management heart failure (papros)

8/8/2019 Management Heart Failure (Papros)

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Contenty Introductiony Epidemiology y

Etiology y Definitiny Prognosisy Pathophysiology y Clinical Characteristics

y Non-Pharmacological Approaches

y

Evidence-basedPharmaceutical Carey Treatment Goalsy Multidisciplinary

Management Approachy Conclusion


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Introductiony H eart failure is a multifaceted syndromey Syndrome of hemodynamic abnormalities?

y

preload, afterload, cardiac outputy Such therapies failed to improve survivaly Pharmacological agents that inhibit neurohormones in the

future?y ACEI, -blocker, aldosterone antagonists

y H eart Failure Society of America ( H FSA) Guidelinesy Pathophysiological mechanisms heart failure progression

y Pharmacological and interventional strategies


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Ep idemiologyy H eart failure is a long-term complication of other cardiovascular

diseasey H eart failure:

y Incidence (10 new cases/1000 >65yrs)y Prevalence (4.6 million in the U.S.)

y Age , post MI survivaly Coronary heart disease 12 million in U.S.

y 28% death (1987-1997)y

H ypertension 50 million in U.S.y 27.4% blood pressure adequately controlledy 75% heart failure cases have hypertension

y H eart failure is the most common cause for hospitalizations amongpatients >65yrs


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Etiologyy Initial insult left ventricular dysfunction (LVD)

neurohormonal activation syndrome of heart failurey H eart failure etiology

y Ischemic (70%)y Myocardial infarction

y Loss of viability, necrosis of myocardiumy Stunned myocardium or H ibernating myocardium

y

Chronic ischemia and reduced mycocardial blood flowy Tissue remain viable (non-necrotic and non-infarcted)y Myocardium are functionally depressed to reduce the

metabolic requirementsy Function generally recovers of adequate flow is restored


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Etiologyy H eart failure etiology

y Non-ischemic (not understood as well)y H ypertentiony Valvular diseasey Alcohol usey Tachyarrhythmiay Myocarditisy Chemotherapy y Viral myopathy y Peri- or postpartum statey Inflammatory cardiomyopathy

y Pharmacological treatment strategy for patients with ischemic etiology is identical for those patients with non ischemic etiology

Modifiable

Mystery?Immunoglobulin?


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D efinitionsy Congection? Chronic?y H eart failure is a syndrome due to alternations in

neurohormonesy Decompensated heart failure: Acute exacerbationy Systolic dysfunction:

y LVEF55% +heart failure symptomsy Stiffness of the chamber, resulting in impaired filling


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P rognosisy 22-46% of patients who had an MI will

develop heart failure within 6 yearsy 5-year mortality rate of 50%y Median survival after onset of heart

failure is 1.7 yrs for men and 3.2 yrs for women


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Pa tho p hysiologyy H emodynamic abnormalitiesy Neurohormonal activation p Progression of heart

failurey R enin-angiotensin aldosterone systemy Sympathetic nervous systemy Natriuretic peptides: NEP-inhibitory Arginine vasopressin : V2-antagonist, under

investigationy Endotheliny Cytokines


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Clinica l Cha ra cteristicsy

NY H

A classy Physical examinationy H eart soundsy JVPy H epatic congestiony Peripheral edemay R alesy Dyspnea on Exertion, Paroxysmal nocturnal dyspnea,

Orthopneay Weight gain

y Diagnostic testsy Echocardiography y 6-minute walk

y Who walk less than 300 m had an almost 4-foldgreater risk of death compared to those who walk450 m or greater


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Criteria for NYHA Functional Classification

for Chronic Heart Failure Patients

y Class I: No limitation of physical activity. Ordinary physical activity does not cause unexpected fatigue,palpitation, or dyspnea

y Class II: Slight limitation of physical activity. Comfortable

at rest, but ordinary physical activity results in fatigue,palpitation or dyspnea

y Class III: Marked limitation of physical activity.Comfortable at rest, but less than ordinary activity causes

fatigue, palpitation or dyspneay Class IV : Unable to carry out any physical activity without

discomfort. Symptoms of cardiac insufficiency at rest. If any physical activity is undertaken, discomfort is increased


