HEART FAILURE Adapted From: American Heart Association HEART FAILURE Adapted From: American Heart Association

Committee on Post Graduate Education, Council on Clinical Cardiology, American Heart Association Developed in collaboration with the Sociedad Española de Cardiología Prepared by: Ann F. Bolger, MD José López-Sendón, MD The content of these slides is current as of March 2003 Future revisions will be posted on the American Heart Association website ( Committee on Post Graduate Education, Council on Clinical Cardiology, American Heart Association Developed in collaboration with the Sociedad Española de Cardiología Prepared by: Ann F. Bolger, MD José López-Sendón, MD The content of these slides is current as of March 2003 Future revisions will be posted on the American Heart Association website (

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

Epidemiology 5,000,000 patients 5,000,000 patients 6,500,000 hospital days / year6,500,000 hospital days / year 300,000 deaths / year 300,000 deaths / year 10% of people > 65 years 10% of people > 65 years 5.4% of healthcare budget ($28 billion) 5.4% of healthcare budget ($28 billion) Incidence x 2 in last ten years Incidence x 2 in last ten years Gottdiener J et al. JACC 2000;35:1628 Haldeman GA et al. Am Heart J 1999;137:352 Kannel WB et al. Am Heart J 1991;121:951 O’Connell JB et al. J Heart Lung Transplant 1993;13:S107

Suspect Heart Failure Assess presence of CARDIAC DISEASE by PE, EKG, CXR, or BNP ABNORMAL Assess LV FUNCTION by Echocardiogram, Nuclear angiography, or MRI if available ABNORMAL NORMAL No Heart Failure NORMAL Heart Failure

Risk Factors Gottdiener J et al. The Cardiovascular Health Study JACC 2000;35:1628

Direct Causes 1- Myocardial Abnormalities (CHD) 2- Hemodynamic Overload 3- Ventricular Filling Abnormalities 4- Ventricular Dyssynergy 5- Changes in Cardiac Rhythm

Aggravating Factors Medications New Heart Disease Myocardial Ischemia Medications New Heart Disease Myocardial Ischemia Endocarditis Obesity Hypertension Physical Activity Dietary Excess Endocarditis Obesity Hypertension Physical Activity Dietary Excess Pregnancy Arrhythmias (AF) Infections Thromboembolism Hyper/hypothyroidism Pregnancy Arrhythmias (AF) Infections Thromboembolism Hyper/hypothyroidism

Clinical Manifestations Dyspnea: First on exertion, then with progressively less strenuous activity Orthopnea: Increased venous return in the recumbent position PND: multiple factors Nocturnal Angina: Increased cardiac workload, 2º to increased venous return Cheyne Stokes Respiration: Alternating phases of apnea and hyperventilation Fatigue: low cardiac output Peripheral Edema

Physical Exam Findings Left Sided Failure Pulmonary Rales Tachypnea S3 Gallop Cardiac Murmurs (AS, AR, MR) Paradoxical Splitting of S2 Right Sided Failure Jugular Venous Distention Peripheral Edema Peripheral/ Perioral cyanosis Hepatomegaly Ascites Hepatojugular Reflux

Assessment of JVD Shasham, Fadi, and Judith Mitchell, M.D. “Essentials of the Diagnosis of Heart Failure.” American Family Physician, March, 2001.

CXR Findings Cardiomegaly (Cardiothoracic ratio >0.5) Large Hila with indistinct margins Prominence of superior pulmonary veins Fluid in intralobar fissures Kerley B lines Alveolar edema Blunting of Angles

Stage A HF Risk Factors No Heart Disease No Symptoms Stage B Asymptomatic Heart Disease Stage D Refractory HF symptoms Stage C Prior or Current HF Symptoms Stages in the Evolution of Heart Failure Definitions

Stage A HTN, DM, CAD, Obesity, Metabolic Syndrome Stage B MI, LV Dysfunction, Valvular Disease Stage D Symptoms at rest despite max. therapy Stage C Dyspnea, Fatigue, Exercise Tolerance Exercise Tolerance Stages in the Evolution of Heart Failure Clinical Characteristics

Stage A Risk Factor Reduction, ACE-I / ARB in DM & Vascular DZ Stage B ACE-I / ARB, B- Blockers Stage D Mechanical Devices, Heart Transplant Stage C Pharmacologic Therapy, Devices Stages in the Evolution of Heart Failure Treatment

