Heart Failure

CHRONIC CONGESTIVE HEART FAILURE
Chronic Congestive Heart Failure
Definition of heart failure

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
AHA / ACC HF guidelines 2008
Clinical symptoms / signs secondary to abnormal ventricular function

ESC HF guidelines 2008
Congestive heart failure

Constellation of symptoms and signs caused for inadequate performance of LV Reduced or preserved LV systolic function Complex blend of structural, functional and biological alterations
LV remodelling, a potential reversible phenomenon, alters size, shape and function
ETIOLOGIES OF HEART FAILURE
Structural and functional abnormalities in left ventricular dysfunction

Systolic dysfunction Preserved systolic function
Low EF Large volumes
Normal EF Small volumes
LV mass hypertrophy Loss of myocytes Interstitial fibrosis
Conditions associated to CHF with and without systolic dysfunction

Systolic dysfunction +++ Preserved systolic function +
Previous MI
Hypertension
Diabetes Obesity Chronic lung dis.
++
++ + -
+++
+++ +++ ++
Natural history of CHF

Neurohormonal adaptative mechanisms SNS SRA Endothelin NPs etc
60%
Secondary damage 20% Time (years)
Mann DL. Circulation 1999
Natural history of CHF in hypertension

Interstitial and perivascular collagen
Left Ventricular Hypertrophy
Diastolic Dysfunction Congestive Heart Failure
Index event High BP Myocardial Ischemia Systolic Dysfunction
Coronary resistance Coronary reserve
Remodelling
Dysfunction
Alterations in the remodelled left ventricle

Alteration Myocytes Dysfunctional phenotype Regression LV assist device -blockers
Myocardium
Loss myocytes Fibrosis

Large and spherical LV assist device -blockers ACEi
Chamber geometry
DIAGNOSTIC ALGORYTHM FOR IDENTIFY PATIENTS WITH SUSPECTED HEART FAILURE
Diagnosis and Investigation

Clinical history, physical examination and laboratory testing Transthoracic echocardiography (ventricular size and function, valves, etc.) Coronary angiography in patients with known/suspected CAD NYHA classification should be used to document functional capacity in all patients
Clinical Presentations of Heart Failure
What is BNP and How Does It Help?

Suspected Heart Failure because of SYMPTOMS and/or SIGNS Assess presence of CARDIAC DISEASE by ECG, X-Ray or BNP (if available)
Tests abnormal
NORMAL No Heart Failure
VENTRICULAR FUNCTION
Imaging by ECHO-Doppler,
Nuclear angiography or MRI if available
Tests abnormal
NORMAL No Heart Failure
Heart Failure: Systolic / Diastolic

Identify etiology, evaluate severity, choose therapy

HF Risk Factors No Heart disease No symptoms Heart disease No symptoms
A
Stages in the evolution of Heart Failure
B C
Prior or current HF Symptoms
Asymptomatic LV dysfunction
D
Refractory HF symptoms

Hypertension Diabetes, Hyperchol. Family Hx Cardiotoxins
A B
Stages in the Evolution of Heart Failure Clinical Characteristics
Heart disease (any)
Asymptomatic LV dysfunction Systolic / Diastolic
Dyspnea, Fatigue Reduced exercise tolerance
D
Marked symptoms at rest despite max. therapy

Treat risk factors Avoid toxics ACE-i in selected p.
A B
Stages in the Evolution of Heart Failure Treatment
ACE-i blockers
In selected patients
C
ACE-i blockers Diuretics / Digitalis
D
Palliative therapy Mech. Assist device Heart Transplant
Treatment Objectives
Survival Morbidity Exercise capacity Quality of life Neurohormonal changes Progression of CHF Symptoms
(Cost)
Treatment
Prevention. Control of risk factors Life style All Treat etiologic cause / aggravating factors Drug therapy Personal care. Team work Revascularization if ischemia causes HF ICD (Implantable Cardiac Defibrillator) Ventricular resyncronization Ventricular assist devices Heart transplant Artificial heart Neoangiogenesis, Gene therapy
Selected patients
Treatment Pharmacologic Therapy
ACE inhibitors / ARBs Beta Blockers Diuretics

