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Heart Failure: Evaluation and Treatment

Anecita Fadol, PhD, RN,FNP-BC Nurse Practitioner Department of Cardiology UT MD Anderson Cancer Center

Objectives
Identify the different types of cardiomyopathy Describe the pathophysiologic mechanism of cardiomyopathy/heart failure Discuss diagnostic testing/procedures for heart failure diagnosis

Discuss the clinical guidelines for the management of heart failure.

Case Examples
A 16 year old male with a history of pneumonia. He was brought to the clinic by his mother because he did not seem to get better after 8 weeks since the initial flu like symptoms. Last night he had severe fatigue and shortness of breath while brushing his teeth.

A 63 year old female with a known history of breast cancer, treated with anthracycline-based chemotherapy 30 years ago. Recently, she noted progressively increasing shortness of breath with exertion, PND and lower extremity swelling.

Cardiomyopathy and Heart Failure

Cardiomyopathy is a weakening or deformity of the heart muscle that causes decreased pumping force.

AHA, 2008a; DeMartinis et al, 2003; Hunt et al, 2005; Yahalom et al, 2005

Risk Factors for Cardiomyopathy/HF


Major causes of CMP/HF
Ischemic heart disease (e.g., coronary artery disease) Nonischemic underlying diseases (e.g., hypertension, valvular heart disease)

Risk factors for cardiomyopathy/HF


History of or active coronary artery disease Hypertension (75% of patients) Genetic predisposition, congenital heart defects Diabetes Valvular heart disease Thyroid disease Hyperlipidemia Sleep apnea Overweight (elevated body mass index [BMI]) Sedentary lifestyle Advanced age Viral Others (e.g., smoking, alcohol, illicit or therapeutic cardiotoxic drugs)

Chang, 2007; DeMartinis et al, 2003; Hunt et al, 2005

Non ischemic Cardiomyopathy

Heart Failure (HF) Definition

A complex clinical syndrome in which the heart is incapable of maintaining a cardiac output adequate to accommodate metabolic requirements and the venous return.

The Donkey Analogy


Ventricular dysfunction limits a patient's ability to perform the routine activities of daily living

Epidemiology of HF in the US
12 10 8 6 4 2 0 1991 2001 2037

10

HF Patients in US (millions)

5 million symptomatic patients in 2001; estimated 10 million in 20371,2 Incidence: about 550,000 new cases/year2 Prevalence is 1% between the ages of 50 and 59 years3; progressively increasing to 10% over age 804

5 3.5

1Adapted

from Gilbert E. Rev Cardiovasc Med. 2002;3:S42-S47. 2American Heart Association. 2004 Heart and Stroke Statistical Update. 2003. 3Ho KKL et al. J Am Coll Cardiol. 1993;22:6A-13A. 4Rich M. J Am Geriatric Soc. 1997;45:968-974.

Part I: Pathophysiology of Heart Failure

Pathological Progression of CV Disease 1


Endothelial Dysfunction CAD CM HTN Valvular Dz Chemo
Neurohormonal stimulation Endothelial dysfunction Myocardial toxicity Vasoconstriction Renal sodium retention
1 Adapted from Cohn JN. N Engl J Med. 1996;335:490498. 2 He J, Ogden LG, Bazzano LA, et al. Risk Factors for Congestive Heart Failure in US Men and women: NHANES I epidemiologic follow-up study. Arch Intern Med 2001, 161: 996-1002.

Arrhythmia

Left ventricular injury

Pathologic remodeling

Low ejection fraction

Death

Pump failure

Symptoms: Dyspnea Fatigue Edema

Chronic heart failure

Left Ventricular Dysfunction


Systolic: Impaired contractility/ejection
Approximately two-thirds of heart failure patients have systolic dysfunction1

Diastolic: Impaired filling/relaxation

30%
(EF > 40 %) (EF < 40%)

70%

Diastolic Dysfunction Systolic Dysfunction


1 Lilly, L. Pathophysiology of Heart Disease. Second Edition p 200

Classification of HF: Comparison Between ACC/AHA HF Stage and NYHA Functional Class
Asymptomatic
ACC/AHA HF Stage1

A At high risk for HF but without structural heart disease or symptoms of HF (eg, patients with HTN or CAD)

NYHA Functional Class2


I Asymptomatic II Symptomatic with moderate exertion

B Structural heart disease but without symptoms of HF

C Structural heart disease with prior or current symptoms of HF

III Symptomatic with minimal exertion

D Refractory HF requiring specialized interventions

IV Symptomatic at rest

Symptomatic
1Hunt

SA et al. J Am Coll Cardiol. 2005;38:2101-2113. 2New York Heart Association/Little Brown and Company, 1964. Adapted from: Farrell MH et al. JAMA. 2002;287:890-897.