New York Heart Association Classification

Goals of Initial / Ongoing Evaluation Identify Heart Disease Identify Heart Disease Assess Functional Capacity (NYHA, 6 min walk) Assess Functional Capacity (NYHA, 6 min walk) Assess Volume Status (edema, crackles, JVD, hepatomegaly, body weight) Assess Volume Status (edema, crackles, JVD, hepatomegaly, body weight) Testing: Initial: CBC, U/A, CMP, HbA1C, FLP, CXR, EKG, TSH, Echo Periodic: electrolytes, RFP, Echocardiogram Testing: Initial: CBC, U/A, CMP, HbA1C, FLP, CXR, EKG, TSH, Echo Periodic: electrolytes, RFP, Echocardiogram Assess Prognosis Assess Prognosis

> Post MI n=196 < % Cardiac Mortality LVEF Brodie B. et al, Am J Cardiol 1992;69:1113 Prognosis

Treatment Objectives Survival Morbidity Exercise Capacity Quality of Life Neurohormonal Changes Progression of CHF Symptoms Survival Morbidity Exercise Capacity Quality of Life Neurohormonal Changes Progression of CHF Symptoms

Treatment Modalities Prevention, Control of Risk Factors Prevention, Control of Risk Factors Lifestyle Lifestyle Treat Cause / Aggravating Factors Treat Cause / Aggravating Factors Pharmacologic Therapy Pharmacologic Therapy Personal Care / Healthcare Team Personal Care / Healthcare Team Revascularization for Ischemic Causes Revascularization for Ischemic Causes ICD ICD Ventricular Resyncronization Ventricular Resyncronization Ventricular Assist Devices Ventricular Assist Devices Heart Transplant Heart Transplant Artificial Heart Artificial Heart Neoangiogenesis, Gene Therapy, Etc. Neoangiogenesis, Gene Therapy, Etc. All Selected Patients

Pharmacologic Therapy Diuretics ACE Inhibitors Beta Blockers Digitalis Spironolactone Others Diuretics ACE Inhibitors Beta Blockers Digitalis Spironolactone Others

Diuretics Essential to Control Symptoms Essential to Control Symptoms Secondary to Fluid Retention Prevent Decompensation Prevent Decompensation Loops Increase Sodium Excretion up to % Loops Increase Sodium Excretion up to % Thiazides Increase Sodium Excretion by 5 – 10% Thiazides Increase Sodium Excretion by 5 – 10%

Cortex Medulla Thiazides Inhibit active exchange of Cl-Na in the cortical diluting segment of the ascending loop of Henle Thiazides 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 K-sparing Inhibit reabsorption of Na in the distal convoluted and collecting tubule Loop diuretics Inhibit exchange of Cl-Na-K in the thick segment of the ascending loop of Henle Loop diuretics Inhibit exchange of Cl-Na-K in the thick segment of the ascending loop of Henle Loop of Henle Loop of Henle Collecting Tubule Collecting Tubule Diuretics

Diuretics: Indications 1.Symptomatic HF, with Fluid Retention Edema Edema Dyspnea Dyspnea Lung Crackles Lung Crackles Jugular Distension Jugular Distension Hepatomegaly Hepatomegaly Pulmonary edema (Xray) Pulmonary edema (Xray)

Loop Diuretics / Thiazides: Practical Use Start with variable dose. Titrate to achieve dry weight.Start with variable dose. Titrate to achieve dry weight. Monitor serum K + at “frequent intervals.”Monitor serum K + at “frequent intervals.” Reduce dose when fluid retention is controlled.Reduce dose when fluid retention is controlled. Teach the patient when, how to adjust dose.Teach the patient when, how to adjust dose. Combine with ACE-I and B-BlockerCombine with ACE-I and B-Blocker

Loop diuretics: Dose (mg) InitialMaximum InitialMaximum Bumetanide 0.5 to 1.0 / 12-24h 10 / day Furosemide 20 to 40 / 12-24h 400 / day Torsemide 10 to 20 / 12-24h 200 / day

Loop Diuretics / Thiazides: Adverse Effects K +, Mg + ( %) K +, Mg + ( %) Na + Na + Stimulation of Neurohormonal Activity Stimulation of Neurohormonal Activity Hyperuricemia ( %) Hyperuricemia ( %) Hypotension, Ototoxicity, Gastrointestinal Sx, Metabolic Alkalosis Hypotension, Ototoxicity, Gastrointestinal Sx, Metabolic Alkalosis 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