Digitalis Spironolactone / Eplerenone Vasodilators Other
THE DONKEY ANALOGY

Ventricular dysfunction limits a patient's ability to perform the routine activities of daily living
CLINICAL EFFICACY OF ACE INHIBITORS, ARBs, DIURETICS AND VASODILATORS
BETA-BLOCKERS EFFICACY
Digitalis Compounds
Like the carrot placed in front of the donkey
Diuretics
Essential to control symptoms secondary to fluid retention
Prevent progression from HT to HF Spironolactone improves survival New research in progress
Diuretics
Thiazides
Cortex
Inhibit active exchange of Cl-Na in the cortical diluting segment of the ascending loop of Henle
K-sparing
Inhibit reabsorption of Na in the distal convoluted and collecting tubule
Medulla
Loop of Henle
Loop diuretics
Inhibit exchange of Cl-Na-K in the thick segment of the ascending loop of Henle
Collecting tubule
Diuretics. Indications
1. Symptomatic HF, with fluid retention Edema Dyspnea Lung Rales Jugular distension Hepatomegaly Pulmonary edema (Xray)
Loop Diuretics / Thiazides. Practical Use Start with variable dose. Titrate to achieve dry weight Monitor serum K+ at frequent intervals
Reduce dose when fluid retention is controlled
Teach the patient when, how to change dose
Combine to overcome resistance

Do not use alone
Loop diuretics. Dose (mg)

Initial Maximum
Bumetanide
Furosemide
0.5 to 1.0 / 12-24h

20 to 40 / 12-24h
10 / day
400 / day
Torsemide
10 to 20 / 12-24h
200 / day
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
ACE-i. Mechanism of Action

VASOCONSTRICTION
ALDOSTERONE VASOPRESSIN SYMPATHETIC
Angiotensinogen RENIN Angiotensin I
VASODILATATION
PROSTAGLANDINS Kininogen tPA
Kallikrein
BRADYKININ
A.C.E.
ANGIOTENSIN II
Inhibitor
Kininase II
Inactive Fragments
ACE-I. Clinical Effects
Improve symptoms
Reduce remodelling / progression
Reduce hospitalization
Improve survival
Mortality Reduction with ACE-i

Study CONSENSUS ACE-i Enalapril Clinical Seting CHF CHF
SOLVD treatment Enalapril
AIRE
Vheft-II TRACE
Ramipril
Enalapril Trandolapril
CHF
CHF CHF / LVD
SAVE
SMILE HOPE
Captopril
Zofenopril Ramipril
LVD
High risk High risk
ACE-i. Indications
Symptomatic heart failure
Asymptomatic ventricular dysfunction - LVEF < 35 - 40 % Selected high risk subgroups
AHA / ACC HF guidelines 2001 ESC HF guidelines 2001
ACE-i. Practical Use

Start with very low dose Increase dose if well tolerated Renal function & serum K+ after 1-2 w
Avoid fluid retention / hypovolemia (diuretic use)
Dose NOT determined by symptoms
Combine to overcome resistance

Do not use alone
ACE-i. Dose (mg)

Initial Captopril 6.25 / 8h Enalapril 2.5 / 12 h Fosinopril 5 to 10 / day Lisinopril 2.5 to 5.0 / day Quinapril 10 / 12 h Ramipril 1.25 to 2.5 / day Maximum 50 / 8h 10 to 20 / 12h 40 / day 20 to 40 / day 40 / 12 h 10 / day
ACE-I. Adverse Effects Hypotension (1st dose effect) Worsening renal function Hyperkalemia Cough Angioedema
Rash, ageusia, neutropenia,
ACE-I. Contraindications
Intolerance (angioedema, anuric renal fail.)
Bilateral renal artery stenosis
Pregnancy
Renal insufficiency (creatinine > 3 mg/dl)
Hyperkalemia (> 5,5 mmol/l)

Severe hypotension
-Adrenergic Blockers Mechanism of action

Density of 1 receptors
Inhibit cardiotoxicity of catecholamines

Neurohormonal activation HR Antiischemic Antihypertensive
Antiarrhythmic
Antioxidant, Antiproliferative
-Adrenergic Blockers Clinical Effects

