Subject: Medicine

Topic: 4.03b Heart Failure II: Management

Lecturer: Dr. Tolentino
Date: November 10, 2015

OUTLINE Nitrates, Nitroprusside and Nesiritide with the latter suggested more
I. General Principles rapid and greater reduction in pulmonary capillary wedge pressure.
A. Acute Decompensated Heart Failure (ADHF) If has a good blood pressure but severely congested give diuretics
II. Heterogeneity of ADHF
which is available in oral and IV (given during acute decompensation).
A. Management Principles
1) Therapeutic goals of ADHF
2) Primary hemodynamic determinants of ADHF
3) Distinctive phenotypes of ADHF, their presentations, and suggested
therapeutic routes
B. Intravenous Therapy in ADHF
1) Inotropic Therapy Figure 2. If severely congested and hypoxemic, give O2 or intubate.
2) Vasodilators
3) Diuretics
III. Management in heart failure with reduced ejection fraction (hfref)
A. Neurohumoral Antagonism
B. Mineralocorticoid Antagnist
C. Arteriovenous Vasodilators Figure 3. For low blood pressure, give positive inotropes such
IV. Other interventions for heart failure
Dobutamine and Milrinone which augment cardiac output, improve
V. Elements of Patient Education
perfusion and relieve congestion acutely. Levosimendan a calcium
References: Harrison’s 18th and 19th Ed. sensitizer provides inotropic and vasodilator effect.

I. GENERAL PRINCIPLES
A. Acute Decompensated Heart Failure (ADHF)
 ADHF is a heterogeneous clinical syndrome most often resulting in
need for hospitalization due to confluence of interrelated
abnormalities of decreased cardiac performance, renal
dysfunction, and alterations in vascular compliance.
 Management:
o Volume control
o Decrease of vascular impedance while maintaining attention
to end-organ perfusion (coronary and renal)
II. HETEROGENEITY OF ADHF
A. Management Principles
1.) Therapeutic goals of ADHF
 Identify and treat the reversible factors that precipitated
decompensation
 Stabilize the hemodynamic derangements that provoked the
symptoms responsible for the hospitalization
 Reestablish an effective outpatient medical regimen that will
prevent progression and relapse
2) Primary hemodynamic determinants of ADHF
 Elevated left ventricular filling pressures
 Depressed cardiac output, frequently accompanied by an increased
in systemic vascular resistance
Figure 4. For very low blood pressure, devices used such as:
 IABP (intra-aortic balloon pump) wherein the balloon is placed
inside the aorta to help in pumping action of the heart. It increases
myocardial oxygen supply and decreases myocardial oxygen
demand.
 VAD (ventricular assist device) serves as alternative to biologic
replacement of the heart. It can also provide a temporary solution
for candidates who eventually fail medical therapy and are waiting
in line for the availability of donor heart.
o Major indications: chronic end stage heart failure and with LV
ejection fraction of <25% or dependent on inotropic and IAB
counter-pulsation
 ECMO (Extracorporeal Membrane Oxygenation) - for pulmonary
and cardiac failure. Unlike standard cardiopulmonary bypass,
which is used for short-term support measured in hours, ECMO is
used for longer-term support ranging from 3-10 days
 The purpose of ECMO is to allow time for intrinsic recovery of the
lungs and heart; a standard cardiopulmonary bypass provides
support during various types of cardiac surgical procedures.

3.) Distinctive phenotypes of ADHF, their presentations, and

suggested therapeutic routes

Figure 5. ECMO - provides long-term breathing and heart support and

Figure 1. If hypertensive, give vasodilators such as Intravenous
is used only when all of the standard treatments for those problems