Diuretics: Resistance Neurohormonal Activation Neurohormonal Activation Rebound Na + uptake after Volume Loss Rebound Na + uptake after Volume Loss Hypertrophy of Distal Nephron Hypertrophy of Distal Nephron Reduced Tubular Secretion (renal failure, Reduced Tubular Secretion (renal failure, NSAIDs) NSAIDs) Decreased Renal Perfusion (low output) Decreased Renal Perfusion (low output) Altered Absortion Altered Absortion Noncompliance Noncompliance Brater NEJM 1998;339:387 Kramer et al. Am J Med 1999;106:90

Managing Resistance to Diuretics Restrict Na + /H 2 O intake Restrict Na + /H 2 O intake Increase Dose Increase Dose Combine: furosemide + thiazide / spiro / metolazone Combine: furosemide + thiazide / spiro / metolazone Dopamine (increase cardiac output) Dopamine (increase cardiac output) Reduce Dose of ACE-I Reduce Dose of ACE-I Ultrafiltration Ultrafiltration Motwani et al Circulation 1992;86:439

VASOCONSTRICTION VASODILATATION Kininogen Kallikrein Inactive Fragments Angiotensinogen Angiotensin I RENIN Kininase II Inhibitor ALDOSTERONE SYMPATHETIC VASOPRESSIN PROSTAGLANDINS tPA ANGIOTENSIN II BRADYKININ ACE-I: Mechanism of Action A.C.E.

ACE-I: Clinical Effects Improve Symptoms Reduce Remodeling / Progression Reduce Hospitalization Improve Survival Improve Symptoms Reduce Remodeling / Progression Reduce Hospitalization Improve Survival

Mortality Reduction with ACE-I StudyACE-IClinical Seting CONSENSUSEnalaprilCHF SOLVD treatment EnalaprilCHF AIRERamiprilCHF Vheft-IIEnalaprilCHF TRACETrandolaprilCHF / LVD SAVECaptoprilLVD SMILEZofenoprilHigh Risk HOPERamiprilHigh Risk

Placebo Enalapril Probability of Death Months p< CONSENSUS N Engl J Med 1987;316:1429

Months p = % Mortality Enalapril n=1285 Enalapril n=1285 Placebo n=1284 Placebo n=1284 N Engl J M 1991;325:293 NYHA II-III EF < 35% NYHA II-III EF < 35% SOLVD (Treatment)

% Mortality 4 4 N Engl J Med 1992;327:669 Years Placebo Captopril 0 0 n=1115 n=1116 p=0.019 ² -19% days post AMI EF < 40% Captopril mg/day days post AMI EF < 40% Captopril mg/day Asymptomatic Ventricular Dysfunction Post MI Asymptomatic Ventricular Dysfunction Post MI SAVE

Months Placebo Ramipril HFS/PAMI p = % Mortality Lancet 1993;342:821 AIRE

Symptomatic Heart Failure Asymptomatic Ventricular Dysfunction - LVEF < 40% Selected High Risk Subgroups Symptomatic Heart Failure Asymptomatic Ventricular Dysfunction - LVEF < 40% Selected High Risk Subgroups ACE-I: Indications

ACE-I: Practical Use Start with very low doseStart with very low dose Increase dose if well toleratedIncrease dose if well tolerated Renal function & serum K + after 1-2 wksRenal function & serum K + after 1-2 wks Avoid fluid retention / hypovolemia (diuretic use)Avoid fluid retention / hypovolemia (diuretic use) Dose NOT determined by symptomsDose NOT determined by symptoms Combine to overcome “resistance”Combine to overcome “resistance”

ACE-I: Dose (mg) InitialMaximum InitialMaximum Captopril 6.25 / 8h 50 / 8h Enalapril 2.5 / 12 h 10 to 20 / 12h Fosinopril 5 to 10 / day 40 / day Lisinopril 2.5 to 5.0 / day 20 to 40 / day Quinapril 10 / 12 h40 / 12 h Ramipril 1.25 to 2.5 / day 10 / day

ACE-I: Adverse Effects Hypotension (1st dose effect) Hypotension (1st dose effect) Worsening Renal Function Worsening Renal Function Hyperkalemia Hyperkalemia Cough Cough Angioedema Angioedema