Improve symptoms (only long term)
Reduce remodelling / progression
Reduce hospitalization
Reduce sudden death
Improve survival
-Adrenergic Blockers Indications

Symptomatic heart failure Asymptomatic ventricular dysfunction - LVEF < 35 - 40 %
After AMI
-Adrenergic Blockers When to start

Patient stable No physical evidence of fluid retention No need for i.v. inotropic drugs Start ACE-I / diuretic first No contraindications In hospital or not
-Adrenergic Blockers Dose (mg)

Initial Bisoprolol Carvedilol Metoprolol tartrate Target 1.25 / 24h 3.125 / 12h 6.25 / 12h 10 / 24h 25 / 12h 75 / 12h
Metoprolol succinnate 12,5-25 / 24h
200 / 24h
Start Low, Increase Slowly

Increase the dose every 2 - 4 weeks
-Adrenergic Blockers Adverse Effects

Hypotension Fluid retention / worsening heart failure Fatigue Bradycardia / heart block
Review treatment (+/-diuretics, other drugs) Reduce dose Consider cardiac pacing Discontinue beta blocker only in severe cases
-Adrenergic Blockers Contraindications

Asthma (reactive airway disease) AV block (unless pacemaker) Symptomatic hypotension / Bradycardia Diabetes is NOT a contraindication
PART II. TREATMENT AND PREVENTION OF CHF
Na-K ATPase
Na+
Digitalis
K+
Na-Ca Exchange
Na+ Ca++
K+ Na+
Myofilaments
Ca++
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 PVCs and VT Marked hypokalemia W-P-W with atrial fibrillation
Aldosterone Inhibitors
Spironolactone
ALDOSTERONE
Competitive antagonist of the aldosterone receptor (myocardium, arterial walls, kidney)
Retention Na+ Retention H2O Excretion K+
Collagen
Edema
deposition
Fibrosis Arrhythmias
- myocardium - vessels
Excretion Mg2+
Spironolactone. Indications
Recent or current symptoms despite ACE-i, diuretics, dig. and -blockers
Recommended in advanced heart failure (III-IV), in addition to ACE-i and diuretics Hypokalemia
Spironolactone. Practical use

Do not use if hyperkalemia, renal insuf.
Monitor serum K+ at frequent intervals

Start ACE-i first
Start with 25 mg / 24h

If K+ >5.5 mmol/L, reduce to 25 mg / 48h
If K+ is low or stable consider 50 mg / day

New studies in progress
Other Drugs. (only in selected patients)

Inotropics: refractory HF Nitrates: ischemia, angina, pulmonary congestion ARB: Contraindications to ACE-i Antiarrhythmics: (only amiodarone) H risk arrhyth. Anticoagulants: High risk of embolysm Ca channel blockers: (only amlodipine) ischemia
Angiotensin II Receptor Blockers (ARB)

RENIN
Angiotensinogen
Other pathways AT1 Receptor Blockers AT1
Vasoconstriction
Angiotensin I ACE ANGIOTENSIN II
RECEPTORS
AT2
Antiproliferative Action
Proliferative Action
Vasodilatation
Angiotensin II Receptor Blockers (ARB) Candesartan, Eprosartan, Irbesartan Losartan, Telmisartan, Valsartan Efficacy not equal / superior to ACE-I
Not indicated with beta blockers

Indicated in patients intolerant to ACE-I
Vasodilators
VENOUS
Nitrates Molsidomine Venous Vasodilatation
MIXED
Calcium antagonists a-adrenergic Blockers ACE-I, ARBs K+ channel activators Nitroprusside Arterial Vasodilatation
ARTERIAL
Minoxidil Hydralazine
NITRATES HEMODYNAMIC EFFECTS 1- VENOUS VASODILATATION Preload

Pulmonary congestion Ventricular size Vent. Wall stress MVO2
2- Coronary vasodilatation
Myocardial perfusion
3- Arterial vasodilatation
Afterload
Cardiac output Blood pressure
4- Others
Nitrates. Clinical Use

