Transcript Document

Management of chest pain and
heart failure. Cardiac rehabilitation
and secondary prevention
WT Bong
Dept of Family Medicine, HUKM
Case scenario 1
• 60 yo gentleman, a known case of DM for the past 2 years
complains of chest pain for the past 2-3 months when he
walks more than 10 minutes. The chest pain radiates to left
arm, lasts 5 min, relieved by rest. Currently during his visit to
the primary care clinic, he has no chest pain. He is a smoker
for the past 40 years. He is on metformin 500mh bd only.
Clinically, BP 120/60mmHg and cardiovascular examination
was unremarkable.
Patient comes in with chest pain..
• ?cardiovascular
– Cardiac.
• MV prolapse.pericarditis
• ischemic
– Non cardiac. Aortic dissection
•
•
•
•
?gastrointestinal. GERD
?Musculoskeletal.fibromyalgia.
?pulmonary
?psychogenic
Patient comes in with chest pain..
• ?cardiovascular
– Cardiac.
• MV prolapse.pericarditis
• ischemic
– Non cardiac. Aortic dissection
•
•
•
•
?gastrointestinal. GERD
?Musculoskeletal.fibromyalgia.
?pulmonary
?psychogenic
We start with stable angina..
• By definition. Clinical syndrome characterised
by
– discomfort in chest, jaw, shoulder, back or arm
– Typically aggravated by exertion or emotional
stress
– Reduced by rest or GTN
• Most common cause for stable angina is
atherosclerotic coronary artery disease (CAD)
• Other causes could be
– Hypertrophic cardiomyopathy
– Aortic stenosis
– Coronary vasospasm etc
Atherosclerosis process in coronary
Stable angina is classified into 4 classes
based on Canadian Cardiovascular
Society Classification (CCS 0-IV)
CLASS
SEVERITY OF EXERTIONL STRESS
INDUCING ANGINA
LIMITATION OF ORDINARY
ACTIVITY
I
STRENUOUS, RAPID OR PROLONGED
EXERTION AT WORK OR RECREATION
NONE
II
WALKING OR CLIMBING STAIRS RAPIDLY,
WALKING UPHILL, CLIMBING STAIRS AFTER
MEAL
SLIGHT
III
WALKING 1-2 BLOCKS ON THE LEVEL AND
CLIMBING ONE FLIGHT OF STAIRS AT
NORMAL PACE
MARKED
IV
INABILITY TO CARRY OUT ANY PHYSICAL
ACTIVITY WITHOUR DISCOMFORT OR
SYMPTOMS PRESENT AT REST
DISCOMFORT IN ALL
ACTIVITY PERFORMED
• However, it might become unstable, which is
unstable angina, with possible progression to
NSTEMI and STEMI too
Diagnosis of stable angina can be
established by
• Clinical assessment
– Look for complication of CAD.murmur(MR).septal
defect.sign of cardiomegaly.CHF
– Other site of atherosclerosis.carotid
bruit.peripheral vascular disease.aortic aneurysm
– Risk factor for atherosclerosis.hpt.metabolic syn
– Other cause of angina.HOCM.aortic stenosis
• Lab test
• Specific cardiac investigation
• Lab test to establish CVS risk factor
– FLP. FBS. homocysteine level
– Determine prognosis, creatinine
– CXR only if suspect CHF if want to see calcification,
cardiomegaly/atrial enlargement, valvular disease,
pulmonary congestion (help establish prognosis)
• Specific cardiac investigation
• Specific cardiac investigation, non invasive
– ECG. See previous ischemia, LVH, BBB, arrhythmia
or conduction defect
– Stress test. More sensitive and specific than
resting ECG
– Echo.when there is abnormal auscultation suggest
valvular, if HCM or prev MI changes on ECG, SSx
CHF , to study diastolic function
Risk-stratify our patient
• For the purpose of prognosis + treatment
(revascularize in high risk patient)
Clinical history – important predictor
of adverse outcome in established CAD
DM
HPT
Metabolic
syndrome
Current smoker
Increasing age
Prior MI
SSx of CHF
Recent onset or
progressive
angina
dyslipidaemia
Responsiveness of
angina to
therapy
Risk stratify .. Higher risk if ECG shows
Evidence of
prior MI
LBBB
LVH
AF
Second of
third degree
AV block
Other aspects to be considered in riskstratifying
• Stress test
• Ventricular function
• COROS
LVEF
< 35 %
12- year
survival rate
(p<0.0001)
21 %
35-49 %
54 %
> 50 %
73 %
Treatment goal
• Prevent MI & death
• Improve SSx of angina & increase QoL
Non pharmacological approach
Life style
• Smoking cessation
– 36 % risk reduction mortality
– 32 % risk reduction non fatal
MI
– Nicotine replacement is safe
and cost effective even for
CAD patient (take into
account risk of depression
and suicidal thought)
diet
• Variety of fruits and
vegetable.legumes.nuts.