Trans Group: Ng, Nicanor, Oblepias, Odrada Page 1 of 8

Edited By: Alie and Kimber
have already been tried.
Figure 6. Hemodynamic profiles in patients with acute heart failure.
Can be categorized by examination of the neck veins, lungs, and
peripheral extremities.
 Normal LV filling pressure with normal perfusion (Profile A)
o Not congested and have normal tissue perfusion, acute HF
with these symptoms are often due to conditions other than
HF (e.g., pulmonary or hepatic disease or transient myocardial
ischemia).
 Elevated LV filling pressure with normal perfusion (Profile B)
o Acute HF present with congestive symptoms in which case
treatment of the elevated filling pressures with diuretics and
vasodilators is warranted to reduce LV filling pressures (e.g.
,acute pulmonary edema).
 Elevated LV filling pressures with decreased perfusion (Profile C)
o Present with congestion and a significantly elevated SVR and
reduction of cardiac output, cardiac output can be increased
and LV filling pressures reduced by using intravenous
vasodilators.
 Normal or low LV filling pressure with decreased tissue perfusion
(Profile L)
o Evaluated by right-heart catheterization for the presence of
an occult elevation of LV filling pressures. If LV filling pressures
are low [pulmonary capillary wedge pressure (PCWP) <12
mmHg], a cautious trial of fluid repletion may be considered.
B. Intravenous Therapy in ADHF
Table 1 Intravenous Therapy in Acute Decompensated Heart Failure
**PLEASE REFER TO APPENDIX FOR BIGGER PICTURE
1. Inotropic Therapy
 Dobutamine – 20-20 ug/kg/min
 Dopamine – will cause tachycardia
 Other medications such as Milirinone and Levosimendan are
not available in the Philippines
Harrison’s:
 Since impairment or myocardial contractlitlity often
accompanies ADHF, positive inotopic agents such as
sympathomimetic amines (dobutamine) and
phosphodiesterase-3 inhibitors (milrinone), increase
intracellular concentration of cyclic adenosine
monophosphate via direct or indirect pathways
 Inotropic therapy in those with a low-output state augments
cardiac output, improves perfusion, and relieves congestion
acutely
 Short-term use of inotropic agents in ADHF is also associated
with increased arrhythmia, hypotension, and no beneficial
effects on hard outcomes
 Inotropic agents are currently indicated as bridge therapy (to
either left ventricular assist device support or to transplant) or
as selectively applied palliation in endstage heart failure
2. Vasodilators
 IV Nitrates – 10-20 ug/min
 If blood pressure is normal or above normal, use vasodilators
 Only IV Nitrates are available in the Philippines
o Nitrates are venodilators: increasing blood flow to the
heart and decreasing preload
Harrison’s:
 Intravenous nitrates, nitroprusside, and nesiritide (a
recombinant brain-type natriuretic peptide) have been
advocated for upstream therapy in an effort to stabilize ADHF
 Nesiritide agent was introduced in a fixed dose for therapy
after a comparison with intravenous nitrates suggested more
rapid and greater reduction in pulmonary capillary wedge
pressure
 However, it was not associated with an increase or a decrease
in the rates of death and rehospitalization and had a clinically
insignificant benefit on dyspnea. Renal function did not
worsen, but increased rates of hypotension were noted;
routine use cannot be advocated due to lack of significant
efficacy
3. Diuretics
 Furosemide – most commonly used
 Bumetanide or Burinex – if resistant to furosemide
 Use IV preparation initially
 Once patient is more stable and less congested, give oral
preparation
Harrison’s:
 Neurohormonal activation results in avid salt and water
retention.
 Loop diuretics are often required because of their increased
potency but frequent dose adjustments may be necessary
because of variable oral absorption and fluctuations in renal
function.
 Diuretic agents should ideally be used in tailored dosing
schedules to avoid excessive exposure but should be noted
that to be essential at the outset to achieve volume control
before neuro-hormonal therapy is likely to be well-tolerated
or titrated.
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 III. MANAGEMENT IN HEART FAILURE WITH REDUCED
EJECTION FRACTION (HFrEF)
 The treatment of symptomatic heart failure evolved from a
renocentric (diuretics) and hemodynamic therapy model (digoxin,
inotropic therapy) ushered in the era of disease-modifying therapy
with neurohormonal antagonism.
 ACEIs and beta blockers form the cornerstone of pharmacotherapy
and lead to attenuation of decline and improvement in cardiac
structure and function with consequent reduction in symptoms,
improvement in quality of life, decreased burden of
hospitalizations, and a decline in mortality from both pump failure