Part II: Assessing Heart Failure

Cardiac Assessment

A comprehensive cardiac assessment includes the following:


Patient history Physical assessment Diagnostic testing

Cardiac Assessment: Diagnostic Testing


Initial diagnostic evaluation for HF patient
Echocardiogram (ECHO) Electrocardiogram Chest x-ray Standard laboratory tests
Blood chemistry, urinalysis Complete blood count (CBC) Renal, liver, thyroid tests

Measures heart size, wall thickness/mobility, flow gradients, valvular function, LVEF
Assesses cardiac rhythm, conduction; can detect myocardial infarction, arrhythmias Detects heart enlargement, fluid around heart or lungs Blood urea nitrogen (BUN), creatinine, albumin (liver function), glucose (diabetes) CBC detects anemia, infection Organ function as a contributing factor or resulting from HF Creatinine kinase (CK, CK-MB), cardiac troponins I and T Brain natriuretic peptide (BNP)

Cardiac enzymes Cardiac markers

Follow-up: Assess signs and symptoms, functional capacity, body weight, understanding of treatment, compliance, exacerbating factors for HF

DeMartinis et al, 2003; Chang, 2007; Fadol, 2006; Hunt et al, 2005

Part III: Current Treatment of Heart Failure

The Vicious Cycle of Heart Failure Management

Chronic HF
Diurese & Home SOB Weight

Hospitalization
IV Lasix or Admit

MDs Office
PO Lasix

Emergency Room

Goals of Heart Failure Therapy


Relieve heart failure symptoms Improve overall clinical status

Stabilize acute episodes of decompensation


Decrease morbidity and mortality Slow and/or reverse disease progression Identify and treat reversible causes of LV dysfunction

General Approach to Treatment


Determine etiology and/or precipitating factors
Avoid drugs which may aggravate HF

Treat underlying disorders


Anemia, hypo/hyperthyroidism, valvular disease Revascularization or anti-ischemic therapy in patients with CAD may reduce symptoms of HF

Physical activity (low-intensity) if stable Restrict fluid (~2 L/day) and sodium intake (<1.5-2 g/day)

Established Therapy: Drugs with a mortality benefit in HF


Beta-blockers

Angiotensin converting enzyme (ACE) inhibitors


Angiotensin Receptor Blocker (Candesartan) Spironolactone or Eplerenone Isordil/Hydralazine

Digoxin
Mechanism of action:
contractility
Inhibition of sodium/potassium ATPase pump which acts to increase intracellular sodium-calcium exchange to increase intracellular calcium leading to increased contractility

Neurohormonal
Blunt SNS activation Increase vagal tone Slow conduction, prolong AV refractoriness, slowing ventricular response in atrial fibrillation

Pharmacologic Management
Digoxin Enhances inotropy of cardiac muscle Reduces activation of SNS and RAAS

Controlled trials have shown long-term digoxin therapy:


Reduces symptoms Increases exercise tolerance Improves hemodynamics Decreases risk of HF progression Reduces hospitalization rates for decompensated HF Does not improve survival

Digoxin
Warnings/Precautions
Acute myocardial infarction Acute myocarditis or amyloid cardiomyopathy

Correct electrolyte imbalances


Adjust dose in renal disease Bradycardia Withdrawal in CHF patients may lead to recurrent CHF symptoms Drug interactions Digoxin toxicity

Digitalis Compounds
Like the carrot placed in front of the donkey

Pharmacologic Management
Diuretics Used to relieve fluid retention

Improve exercise tolerance


Facilitate the use of other drugs indicated for heart failure Patients can be taught to adjust their diuretic dose based on changes in body weight Electrolyte depletion a frequent complication Should never be used alone to treat heart failure