Soy products.low fat
dairy.whole grain
• Replace saturated & transfat (red meat.whole milk .
Pastries) with polysaturated
fat (oily fish,walnut,sesame.
Pumpkin seed.vegetable oil)
• Soluble fibre.oat.peas.bean
Alcohol restriction.
Moderate/beneficial.
Insufficient evidence
Physical activity.
30min
3-4x/week
Target BP <130/80
DM
Generally target HbA1c <
6.5 %. Individualize as
Keep waist circumference
< 85 cm for men
< 80 cm for women
Correct anaemia
Correct hyperthyroid state
HDL > 1.0 male, 1.2 female
( secondary target)
TG < 1.7
(secondary target)
hypoglycemia worsen angina &
increase mortality
LDL < 1.8 ( primary target)
education
Self management
During acute anginal
attack
-Restrain activity
-GTN S/L or spray
-Sit . Hypotension.
Headache after GTN
Can also take GTN as
preventive measure if
patient know he is going to
have attack while carrying
out some activity
If SSx persist more than
10min at rest or not
improved after 3 tablet of
GTN, advice to go to
hospital
Antithrombotic
Antithrombotic
ASA 75-150mg od. Lower MI, cardiac death
Clopidogrel 75mg
-more effective than ASA in peripheral
vascular disease
or stroke
Take into account GI side effect
*double antiplatelet not warranted in
angina
Ticlopidine – proven efficacy in stroke
and post-PCI, no evidence in angina
Lipid lowering
ACEi
Statin reduce mortality & CV event by
20 – 30 %
For secondary prevention in post MI +
reduced EF < 40 %
Can add ezetimide if target not
reached with statin
Recommended for all patients with
CAD esp with concomitant LV
dysfunction/DM
ARB
Beta blocker
\as secondary prevention in CAD with Hpt/
CHF / post MI + LV dysfunction / DM if not
tolerable to ACEi
First line treatment in angina
- 30 % reduction risk of CV death / MI (beta
blocker in post MI trials)
-Beta1 blockade by Metoprolol/bisoprolol reduce cardiac
event in CHF
-Non selective beta blockade by carvedilol reduce death
& CV hospitalisation in CHF
Ivabradine
Calcium Channel Blocker
HR reducing, acting on SA node
-non dihydropyridine – diltiazem/verapamil,
Symptomatic treatment in patient with N`SR, as alternative to beta blocker
esp with contraindication for beta blocker
-dihydropyridine (long acting) –amlodipine No significant interaction with other cardiac use in patient reduce coronary intervention
but no reduction in treatment endpoints (ie death , MI)
drugs
Nitrates
Trimetazidine
(long acting – isordil,imdur)
(Vasteral MR)
Symptomatic improvement of angina
No prognostic benefit
symptomatic relief of angina
Safe and effective in patient with ED
Dipyridamole
Anticoagulant
Not indicated unless has AF
(Persanthine)
not recommended, poor antithrombotic
efficacy in angina
revascularization
• PCI or CABG
– In high risk group it is firstline treatment
• Significant LMS ( > 50% stenosis)
• Significant proximal mutivessel involvement
• Multivessel disease with impaired LV function with
proven viable myocardium
– Or if failed medical treatment to control angina
SSx
– In asymptomatic patient, consider if there is
extensive inducible ischaemia (stress test)
What if it is aMI ?
