitroprusside

Arterial ARTERIAL
Vasodilatation Minoxidil
Hydralazine

NITRATES
HEMODYNAMIC EFFECTS

1- VENOUS VASODILATATION
Pulmonary congestion
Ventricular size
Preload Vent. Wall stress
MVO2

2- Coronary vasodilatation
Myocardial perfusion
3- Arterial vasodilatation • Cardiac output
Afterload • Blood pressure

4- Others

Mechanism of action of digoxin. Digoxin inhibits Na+/K+ ATPase. As a consequence of an increased
intercellular Na+ concentration, Ca2+ extrusion (via Na+/Ca2+ exchange) is reduced. The result is an increase
in cellular Ca2+.

Digitalis
-
Na-K ATPase
Na+ Na-Ca Exchange
K+ Na+ Ca++

Myofilaments Ca++
K+ Na+

CONTRACTILITY

Digitalis. Mechanism of Action
Blocks Na+ / K+ ATPase => Ca+ +
• Inotropic effect
• Natriuresis
• Neurohormonal control
- Plasma Noradrenaline
- Peripheral nervous system activity
- RAAS activity
- Vagal tone
- Normalizes arterial baroreceptors
NEJM 1988;318:358

Digitalis. Clinical Effects

• Improve symptoms
• Modest reduction in hospitalization
• Does not improve survival

Digitalis. Indications
• When no adequate response to
ACE-i + diuretics + beta-blockers
AHA / ACC Guidelines 2001

• In combination with ACE-i + diuretics
if persisting symptoms
ESC Guidelines 2001

• AF, to slow AV conduction

Dose 0.125 to 0.250 mg / day

Digoxin. Contraindications
• Digoxin toxicity
• Advanced A-V block without pacemaker
• Bradycardia or sick sinus without PM
• PVC’s and VT
• Marked hypokalemia
• W-P-W with atrial fibrillation

Device Therapy

1.Implantable Cardioverter- Defibrillators (ICD)
2.Cardiac Resynchronization Therapy or
Biventricular Pacing
3.Ventricular Assist Devices

CRT: cardiac resynchronization therapy

Chronic Heart Disease
Aims of treatment

Prevention
Prevention and / or controlling of disease leading to cardiac dysfunction and heart
disease
Prevention of progression to heart failure once cardiac dysfunction is established
Morbidity
Maintenance or improvement in quality of life
Avoid re-admissions
Mortality
Increased duration of life
Non-pharmacological management

The ESC Guidelines for the Diagnosis & Treatment of Chronic Heart Failure

General advice and measures
Patient and family education
-Explain what HF is and why symptoms occur
-Causes of HF
-How to recognize symptoms and what to do when they occur
-Daily self-weighing and what to do in case of weight gain
-Rationale for treatments
-Importance of adhering to pharmacological and non-pharmacological prescriptions
-Refrain from smoking
-Prognosis
Drug counselling
-Effects
-Doses and times of administration
-Side-effects and adverse effects
-What to do in case of skipped doses
-Self-management


General advice and measures (continued…)
Dietary and social habits
-Control sodium intake when necessary (e.g. some patients with advanced HF)
-Avoid excessive fluid intake (e.g. >1.5 L/day) in severe HF
-Avoid excessive alcohol fluid intake
-Reduce weight in obese patients
-Assess malnutrition and cardiac cachexia
Rest and exercise
-Rest recommended only in AHF or decompensated CHF
-Encourage daily physical activities that do not induce symptoms
-Recommended exercise training programme in stable NYHA class II-III patients
-Work counselling
Sexual activity
-Phosphodiesterase-5 inhibitors are not recommended in advance heart failure. It used
, they should be avoided < 24-48 h of nitrate intake depending on agent.