ACE-I: Contraindications Intolerance (angioedema, anuric renal failure) Bilateral Renal Artery Stenosis Pregnancy Renal Insufficiency (creatinine > 2 mg/dL) Hyperkalemia (> 5.5 mmol/l) Severe Hypotension ACE-I: Contraindications Intolerance (angioedema, anuric renal failure) Bilateral Renal Artery Stenosis Pregnancy Renal Insufficiency (creatinine > 2 mg/dL) Hyperkalemia (> 5.5 mmol/l) Severe Hypotension

RENIN Angiotensinogen Angiotensin I ANGIOTENSIN II Angiotensin I ANGIOTENSIN II ACE Other pathways Vasoconstriction Proliferative Action Proliferative Action Vasodilatation Antiproliferative Action Antiproliferative Action AT1 AT2 AT1 Receptor Blockers AT1 Receptor Blockers RECEPTORS Angiotensin II Receptor Blockers (ARB)

For Patients who can not take ACE-I “Reasonable Alternative” to ACE-I Similar in Benefit to ACE-I –CHARM Less Studied than ACE-I Combined with ACE-I may Decrease Morbidity and Mortality???

ARB: Indications StageA B C

ARB: Dose (mg) InitialTarget Candesartan4 – 8 / d32 / d Losartan25 – 50 / d50 – 100 / d Valsartan20 – 40 BID160 BID

ß-Blockers: Mechanism of action Density of ß 1 Receptors Inhibit Cardiotoxicity of Catecholamines Neurohormonal Activation HR Antiischemic Antihypertensive Antiarrhythmic Antioxidant, Antiproliferative Density of ß 1 Receptors Inhibit Cardiotoxicity of Catecholamines Neurohormonal Activation HR Antiischemic Antihypertensive Antiarrhythmic Antioxidant, Antiproliferative

ß-Blockers: Clinical Effects Improve Symptoms (only long term) Reduce Remodelling / Progression Reduce Hospitalization Reduce Sudden Death Improve Survival Improve Symptoms (only long term) Reduce Remodelling / Progression Reduce Hospitalization Reduce Sudden Death Improve Survival

NEJM 1996; 334: Carvedilol(n=696) Placebo(n=398) Risk Reduction = 65% p< US Carvedilol HF % Survival Days NYHAI-II

P< Days Bisoprolol11.8% Placebo17.3% Survival NYHAIII-IV Lancet 1999;353:9 CIBIS-II

Lancet 1999; 353: 2001 Months % Mortality Placebo Metoprolol p= Risk Reduction 34% MERIT-HF NYHAII-IV

Placebo Carvedilol Months NYHAIII-IV NEJM 2001;344:1651 % Survival COPERNICUS p= Risk Reduction 34%

1 Survival Years Carvedilol 116 / 975 (12%) Placebo 151 / 984 (15%) HR 0.77 ( ) p<0.031 Lancet 2001;357:1385 CAPRICORN HFPostAMI

Symptomatic Heart Failure Asymptomatic Ventricular Dysfunction - LVEF < 35% After AMI Symptomatic Heart Failure Asymptomatic Ventricular Dysfunction - LVEF < 35% After AMI ß-Blockers: Indications Stage AB C

Patient Stable Patient Stable No physical evidence of fluid retention No physical evidence of fluid retention No need for IV inotropic drugs No need for IV inotropic drugs Start ACE-I / Diuretic First Start ACE-I / Diuretic First No Contraindications No Contraindications In Hospital or not In Hospital or not ß-Blockers: When to Start

InitialTarget Bisoprolol 1.25 / 24h 10 / 24h Carvedilol / 12h25 / 12h Metoprolol tartrate6.25 / 12h 75 / 12h Start Low, Increase Slowly Start Low, Increase Slowly Increase the dose every weeks Increase the dose every weeks ß-Blockers: Dose (mg)

Hypotension Hypotension Fluid Retention / Worsening Heart Failure Fluid Retention / Worsening Heart Failure Fatigue Fatigue Bradycardia / Heart Block Bradycardia / Heart Block ß-Blockers: Adverse Effects Review Treatment (+/-diuretics, other drugs) Review Treatment (+/-diuretics, other drugs) Reduce Dose Reduce Dose Consider Cardiac Pacing Consider Cardiac Pacing Discontinue Beta Blocker only in Severe Cases Discontinue Beta Blocker only in Severe Cases

ß-Blockers: Contraindications Asthma (reactive airway disease) Asthma (reactive airway disease) AV block (unless pacemaker) AV block (unless pacemaker) Symptomatic Hypotension / Bradycardia Symptomatic Hypotension / Bradycardia Diabetes is NOT a contraindication Diabetes is NOT a contraindication