CHF with myocardial ischemia Orthopnea and paroxysmal nocturnal dyspnea In acute CHF and pulmonary edema:NTG sl / iv Nitrates + Hydralazine in intolerance to ACE-I (hypotension, renal insufficiency)
Positive Inotropes
Digitalis Sympathomimetics Catecholamines B-adrenergic agonists Phosphodiesterase inhibitors Amrinone, Milrinone, Enoximone Calcium sensitizers Levosimendan, Pimobendan
Positive Inotropic Therapy May increase mortality Exception: Digoxin, Levosimendan Use only in refractory CHF
NOT for use as chronic therapy
Drugs to Avoid (may increase symptoms, mortality)

Inotropes, long term / intermittent Antiarrhythmics (except amiodarone)
Calcium antagonists (except amlodipine)

Non-steroidal antiinflammatory drugs (NSAIDS) Tricyclic antidepressants Corticosteroids Lithium
NEW DRUGS (ongoing research) 1. New neurohormonal modulators 2. New inotropics 3. Gene therapy
4. Myocyte transplant and mitosis

5. Neoangiogenesis / Growth factors
New Drugs (ongoing research) 1. New neurohormonal modulators Beta-blockers Aldosterone receptor antagonists Angiotensin II receptor antagonists Endothelin inhibitors Vasopresin inhibitors Natriuretic Peptides Endopeptidase inhibitors Vasopeptidase inhibitors
Other Drugs (ongoing research) Erythropoietin Ranolazine Matrix metalloproteinases Growth Hormone L-Thyroxine Inhibitors of carnitine palmitoyltransferse-I Dopamine--hyydroxylase inhibitors Antithrombotics
Refractory End-Stage HF
Review etiology, treatment & aggrav. factors Control fluid retention Resistance to diuretics Ultrafiltration ? iv inotropics / vasodilators during decompensation Consider resynchronization Consider mechanical assist devices Consider heart transplantation
Heart Transplant. Indications

Refractory cardiogenic shock Documented dependence on IV inotropic support to maintain adequate organ perfusion Peak VO2 < 10 ml / kg / min
Severe symptoms of ischemia not amenable to revascularization

Recurrent symptomatic ventricular arrhythmias refractory to all therapeutic modalities Contraindications: age, severe comorbidity
Heart Failure and Myocardial Ischemia

Coronary HD is the cause of 2/3 of HF Segmental wall motion abnormalities are not specific if ischemia Angina coronary angio and revascularization
No angina Search for ischemia and viability in all ? Coronary angiography in all ?
Supraventricular Arrhythmias
Risk of embolization (AF)
Anticoagulation in AF Systolic & diastolic dysfunction Digoxin, beta blockers Amiodarone if b-blocker ineffective/ contraind. Conversion to sinus rhythm in all ? ongoing research
Ventricular Arrhythmias / Sudden Death

Antiarrhythmics ineffective (may increase mortality) Amiodarone do not improve survival
-blockers reduce all cause mortality and SD Control ischemia Control electrolyte disturbances ICD (Implantable Cardiac Defibrillator) In secondary prevention of SD
In sustained, hemodynamic destabilizing VT Ongoing research will establish new indications
Diastolic Heart Failure

Incorrect diagnosis of HF Inaccurate measurement of LVEF Primary valvular disease Restrictive (infiltrative) cardiomyopathies (Amyloidosis) Pericardial constriction Episodic or reversible LV systolic dysfunction Severe hypertension, ischemia High output states: Anemia, thyrotoxicosis, etc Chronic pulmonary disease with right HF Pulmonary hypertension Atrial myxoma LV Hypertrophy Diastolic dysfunction of uncertain origin
Diastolic Heart Failure Treat as HF with low LVEF Control: Hypertension Tachycardia Fluid retention Myocardial ischemia Ongoing research
HEART FAILURE MODELS