and arrhythmic deaths
A. Neuro-hormonal Antagonism
 Meta-analyses suggest a 23% reduction in mortality and a 35%
reduction in the combination endpoint of mortality and
hospitalizations for heart failure in patients treated with ACEIs.
 Patients treated with beta blockers provide a further 35%
reduction in mortality on top of the benefit provided by ACEIs
alone.
 Increased experience with both agents in a broad range of patients
with HFrEF has demonstrated the safety of ACEIs in treating
patients with mild renal insufficiency and the tolerability of beta
blockers in patients with moderately controlled diabetes, asthma,
and obstructive lung disease.
 The benefits of ACEIs and beta blockers extend to advanced
symptoms of disease (NYHA class IIIb–IV).
Class Effect, Sequence of Administration, Dose and Outcome
 ACEIs exert their beneficial effects in HFrEF as a class; however, the
beneficial effects of beta blockers are thought to be limited to
specific drugs.
 Beta blockers with intrinsic sympathomimetic activity (Xamoterol)
and other agents, including Bucindolol, have not demonstrated a
survival benefit.
 Beta blocker use in HFrEF should be restricted to Carvedilol,
Bisoprolol, and Metoprolol Succinate—agents tested and proven to
improve survival in clinical trials.
 Whether beta blockers or ACEIs should be started first was
answered by the Cardiac Insufficiency Bisoprolol Study (CIBIS) III, in
which outcomes did not vary when either agent was initiated first.
 Thus, it matters little which agent is initiated first; what does
matter is that optimally titrated doses of both ACEIs and beta
blockers be established in a timely manner.
 Beta blockers demonstrate a dose-dependent improvement in
cardiac function and reductions in mortality and hospitalizations.
 In the absence of symptoms to suggest hypotension (fatigue and
dizziness), pharmacotherapy may be up-titrated every 2 weeks in
hemodynamically stable and euvolemic ambulatory patients as
tolerated.
B. Mineralocorticoid Antagonists
 Aldosterone antagonism is associated with a reduction in mortality
in all stages of symptomatic NYHA class II to IV HFrEF.
 Elevated aldosterone levels in HFrEF promote sodium retention,
electrolyte imbalance, and endothelial dysfunction and may
directly contribute to myocardial fibrosis.
C. Arteriovenous Vasodilators
 The combination of hydralazine and nitrates has been
demonstrated to improve survival in HFrEF.
 Hydralazine reduces systemic vascular resistance and induces
arterial vasodilatation by affecting intracellular calcium kinetics;
nitrates are transformed in smooth muscle cells into nitric oxide,
which stimulates cyclic guanosine monophosphate production and
consequent arterial-venous vasodilation.
 This combination improves survival, but not to the magnitude
evidenced by ACEIs or ARBs.
 However, in individuals with HFrEF unable to tolerate renin-
angiotensin-aldosterone–based therapy for reasons such as renal
insufficiency or hyperkalemia, this combination is preferred as a
disease-modifying approach
 A trial conducted in self-identified African Americans, the African-
American Heart Failure Trial (A-Heft), studied a fixed dose of
isosorbide dinitrate with hydralazine in patients with advanced
symptoms of HFrEF who were receiving standard background
therapy. The study demonstrated benefit in survival and
hospitalization recidivism in the treatment group
Table 2. List of common neuro-hormonal and vasodilator regimens
for HFrEF (REFER to APPENDIX for bigger photo)
From the lecturer (additional): Oral medications are given once
patient is stable, this table shows the list of medications that have
proven mortality and morbidity benefit. ACE inhibitors (Lisinopril,
Enalapril, Captopril, Trandolapril) provides the most benefit which
have reverse remodeling effect, other than its vasodilating effect.
ARBs are substitute to ACE inhibitors when patients present with
coughing which is the most common side effect due to ACE inhibitor.
Aldosterone antagonists also have reverse remodelling effect, where
spironolactone is used in our country. In addition to beta blockers,
they are preferred more than ACE inhibitors when the patient is
tachycardic. Hydralazine and nitrates are used for African American
because they do not respond to ACE inhibitors.
D. Heart Rate Modification
 Ivabradine, an inhibitor of the If current in the sinoatrial node slows
the heart rate without negative inotropic effect. It lowers heart
rate at concentrations that do not affect other cardiac ionic
currents.
 Ivabradine reduced hospitalization and the combined endpoint of
cardiovascular related death and heart failure hospitalization
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E. Digoxin/Digitalis G. Aspirin
