Management of chest pain and heart failure. Cardiac rehabilitation and secondary prevention

Lindenfeld J, et al. HFSA 2010 Comprehensive Heart Failure Guideline. J Card Fail 2010;16:e1-e194.

Management of chest pain and heart failure. Cardiac rehabilitation

and secondary prevention

WT BongDept 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


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 ANGINALIMITATION 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


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

Responsiveness of angina to therapy

dyslipidaemia


Risk stratify .. Higher risk if ECG shows

Evidence of prior MI

LBBB Second of third degree

AV block

LVH AF


Other aspects to be considered in risk-stratifying

• Stress test• Ventricular function• COROS LVEF 12- year

survival rate (p<0.0001)

< 35 % 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 & trans-fat (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

DMGenerally target HbA1c < 6.5 %. Individualize as hypoglycemia worsen angina & increase mortality

Keep waist circumference< 85 cm for men< 80 cm for women

Correct anaemiaCorrect hyperthyroid state

LDL < 1.8 ( primary target) HDL > 1.0 male, 1.2 female( secondary target)

TG < 1.7(secondary target)


education

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

Self management

During acute anginal attack-Restrain activity-GTN S/L or spray-Sit . Hypotension. Headache after GTN


Antithrombotic

ASA 75-150mg od. Lower MI, cardiac death or strokeTake into account GI side effect

*double antiplatelet not warranted in angina

Antithrombotic

Clopidogrel 75mg -more effective than ASA in peripheral vascular disease

Ticlopidine – proven efficacy in stroke and post-PCI, no evidence in angina

Lipid lowering

Statin reduce mortality & CV event by 20 – 30 %

Can add ezetimide if target not reached with statin

ACEi

For secondary prevention in post MI + reduced EF < 40 %

Recommended for all patients with CAD esp with concomitant LV dysfunction/DM


ARB

\as secondary prevention in CAD with Hpt/ CHF / post MI + LV dysfunction / DM if not tolerable to ACEi

Beta blocker

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

HR reducing, acting on SA nodeSymptomatic treatment in patient with N`SR, esp with contraindication for beta blocker

No significant interaction with other cardiac drugs

Calcium Channel Blocker

-non dihydropyridine – diltiazem/verapamil, as alternative to beta blocker

-dihydropyridine (long acting) –amlodipine - use in patient reduce coronary intervention but no reduction in treatment endpoints (ie death , MI)


Nitrates

(long acting – isordil,imdur)

Symptomatic improvement of anginaNo prognostic benefit

Trimetazidine

(Vasteral MR)

symptomatic relief of anginaSafe and effective in patient with ED

Dipyridamole

(Persanthine)

not recommended, poor antithrombotic efficacy in angina

Anticoagulant

Not indicated unless has AF


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 (preferred in high risk patient or contraindicated for thrombolytic) or fibrinolytic

Primary PCI (if door to balloon time < 90min)

Medical therapy +/- anti thrombotics

Second options fibrinolytics Primary PCI ( if clinically indicated)

Concomitant therapy

Anti thromboticsBeta blockers

ACEi / ARBStatins

NitratesCCB


Secondary prevention

• Basically similar to angina which includeSmoking 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

• 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 FailureClassification Ejection

FractionDescription

I. Heart Failure with Reduced Ejection Fraction (HFrEF)

≤40% 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.

II. Heart Failure with Preserved Ejection Fraction (HFpEF)

≥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.


Stages, Phenotypes and Treatment of HF ACC AHA 2013

STAGE AAt high risk for HF but without structural heart

disease or symptoms of HF

STAGE BStructural heart disease

but without signs or symptoms of HF

THERAPYGoals· 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

STAGE CStructural heart disease

with prior or current symptoms of HF

THERAPYGoals· 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

STAGE DRefractory HF

THERAPYGoals· 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

e.g., Patients with:· Known structural heart disease and· HF signs and symptoms

HFpEF HFrEF

THERAPYGoals· 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

THERAPYGoals· Control symptoms· Improve HRQOL· Reduce hospital

readmissions· Establish patient’s end-

of-life goals

Options· Advanced care

measures· Heart transplant· Chronic inotropes· Temporary or permanent

MCS· Experimental surgery or

drugs· Palliative care and

hospice· ICD deactivation

Refractory symptoms of HF at rest, despite GDMT

At Risk for Heart Failure Heart Failure

e.g., Patients with:· Marked HF symptoms at

rest · Recurrent hospitalizations

despite GDMT

e.g., Patients with:· Previous MI· LV remodeling including

LVH and low EF· Asymptomatic valvular

disease

e.g., Patients with:· HTN· Atherosclerotic disease· DM· Obesity· Metabolic syndrome orPatients· Using cardiotoxins· With family history of

cardiomyopathy

Development of symptoms of HF

Structural heart disease


Classification of Heart FailureACCF/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.