CONGESTIVE - Digoxin, Diurtics
HEMODYNAMIC - Vasodilators NEUROHUMORAL - ACE inhibitors, - Blockers, Spironolactone IMMUNOLOGICAL - Cytokine inhibitors
TREATMENT STRATEGIES
Diuretics Vasodilators Inotropics Symptom relief
Neurohumoral activation ACE-is, -blockers Spironolatone ARBs?, ANP? ET-1? Gene therapy?
Prevention of disease progression
Anti-remodeling Reversal strategies of HF
Mann. Circulation 1999; 100: 999-1008
RESYNCHRONISATION THERAPY
2D echo
Chronic Congestive Heart Failure REVERCE OF MITRAL REGURGITATION AFTER RESYNCHRONICATION THERAPY
Cardiac Resynchronization Therapy

Increase the donkeys (heart) efficiency

AHA / ACC Recommendations for the Evaluation of Patients Class I 1. Thorough history and physical examination 2. Patients ability to perform desired activities
3. Volume status (fluid retention, edema)

4. Lab: blood count, electrolytes, creatinine, glucose, 5. Initial 12-lead ECG and chest radiograph 7. Initial 2-D ECHO or radionuclide ventriculography to assess left ventricular systolic function 8. Coronary arteriography in patients with angina
AHA / ACC HF guidelines 2001 http://www.americanheart.org/presenter.jhtml?identifier=11841

AHA / ACC Recommendations for the Evaluation of Patients Class III 1. Routine endomyocardial biopsy 2. Routine Holter monitoring or signal-averaged electrocardiography. 3. Repeat coronary arteriography or noninvasive testing for ischemia in patients with already excluded coronary artery disease 4. Routine measurement of norepinephrine or endothelin

AHA / ACC Recommendations for Patients at High Risk of Developing HF (Stage A) Class I 1. Control of systolic and diastolic hypertension
2. Treatment of lipid disorders 3. Control other risk factors (e.g., smoking, alcohol, drugs)
4. ACE inhibition in patients with a history of atherosclerotic vascular disease, diabetes mellitus, or hypertension
5. Control of ventricular rate in supraventricular arrhythmias
6. Treatment of thyroid disorders

7. Periodic evaluation for signs and symptoms of HF

AHA / ACC Recommendations for Patients at High Risk of Developing HF (Stage A) Class IIa 1. Noninvasive evaluation of left ventricular function in patients with a strong family history of cardiomyopathy or in those receiving cardiotoxic interventions Class III 1. Exercise to prevent the development of HF 2. Reduction of dietary salt beyond that which is prudent 3. Routine testing to detect left ventricular dysfunction 4. Routine use of nutritional supplements

AHA / ACC Recommendations for Patients With Asymptomatic Left Ventricular Systolic Dysfunction (Stage B) Class I 1. ACE inhibition in patients with previous AMI 2. ACE inhibition in patients with a reduced LVEF 3. Beta-blockade in patients with a recent AMI 4. Beta-blockade in patients with a reduced LVEF 5. Valve repair for significant valvular stenosis / regurgitation 6. Regular evaluation for signs and symptoms of HF 7. Also Class I recommendations for patients in Stage A

AHA / ACC Recommendations for Patients With Asymptomatic Left Ventricular Systolic Dysfunction (Stage B)
Class IIb 1. Systemic vasodilators in severe aortic regurgitation Class III
1. Digoxin in patients in sinus rhythm

2. Reduction of dietary salt beyond that which is prudent 3. Exercise to prevent the development of HF
4. Routine use of nutritional supplements


AHA / ACC Recommendations for Treatment of Symptomatic Left Ventricular Systolic Dysfunction (Stage C) Class I 1. Diuretics in patients with fluid retention.
2. ACE inhibition in all patients 3. Beta-blockers in all stable patients 4. Digitalis for the treatment of symptoms of HF 5. Withdrawal of drugs adversely affecting clin. status (most antiarrhythmics, most calcium channel blockers, nonsteroidal anti-inflammatory drugs, )

AHA / ACC Recommendations for Treatment of Symptomatic Left Ventricular Systolic Dysfunction (Stage C) Class IIa 1. Spironolactone in patients with recent or current Class IV symptoms 2. Exercise training to improve clinical status 3. Angiotensin receptor blockade in patients who cannot be given ACE-I because of cough or angioedema 4. Hydralazine and a nitrate in patients who cannot be given ACE-i because of hypotension or renal insufficiency

