HEART FAILURE

Abate W, Clinical Pharmacist

Debre Berhan University
Asrat Woldeyes Health Sciences
Campus
Pharmacy Dept
 Presentation Outline
Definition of HF
Etiology of HF
Type of HF
Pathogenesis of HF
Dx of HF
Non-pharmacological and pharmacological
treatment of HF
Treatment monitoring parameter of HF
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 Enabeling Objectives
At the end of this session
The students will be expected to define
HF, understand the etiology,
pathogenesis, types, and clinical
manifestation of HF.
 Identify the DX principle, the non-
pharmacological, and pharmacological
treatment choices of HF.

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 Introduction
 Cardiovascular diseases (CVDs) are the leading cause
of death globally.
 CVD accounted for approximately 19.91 million
global deaths in 2021.
 CVD cause 931,578 deaths in the US in 2021
 CVD accounted for 12% of total US health
expenditures in 2019 to 2020.

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 Patient Evaluation Case 1
• K.M. a 48-year-old male, is admitted with a chief complaint of increasing
SOB and an 8-kg weight gain. Two weeks before admission, he noted the
onset of dyspnea on exertion (DOE) after one flight of stairs, orthopnea,
and ankle edema. Since then, his symptoms have worsened. He has also
noted episodic bouts of paroxysmal nocturnal dyspnea (PND), and he has
been able to sleep only in a sitting position.
• K.M. reports a productive cough, nocturia (two to three times a night),
and edema. K.M.’s other medical problems include a long history of
heartburn, a 10-year history of osteoarthritis, depression, and poorly
controlled HTN. A family history of diabetes mellitus is also present.
• Physical examination reveals dyspnea, cyanosis, and tachycardia. K.M. has
the following vital signs: BP, 160/100 mm Hg; pulse, 90 bpm; and
respiratory rate, 28 breaths/minute. He is 5 feet 11 inches tall and weighs
78 kg. His neck veins are distended.
• On cardiac examination, an S3 gallop is heard. His liver is enlarged and
tender to palpation, and a positive hepatojugular reflux is observed. He is
noted to have 3+ pitting edema of the extremities and sacral edema.
Chest examination reveals inspiratory rales and rhonchi bilaterally.
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• The medication history reveals the following current medications:
hydrochlorothiazide (HCT) 25 mg every day, ibuprofen 600 mg 4 times a
day (QID), ranitidine 150 mg every night at bedtime, and citalopram 20 mg
every day. He has no allergies and no dietary restrictions.
 Admitting laboratory values include the following:
• Hematocrit, 41.1%
• White blood cell count, 5,300/μL
• Sodium (Na), 132 mEq/L
• Potassium (K), 3.2 mEq/L
• Chloride (Cl), 100 mEq/L
• Bicarbonate, 30 mEq/L
• Magnesium, 1.5 mEq/L
• Fasting blood sugar, 100 mg/dL
• Uric acid, 8 mg/dL
• Blood urea nitrogen (BUN), 40 mg/dL
• Serum creatinine (SCr), 0.8 mg/dL
• Alkaline phosphatase, 44 units/L
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• Aspartate aminotransferase, 30 units/L
• BNP, 1,364 pg/mL (normal <100 pg/mL)
• Thyroid-stimulating hormone, 2.0 microunits/mL
• The chest-x-Ray shows bilateral pleural effusions and cardiomegaly.
 Questions
1. What signs, symptoms, and laboratory abnormalities of HF does K.M. .
exhibit?
2. Relate these clinical findings to the pathogenesis of the disease?
3. Which type of HF K.M. has?
4. Which stage and NYHA class of this patient?
5. List the non-pharmacological treatment for this patient.
6. List Pharmacological treatment options for this patient.
7. How long he should take medication?
8. Is his medical problem curable? 7
Definition 0f Heart Failure(HF)
 The current American College of Cardiology Foundation
(ACCF)/American Heart Association (AHA) guidelines
define HF as a complex clinical syndrome that results
from structural or functional impairment of ventricular
filling or ejection of blood, which in turn leads to the
cardinal clinical symptoms of dyspnea and fatigue and
signs of HF, namely edema and rales.
 Currently, many patients present without signs or
symptoms of volume overload, the term “heart failure” is
preferred over the older term “congestive heart failure.”
 HF is the final common pathway for numerous cardiac
disorders including those affecting the pericardium, heart
valves, and myocardium.
 Epidemiology
• HF is an increase rapidly problem worldwide, with >20
million people affected.
• HF may be caused by an abnormality in systolic
function(contraction), diastolic function(relaxation or filling),
or both (making the distinction is important because the
treatment may be quite different).
• The historical terms ―systolic‖ and ―diastolic‖ HF have been
abandoned, and HF patients are now broadly categorized into
HF with a reduced ejection fraction( EF˂ 40%) (HFrEF;
formerly systolic failure) or HF with a preserved EF≥ 50%
(HFpEF; formerly diastolic failure).
• Patients with a LV EF between 40 and 50% have been
considered as having a borderline or midrange EF.
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 ACUTE vs CHRONIC HF
ACUTE HEART FAILURE
- Sudden reduction in COP → often systemic hypotension without
peripheral edema
- Usually predominantly systolic
Causes: e.g.
- sudden dev’t of a large myocardial infarction
- rupture of a cardiac valve
CHRONIC HEART FAILURE
- Progresses slowly
- Unlike acute HF:
Arterial pressure is ordinarily well maintained
until very late in the course
Often accumulation of edema
Causes: e.g.
Dilated cardiomyopathy
Multivalvular heart disease/chronic rehumatic valvular10
hear disease(CRVHD)
 SYSTOLIC vs DIASTOLIC
Systolic failure:
FAILURE
Systolic Failure - the inability of the ventricle to contract normally and
expel sufficient blood