Digitalis: Mechanism of Action Blocks Na + / K + ATPase => Ca + + Inotropic effect Inotropic effect Natriuresis Natriuresis Neurohormonal control Neurohormonal control - Plasma Noradrenaline - Peripheral Nervous System Activity - RAAS Activity - Vagal Tone - Normalizes Arterial Baroreceptors NEJM 1988;318:358

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

Digitalis: Clinical Effects Improve Symptoms Modest Reduction in Hospitalization Does Not Improve Survival Improve Symptoms Modest Reduction in Hospitalization Does Not Improve Survival

Placebo n=3403 Placebo n=3403 Digoxin n=3397 Digoxin n= % Mortality N Engl J Med 1997;336:525 Months p = 0.8 DIG NYHA II-III NYHA II-III

Digitalis: Indications When no adequate response to When no adequate response to ACE-I + diuretics + beta-blockers ACE-I + diuretics + beta-blockers In combination with ACE-I + diuretics In combination with ACE-I + diuretics if persisting symptoms if persisting symptoms AFib, to slow AV conduction AFib, to slow AV conduction Dose to mg / day

Digoxin toxicity Advanced A-V block without pacemaker Bradycardia or sick sinus without PM PVC’s and VT Marked hypokalemia WPW with atrial fibrillation Digoxin toxicity Advanced A-V block without pacemaker Bradycardia or sick sinus without PM PVC’s and VT Marked hypokalemia WPW with atrial fibrillation Digitalis: Contraindications

ALDOSTERONE Retention Na + Retention H 2 O Excretion K + Excretion Mg 2+ Retention Na + Retention H 2 O Excretion K + Excretion Mg 2+ Collagen depositionFibrosis - myocardium - myocardium - vessels - vessels Spironolactone Edema Arrhythmias Competitive antagonist of the aldosterone receptor (myocardium, arterial walls, kidney) Competitive antagonist of the aldosterone receptor (myocardium, arterial walls, kidney) Aldosterone Inhibitors -

Aldactone Placebo Survival months p < Annual Mortality Aldactone 18%; Placebo 23% NYHAIII-IV NEJM 1999;341:709 RALES

Spironolactone: Indications LV Dysfunction Early After MILV Dysfunction Early After MI Moderately Severe or Severe HF with Recent DecompensationModerately Severe or Severe HF with Recent Decompensation HypokalemiaHypokalemia

Spironolactone: Practical Use Do not use if hyperkalemia, renal insuf.Do not use if hyperkalemia, renal insuf. Monitor serum K + at “frequent intervals”Monitor serum K + at “frequent intervals” Start ACE-I firstStart ACE-I first Start with mg / 24hStart with mg / 24h If K + >5.5 mmol/L, reduce to 25 mg / 48hIf K + >5.5 mmol/L, reduce to 25 mg / 48h If K + is low or stable consider 50 mg / dayIf K + is low or stable consider 50 mg / day

1- VENOUS VASODILATATION Preload 2- Coronary vasodilatation Myocardial perfusion 3- Arterial vasodilatation Afterload 4- Others 1- VENOUS VASODILATATION Preload 2- Coronary vasodilatation Myocardial perfusion 3- Arterial vasodilatation Afterload 4- Others Pulmonary congestion Ventricular size Vent. Wall stress MVO 2 NITRATES HEMODYNAMIC EFFECTS Cardiac output Blood pressure

0.6 Probability of Death Probability of Death 0 0 Placebo (273) Prazosin (183) Hz + ISDN (186) Months N Engl J Med 1986;314:1547 VHefT-1 ( Nitrates)

0,54 0, Months p = 0.08 Enalapril HZ + ISDN n = 804 p = ProbabilityofDeath V-HeFT II Nitrate + Hydralazine) V-HeFT II ( Nitrate + Hydralazine) N Engl J Med 1991; 325:303

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) 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 Digitalis Sympathomimetics Sympathomimetics Catecholamines Catecholamines B-adrenergic agonists B-adrenergic agonists Phosphodiesterase inhibitors Phosphodiesterase inhibitors Amrinone, Milrinone, Enoximone Amrinone, Milrinone, Enoximone Calcium sensitizers Calcium sensitizers Levosimendan, Pimobendan Levosimendan, Pimobendan

May increase mortality Exception: Digoxin, Levosimendan Use only in refractory CHF NOT for use as chronic therapy May increase mortality Exception: Digoxin, Levosimendan Use only in refractory CHF NOT for use as chronic therapy Positive Inotropic Therapy