General advice and measures (continued…)
Travelling
- Discourage long journeys, high altitudes, very hot or humid places
Vaccinations- Advice on immunizations
-Immunization for influenza is widely used
Drugs to avoid or use with caution
-Non-steroidal anti-inflammatory drugs (NSAIDs) & coxibs
-Class I anti-arhythmics
-Calcium-antagonists
-Tricyclic antidepressants
-Lithium
-Corticosteroids


50 – 60%

< 5%. Normal blood pressure: Vasodilators

Reduced blood pressure :
Inotropics or vasopressors 20%,

Dec G.W. Management of Acute Decompensated Heart Failure. Curr Probl Cardiol 2007; 32: 319 - 366

http://www.biomerieux-diagnostics.com/servlet/srt/bio/clinical-
diagnostics/dynPage?node=Heart_Failure

Ventricular Stretch

Enzyme corin

T ½ 1.5 to 2 hours
T ½ 20 minutes

Heart Failure Clin 2 (2006)-291-298

The prognostic power of BNP &ø Troponins

 30–70% of patients hospitalized with AHFS have
detectable plasma levels of cardiac troponin( Troponin I or
Troponin T*)
 Associated with a 2-fold increase in postdischarge mortality
and a 3-fold increase in rehospitalization rate
 elevated cTnI and elevated BNP identified patients with advanced HF with a
markedly increased risk of death (12-fold increase) **

* Gheorghiade M et al. Circulation 2005; 112: 3958 – 3968
** Horwich TB et al. Circulation 2003; 108: 833 - 838

Gheorghiade M et al. Circulation 2005; 112: 3958 – 3968

Predictor Points
Elevated NT-proBNP 4

Interstitial edema on chest X-ray 2

Orthopnea 2
Absence of fever 2

Current loop diuretic use 1

Age > 75 years 1

Rales on lung examination 1

Absence of cough 1

A total score of ≥ 6 has a high
Interpretation predictive accuracy for the
diagnosis of acute HF

http://www.biomerieux-diagnostics.com/servlet/srt/bio/clinical-
diagnostics/dynPage?node=Heart_Failure

Evaluation
and Management
of Heart Failure

B-type Natriuretic Peptide
(BNP)
 BNP is a neurohormone secreted by the
myocardium in response to stretch
 Elevated BNP levels are associated with elevated
ventricular filling pressures
 Large variation in “normal” or optimal level
 Obesity
 Age

 Gender

BNP Levels in Patients With Dyspnea
Secondary to COPD or CHF

1200 1076 +/- 138

1000
p < 0.001
BNP pg/mL

800
600
400
86 +/- 39
200
0
COPD CHF
N=56 N=94
Cause of Dyspnea

Dao Q et al, JACC 2001

BNP Levels for Types of Lung
Disease
207 272

Morrison KL et al, JACC 2002

How do I monitor
response to treatment?

Echocardiography

 Once the diagnosis of heart failure due to
systolic dysfunction is established, repeat
echocardiography is indicated only
 For significant change in functional status
 To assess response to beta blockade

Uses of BNP levels
 DIAGNOSIS
 Levels less than 100 pg/ml generally exclude a
cardiac cause of dyspnea
 PROGNOSIS
 Failure to lower BNP level during hospitalization
suggests an increased risk of early readmission
 Elevation of BNP during hospitalization suggests
increased mortality

Uses of BNP levels

 On admission
 During course of therapy
 When euvolemic
 Clinically
 By right heart catheterization

 On discharge

BNP Predicts Outcome

1506
BNP Level

690
2009
2

•Of the 72 patients admitted with CHF, 22 endpoints occurred
•In these patients BNP increased by a mean of 233 pg/ml, p<0.001
•In patients without death or readmission BNP decreased by 215 pg/ml
•The last BNP level measured was the strongest predictor of events, if the
level was <1200 (in this population) 90% chance of no adverse events

BNP Concentration for the
Prediction of Clinical Events
CHF Death, Hospitalization, or ED visit
50%
45
40
35
30 BNP > 480 pg/ml
25 RR CHF death
20 24.1
15
BNP 230-480 pg/ml
10
5 BNP < 230 pg/ml
0
0 20 40 60 80 100 120 140 160 180
Days
Harrison A, et al, Annals of Emergency Medicine 2002

Conclusions

• NT-Pro BNP & BNP are valuable adjuncts for the
diagnosis & prognosis of decompensated HF in patients
with dyspnea
• Elevated natriuretic levels in the absence of HF may
often represent other acute or chronic heart disease
including ischemia
• Additional applications may include risk stratification in
patients with renal disease

Heartfailure

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