Higher doses of diuretics are associated with increased mortality

Diuretics
Diuretics and salt restriction are indicated in patients with current or prior symptoms of HF and reduced LVEF who have evidence of fluid retention (Class I; LOE C)
Use until euvolemic stage is achieved
Continue to prevent recurrence of fluid retention

Increase urinary sodium excretion

Improve pulmonary and peripheral congestion


Decrease preload

No long-term studies
Effects on morbidity and mortality are unknown
ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult http://www.acc.org/clinical/guidelines/failure/hf_index.htm

Dosing Oral Diuretics

ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult http://www.acc.org/clinical/guidelines/failure/hf_index.htm

Dosing IV Diuretics

ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult http://www.acc.org/clinical/guidelines/failure/hf_index.htm

ACE inhibitors
Mechanism of action:
preload and afterload Arterial and venous dilatation
Reduces formation of Angiotension II (vasoconstrictor) Reduces breakdown of bradykinin (vasodilator)

Clinical Effects:
Improve symptoms Reduce remodeling / progression Reduce hospitalization Improve survival

Ace Inhibitors
Recommendations
ACEIs are recommended for all patients with current or prior symptoms of HF and reduced LVEF , unless contraindicated (Class I; LOE A) ACEIs should be used in all patients with reduced LVEF and no symptoms of HF, even if they have not experienced MI (Class I; LOE A) ACEIs or ARBs can be beneficial in patients with HTN and LVH and no symptoms of HF (Class IIa; LOE B)

ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult

http://www.acc.org/clinical/guidelines/failure/hf_index.htm

Effect of ACE Inhibitors on Survival in Heart Failure

Cumulative Mortality

20 15 10 5 0
Placebo Enalapril

Cumulative Predictability of Death

25
Mortality From All Causes (%)

P=0.30

0.75 0.5
Enalapril

P<0.0036

0.8 0.6 0.4 0.2 0


Placebo

P<0.003

0.25
Hydralazine Isosorbide Dinitrate

Enalapril

12

24

36

48

0
0 6 12 18 24 30 36 42 48 54 60 Months

0 1 2 3 4 5 6 7 8 910 11 12
Months

Months

SOLVD-P NYHA Class Treatment Results


1The

SOLVD-T Class II-III (N=2569) Enalapril 16%

CONSENSUS Class IV (N=253) Enalapril 27%

Class I-II (N=4228) Enalapril 8% (% reduction in all-cause mortality)

SOLVD Investigators. N Engl J Med. 1991;325:293-302. 2Cohn J et al. N Engl J Med. 1991;325:303-310. 3The CONSENSUS Trial Study Group. N Engl J Med. 1987;316;1429-1435.

ACE inhibitors
ACEI
Captopril

Initial Dose
6.25 mg tid

Maximum Dose
50 mg tid

Enalapril
Fosinopril Lisinopril Quinapril Ramipril Trandolapril

2.5 mg bid
5-10 mg daily 2.5-5 mg daily 5 mg bid 1.25-2.5 mg daily 1 mg daily

10-20 mg bid
40 mg daily 20-40 mg daily 20 mg bid 10 mg daily 4 mg daily

ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult

http://www.acc.org/clinical/guidelines/failure/hf_index.htm

Ace Inhibitors
Contraindications:
Hypersensitivity Angioedema related to previous treatment with ACEI

Warnings/Precautions:
Anaphylactic reactions can occur Angioedema can occur at any time during treatment, especially after 1st dose

Hereditary angioedema
Bilateral renal artery stenosis Pregnancy (2nd and 3rd trimester)

Careful BP monitoring with 1st dose (hypotension)


Captopril>Lisinopril>Enalapril

May cause hyperkalemia, rise in Scr

Principles of ACEI therapy


Occurrence of ARF should prompt a search for:
Hypotension (MAP <65 mmHg), volume depletion, or nephrotoxin administration
Correct or remove these factors

Consider bilateral renal artery stenosis

ACEIs should be discontinued temporarily while precipitating factors for ARF are corrected
ARBs are not an appropriate substitute under these conditions!!! ACEI therapy can be reinstituted once these factors are corrected