inadequate cardiac output

symptoms of hypoperfusion
- weakness,
- fatigue,
- reduced exercise tolerance, & etc.
Diastolic failure:
Inability of the ventricle to relax and/or fill normally

Manifestations relate principally to the elevation of filling pressures.
• Many pts, have both ventricular hypertrophy and dilatation

Exhibit abnormalities both of contraction & relaxation
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 ETIOLOGY
 Etiology of HF in patients with a preserved EF differs from
patients with depressed EF….sometimes overlap.
 In industrialized countries, coronary artery disease (CAD) has
become the predominant cause and is responsible for 60–75%
of cases of HF. Hypertension cause responsible for 75% of
patients, including most patients with CAD.
 Dilated cardiomyopathy is may be caused by prior viral
infection or toxin exposure (e.g., alcoholic or
chemotherapeutic).
 Infections: Viral infections, such as myocarditis, or bacterial
infections, such as endocarditis.
 MI, Arrhythmias,
 Congenital heart defects
 Rheumatic heart disease(RHD) is a major cause of HF in
Africa and Asia, especially in the young.
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 Others: diabetes, obesity, smoking
 ARF
 Acute rheumatic fever (ARF) is a nonsuppurative complication
of pharyngeal infection with group A Streptococcus (GAS).
• Signs and symptoms of ARF develop two to three weeks
following pharyngitis
 Clinical Manifestations
 The five major manifestations
● Carditis and valvulitis (eg, pancarditis) that is clinical or
subclinical
● Arthritis (usually migratory polyarthritis predominantly
involving the large joints)
● Central nervous system involvement (eg, Sydenham chorea)
● Subcutaneous nodules
● Erythema marginatum
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 ARF Conti…

 The four minor manifestations are:

● Arthralgia
● Fever
● Elevated acute phase reactants (erythrocyte sedimentation rate
[ESR], C-reactive protein [CRP])
● Prolonged PR interval on electrocardiogram(ECG).
 Treatment of ARF consists of anti-inflammatory therapy,
antibiotic therapy, and heart failure management.