D Refractory HF requiring specialized interventions.


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 thyroid-stimulating 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 HFBiomarker, Application Setting COR LOE

Natriuretic peptides

Diagnosis or exclusion of HFAmbulatory,

AcuteI A

Prognosis of HFAmbulatory,

AcuteI A

Achieve GDMT Ambulatory IIa BGuidance of acutely decompensated HF therapy

Acute IIb C

Biomarkers of myocardial injury

Additive risk stratificationAcute,

Ambulatory I A

Biomarkers of myocardial fibrosis

Additive risk stratification

Ambulatory

IIb B

AcuteIIb A


Recommendations for Noninvasive Imaging

Recommendation COR LOE

Patients with suspected, acute, or new-onset HF should undergo a chest x-ray

I C

A 2-dimensional echocardiogram with Doppler should be performed for initial evaluation of HF

I C

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

I C

Noninvasive imaging to detect myocardial ischemia and viability is reasonable in HF and CAD

IIa C

Viability assessment is reasonable before revascularization in HF patients with CAD

IIa B

Radionuclide ventriculography or MRI can be useful to assess LVEF and volume

IIa C

MRI is reasonable when assessing myocardial infiltration or scar IIa B

Routine repeat measurement of LV function assessment should not be performed

III: No Benefit

B

HFSA 2010 Comprehensive Heart Failure Practice Guideline

Key Recommendations


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:



HF Risk Factor Treatment GoalsRisk 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 Care 2006; 29: S4-S42

2JAMA 2001; 285:2486-97

Adapted from:

Treating Hypertension to Prevent HF

Aggressive blood pressure control:

Aggressive BP control in patients with prior MI:

Decreasesrisk of new HF

by ~ 80%


by ~ 50%56% in DM2


by ~ 50%56% in DM2

Lancet 1991;338:1281-5 (STOP-HypertensionJAMA 1997;278:212-6 (SHEP)UKPDS Group. UKPDS 38. BMJ 1998;317:703-713


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.


Management of Patients with Known Atherosclerotic Disease But No HF

Treatment with ACE inhibitors decreases the risk of CV death, MI, stroke, or cardiac arrest.

NEJM 2000;342:145-53 (HOPE)Lancet 2003;362:782-8

(EUROPA)

02468

10121416

0 1 2 3 4

Years

% MI,Stroke,

CV Death

0

3

6

9

12

15

0 1 2 3 4 5

Years

% MI, CV Death, Cardiac Arrest

Placebo

Ramipril

Placebo

Perindopril

20% rel. risk red. p = .0003

22% rel. risk red. p < .001

HOPE

EUROPA

Treatment of Post-MI Patients with Asymptomatic LV Dysfunction (LVEF ≤ 40%)

SAVE Study

All-cause mortality ↓19%

CV mortality ↓21%

HF development ↓37%

Recurrent MI ↓25% 0

0.1

0.2

0.3

0 0.5 1 1.5 2 2.5 3 3.5 4

Placebo

Captopril

Years

MortalityRate

19% rel. risk reduction

p = 0.019

Pfeffer et al. NEJM 1992;327:669-77


HFSA 2010 Practice Guideline (4.8, 4.10)

Heart Failure Patient EvaluationRecommended 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:



Evaluation—Follow Up AssessmentsRecommended Components of Follow-Up Visits

Signs and symptoms evaluated during initial visit

Functional capacity and activity level

Changes in body weight

Patient understanding of and compliance with dietary sodium restriction and medical regimen

History of arrhythmia, syncope, pre-syncope, palpitation, or ICD discharge

Adherence and response to therapeutic interventions

Exacerbating factors for HF, including worsening ischemic heart disease, hypertension, and new or worsening valvular disease Strength of Evidence = B



Pharmacologic Therapy: ACE Inhibitors

ACE inhibitors are recommended for symptomatic and asymptomatic patients with an LVEF ≤ 40%.


ACE inhibitors should be titrated to doses used in clinical trials (as tolerated during uptitration of other medications, such as beta blockers). Strength of Evidence = C

ACE inhibitors are recommended as routine therapy for asymptomatic patients with an LVEF ≤ 40%.