Chest pain
ECG ,cardiac biomarker
STEMI
Concomitant initial
management
Sublingual GTN, continuous ECG
monitoring, oxygen, ASA, clopidogrel,
analgesia
Assessment for reperfusion
< 3hrs
3-12hrs
> 12 hrs
Onset of symptoms < 3 hrs
3-12 hrs
> 12 hrs
Preferred options
Primary PCI
(if door to balloon time <
Medical therapy +/anti thrombotics
Primary PCI
(preferred in high risk
patient or
contraindicated for
thrombolytic) or
90min)
fibrinolytic
Second options
fibrinolytics
Primary PCI
( if clinically indicated)
Concomitant
therapy
Anti thrombotics
Beta blockers
ACEi / ARB
Statins
Nitrates
CCB
Secondary prevention
• Basically similar to angina which include
Smoking cessation
diet
Regular exercise
BP control
Glycemic control
Antiplatelet agent
*consider dual antiplatelet
1mth-1yr depend on stent
used
Beta blocker
ACEi and ARB
Lipid lowering
• Oral Anticoagulant (warfarin)
– If AF
– LV thrombus for 3-6mths
Secondary prevention
• Hormone replacement therapy is not
beneficial for secondary prevention
• Postmenopausal women who were taking HRT
at the time of STEMI should discontinue it
• Vitamin E and antioxidants have no clinical
benefit
• Garlic, lecithin, vitamin A and C are not
beneficial
Heart failure
Heart failure
• Is a complex clinical syndrome results from
structural or functional impairment of
ventricular filling or ejection of blood
• Cardinal manifestation are dyspnea, fatigue,
which may limit effort tolerance, and fluid
retention, which may lead to pulmonary or
splanchnic congestion or peripheral edema.
Definition of Heart Failure
Classification
I. Heart Failure with
Reduced Ejection Fraction
(HFrEF)
Ejection
Fraction
≤40%
Description
Also referred to as systolic HF. Randomized clinical trials have
mainly enrolled patients with HFrEF and it is only in these patients
that efficacious therapies have been demonstrated to date.
≥50%
Also referred to as diastolic HF. Several different criteria have been
used to further define HFpEF. The diagnosis of HFpEF is
challenging because it is largely one of excluding other potential
noncardiac causes of symptoms suggestive of HF. To date,
efficacious therapies have not been identified.
a. HFpEF, Borderline
41% to 49%
These patients fall into a borderline or intermediate group. Their
characteristics, treatment patterns, and outcomes appear similar to
those of patient with HFpEF.
b. HFpEF, Improved
>40%
It has been recognized that a subset of patients with HFpEF
previously had HFrEF. These patients with improvement or recovery
in EF may be clinically distinct from those with persistently
preserved or reduced EF. Further research is needed to better
characterize these patients.
II. Heart Failure with
Preserved Ejection
Fraction (HFpEF)
Stages, Phenotypes and Treatment of
HF
At Risk for Heart Failure
Heart Failure
STAGE A
STAGE B
STAGE C
At high risk for HF but
without structural heart
disease or symptoms of HF
Structural heart disease
but without signs or
symptoms of HF
Structural heart disease
with prior or current
symptoms of HF
e.g., Patients with:
· HTN
· Atherosclerotic disease
· DM
· Obesity
· Metabolic syndrome
or
Patients
· Using cardiotoxins
· With family history of
cardiomyopathy
Structural heart
disease
e.g., Patients with:
· Previous MI
· LV remodeling including
LVH and low EF
· Asymptomatic valvular
disease
Development of
symptoms of HF
e.g., Patients with:
· Known structural heart disease and
· HF signs and symptoms
HFpEF
THERAPY
Goals
· Heart healthy lifestyle
· Prevent vascular,
coronary disease
· Prevent LV structural
abnormalities
Drugs
· ACEI or ARB in
appropriate patients for
vascular disease or DM
· Statins as appropriate
THERAPY
Goals
· Prevent HF symptoms
· Prevent further cardiac
remodeling
Drugs
· ACEI or ARB as
appropriate
· Beta blockers as
appropriate
In selected patients
· ICD
· Revascularization or
valvular surgery as
appropriate
STAGE D
Refractory HF
THERAPY
Goals
· Control symptoms
· Improve HRQOL
· Prevent hospitalization
· Prevent mortality
Strategies
· Identification of comorbidities
Treatment
· Diuresis to relieve symptoms
of congestion
· Follow guideline driven
indications for comorbidities,
e.g., HTN, AF, CAD, DM
· Revascularization or valvular
surgery as appropriate
Refractory
symptoms of HF
at rest, despite
GDMT
e.g., Patients with:
· Marked HF symptoms at
rest
· Recurrent hospitalizations
despite GDMT
HFrEF
THERAPY
Goals
· Control symptoms
· Patient education
· Prevent hospitalization
· Prevent mortality
Drugs for routine use
· Diuretics for fluid retention
· ACEI or ARB
· Beta blockers
· Aldosterone antagonists
Drugs for use in selected patients
· Hydralazine/isosorbide dinitrate
· ACEI and ARB
· Digoxin
In selected patients
· CRT
· ICD
· Revascularization or valvular
surgery as appropriate
THERAPY
Goals
· Control symptoms
· Improve HRQOL
· Reduce hospital
readmissions
· Establish patient’s endof-life goals
Options
· Advanced care
measures
· Heart transplant
· Chronic inotropes
· Temporary or permanent
MCS
· Experimental surgery or
drugs
· Palliative care and
hospice
· ICD deactivation
Classification of Heart Failure
A
B
C
ACCF/AHA Stages of HF
At high risk for HF but without structural
heart disease or symptoms of HF.