AHA / ACC Recommendations for Treatment of Symptomatic Left Ventricular Systolic Dysfunction (Stage C) Class IIb 1. Addition of angiotensin receptor blocker to ACE-i 2. Addition of a nitrate to ACE-I in patients Class III 1. Long-term intermittent use inotropics infusion 2. Use of angiotensin blocker instead of ACE-i 3. Use of angiotensin blocker before a beta-blocker 4. Use of Ca channel blocker for HF 5. Routine use of nutritional supplements

AHA / ACC Recommendations for Patients With Refractory End-Stage HF (Stage D) Class I 1. Meticulous identification and control of fluid retention 2. Referral for cardiac transplantation in eligible patients 3. Referral to an HF program 4. Other class I recommendations for Stages A, B, and C

AHA / ACC Recommendations for Patients With Refractory End-Stage HF (Stage D)
Class IIb 1. Pulmonary artery catheter to guide therapy 2. Mitral valve repair for severe secondary mitral regurg. 3. Continuous infusion of inotropics for symptoms
Class III 1. Partial left ventriculectomy 2. Routine intermittent infusions of inotropics

Heart Failure

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Heart Failure

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CHRONIC CONGESTIVE HEART FAILURE

Chronic Congestive Heart Failure

Definition of heart failure

Clinical symptoms / signs secondary to abnormal ventricular function

Chronic Congestive Heart Failure

Congestive heart failure

LV remodelling, a potential reversible phenomenon, alters size, shape and function

Chronic Congestive Heart Failure

ETIOLOGIES OF HEART FAILURE

Chronic Congestive Heart Failure

Structural and functional abnormalities in left ventricular dysfunction

Low EF Large volumes

Normal EF Small volumes

LV mass hypertrophy Loss of myocytes Interstitial fibrosis

Chronic Congestive Heart Failure

Conditions associated to CHF with and without systolic dysfunction

Chronic Congestive Heart Failure

Natural history of CHF

Secondary damage 20% Time (years)

Mann DL. Circulation 1999

Chronic Congestive Heart Failure

Natural history of CHF in hypertension

Left Ventricular Hypertrophy

Diastolic Dysfunction Congestive Heart Failure

Index event High BP Myocardial Ischemia Systolic Dysfunction

Coronary resistance Coronary reserve

Chronic Congestive Heart Failure

Alterations in the remodelled left ventricle

Loss myocytes Fibrosis

Chronic Congestive Heart Failure

DIAGNOSTIC ALGORYTHM FOR IDENTIFY PATIENTS WITH SUSPECTED HEART FAILURE

Chronic Congestive Heart Failure

Diagnosis and Investigation

Chronic Congestive Heart Failure

Clinical Presentations of Heart Failure

Chronic Congestive Heart Failure

What is BNP and How Does It Help?

Chronic Congestive Heart Failure

NORMAL No Heart Failure

NORMAL No Heart Failure

Heart Failure: Systolic / Diastolic

Chronic Congestive Heart Failure

AHA / ACC HF guidelines 2008

Chronic Congestive Heart Failure

Heart disease (any)

Asymptomatic LV dysfunction Systolic / Diastolic

Dyspnea, Fatigue Reduced exercise tolerance

AHA / ACC HF guidelines 2008

Chronic Congestive Heart Failure

AHA / ACC HF guidelines 2008

Chronic Congestive Heart Failure

Chronic Congestive Heart Failure

Chronic Congestive Heart Failure

Treatment Pharmacologic Therapy

ACE inhibitors / ARBs Beta Blockers Diuretics

Chronic Congestive Heart Failure

THE DONKEY ANALOGY

Chronic Congestive Heart Failure

CLINICAL EFFICACY OF ACE INHIBITORS, ARBs, DIURETICS AND VASODILATORS

Chronic Congestive Heart Failure

Chronic Congestive Heart Failure

Chronic Congestive Heart Failure

Chronic Congestive Heart Failure