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 ARF Conti…
 Prevention; primary and secondary.
 Primary prevention: is accomplished by prompt diagnosis
and antibiotic treatment of GAS tonsillopharyngitis.
 Secondary prevention(antibiotic prophaylaxis); secondary
prevention for recurrent ARF consists of years of prophylactic
antibiotic administration.
• Continuous prophylaxis is warranted for patients with a well-
documented history of ARF (including cases with Sydenham
chorea as the sole manifestation), as well as those with definite
evidence of RHD.
• Patients with breakthrough GAS pharyngitis on penicillin
should be treated with an alternative agent such
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as clindamycin.
 ARF Conti…
 Duration —The total duration of secondary prophylaxis
depends upon risk of recurrent ARF and severity of disease.
 In the setting of carditis, prophylaxis should continue until the
patient is a young adult (21 years of age), which is usually
approximately 10 years from the initial acute attack with no
recurrence.
 Antibiotic prophylaxis should continue even after valve
surgery, including prosthetic valve replacement.
 Antibiotic selection — Parenteral prophylaxis with penicillin
G benzathine is preferred for all patients.
• Oral agents are used in the case of shortages of penicillin G
benzathine and are also appropriate for patients who are
allergic to penicillin.
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Dosing
 Penicillin G benzathine intramuscular: 1.2 million units every 21 to
28 days* for adults ˃ 27kg and for adults < 27kg use 600,000 units
every 21 to 28 days*.
 Allergy to penicillin and sulfonamide antimicrobials: azithromycin 250
mg po once per day for adults >27kg and for adults <27kg 5 mg/kg po
once daily (up to 250 mg).
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 HF PROGNOSIS
• Despite recent advances in the management of HF, the
development of symptomatic HF still carries a poor
prognosis.
• Community-based studies indicate that 30–40% of
patients die within 1 year of diagnosis and 60–70% die
within 5 years, mainly from worsening HF or as a sudden
event.

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 HF Pathophysiology
Normal Cardiac Function
 Cardiac output(CO) is defined as the volume of blood
ejected per unit time (L/min) and is the product of heart
rate (HR) and stroke volume (SV): CO = HR × SV
 The relationship between CO and mean arterial pressure
(MAP) is: MAP = CO × systemic vascular resistance
(SVR)
 Stroke volume is the amount of blood ejected from each
ventricle with each beat.
- SV= End-diastolic volume - end-systolic volume
C:\Users\hp\Desktop\cardiovascular system： cardiac
output.mp4 19
The Normal Myocardial function
Cardiac output is a function of : -
1. The volume and pressure of blood in the
ventricle at the end of diastole → PRELOAD
2. Myocardial contractility → the force generated
at any given end–diastolic volume
3. The volume and pressure of blood in the
ventricle during systole → AFTERLOAD
The interaction of these variables is based on Frank-
Starling curves or Starling's Law of the
heart.
 Normal

Mild HF
Moderate HF
Severe HF

Starling's Law.
Ventricular performance is related to the degree of myocardial stretching.
An increase in preload (EDV, EDP, filling pressure or atrial pressure) will
↑ function; however, overstretching causes marked deterioration.
In HF the curve moves to the right and becomes flatter.
An increase in myocardial contractility or a reduction in afterload will shift
the curve upwards and to the left.
 An increase in (-)inotropic agents and decrease contractility will shift the21
cure downwards and to the right
MAJOR DETERMINANTS OF
CARDIAC PERFORMANCE

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 PATHOGENESIS
 Pathogenesis of HFrEF… HF begins after an
index event produces an initial decline in the
heart’s pumping capacity…. then a variety of
compensatory mechanisms are activated,
including the adrenergic nervous system, the
renin-angiotensin-aldosterone system, and the
cytokine system.
 In the short term, these systems are able to
restore cardiovascular function to a normal
homeostatic range. However, sustained activation
of these systems leads to secondary end-organ
damage within the ventricle, with worsening left
ventricular remodeling and subsequent cardiac
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decompensation.
 Compensatory mechanisms of HF
(1) Activation of the renin angiotensin-aldosterone system
(RAAS) and the adrenergic nervous system, which are
responsible, for maintaining cardiac output through
increased retention of salt and water.
(2) Increased myocardial contractility
(3) Vasodilator molecules are activated, including the atrial
and brain natriuretic peptides (ANP and BNP), bradykinin,
prostaglandins (PGE2 and PGI2), and nitric oxide (NO),
that offset the excessive peripheral vascular
vasoconstriction.
 Symptomatic HF is accompanied by increasing
activation of neurohormonal, adrenergic, and cytokine
systems that lead to a series of adaptive changes within
the myocardium collectively referred to as LV remodeling 25.
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 Compensatory Hypertrophy

• Two basic patterns of cardiac

hypertrophy occur in response to
hemodynamic overload.
–Concentric(pressure overloaded)
–Eccentric (volume overloaded)

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 Ventricular remodeling
• Cardiac or ventricular remodeling is changes in both
myocardial cells and the extracellular matrix that result in
changes in the size, shape, structure, and function of the
heart.
• Ventricular Hypertrophy and Remodeling; an increase in
ventricular muscle mass.
• These progressive changes in ventricular structure and
function ultimately result in a change in the shape of the
left ventricle from an ellipse to a sphere.