Structural heart disease but without signs
or symptoms of HF.
Structural heart disease with prior or
current symptoms of HF.
NYHA Functional Classification
None
I
I
II
III
IV
D
Refractory HF requiring specialized
interventions.
No limitation of physical activity.
Ordinary physical activity does not cause
symptoms of HF.
No limitation of physical activity.
Ordinary physical activity does not cause
symptoms of HF.
Slight limitation of physical activity.
Comfortable at rest, but ordinary physical
activity results in symptoms of HF.
Marked limitation of physical activity.
Comfortable at rest, but less than ordinary
activity causes symptoms of HF.
Unable to carry on any physical activity
without symptoms of HF, or symptoms of
HF at rest.
Physical examination
•
•
•
•
•
•
•
•
BMI and evidence of weight loss
Bp, supine and upright( orthostatic changes – volume depletion)
Pulse – strength and regularity
JVP
Extra heart sound, murmur, apex beat displacement, RV heave
Pulmonary status
Hepatomegaly
Peripheral edema
Lab investigation
•
•
•
•
•
•
•
Class I
1.Initial laboratory evaluation of patients presenting with HF should include complete
blood count, urinalysis, serum electrolytes (including calcium and magnesium), blood urea
nitrogen, serum creatinine, glucose, fasting lipid profile, liver function tests, and thyroidstimulating hormone. (Level of Evidence: C)
2.Serial monitoring, when indicated, should include serum electrolytes and renal function.
(Level of Evidence: C)
3.A 12-lead ECG should be performed initially on all patients presenting with HF. (Level of
Evidence: C)
Class Iia
1.Screening for hemochromatosis or HIV is reasonable in selected patients who present
with HF (Level of Evidence: C)
2.Diagnostic tests for rheumatologic diseases, amyloidosis, or pheochromocytoma are
reasonable in patients presenting with HF in whom there is a clinical suspicion of these
diseases. (Level of Evidence: C)
Recommendations for Biomarkers in HF
Biomarker, Application
Setting
COR
LOE
Diagnosis or exclusion of HF
Ambulatory,
Acute
I
A
Prognosis of HF
Ambulatory,
Acute
I
A
Ambulatory
IIa
B
Acute
IIb
C
Acute,
Ambulatory
I
A
IIb
B
IIb
A
Natriuretic peptides
Achieve GDMT
Guidance of acutely decompensated
HF therapy
Biomarkers of myocardial injury
Additive risk stratification
Biomarkers of myocardial fibrosis
Ambulatory
Additive risk stratification
Acute
Recommendations for Noninvasive Imaging
Recommendation
Patients with suspected, acute, or new-onset HF should undergo a chest xray
A 2-dimensional echocardiogram with Doppler should be performed for
initial evaluation of HF
Repeat measurement of EF is useful in patients with HF who have had a
significant change in clinical status or received treatment that might affect
cardiac function, or for consideration of device therapy
Noninvasive imaging to detect myocardial ischemia and viability is
reasonable in HF and CAD
Viability assessment is reasonable before revascularization in HF patients
with CAD
Radionuclide ventriculography or MRI can be useful to assess LVEF and
volume
MRI is reasonable when assessing myocardial infiltration or scar
Routine repeat measurement of LV function assessment should not be
performed
COR
LOE
I
C
I
C
I
C
IIa
C
IIa
B
IIa
C
IIa
B
III: No
Benefit
B
ACC AHA heart failure 2013
• Treament based on stages of heart failure
ACCF/AHA Stages of HF
NYHA Functional Classification
A
At high risk for HF but without structural
heart disease or symptoms of HF
none
B
Structural heart disease but without
signs or symptoms of HF
I
No limitation of physical activity. Ordinary
physical activity does not cause symptoms of
HF.
C
Structural heart disease with prior or
current symptoms of HF
I
No limitation of physical activity. Ordinary
physical activity does not cause symptoms of
HF.
II
Slight limitation of physical activity.
Comfortable at rest, but ordinary physical
activity results in symptoms of HF.
III
Marked limitation of physical activity.
Comfortable at rest, but less than ordinary
activity causes symptoms of HF.
IV
Unable to carry on any physical activity
without symptoms of HF, or symptoms of HF
at rest.
IV
Unable to carry on any physical activity
without symptoms of HF, or symptoms of HF
at rest.