Post MI Strength of Evidence = B

Non Post-MI Strength of Evidence = C

Adapted from:


ACE Inhibitors Used in Clinical Trials

Generic Name Trade Name Initial Daily Dose

Target Dose Mean Dose in Clinical Trials

Captopril Capoten 6.25 mg tid 50 mg tid 122.7 mg/day

Enalapril Vasotec 2.5 mg bid 10 mg bid 16.6 mg/day

Fosinopril Monopril 5-10 mg qd 80 mg qd N/A

Lisinopril Zestril, Prinivil

2.5-5 mg qd 20 mg qd 4.5 mg/day, 33.2 mg/day*

Quinapril Accupril 5 mg bid 80 mg qd N/A

Ramipril Altace 1.25-2.5 mg qd 10 mg qd N/A

Trandolapril Mavik 1 mg qd 4 mg qd N/A

*No mortality difference between high and low dose groups, but 12% lower risk of death or hospitalization in high dose group vs. low dose group.



Pharmacologic Therapy: Substitutes for ACEI

It is recommended that other therapy be substituted for ACE inhibitors in the following circumstances:

In patients who cannot tolerate ACE inhibitors due to cough, ARBs are recommended. Strength of Evidence = A

The combination of hydralazine and an oral nitrate may be considered in such patients not tolerating ARBs.

Strength of Evidence = C

Patients intolerant to ACE inhibitors from hyperkalemia or renal insufficiency are likely to experience the same side effects with ARBs. In these cases, the combination of hydralazine and an oral nitrate should be considered. Strength of Evidence = C



Pharmacologic Therapy: Beta Blockers

Beta blockers shown to be effective in clinical trials are recommended for symptomatic and asymptomatic patients with an LVEF ≤ 40%.


Beta blockers are recommended as routine therapy for asymptomatic patients with an LVEF ≤ 40%.

Post MI Strength of Evidence = B

Non Post-MI Strength of Evidence = C

Effect of Beta Blockade on Outcome in Patients With HF and Post-MI LVD

Study Drug

HF Severity

Target Dose (mg)

Outcome

US Carvedilol1 carvedilol mild/ moderate

6.25- 25 BID

↓48% disease progression (p= .007)

CIBIS-II2 bisoprolol moderate/ severe

10 QD ↓34% mortality (p <.0001)

MERIT-HF3 metoprolol succinate

mild/ moderate

200 QD ↓34% mortality (p = .0062)

COPERNICUS4 carvedilol severe 25 BID ↓35% mortality (p = .0014)

CAPRICORN5 carvedilol post-MI LVD

25 BID ↓23% mortality (p =.031)

1Colucci WS et al. Circulation 1196;94:2800-6. 2CIBIS II Investigators. Lancet 1999;353:9-13.3MERIT-HF Study Group. Lancet 1999;353:2001-7. 4Packer M et al. N Engl J Med 2001;3441651-8. 5The CAPRICORN Investigators. Lancet 2001;357:1385-90.




CONCOMITANT DISEASE

Beta blocker therapy is recommended in the great majority of patients with HF and reduced LVEF—even if there is concomitant diabetes, chronic obstructive lung disease or peripheral vascular disease.

Use with caution in patients with: Diabetes with recurrent hypoglycemia Asthma or resting limb ischemia.

Use with considerable caution in patients with marked bradycardia (<55 bpm) or marked hypotension (SBP < 80 mmHg).

Not recommended in patients with asthma with active bronchospasm. Strength of Evidence = C




PRESERVED LVEF

Beta blocker treatment is recommended in patients with HF and preserved LVEF who have:

Prior MI Strength of Evidence = A

Hypertension Strength of Evidence = B

Atrial fib. requiring control of ventricular rate Strength of Evidence =

B

THE ELDERLY

Beta-blocker and ACE inhibitor therapy is recommended as standard therapy in all elderly patients with HF due to LV systolic dysfunction.

Strength of Evidence = B

In the absence of contraindications, these therapies are also recommended in the very elderly (age > 80 years).



Beta Blockers Used in Clinical Trials



Bisoprolol Zebeta 1.25 mg qd 10 mg qd 8.6 mg/day

Carvedilol Coreg 3.125 mg bid 25 mg bid 37 mg/day

Carvedilol Coreg CR 10 mg qd 80 mg qd

Metoprolol succinate CR/XL

Toprol XL 12.5-25 mg qd 200 mg qd 159 mg/day



Pharmacologic Therapy: Angiotensin Receptor Blockers

ARBs are recommended for routine administration to symptomatic and asymptomatic patients with an LVEF ≤ 40% who are intolerant to ACE inhibitors



Angiotensin Receptor Blockers Used in Clinical Trials



Candesartan Atacand 4-8 mg qd 32 mg qd 24 mg/day

Losartan Cozaar 12.5-25 mg qd 150 mg qd 129 mg/day

Valsartan Diovan 40 mg bid 160 mg bid 254 mg/day



Pharmacologic Therapy: Aldosterone Antagonists

An aldosterone antagonist is recommended for patients on standard therapy, including diuretics, who have:

NYHA class IV HF (or class III, previously class IV) HF from

reduced LVEF (≤ 35%)

One should be considered in patients post-MI with clinical HF or diabetes and an LVEF < 40% who are on standard therapy, including an ACE inhibitor (or ARB) and a beta blocker.