Hyperkalemia is a potential complication, particularly in patients with DM or CRF


Monitor K+ early after initiation of therapy, reduce dietary K+, avoid agents that aggravate hyperkalemia

ACE inhibitors
Start with a low dose Increase dose if well tolerated (hold parameters for BP and HR) Dose NOT determined by symptoms, titrate to target dose

Monitor renal function & serum K+


Avoid initiating while volume depleted

Diuretics, ACE Inhibitors


Reduce the number of sacks on the wagon

ARBs
Recommendations
ARBs approved for the treatment of HF are recommended in patients with current or prior symptoms of HF and reduced LVEF who are ACEI intolerant (Class I; LOE A) ARBs are reasonable to use as alternatives to ACEIs as 1st line therapy for patients with mild to moderate H F and reduced LVEF, especially for patients already taking ARBs for other indications (Class IIa; LOE A) The addition of an ARB may be considered in persistently symptomatic patients with reduced LVEF who have already been treated with conventional therapy (Class IIb; LOE B)
ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult

http://www.acc.org/clinical/guidelines/failure/hf_index.htm

ARBs

ARB Candesartan Losartan


Not FDA approved

Initial Dose 4-8 mg daily 25-50 mg day


20-40 mg bid

Maximum Dose 32 mg daily 50-100 mg day


160 mg bid

Valsartan

ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult

http://www.acc.org/clinical/guidelines/failure/hf_index.htm

Beta-blockers
Recommendations
Beta-blockers and ACEIs should be used in all patients with recent or remote history of MI regardless of EF or presence of HF (Class I: LOE A) Beta-blockers are indicated in all patients without a history of MI who have reduced LVEF with no HF symptoms(Class I: LOE C)

ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adul

http://www.acc.org/clinical/guidelines/failure/hf_index.htm

Pharmacologic Management
Beta-Blockers Cardioprotective effects due to blockade of excessive SNS stimulation In the short-term, beta blocker decreases myocardial contractility; increase in EF after 1-3 months of use Long-term, placebo-controlled trials have shown symptomatic improvement in patients treated with certain beta-blockers1 When combined with conventional HF therapy, betablockers reduce the combined risk of morbidity and mortality, or disease progression1
1 Hunt, SA, et al ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult, 2001 p. 20.

Beta-blockers
Mechanism of action:
Density of 1 receptors Neurohormonal activation

Slow/reverse ventricular remodeling


Decreased myocyte death from catecholamine- induced necrosis or apoptosis HR Symptomatic worsening of HF Low doses, slow upward titration

Antiischemic Antihypertensive

Antiarrhythmic
Antioxidant, Antiproliferatiev

Beta-blockers
Increase EF Decrease ventricular mass

Reduce systolic and diastolic volumes


Decrease hospitalization and mortality
Greater benefit seen at higher doses

Even low doses of B-blockade can have a dramatic effect


Ejection Fraction*
8 LVEF (EF units) 6

2 0 Placebo 6.25 mg bid 12.5 mg bid Carvedilol


Patients receiving diuretics, ACE inhibitors, digoxin; follow-up 6 months; placebo (n=84), carvedilol (n=261). *Results from the Multicenter Oral Carvedilol Heart Failure Assessment (MOCHA) trial (n=345).
P.005

25 mg bid

vs placebo. vs placebo. Adapted from Bristow MR et al. Circulation. 1996;94:28072816.


P.0001

Effects of Beta-Blockers on Mortality


1.0
b -blocker 1.0 b -blocker 1.0 b -blocker

Mortality

0.8

Placebo Risk 34 %

Placebo 0.8 Risk 34 % 0.6 P <0.0001 P=0.006 0 1 MERIT-HF II - IV (N=3391) LVEF 40% Metoprolol CR/XL 34% 2 0.6 0.8

Placebo

Risk 35 %

0.6

P<0.00013 0 1 2

Time (years)

1 CIBIS II

COPERNICUS IV (N=2289) LVEF 25% Carvedilol 35%

NYHA Class III-IV (N=2647) Entry criteria LVEF 35% Treatment Bisoprolol Results 34% (% reduction in death)

1. CIBIS II Investigators and Committees. Lancet. 1999;353:9-13. 2. MERIT-HF Study Group. Lancet. 1999;353:2001-2007. 3. Packer M et al. N Engl J Med. 2001;344:1651-1658.