D
Refractory HF requiring specialized
interventions
ACC AHA heart failure 2013
• Stage A: Recommendations
• Class I
• 1.Hypertension and lipid disorders should be controlled in
accordance with contemporary guidelines to lower the risk
of HF(Level of Evidence: A)
• 2.Other conditions that may lead to or contribute to HF, such
as obesity, diabetes mellitus, tobacco use, and known
cardiotoxic agents, should be controlled or avoided. (Level of
Evidence: C)
HFSA 2010 Practice Guideline (3.1)
Heart Failure Prevention
A careful and thorough clinical
assessment, with appropriate
investigation for known or potential risk
factors, is recommended in an effort to
prevent development of LV remodeling,
cardiac dysfunction, and HF.
Strength of Evidence = A
Adapted from:
HFSA 2010 Practice Guideline (3.2)
HF Risk Factor Treatment Goals
Risk Factor
Goal
Hypertension
Generally < 130/80
Diabetes
See ADA guidelines1
Hyperlipidemia
See NCEP guidelines2
Inactivity
20-30 min. aerobic 3-5 x wk.
Obesity
Weight reduction < 30 BMI
Alcohol
Men ≤ 2 drinks/day, women ≤ 1
Smoking
Cessation
Dietary Sodium
Maximum 2-3 g/day
1Diabetes
2JAMA
Adapted from:
Care 2006; 29: S4-S42
2001; 285:2486-97
Treating Hypertension to Prevent HF
Aggressive blood
pressure control:
Decreases
risk of
new HF
by ~ 50%
56% in T2DM
Lancet 1991;338:1281-5 (STOP-Hypertension
JAMA 1997;278:212-6 (SHEP)
UKPDS Group. UKPDS 38. BMJ 1998;317:703-713
Aggressive BP control in
patients with prior MI:
Decreases
risk of
new HF
by ~ 80%
HFSA 2010 Practice Guideline (3.3-3.4)
Prevention—ACEI and Beta Blockers
ACE inhibitors are recommended for prevention of HF in patients at
high risk for this syndrome, including those with:
– Coronary artery disease
– Peripheral vascular disease
– Stroke
– Diabetes and another major risk factor
Strength of Evidence = A
ACE inhibitors and beta blockers are recommended for all patients
with prior MI.
Strength of Evidence = A
HFSA 2010 Practice Guideline (4.8, 4.10)
Heart Failure Patient Evaluation
Recommended evaluation for patients with a diagnosis of HF:
– Assess clinical severity and functional limitation by history, physical
examination, and determination of functional class*
–
–
–
–
–
–
–
Assess cardiac structure and function
Determine the etiology of HF
Evaluate for coronary disease and myocardial ischemia
Evaluate the risk of life threatening arrhythmia
Identify any exacerbating factors for HF
Identify co-morbidities which influence therapy
Identify barriers to adherence and compliance Strength of Evidence = C
*Metrics to consider include the 6-minute walk test and NYHA functional class
Adapted from:
Recommendations for Treatment of Stage B HF
Recommendations
In patients with a history of MI and reduced EF, ACE inhibitors or
ARBs should be used to prevent HF
In patients with MI and reduced EF, evidence-based beta blockers
should be used to prevent HF
In patients with MI, statins should be used to prevent HF
Blood pressure should be controlled to prevent symptomatic HF
ACE inhibitors should be used in all patients with a reduced EF to
prevent HF
Beta blockers should be used in all patients with a reduced EF to
prevent HF
An ICD is reasonable in patients with asymptomatic ischemic
cardiomyopathy who are at least 40 d post-MI, have an LVEF ≤30%,
and on GDMT
Nondihydropyridine calcium channel blockers may be harmful in
patients with low LVEF
COR
LOE
I
A
I
B
I
A
I
A
I
A
I
C
IIa
B
III: Harm
C
Treatment of Stages A to D
Stage C
Treatment of Stages A to D
Nonpharmacological
Interventions
I
IIa
Stage C: Nonpharmacological
Interventions
IIb
III
Patients with HF should receive specific education to
facilitate HF self-care.
I
IIa
IIb
III
Exercise training (or regular physical activity) is
recommended as safe and effective for patients with HF who
are able to participate to improve functional status.
I
IIa
IIb
III
Sodium restriction is reasonable for patients with
symptomatic HF to reduce congestive symptoms.