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 Factors Precipitating/Exacerbating HF

 There are many aggravating or precipitating factors that may

cause a previously compensated patient to develop worsened
symptoms necessitating hospitalization.
 Myocardial ischemia and infarction
 Atrial fibrillation
 Uncontrolled HTN
 Pulmonary embolus, diabetes, chronic kidney disease,
hypothyroidism, and hyperthyroidism
 Non-adherence with prescribed HF medications(poly-
pharmacy) or with dietary recommendations (eg, sodium
intake and fluid restriction).
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 A number of drugs can precipitate or exacerbate HF by
one or more of the following mechanisms:
(a) Negative inotropic effects
• BB: eg, propranolol, metoprolol, carvedilol
• CCB; eg, verapamil, diltiazem
• Antiarrhythmics (disopyramide, dronedarone, flecainide,
propafenone, sotalol)
(b) Direct cardiotoxicity
 Anticancer, carbamazepine, amphetamine ,ethanol
(c) Increased sodium and/or water retention; NSAID,
rosiglitazone and pioglitazone, glucocorticoids, androgens
and estrogens, Salicylates (high dose),sodium-containing
drugs 30
 Clinical Manifestations
 General: patient presentation may range from
asymptomatic to cardiogenic shock.
 Symptoms
 The cardinal symptoms of HF are fatigue and shortness
of breath.
 Orthopnea, defined as dyspnea occurring in the
recumbent(lying down) position, is usually a later
manifestation of HF than is exertional dyspnea.
 Paroxysmal Nocturnal Dyspnea (PND):This refers to
acute episodes of severe shortness of breath and
coughing that generally occur at night and awaken the
patient from sleep.
 Exercise intolerance, weight gain or loss, nocturia, 31
 Acute pulmonary edema, early satiety, anorexia, Ab pain
Clinical Manifestation

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 DIAGNOSIS
 No single test is available to confirm the diagnosis of HF.
 With few exceptions, HFpEF cannot be distinguished
from HFrEF on the basis of the history, physical
examination, chest x-ray, and ECG alone
 The echocardiogram(ECHO) is used to assess
abnormalities in cardiac structure, function and
evaluation of the pericardium, myocardium, and heart
valves, and quantification of the LVEF to determine if
systolic or diastolic dysfunction is present.
 A complete history, physical examination, and
medication history
 CBC, serum electrolytes (including calcium and
magnesium), renal and hepatic function, urinalysis, lipid
profile, hemoglobin A1C, thyroid function tests, iron
studies, chest x-ray, and 12-lead ECG.
 Measurement of BNP or NT-proBNP assist in dyspnea 33
caused by HF or other causes.
 Differential DX
 Cor Pulmonale; referred to as pulmonary heart disease,
is broadly defined by altered right ventricle (RV) structure
and/or function in the context of chronic lung disease
and is triggered by the presence of pulmonary
hypertension(PHT) or pulmonary arterial
hypertension(PAH).

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 Treatment of Heart Failure
Desired Outcomes
The goals of therapy in the management
of chronic HF are
To improve the patient's quality of life,
To relieve or reduce symptoms,
 To prevent or minimize hospitalizations,
To slow progression of the disease, and
To prolong survival.
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 ACC/AHA heart failure staging
system.
 The American College of Cardiology (ACC)/American
Heart Association (AHA) guidelines for the evaluation and
management of HF utilize a staging system.
- The four stages of this system differ from the NYHA functional
classification.
 The NYHA system is primarily intended to classify symptoms.
 A patient's symptoms can change frequently over a short period of
time due to changes in medications, diet, intercurrent illnesses, etc.
o For example, a patient with ACC/AHA Stage C HF with NYHA class
IV symptoms such as marked volume overload could rapidly
improve to class I or II with aggressive diuretic therapy. In contrast,
a patient's ACC/AHA HF stage could not improve (eg, go from Stage
C to Stage B).
o ACC/AHA heart failure staging system as follows below….
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37
NYHA Classification

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General Approach to Treatment
 Non-pharmacological
• Restriction of dietary sodium and fluid intake is an
important lifestyle intervention for both HFrEF and
HFpEF.
• Mild HF (<3 g/day) to moderate HF (<2 g/day) sodium
restriction, in conjunction with daily measurement of
weight.
• Fluid restriction( less than 2L/day of all fluids)
• Eat fruits and vegetables
• Avoid fatty meals