Beta-blockers
Recommendations

Beta-blockers and ACEIs should be used in all patients with recent or remote history of MI regardless of EF or presence of HF (Class I: LOE A) Beta-blockers are indicated in all patients without a history of MI who have reduced LVEF with no HF symptoms(Class I: LOE C)

ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult http://www.acc.org/clinical/guidelines/failure/hf_index.htm

Beta-blockers
Medication Mechanism of action b1-selective NYHA Class III-IV Initial dose Target Dose

Bisoprolol (Zebeta)
not FDA-approved

1.25 mg/day

10 mg/day

Carvedilol (Coreg) Coreg CR Metoprolol succinate (Toprol XL)

Non-selective b-blocker, 1blocker b1-selective

II-IV

3.125 mg bid

25 mg bid (< 85 kg) 50 mg bid (> 85 kg)

II-III

10 mg/day 12.5-25 mg day

80 mg/day 200 mg/day

-Blockers
Limit the donkeys speed, thus saving energy

Beta-blockers
Contraindications:
Cardiogenic shock, symptomatic hypotension Hypersensitivity Bradycardia HR<45 2nd and 3rd degree heart block; (P-R interval greater than or equal to 0.24 sec) unless pacemaker places

Beta-blockers
Warnings/Precautions:
Anesthesia/surgery (myocardial depression) Bronchospastic disease (less with cardioselective agents)

Decompensated HF
May mask s/sx hypoglycemia May mask signs of hyperthyroidism/thyrotoxicosis PVD use with caution since may aggravate arterial insufficiency Avoid abrupt withdrawal (may result in hypertension, tachycardia, ischemia, angina, MI, and sudden death) discontinue over 1-2 weeks

Pharmacologic Management
Aldosterone Antagonists Generally well-tolerated Shown to reduce heart failure-related morbidity and mortality Generally reserved for patients with NYHA Class III-IV HF Side effects include hyperkalemia and gynecomastia. Potassium and creatinine levels should be closely monitored

Aldosterone Antagonists
Randomized Aldactone Evaluation Study (RALES)
30% relative risk reduction in all-cause mortality and 35% reduction in hospitalizations

The Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival (EPHESUS) Trial
15% relative risk reduction in all-cause mortality and hospitalizations for HF

N Engl J Med. 1999;341(10):709-17. N Engl J Med. 2003;348(14):1309-21.

Effect of Spironolactone on Survival (Aldosterone blockade)


1.00

P<0.001
Probability of Survival 0.90 Spironolactone 0.80 0.70 0.60 Placebo 0.50 0.00 0 3 6 9 12 15 18 21 24 27 30 33 36 Months

Study Design NYHA Class III-IV (N= 1663) EF 35% Frequent monitoring of potassium Result: 30% reduction in death

Pitt B et al. N Engl J Med. 1999;341:709-717.

Effect of Eplerenone on Sudden Cardiac Death

Pitt,NEJM 2003,348,p.1309

Aldosterone Antagonists
Recommendations
Addition of an aldosterone antagonist is reasonable in selected patients with moderately severe to severe symptoms of HF and reduced LVEF who can be carefully monitored for preserved renal function and normal potassium concentration.
Creatinine should be 2.5 mg/dL in men or 2.0 mg/dL in women and potassium should be 5.0 mEq/L (Class I; LOE B)

ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult

http://www.acc.org/clinical/guidelines/failure/hf_index.htm

Aldosterone Antagonists

ARB
Spironolactone Eplerenone

Initial Dose
12.5-25 mg daily 25 mg daily

Maximum Dose
25 mg daily or bid 50 mg daily

ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult

http://www.acc.org/clinical/guidelines/failure/hf_index.htm

Vasodilators
Hydralazine + Nitrates
Nitrates
Activate guanylate cyclase to cGMP in vascular smooth muscle venodilation preload Inhibit ventricular remodeling process

Hydralazine
Direct-acting vasodilator on predominantly arterial smooth muscle SVR (afterload) Prevent nitrate tolerance, antioxidant effects