Treatment of Stages A to D
Pharmacological Treatment for
Stage C HFrEF
Pharmacologic Treatment for Stage C HFrEF
HFrEF Stage C
NYHA Class I – IV
Treatment:
Class I, LOE A
ACEI or ARB AND
Beta Blocker
For all volume overload,
NYHA class II-IV patients
For persistently symptomatic
African Americans,
NYHA class III-IV
For NYHA class II-IV patients.
Provided estimated creatinine
>30 mL/min and K+ <5.0 mEq/dL
Add
Add
Add
Class I, LOE C
Loop Diuretics
Class I, LOE A
Hydral-Nitrates
Class I, LOE A
Aldosterone
Antagonist
Pharmacological Treatment for
Stage C HFrEF (cont.)
I
IIa
IIb
III
Diuretics are recommended in patients with HFrEF who have
evidence of fluid retention, unless contraindicated, to improve
symptoms.
I
IIa
IIb
III
ACE inhibitors are recommended in patients with HFrEF and
current or prior symptoms, unless contraindicated, to reduce
morbidity and mortality.
I
IIa
IIb
III
ARBs are recommended in patients with HFrEF with current or
prior symptoms who are ACE inhibitor-intolerant, unless
contraindicated, to reduce morbidity and mortality.
Drugs Commonly Used for HFrEF
(Stage C HF)
Drug
ACE Inhibitors
Captopril
Enalapril
Fosinopril
Lisinopril
Perindopril
Quinapril
Ramipril
Trandolapril
ARBs
Candesartan
Losartan
Valsartan
Aldosterone Antagonists
Spironolactone
Eplerenone
Initial Daily Dose(s)
Maximum Doses(s)
Mean Doses Achieved in
Clinical Trials
6.25 mg 3 times
2.5 mg twice
5 to 10 mg once
2.5 to 5 mg once
2 mg once
5 mg twice
1.25 to 2.5 mg once
1 mg once
50 mg 3 times
10 to 20 mg twice
40 mg once
20 to 40 mg once
8 to 16 mg once
20 mg twice
10 mg once
4 mg once
122.7 mg/d (421)
16.6 mg/d (412)
--------32.5 to 35.0 mg/d (444)
---------------------------------
4 to 8 mg once
25 to 50 mg once
20 to 40 mg twice
32 mg once
50 to 150 mg once
160 mg twice
24 mg/d (419)
129 mg/d (420)
254 mg/d (109)
12.5 to 25 mg once
25 mg once
25 mg once or twice
50 mg once
26 mg/d (424)
42.6 mg/d (445)
Drugs Commonly Used for HFrEF
(Stage C HF) (cont.)
Drug
Initial Daily Dose(s)
Beta Blockers
Bisoprolol
1.25 mg once
Carvedilol
3.125 mg twice
Carvedilol CR
10 mg once
Metoprolol succinate
extended release
12.5 to 25 mg once
(metoprolol CR/XL)
Hydralazine & Isosorbide Dinitrate
37.5 mg hydralazine/
Fixed dose combination
20 mg isosorbide
(423)
dinitrate 3 times daily
Hydralazine and
Hydralazine: 25 to 50
isosorbide dinitrate (448)
mg, 3 or 4 times daily
and isorsorbide
dinitrate:
20 to 30 mg
3 or 4 times daily
Maximum Doses(s)
Mean Doses Achieved in
Clinical Trials
10 mg once
50 mg twice
80 mg once
8.6 mg/d (118)
37 mg/d (446)
---------
200 mg once
159 mg/d (447)
75 mg hydralazine/
40 mg isosorbide
dinitrate 3 times daily
Hydralazine: 300 mg
daily in divided doses
and isosorbide dinitrate
120 mg daily in
divided doses
~175 mg hydralazine/90 mg
isosorbide dinitrate daily
---------
Pharmacological Treatment for
Stage C HFrEF (cont.)
I
IIa
IIb
III
ARBs are reasonable to reduce morbidity and mortality as
alternatives to ACE inhibitors as first-line therapy for patients
with HFrEF, especially for patients already taking ARBs for other
indications, unless contraindicated.
I
IIa
IIb
III
Addition of an ARB may be considered in persistently
symptomatic patients with HFrEF who are already being treated
with an ACE inhibitor and a beta blocker in whom an
aldosterone antagonist is not indicated or tolerated.
Pharmacological Treatment for
Stage C HFrEF (cont.)
I
IIa
IIb
III
Routine combined use of an ACE inhibitor, ARB, and aldosterone
antagonist is potentially harmful for patients with HFrEF.
Harm
I
IIa
IIb
III
Use of 1 of the 3 beta blockers proven to reduce mortality (i.e.,
bisoprolol, carvedilol, and sustained-release metoprolol
succinate) is recommended for all patients with current or prior
symptoms of HFrEF, unless contraindicated, to reduce morbidity
and mortality.