 Recommended for patients with symptomatic LV systolic
dysfunction who have concomitant atrial fibrillation, and it should  Routine use of aspirin is NOT recommended in patients with HF
be considered for patients with reduced LVEF (≤ 40) who have without atherosclerotic vascular disease
signs or symptoms of HF while receiving standard therapy,
including ACE inhibitors and beta blockers. LONG- TERM ANTITHROMBOTIC THERAPY
o NYHA class II-III  Long- term treatment with an antiplatelet agent, generally aspirin
o NYHA class IV in doses of 75-81 mg, is recommended for patients with HF due to
 Commonly initiated and maintained at a dose of 0.125–0.25 mg ischemic cardiomyopathy, whether or not they are receiving ACE
daily. For the great majority of patients, the dose should be 0.125 inhibitors
mg daily, and the serum digoxin level should be <1 ng/mL,  Warfarin and Clopidogrel (75 mg) also have prevented vascular
especially in elderly patients, patients with impaired renal function, events in post-MI patients and may be considered as alternatives
and patients with a low lean body mass. Higher doses (and serum to aspirin
concentrations) appear to be less beneficial. There is no indication
for using loading doses of digoxin to initiate therapy in patients IV. OTHER INTERVENTIONS FOR HEART FAILURE
with HF.
 In the past, digoxin was a mainstay for the treatment of heart A. CORONARY ARTERY REVASCULARIZATION VERSUS MEDICAL
failure because as an inotropic agent, it improved heart contraction THERAPY IN PATIENTS WITH HEART FAILURE
 May be considered to reduce the signs and symptoms of heart
failure even if you have already started the patient on the standard
treatments such as ace inhibitors, beta blockers, and diuretics, and
thus, digoxin is mainly for symptomatic relief
 Generally, digoxin is now used as therapy for patients who remain
profoundly symptomatic despite adequate neuro-hormonal
blockade and adequate volume control.
 It is recommended that the dose of digoxin, which should be based
on lean body mass, renal function and concomitant medications,
should be 0.125 mg daily in the majority of patients.
 The serum digoxin level should be < 1.0 ng/mL, generally 0.7- 0.9
ng/mL Figure 7. Comparison of coronary artery bypass grafting versus medical
 If you maintained the serum level at 0.8 ng/mL, the mortality therapy on long-term outcome in patients with ischemic cardiomyopathy: A
among the patients lowered compared to those in placebo. 25-year experience from the Duke Cardiovascular Disease Databank
 It might just be a problem of dosing and the right plasma level.
 Digoxin should be considered for achieving adequate control of  If you have a patient with coronary artery disease and you were
the ventricular response to atrial fibrillation in patients with HF able to demonstrate that the tissues are still viable, subjecting
 High doses of digoxin (maintenance dose > 0.25) them to revascularization will increase survival rate compared to
just giving medical treatment.
F. Warfarin  If there are no more viable tissues, don’t do revascularization. You
might kill the patient on the table.
 A patient who has heart failure with atrial fibrillation is at a higher
risk of developing an embolic event so they must be placed on an B. CORONARY ANGIOGRAPHY IN PATIENTS WITH HEART FAILURE
anti-coagulation, whether it is a permanent or transient atrial Current indications:
fibrillation.  Heart failure patients with angina
 If NOT at risk, NO need for warfarin, no need to anti-coagulate  Patients with prior myocardial infarction or known coronary artery
them. disease
 Treatment with warfarin (goal INR 2.0- 3.0) is recommended for all  Patients (younger than 65 years) with unexplained heart failure –
patients with: reasonable to consider
 HF and chronic or documented paroxysmal, persistent or long-  Positive exercise test in patients with cardiovascular risk factors
standing atrial fibrillation  Heart failure patients with positive scintigraphy, stress
 Or a history of systemic or pulmonary emboli, including stroke or echocardiography, or positron emmision tomography results
transient ischemic attack, unless contraindicated  Heart failure patients with severely dyskinetic myocardium
 It is recommended that patients with symptomatic or
asymptomatic ischemic cardiomyopathy and documented recent
large anterior MI or recent MI with documented LV thrombus be
treated with warfarin for the initial 3 months post-MI, unless
contraindicated.
 Other patients with ischemic or non-ischemic cardiomyopathy and
LV thrombus should be considered for chronic anticoagulation,
depending on the characteristics of the thrombus, such as its size,
mobility, and degree of calcification.