Vasodilators: Clinical Data


Veteran Affairs Cooperative Studies V-HeFT-I
Hydralazine 75 mg po qid + ISDN 40 mg qid vs prazosin 5 mg qd in addition to std therapy
Hydralzine + nitrates mortality by 38% , 25%, and 23% at 1, 2, and 3 years

V-HeFT-II
Hydralazine 75 mg po qid + ISDN 40 mg qid vs. enalapril and enalapril was superior

Vasodilators: Clinical Data


A-HeFT
Randomized, placebo-controlled, double-blind clinical trial2 1,050 pts, self-identified as black2 with stable symptomatic HF

LVEF <35% or left ventricular internal diastolic dimension >2.9 cm/m2 plus LVEF <45%2
1% NYHA class II, 95% NYHA class III , 4% NYHA class IV Mean age upon entry: 571

60% men, 40% women

Patients randomized to receive either their current standard therapies + BiDil (n=518) or their current standard therapies + placebo1 (n=532) BiDil tablet = Hydralazine 37.5 mg/ISDN 20 mg 2 tablets po tid

Vasodilators: Clinical Data


A-HeFT Results
Additional 43% reduction in mortality beyond current standard therapies (P=0.012)1

Additional 39% risk reduction in first hospitalization for heart failure beyond current standard therapies (P<0.001)
Significant additional improvement in symptoms of heart failure1

Vasodilators
Recommendations
The addition of a combination of hydralazine and a nitrate is reasonable for patients with reduced LVEF who are already taking an ACEI and beta-blocker for symptomatic HF and who have persistent symptoms (Class IIa; LOE A) A combination of hydralazine and a nitrate might be reasonable in patients with current or prior symptoms of HF and reduced LVEF who are who cannot be given a ACEI or ARB because of drug intolerance, hypotension, or renal insufficiency (Class IIb; LOE C)

ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult

http://www.acc.org/clinical/guidelines/failure/hf_index.htm

Vasodilators: Precautions
Hydralazine
Systemic lupus erythematosus Hypotension

Nitrates
Hypotension Headaches

Tachycardia
Peripheral neuritis, evidenced by paresthesia, numbness, and tingling, which may be related to an antipyridoxine effect.
Pyridoxine should be added to therapy if such symptoms develop.

Tolerance separate dosing by 10-12 hours


Example: Dose at 9am, 3pm, 9 pm

Drug interactions with Viagra- like drugs

Treatment Approach for the Patient with Heart Failure


Stage A Stage B Stage C Stage D

At high risk, no structural disease

Structural heart disease, asymptomatic

Structural heart disease with prior/current symptoms of HF


Therapy All measures under stage A Drugs: Diuretics ACE inhibitors Beta-blockers Digitalis Dietary salt restriction

Refractory HF requiring specialized interventions


Therapy All measures under stages A,B, and C Mechanical assist devices Heart transplantation Continuous (not intermittent) IV inotropic infusions for palliation Hospice care

Therapy Treat Hypertension Treat lipid disorders Encourage regular exercise Discourage alcohol intake ACE inhibition

Therapy All measures under stage A ACE inhibitors in appropriate patients Beta-blockers in appropriate patients

Hunt, SA, et al ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult, 2005

Current Treatment Options

Cardiac Resynchronization Therapy (CRT)


Symptomatic heart failure despite OPT
Wide QRS complex LV dysfunction EF < 35% NYHA Class III/IV

Cardiac Resynchronization Therapy


Increase the donkeys (heart) efficiency

Reverse Remodeling in HF

10/10/03

8/13/07

Implanted Cardioverter Defibrillator (ICD)


ICD prevents SCD CRT improves Quality of Life and NYHA Heart Failure patients should be managed on optimal background therapy

Assist Devices: Bridge to Transplant

Other New Modalities Research Stage


Cell and Gene Therapy
* Utility in treating acute myocardial infarction -we cannot limit infarct size -we can rebuild infarcted muscle Potential Cells to use: * cardiac myocytes * skeletal muscle cells * endothelial cells * progenitor cells

* pluripotent cells

Knowing is not enough; we must apply. Willing is not enough; we must do.
- Goethe

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