Pharmacological Treatment for
Stage C HFrEF (cont.)
I
IIa
IIb
III
Aldosterone receptor antagonists [or mineralocorticoid receptor
antagonists (MRA)] are recommended in patients with NYHA class
II-IV and who have LVEF of 35% or less, unless contraindicated, to
reduce morbidity and mortality. Patients with NYHA class II should
have a history of prior cardiovascular hospitalization or elevated
plasma natriuretic peptide levels to be considered for aldosterone
receptor antagonists.
Pharmacological Treatment for
Stage C HFrEF (cont.)
I
IIa
IIb
III
Aldosterone receptor antagonists are recommended to reduce
morbidity and mortality following an acute MI in patients who
have LVEF of 40% or less who develop symptoms of HF or who
have a history of diabetes mellitus, unless contraindicated.
I
IIa
IIb
Harm
III
Inappropriate use of aldosterone receptor antagonists is
potentially harmful because of life-threatening hyperkalemia or
renal insufficiency when serum creatinine greater than 2.5
mg/dL in men or greater than 2.0 mg/dL in women (or
estimated glomerular filtration rate <30 mL/min/1.73m2),
and/or potassium above 5.0 mEq/L.
Pharmacological Treatment for
Stage C HFrEF (cont.)
I
IIa
IIb
III
The combination of hydralazine and isosorbide dinitrate is
recommended to reduce morbidity and mortality for patients
self-described as African Americans with NYHA class III–IV
HFrEF receiving optimal therapy with ACE inhibitors and beta
blockers, unless contraindicated.
I
IIa
IIb
III
A combination of hydralazine and isosorbide dinitrate can be
useful to reduce morbidity or mortality in patients with current
or prior symptomatic HFrEF who cannot be given an ACE
inhibitor or ARB because of drug intolerance, hypotension, or
renal insufficiency, unless contraindicated.
Pharmacological Treatment for
Stage C HFrEF (cont.)
I
IIa
IIb
III
Digoxin can be beneficial in patients with HFrEF, unless
contraindicated, to decrease hospitalizations for HF.
I
IIa
IIb
III
Patients with chronic HF with permanent/persistent/
paroxysmal AF and an additional risk factor for cardioembolic
stroke (history of hypertension, diabetes mellitus, previous
stroke or transient ischemic attack, or ≥75 years of age) should
receive chronic anticoagulant therapy (in the absence of
contraindications to anticoagulation).
Pharmacological Treatment for
Stage C HFpEF (cont.)
I
IIa
IIb
III
I
IIa
IIb
III
Management of AF according to published clinical practice
guidelines in patients with HFpEF is reasonable to improve
symptomatic HF.
The use of beta-blocking agents, ACE inhibitors, and ARBs in
patients with hypertension is reasonable to control blood
pressure in patients with HFpEF.
Medical Therapy for Stage C HFrEF:
Magnitude of Benefit Demonstrated in RCTs
GDMT
ACE inhibitor or
ARB
Beta blocker
Aldosterone
antagonist
Hydralazine/nitrate
(Standardized to 36 mo)
RR Reduction
in HF
Hospitalizations
17%
26
31%
34%
9
41%
30%
6
35%
43%
7
33%
RR Reduction
in Mortality
NNT for Mortality
Reduction
Treatment of Stages A to D
Treatment for Stage C HFpEF
Treatment of HFpEF
Recommendations
Systolic and diastolic blood pressure should be controlled
according to published clinical practice guidelines
Diuretics should be used for relief of symptoms due to
volume overload
Coronary revascularization for patients with CAD in
whom angina or demonstrable myocardial ischemia is
present despite GDMT
Management of AF according to published clinical
practice guidelines for HFpEF to improve symptomatic
HF
Use of beta-blocking agents, ACE inhibitors, and ARBs
for hypertension in HFpEF
ARBs might be considered to decrease hospitalizations in
HFpEF
Nutritional supplementation is not recommended in
HFpEF
COR
LOE
I
B
I
C
IIa
C
IIa
C
IIa
C
IIb
B
III: No
Benefit
C
Treatment of Stages A to D
Device Treatment for Stage C
HFrEF
Device Therapy for Stage C HFrEF
I
IIa
IIb
III
ICD therapy is recommended for primary prevention of SCD to reduce
total mortality in selected patients with nonischemic DCM or ischemic
heart disease at least 40 days post-MI with LVEF of 35% or less, and
NYHA class II or III symptoms on chronic GDMT, who have reasonable
expectation of meaningful survival for more than 1 year.