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 Surgical Therapy In Heart Failure
 Coronary artery bypass grafting (CABG)
 Mitral regurgitation (MR)
 Surgical ventricular restoration (SVR),
o Implantation of a specialized biventricular pacemaker to
restore activation of the ventricles improves ventricular
function and hemodynamics and is associated with
reverse remodeling and increased LVEF

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Pharmacological RX

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 Treatment of Stage D HFrEF

• Stage D HF includes patients receiving maximally

tolerated GDMT that have persistent symptoms. This is
often referred to as advanced, refractory, or end-stage
HF.
• These patients often undergo recurrent hospitalizations
or cannot be discharged from the hospital without special
interventions, have a poor quality of life, and are at high
risk for morbidity and mortality.
• specialized therapies including mechanical circulatory
support, continuous IV positive inotropic therapy, and
cardiac transplantation can be considered in addition to
standard treatments outlined in Stages A to C.
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 HFpEF
• Less information on the treatment of HFpEF is available
in ACC/AHA, the ESC, and the HFSA.
• In general, all three guidelines recommend treating
comorbid conditions by controlling HR and BP,
alleviating causes of myocardial ischemia, reducing
volume, and restoring and maintaining sinus rhythm in
patients with atrial fibrillation.

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Neurohormonal activation and sites of action of
drugs used in the treatment of heart failure.

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 Diuretics
• Diuretics are used for relief of acute symptoms of
congestion and maintenance of euvolemia.
• The rationale for the use of diuretic therapy is to
maintain euvolemia in symptomatic or stages C and D
heart failure.
• Diuretic therapy is recommended for all patients with
clinical evidence of fluid overload retention.
• Thiazides are weaker than loop diuretics in terms of
effecting an increase in urine output and therefore are
not utilized frequently as monotherapy in HF.
• Loop diuretics are the most widely used diuretics in HF.
• If there is diuretic resistance?( combine loop with
thiazide or continuous infusion of Loop..). 46
Neurohormonal Blocking Agents

Agents with proven benefits in improving

symptoms, slowing disease progression, and
improving survival target neurohormonal
blockade.

ACE inhibitors, ARBs, β-adrenergic blockers,

and aldosterone antagonists.

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 ACE – Inhibitors [1]
ACE inhibitors demonstrate favorable effects on
cardiac hemodynamics, such as:

Long-term increases in cardiac index (CI),

stroke work index, and SV index,

Significant reductions in LV filling pressure, SVR,

mean arterial pressure, and HR.

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 ACE – Inhibitors [2]
Initiated using low doses and titrated up to target
doses over several weeks depending on
tolerability (adverse effects and blood pressure).
Absolute contraindications include a history of
angioedema, bilateral renal artery stenosis, and
pregnancy.
Relative contraindications include unilateral renal
artery stenosis, renal insufficiency, hypotension,
hyperkalemia, and cough.
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Hydralazine and Isosorbide Dinitrate [1]

Complementary hemodynamic actions originally led

to the combination of nitrates with hydralazine.

Nitrates reduce preload by causing primarily venous

vasodilation.

Hydralazine reduces afterload through direct arterial

smooth muscle relaxation.

Hydralazine may reduce the development of nitrate

tolerance when nitrates are given chronically.

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Hydralazine and Isosorbide Dinitrate [2]

Appropriate substitute for angiotensin II antagonism

in those unable to tolerate an ACE inhibitor or ARB.

Adverse effects such as hypotension and headache

cause frequent discontinuations in patients taking
this combination.

Patients should be monitored for headache, hypotension,

and tachycardia.

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 β-Adrenergic Antagonists [1]
Reduces ventricular mass, improves ventricular shape, and
reduces LV end-systolic and diastolic volumes.

Exhibit antiarrhythmic effects, slow or reverse

catecholamine-induced ventricular remodeling, decrease
myocyte death from catecholamine-induced necrosis or
apoptosis.

Three β-blockers shown to reduce mortality in systolic

HF, including the selective β1-antagonists bisoprolol
and metoprolol, and the non-selective β1-, β2-, and
α1-antagonist carvedilol.
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 β-Adrenergic Antagonists [2]
β-blocker need to be initiated when a patient is
clinically stable and euvolemic.