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 META-ANALYSIS OF CLINICAL OUTCOMES IN PATIENTS WITH AND D. EFFECT OF CARDIAC RESYNCHRONIZATION ON MORBIDITY AND
WITHOUT VIABLE MYOCARDIAL TISSUE MORTALITY IN HEART FAILURE

Figure 10. Kaplan-Meier analysis of the time to death from any cause or an
unplanned hospitalization for a major cardiovascular event
Figure 8. Death rates for patients with and without myocardial viability  If you put the patients in cardiac resynchronization, the patient is
treated by revascularization or medical therapy
free from death from any cause compared to medical treatment
alone.
 There was a 79.6 percent reduction in mortality for patients with
E. INTRAAORTIC BALLOON PUMP AND CONSOLE
myocardial viability treated by revascularization (P < 0.0001). In
patients without myocardial viability, there was NO significant
difference in mortality with revascularization versus medical
therapy.
 Comparisons are based on treatment strategy in patients with and
without myocardial viability. Annual mortality was lower in
revascularized patients when viability was present versus absent
(3.2 versus 7.7 percent; P < 0.0001). Annual mortality was
significantly higher in medically treated patients when viability was
present versus absent (16 versus 6.2 percent; P = 0.001).

C. SURVIVAL AFTER AORTIC VALVE REPLACEMENT FOR SEVERE Figure 11. Intra-aortic balloon pump and console is a mechanical
AORTIC STENOSIS circulatory support in patients with heart failure
 Every time the heart contracts, the balloon deflates and sucks
blood out of the heart into the circulation. During diastole when the
myocardium is being perfused, the balloon inflates and pushes
blood back into the aorta and supply the myocardium.
F. STEM CELL

Figure 9. Kaplan-Meier survival analysis of patients with low gradient aortic

stenosis treated with aortic valve replacement (AVR)
versus medical therapy (No AVR)
 With patients with severe aortic stenosis, if you replace their valve,
their survival is higher.

Figure 12. Stem Cell

 Stem cells induce regeneration of the myocardium. However, this

is still experimental.