Inotropes, long term / intermittent Inotropes, long term / intermittent Antiarrhythmics (except amiodarone) Antiarrhythmics (except amiodarone) Calcium Channel Blockers Calcium Channel Blockers Non-steroidal antiinflammatory drugs (NSAIDS) Non-steroidal antiinflammatory drugs (NSAIDS) Tricyclic antidepressants Tricyclic antidepressants Corticosteroids Corticosteroids Lithium Lithium Drugs to Avoid (may increase symptoms, mortality)

Refractory End-Stage HF Review etiology, treatment & aggrav. factors Review etiology, treatment & aggrav. factors Control fluid retention Control fluid retention Resistance to diuretics Resistance to diuretics Ultrafiltration ? Ultrafiltration ? IV inotropics / vasodilators during decompensation IV inotropics / vasodilators during decompensation Consider resynchronization Consider resynchronization Consider mechanical assist devices Consider mechanical assist devices Consider heart transplantation Consider heart transplantation

Heart Transplant: Indications Refractory cardiogenic shock Refractory cardiogenic shock Documented dependence on IV inotropic support to maintain adequate organ perfusion Documented dependence on IV inotropic support to maintain adequate organ perfusion Peak VO2 < 10 ml / kg / min Peak VO2 < 10 ml / kg / min Severe symptoms of ischemia not amenable to revascularization Severe symptoms of ischemia not amenable to revascularization Recurrent symptomatic ventricular arrhythmias refractory to all therapeutic modalities Recurrent symptomatic ventricular arrhythmias refractory to all therapeutic modalities Contraindications: age, severe comorbidity

Supraventricular Arrhythmias Risk of embolization (AF) Risk of embolization (AF) Anticoagulation in AF Anticoagulation in AF Systolic & diastolic dysfunction Systolic & diastolic dysfunction Digoxin, beta blockers Digoxin, beta blockers Amiodarone if b-blocker ineffective/ contraind. Amiodarone if b-blocker ineffective/ contraind.

Ventricular Arrhythmias / Sudden Death Antiarrhythmics ineffective (may increase mortality) Antiarrhythmics ineffective (may increase mortality) Amiodarone does not improve survival  -blockers reduce all cause mortality and SD  -blockers reduce all cause mortality and SD Control ischemia Control ischemia Control electrolyte disturbances Control electrolyte disturbances ICD (Implantable Cardiac Defibrillator) ICD (Implantable Cardiac Defibrillator) In secondary prevention of sudden death In secondary prevention of sudden death In sustained, hemodynamic destabilizing VT In sustained, hemodynamic destabilizing VT In LVEF < 30% and mild - moderate HF symptoms In LVEF < 30% and mild - moderate HF symptoms

Diastolic Heart Failure Incorrect diagnosis of HF Incorrect diagnosis of HF Inaccurate measurement of LVEF Inaccurate measurement of LVEF Primary valvular disease Primary valvular disease Restrictive (infiltrative) cardiomyopathies (Amyloidosis…) Restrictive (infiltrative) cardiomyopathies (Amyloidosis…) Pericardial constriction Pericardial constriction Episodic or reversible LV systolic dysfunction Episodic or reversible LV systolic dysfunction Severe hypertension, ischemia Severe hypertension, ischemia High output states: Anemia, thyrotoxicosis, etc High output states: Anemia, thyrotoxicosis, etc Chronic pulmonary disease with right HF Chronic pulmonary disease with right HF Pulmonary hypertension Pulmonary hypertension Atrial myxoma Atrial myxoma LV Hypertrophy LV Hypertrophy Diastolic dysfunction of uncertain origin Diastolic dysfunction of uncertain origin

Diastolic Heart Failure Treat as HF with low LVEF Treat as HF with low LVEF Control: Control: Hypertension Hypertension Tachycardia Tachycardia Fluid Retention Fluid Retention Myocardial Ischemia Myocardial Ischemia Ongoing Research Ongoing Research

Treatment Summary SymptomsMorbidityMortality Increase Dose of ACEI No effect ↓ 10-15% No effect Add ARB ↓↓ 10-15% No effect Add ß- blocker ↓↓ 20-35%↓ 35%+ Add Aldactone ↓↓ 20%↓ 16-25% Add ISDN+ Hydralazine ↓↓ 30%↓ 40% AHA Scientific Sessions, 2004 (Lachel et al)