I
IIa
IIb
III
NYHA Class III/IV
I
IIa
IIb
III
NYHA Class II
CRT is indicated for patients who have LVEF of 35% or less, sinus
rhythm, left bundle-branch block (LBBB) with a QRS duration of 150 ms
or greater, and NYHA class II, III, or ambulatory IV symptoms on GDMT.
Treatment of Stages A to D
Stage D
Clinical Events and Findings Useful for
Identifying Patients With Advanced HF
Repeated (≥2) hospitalizations or ED visits for HF in the past year
Progressive deterioration in renal function (e.g., rise in BUN and creatinine)
Weight loss without other cause (e.g., cardiac cachexia)
Intolerance to ACE inhibitors due to hypotension and/or worsening renal function
Intolerance to beta blockers due to worsening HF or hypotension
Frequent systolic blood pressure <90 mm Hg
Persistent dyspnea with dressing or bathing requiring rest
Inability to walk 1 block on the level ground due to dyspnea or fatigue
Recent need to escalate diuretics to maintain volume status, often reaching daily
furosemide equivalent dose >160 mg/d and/or use of supplemental metolazone therapy
Progressive decline in serum sodium, usually to <133 mEq/L
Frequent ICD shocks
Adapted from Russell et al. Congest Heart Fail. 2008;14:316-21.
Treatment of Stages A to D
Water Restriction
Water Restriction
I
IIa
IIb
III
Fluid restriction (1.5 to 2 L/d) is reasonable in stage
D, especially in patients with hyponatremia, to
reduce congestive symptoms.
Surgical/Percutaneous/Transcatheter
Interventional Treatment of HF
I
IIa
IIb
III
I
IIa
IIb
III
Coronary artery revascularization via CABG or percutaneous
intervention is indicated for patients (HFpEF and HFrEF) on
GDMT with angina and suitable coronary anatomy, especially for
a left main stenosis (>50%) or left main equivalent disease.
CABG to improve survival is reasonable in patients with mild to
moderate LV systolic dysfunction (EF 35% to 50%) and significant
(≥70% diameter stenosis) multivessel CAD or proximal LAD
coronary artery stenosis when viable myocardium is present in
the region of intended revascularization.
Heart failure with preserved EF
or diastolic heart failure
Heart failure with preserved EF
Case scenario 2
• A 55 yo man presents with gradually increasing shortness of breath and
leg swelling that occurred while on a business trip. He has congestive
heart failure, which has caused fatigue and shortness of breath if he walks
a block or climbs a flight of stairs. BP is 140/ 90; there is no jugular venous
distension or gallop, and only minimal pedal edema. AN echo shows left
ventricular EF 45 %. Current medication include aspirin and simvastatin.
The patient desires to keep medications to a minimum. What additional
treatments are indicated at this time?
• A. Spironolactone
• B. ACE inhibitor and beta blocker
• C. Digoxin
• D. Frusemide
• E. An implantable defibrillator
Cardiac rehabilitation
• Coordinated interventions designed to
optimize a cardiac patient’s physical,
psychological, and social functioning, in
addition to stabilizing or slowing the progress
of underlying atherosclerotic process, thereby
reducing morbidity and mortality.
• Answer is B
• ACE inhibitor is recommended in both symptomatic n
asymptomatic heart failure
• Beta blocker stabilize left ventricular remodeling
• Spironolactone recommended for NYHA III-IV with EF <35%
despite on loop diuretic + ACEi + b blocker
• Frusemide can improve SSx but patient wants to keep
medication to minimal
• Defibrillator not indicated yet
Cardiac rehabilitation
• Include
– baseline patient assesssment,
– nutritional counselling,
– aggressive risk factor management ie
• lipid, hpt, weight, diabetes and smoking,
– psychosocial and vocational counseling , and
– physical activity counseling and exercise training, in
addition to
– appropriate use of cardioprotective drugs that have
evidence-based efficacy for secondary prevention
Who should be included in cardiac
rehab ?
•
•
•
•
•
Patient with previous MI
Who had undergone CABG
Those with PCI done
Heart transplant candidate or recipient
Who has stable chronic heart failure,
peripheral arterial disease
Exercise training
intervention
Return to work
Cardioprotective mechanism (improve endothelial function)
Risk factor
modification &
intervention
Aggresive reduction of risk factors via nutritional
counselling, weight management, adherence to drug
therapy
Psychosocial
intervention (address depression,
anxiety, social isolation. Consider SSRI, cognitive
behavioral therapy.
Thank you for your kind
attention