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
HF Patients in US
(millions)
10
8
6
4
• 5 million symptomatic patients
in 2001; estimated 10 million in
20371,2
• Incidence: about 550,000 new
cases/year2
5
• Prevalence is 1% between the
ages of 50 and 59 years3;
progressively increasing to
10% over age 804
3.5
2
0
1991
1Adapted
2001
2037
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
Arrhythmia
CM
HTN
Left ventricular
injury
Pathologic
remodeling
Low ejection
fraction
Death
Valvular Dz
Pump
failure
Chemo
• Neurohormonal
stimulation
• Endothelial
dysfunction
• Myocardial toxicity
• Vasoconstriction
• Renal sodium retention
Symptoms:
Dyspnea
Fatigue
Edema
1 Adapted from Cohn JN. N Engl J Med. 1996;335:490–498.
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.
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)
B Structural heart disease but without
symptoms of HF
NYHA Functional Class2
I Asymptomatic
II Symptomatic with moderate exertion
C Structural heart disease with prior or
current symptoms of HF
D Refractory HF requiring
specialized interventions
III Symptomatic with minimal exertion
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)
Measures heart size, wall thickness/mobility, flow gradients,
valvular function, LVEF
Electrocardiogram
Assesses cardiac rhythm, conduction; can detect myocardial
infarction, arrhythmias
Chest x-ray
Detects heart enlargement, fluid around heart or lungs
Standard laboratory tests
• Blood chemistry, urinalysis
• Complete blood count (CBC)
• Renal, liver, thyroid tests
• Blood urea nitrogen (BUN), creatinine, albumin (liver
function), glucose (diabetes)
• CBC detects anemia, infection
• Organ function as a contributing factor or resulting from HF
Cardiac enzymes
Cardiac markers
Creatinine kinase (CK, CK-MB), cardiac troponins I and T
Brain natriuretic peptide (BNP)
• 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
Hospitalization
IV Lasix
or Admit
Emergency
Room
SOB
 Weight
MD’s Office
PO Lasix
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
Placebo
Enalapril
5
Cumulative Mortality
15
10
0.75
P=0.30
20
P<0.0036
0.5
Enalapril
0.25
Hydralazine
Isosorbide Dinitrate
48
36
24
12
0
0
Mortality From All Causes (%)
25
Months
0
0 6 12 18 24 30 36 42 48 54 60
Months
SOLVD-P
NYHA Class
Treatment
Results
Class I-II (N=4228)
Enalapril
8%
(% reduction in all-cause mortality)
1The
Cumulative Predictability of Death
Effect of ACE Inhibitors on Survival
in Heart Failure
0.8
0.6
P<0.003
Placebo
0.4
0.2
Enalapril
0
0 1 2 3 4 5 6 7 8 9101112
Months
SOLVD-T
CONSENSUS
Class II-III (N=2569)
Enalapril
16%
Class IV (N=253)
Enalapril
27%
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
Initial Dose
Maximum Dose
Captopril
6.25 mg tid
50 mg tid
Enalapril
2.5 mg bid
10-20 mg bid
Fosinopril
5-10 mg daily
40 mg daily
Lisinopril
2.5-5 mg daily
20-40 mg daily
Quinapril
5 mg bid
20 mg bid
Ramipril
1.25-2.5 mg daily
10 mg daily
Trandolapril
1 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:
• Warnings/Precautions:
– Hypersensitivity
– Anaphylactic reactions can occur
– Angioedema related to
previous treatment with
ACEI
– Angioedema can occur at any
time during treatment, especially
after 1st dose
– Hereditary angioedema
– Careful BP monitoring with 1st
dose (hypotension)
– Bilateral renal artery
stenosis
– Pregnancy (2nd and 3rd
trimester)
• 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
Initial Dose
Maximum Dose
Candesartan
4-8 mg daily
32 mg daily
Losartan
25-50 mg day
50-100 mg day
20-40 mg bid
160 mg bid
Not FDA approved
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 ß1 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*
‡
LVEF (EF units)
8
†
6
†
4
2
0
Placebo
6.25 mg bid
12.5 mg bid
25 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
vs placebo.
vs placebo.
Adapted from Bristow MR et al. Circulation. 1996;94:2807–2816.
‡P.0001
Effects of Beta-Blockers on Mortality
Mortality
1.0
1.0
b -blocker
0.8
0.8
Risk
 34 %
Placebo
Risk
 35 %
0.6
0.6
P <0.0001
0
b -blocker
Risk
 34 %
0.6
Time (years)
1.0
Placebo
Placebo
0.8
b -blocker
1
CIBIS II
NYHA Class
III-IV (N=2647)
Entry criteria LVEF 35%
Treatment
Bisoprolol
Results
34%
(% reduction in death)
2
P=0.006
0
1
2
MERIT-HF
II - IV (N=3391)
LVEF 40%
Metoprolol CR/XL
34%
P<0.00013
0
1
2
COPERNICUS
IV (N=2289)
LVEF  25%
Carvedilol
35%
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
NYHA
Class
Initial dose
Target Dose
Bisoprolol
(Zebeta®)
b1-selective
III-IV
1.25 mg/day
10 mg/day
Non-selective
b-blocker, 1blocker
II-IV
3.125 mg bid
25 mg bid (< 85 kg)
not FDA-approved
Carvedilol
(Coreg®)
Coreg CR
Metoprolol
succinate
(Toprol
XL®)
b1-selective
50 mg bid (> 85 kg)
II-III
10 mg/day
12.5-25 mg
day
80 mg/day
200 mg/day
ß-Blockers
Limit the donkey’s 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
Probability of Survival
P<0.001
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
Pitt B et al. N Engl J Med. 1999;341:709-717.
Study Design
 NYHA Class III-IV (N= 1663)
 EF 35%
 Frequent monitoring of
potassium
 Result: 30% reduction in death
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
Initial Dose
Maximum Dose
Spironolactone
12.5-25 mg daily
25 mg daily or bid
Eplerenone
25 mg daily
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
• Nitrates
– Systemic lupus erythematosus
– Hypotension
– 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
Refractory HF
requiring
specialized
interventions
Therapy
Therapy
Therapy
Therapy
• Treat Hypertension
• All measures under
stage A
• All measures under
stage A
• All measures under
stages A,B, and C
• ACE inhibitors in
appropriate
patients
Drugs:
• Mechanical assist
devices
• Treat lipid
disorders
• Encourage regular
exercise
• Discourage alcohol
intake
• ACE inhibition
• Beta-blockers in
appropriate
patients
• Diuretics
• ACE inhibitors
• Beta-blockers
• Digitalis
• Dietary salt
restriction
• Heart
transplantation
• Continuous (not
intermittent) IV
inotropic infusions
for palliation
• Hospice care
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 donkey’s (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