Adapted from:




Pharmacologic Therapy: Diuretics

Diuretic therapy is recommended to restore and maintain normal volume status in patients with clinical evidence of fluid overload, generally manifested by:

Congestive symptoms

Signs of elevated filling pressures Strength of Evidence = A

Loop diuretics rather than thiazide-type diuretics are typically necessary to restore normal volume status in patients with HF.

Strength of Evidence = B



Pharmacologic Therapy: Diuretics Restoration of normal volume status may require multiple

adjustments.

Once a diuretic effect is achieved with short-acting loop diuretics, increase frequency to 2-3 times a day if necessary, rather than increasing a single dose. Strength of Evidence = B

Diuretic refractoriness may represent patient nonadherence or progression of underlying dysfunction.

Adapted from:


Loop Diuretics

Agent Initial Daily Dose

Max Total Daily Dose

Elimination: Renal – Met.

Duration of Action

Furosemide 20-40mg qd or bid

600 mg 65%R-35%M 4-6 hrs

Bumetanide 0.5-1.0 mg qd or bid

10 mg 62%R/38%M 6-8 hrs

Torsemide 10-20 mg qd 200 mg 20%R-80%M 12-16 hrs

Ethacrynic acid

25-50 mg qd or bid

200 mg 67%R-33%M 6 hrs


Potassium-Sparing Diuretics

Agent Initial Daily Dose

Max Total Daily Dose

Elimination Duration of Action

Spironolactone 12.5-25 mg qd

50 mg Metabolic 48-72 hrs

Eplerenone 25-50 mg qd

100 mg Renal, Metabolic

Unknown

Amiloride 5 mg qd 20 mg Renal 24 hrs

Triamterene 50-75 mg bid

200 mg Metabolic 7-9 hrs



Device Therapy:Prophylactic ICD Placement

Prophylactic ICD placement should be considered in patients with an LVEF ≤35% and mild to moderate HF symptoms: Ischemic etiology Strength of Evidence = A

Non-ischemic etiology Strength of Evidence = B

Decisions should be made in light of functional status and prognosis based on severity of underlying HF and comorbid conditions, ideally after 3-6 mos. of optimal medical therapy.


Adapted from:



HF with Preserved LVEF—Diagnosis

Careful attention to differential diagnosis is recommended in patients with HF and preserved LVEF.

Treatments may differ based on cardiac disorder.

Evaluation for ischemic disease and inducible myocardial ischemia should be included.

Recommended diagnostic tools:

Echocardiography

Electrocardiography

Stress imaging (via exercise or pharmacologic means, using myocardial perfusion or echocardiographic imaging)

Cardiac catheterization

Adapted from:



Figure 11.3. Diagnostic Algorithmfor HF with Preserved LVEF

HF with Preserved LVEF

Dilated LV Non-dilated LV

Valvular diseaseAR, MR

No valvular dis.High output HF

Increasedthickness

NormalThickness

Right vent.dysfunction

Pulmonaryhypertension

Isolated pre-dominant RVMI

No mitralobstruction

Mitral obstructionMS, atrial myxoma

Pericardial dis.Tamponade Constriction

No pericardial disease

Inducible ischemiaIntermittent/active

ischemia

Normal or increased QRS

Hypertrophic dis.

Low QRS voltageInfiltrative myopathy

No aortic valve disease

Aortic valve dis.Aortic stenosis

No hypertensive history of PE

HCM, Fabry dis.

Hypertensive history of PE

Hypertensive-HCM

Some patients with RV dysfunction have LV dysfunction due to ventricular interaction.

No inducible ischemia, fibrotic, collagen-Vascular, RCM, cardinoid, diabetes,Radiation or chemotherapy induced heart disease, infiltrative disease, co-morbid conditions, reconsider diagnosisof HF


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


• 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

• 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.


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


Psychosocial intervention (address depression,

anxiety, social isolation. Consider SSRI, cognitive behavioral therapy.

Risk factor modification & interventionAggresive reduction of risk factors via nutritional counselling, weight management, adherence to drug therapy

Exercise training interventionReturn to workCardioprotective mechanism (improve endothelial function)


Thank you for your kind attention

Management of chest pain and heart failure. Cardiac rehabilitation and secondary prevention

Documents

Transcript of Management of chest pain and heart failure. Cardiac rehabilitation and secondary prevention