Volume overload at the time of β-blocker

initiation increases the risk for worsening
symptoms.

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 Aldosterone Antagonists
• Aldosterone exerts multiple detrimental effects in HF.
• Mediates pathologic ventricular remodeling by causing
increased extracellular matrix collagen deposition and
cardiac fibrosis.
• Contributes to disease progression via sympathetic
potentiation and ventricular remodeling.
• Before and within one week of initiating therapy, two
parameters must be assessed: serum potassium and
creatinine clearance (or serum creatinine).
• Other adverse effects observed mainly with
spironolactone include gynecomastia for men and
breast tenderness and menstrual irregularities for
women.
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 Digoxin [1]
• Traditionally, useful for its positive inotropic effects, but
more recently its benefits related to neurohormonal
modulation.
• Decrease HF-related hospitalizations but did not decrease
HF progression or improve survival.
• Current recommendations are for the addition of digoxin
for patients who remain symptomatic despite an optimal
HF regimen consisting of an ACE inhibitor or ARB, β-
blocker, and diuretic.
• In patients with concomitant atrial fibrillation, digoxin may
be added to slow ventricular rate regardless of HF
symptomology.

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 Digoxin [2]
• Toxicity may manifest as non-specific findings such as
fatigue or weakness, and other CNS effects such as
confusion, delirium, and psychosis. Gastrointestinal
manifestations include nausea, vomiting, or anorexia, and
visual disturbances may occur such as halos,
photophobia, and color perception problems (red-green or
yellow-green vision).
• Cardiac findings include numerous types of arrhythmias
related to enhanced automaticity, slowed or accelerated
conduction, or delayed afterdepolarizations.
• These include ventricular tachycardia and fibrillation,
atrioventricular nodal block, and sinus bradycardia.

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 Digoxin [3]
Risk of cardiac digoxin toxicity are increased with
electrolyte disturbances such as hypokalemia,
hypercalcemia, and hypomagnesemia.

To reduce the proarrhythmic risk of digoxin,

serum potassium and magnesium should be
monitored closely to ensure adequate
concentrations.

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Antiplatelets and Anticoagulation
• Patients with HF are at an increased risk of
thromboembolic events secondary to a combination of
hypercoagulability, relative stasis of blood, and
endothelial dysfunction.
• Aspirin is generally used in HF patients with an
underlying ischemic etiology, a history of ischemic
heart disease, or other compelling indications such as
history of embolic stroke.
• Current consensus recommendations support the use
of warfarin in patients with reduced LV systolic
dysfunction.

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Guideline Recommended Drug Therapy and
dose of HFrEF

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Novel Neurohormonal Antagonism

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61
Hear Rate modifications

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 Heart Failure with Preserved Left
Ventricular Ejection Fraction [1]
• A significant number of patients exhibiting HF symptoms
have normal systolic function or preserved LVEF (40% to
60%).
• The primary defect is impaired ventricular relaxation and
filling, referred to as diastolic dysfunction or diastolic HF.
• The current treatment approach for diastolic dysfunction or
preserved LVEF is:
(1) correction or control of underlying etiologies (including
optimal treatment of hypertension and CAD and maintenance
of normal sinus rhythm);
(2) reduction of cardiac filling pressures at rest and during
exertion; and
(3) increased diastolic filling time.
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 Heart Failure with Preserved Left
Ventricular Ejection Fraction [2]
• Diuretics, ACE inhibitors, and ARBs are frequently
used to control congestion.
• β-Blockers and CCBs can improve ventricular
relaxation through negative inotropic and chronotropic
effects.
• Nondihydropyridine CCBs (diltiazem and verapamil)
may be especially useful in improving diastolic function
by limiting the availability of calcium that mediates
contractility.
• The role of digoxin for symptom management and
HR control in these patients is not well established.

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 Outcome Evaluation of
Heart Failure
• The evaluation of therapy is influenced by the ability of
treatment to succes drugs fully reduce symptoms,
improve quality of life, decrease frequency of
hospitalizations for HF, reduce disease progression, and
prolong survival.
• The major outcome parameters focus on:
(1) volume status;
(2) exercise tolerance;
(3) overall symptoms/quality of life;
(4) adverse reactions; and
(5) disease progression and cardiac function.

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THANK YOU!!

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