Page 5 of 8
 G. SURGICAL TREATMENT OF CHRONIC CONGESTIVE HEART FAILURE
Figure 13. Secondary mitral regurgitation and left ventricular dilation
 Ventricular dilation displaces the papillary muscles, decreases
coaptation of the mitral leaflets, and leads to a central jet of
mitral regurgitation recognizable on echocardiography.
 If you have a patient with mitral regurgitation, you can repair in
order to diminish the wall stress.
H. LEFT VENTRICULAR ASSIST DEVICE
Figure 14. Left ventricular asst device
Components of the left ventricular assist device:
 The inflow cannula is inserted into the apex of the left ventricle
and the outflow cannula is anastomosed to the ascending aorta.
Blood returns from the lungs to the left side of the heart and exits
through the left ventricular apex and across an inflow valve into
the prosthetic pumping chamber. Blood is then actively pumped
through an outflow valve into the ascending aorta. The pumping
chamber is placed within the abdominal wall or peritoneal cavity. A
percutaneous driveline carries the electrical cable and air vent to
the battery packs (only the pack on the right side is shown) and
electronic controls, which are worn on a shoulder holster or belt,
respectively.
 The use of this device is limited mainly to patients with post-
cardiac surgery shock and to those who are bridged to
transplantation.
[4]
 The results of bridging to transplantation with the available devices
are quite good, with nearly 75% of younger patients receiving a
transplant by 1 year and having excellent post-transplant survival
rates.
[4]
 The early bridge-to-transplantation experience demonstrated
reduced post-transplantation survival when compared with
medical management; however, more recent experience has
shown equivalent outcomes following transplantation.
H. SURGICAL TECHNIQUES FOR CARDIAC TRANSPLANTATION
 Increasing numbers of heart transplant patients are surviving for
years following transplantation.
 The most recent update reveals 83% and 76% survival 1 and 3
years post-transplant, or a post-transplant “half-life” of 10.00
years. The quality of life in these patients is generally excellent,
with well over 90% of patients in the registry returning to normal
[4]
and unrestricted function following transplantation.
I. NON-PHARMACOLOGIC
 Dietary instruction regarding sodium intake is recommended in all
patients with HF.
 Patients with HF and diabetes, dyslipidemia or severe obesity
should be given specific dietary instructions
 Dietary sodium restriction (2-3 g daily) is recommended for
patients with the clinical syndrome of HF and preserved or
depressed LVEF.
 Further restriction (< 2 g daily) may be considered in moderate to
severe HF.
 Restriction of daily fluid intake to < 2 liters:
o is recommended in patients with severe hyponatremia (serum
sodium < 130 mEq/L)
o should be considered for all patients demonstrating fluid retention
that is difficult to control despite high doses of diuretic and sodium
restriction.
 It is recommended that patients with HF be advised to stop
smoking and to limit alcohol consumption to ≤ 2 standard drinks
per day in men or ≤ 1 standard drink per day in women.
 Patients suspected of having an alcohol-induced cardiomyopathy
should be advised to abstain from alcohol consumption.
 Patients suspected of using illicit drugs should be counseled to
discontinue such use.
 Pneumococcal vaccine and annual influenza vaccination are
recommended in all patients with HF in the absence of known
contraindications.
 NSAIDs, including COX-2 inhibitors, are NOT recommended in
patients with chronic HF because of blockage of COX-1 and COX-2
that decreases the production of prostaglandin leading to
peripheral vasoconstriction.
o The risk of renal failure and fluid retention is markedly
increased in the setting of reduced renal function or ACE
inhibitor therapy.
 It is recommended that patients with HF undergo exercise testing
to determine suitability for exercise training (patient does not
develop significant ischemia or arrhythmias). If deemed safe,
exercise training should be considered for patients with HF in order
to:
o Facilitate understanding of exercise expectations (heart rate
ranges and appropriate levels of exercise training)
o Increase exercise duration and intensity in a supervised
setting
o Promote adherence to a general exercise goal of 30 minutes
of moderate activity/exercise, 5 days per week with warm up
and cool down exercises
 Address the following issues:
o Stress/ depression o Employability
o Nutrition o Patient and family
o Sexual dysfunction education and counseling
(Sildenafil can be given but o Team management
do not use this with o End-of-life care
nitrates.)
Page 6 of 8
 V. ELEMENTS OF PATIENT EDUCATION CASE
ELEMENT SKILLS AND TARGET BEHAVIORS A 67 y/o man with long standing hypertension presents to the ER with
sudden onset chest pain described as ripping in quality which has
Definition of HF Discuss basic HF information, cause of patient’s
subsided since its onset. He was previously diagnosed with CAD where
and cause of HF, and how symptoms relate to HF status
angiogram only showed an insignificant lesion. His medications include
patient’s HF
ASA, Atorvastatin and Nifedipine. He appears diaphoretic with BP of
Recognition of Identify specific signs and symptoms (e.g.
110/50 on right arm, and 70/40 mmHg on left arm. JVP is elevated.
escalating increasing fatigue or shortness of breath,
Heart sounds are muffled. ECG showed non-specific findings and CXR
symptoms and edema, increasing fatigue)
showed cardiomegaly with globular shaped heart.
concrete plan for Perform daily weights and know how to respond
response to to evidence of volume overload
particular 1. What is the medication/ intervention that should be given to this
symptoms Develop action plan for notifying provider, patient?
changing diet, fluid and diuretics A. IV ganglionic blocking agent
Indications and use Reiterate dosing schedule, basic reason for B. Sodium nitroprusside
of each specific medications, what to do if a dose is C. Start IV fluids
medication missed D. Thrombolytic therapy
Modify risks for HF Initiate smoking cessation
progression Maintain BP in target range 2. Which of the following is the first diagnostic test that should be
performed?
Maintain normal HgA1c if diabetic
A. Cardiac enzymes
Maintain specific body weight B. CT scan of the Aorta
Specific activity/ Comply with prescribed exercise C. MRI of the aorta
exercise D. TEE/TTE
recommendations
Specific diet, Understand and comply with sodium restriction APPENDIX
sodium, and Demonstrate ability to read food label for
alcohol sodium per serving and sort into high- and low-
recommendations sodium
Reiterate limits for alcohol consumption or
abstinence if history of abuse
Treatment Plan and use a medication system that
adherence promotes adherence
Plan for refills

Figure 15. Outcome with a cardiomyopathy relating to etiology

In a study of 1230 patients with a cardiomyopathy of various
etiologies, the adjusted Kaplan-Meier estimates of survival is related
to the underlying cause of cardiomyopathy. Only idiopathic
cardiomyopathy and cardiomyopathy due to causes for which
survival was significantly different from that in patients with
idiopathic cardiomyopathy are shown. The best outcome is in those
with a Peripartum Cardiomyopathy, and the worst outcome is in
those with an infiltrative cardiomyopathy or that due to HIV
infection.

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 Subject: Medicine
Topic: 4.03b Heart Failure II: Management
Lecturer: Dr. Tolentino
Date: November 10, 2015

APPENDIX

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Edited By: Alie and Kimber