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N on- P h a rm a cologic a l App ro a chesy Compliance and dietary indiscretion account for the

majority of heart failure exacerbationy Provide patient with mg of sodium per serving guielines

y 2000 mg/day of sodium is often set as the sodium goaly Modest reductions (3000-4000 mg/day) should be made

initially y Potassium, Cholesterol and saturated fats, Alcoholy Free water restriction

y 1.5 L/day or less may be required in patient withhyponatremia

y

2 L/day for NY H

A IV y Patient should be encouraged to remain active and performactivities as tolerated without overexerting themselves

y Surgery y Transplant still remains an option for patients with

advanced NY H

A class IV


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Evidence-b a sed P h a rm a ceutic a l Ca reACE Inhibitor

y ACEI as Cornerstone: V- H eFT, SOLVD in the early 1990sy ACEI should be prescribed to all patients with systolic

dysfunction unless they are absolutely intoleranty Underuse of ACEI? 30%-80%?y Contraindications to ACEI

y Absolute: H istory of angioedema, bilateral renal artey

stenosis, pregnancy y R elative: Unilateral renal artery stenosis, renal

insufficiency, hyperkalemia, hypotension, cough


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y R enal insufficiency:y SCr oq ?y If SCr continues to rise, patient should

discontinue the ACE inhibitory Even patient with baseline renal insufficiency

(SCr


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y H yperkalemiay Serum potassium increases on average 0.3-0.5 mmol/L when

initiating ACE inhibitor therapy y

Baseline renal insufficiency y Treatment with potassium-sparing diuretics such as spironolactoney External potassium sources (food, supplements, salt substitutes)

y Coughy Dry and hackingy

Pulmonary volume overload?y If an ACE inhibitor is discontinued, the cough should generally

resolve within 1 week or lessy Optimal dose of an ACEI: ?ATLAS (higher dose of lisinopril reduce

hospitalizations), captopril 50 mg tid ?, enalapril 10 mg bid?


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y Alternative therapy to ACE inhibitor:y A R Bs

y ELITE: Incidence of renal insufficiency and hyperkalemia are

similar captopril V.S. losartany ELITE II:

y No difference in all-cause mortality captopril V.S. losartany Lower incidence of cough with losartan

y 32% ACEI related angioedema p A R Bs related angioedemay

A R Bs may be the choice if intolerance is due to coughy H ydralazine + Nitrates (V- H eFT II study)

y Mortality q , norepinephrine o , compliance, neurohormone oy Used in patients with ACE inhibitor intolerance secondary to

renal insufficiency, angioedema, or hyperkalemia


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Evidence-b a sed P h a rm a ceutic a l Ca re F-Blockers

y Carvedilol: 35% mortality reduction, 1996y Patient selectiony The safety and efficacy in the patient with active volume overload or

acute exacerbations of chronic heart failure is unknowny Used in all patients with stable NY H A class II-III ischemic and non-

ischemic heart failure without contraindicationsy COPER NICUS: Carvedilol is beneficial in patients with symptomatic

heart failurey Carvedilol (FDA), metoprolol and bisoprolol are the only F-Blockers

which should be used in treating heart failurey H ypertensive cardiomyopathy or persistent hypertension p Carvediloly Borderline hypotension, reactive airway disease p metoprololy The optimal dose of F-Blockers is not known


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Evidence-b a sed P h a rm a ceutic a l Ca re F-Blockers

y F-Blockers must be initiated at low doses and titratedslowly for a period of monthes

y

Blood pressure, heart rate, and heart failure symptoms(weight gain, shortness of breath, orthopnea) should beclosely monitored

D rug Initial D ose Target

Carvedilol 3.125 mg bid 25 mg bid

Metoprolol 12.5 mg Q D (NYHA III)25 mg Q D (NYHA II)

150-200 mg Q D

B isoprolol 1.25 mg Q D 5 mg Q D


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Evidence-b a sed P h a rm a ceutic a l Ca reSp ironol a ctone

y R ALES:y 40% mortality reduction among patients with advanced

heart failure (NY H A III-IV)y Background therapy : ACE inhibitors, F-Blockers,

digoxin, diureticsy Potassium supplements should be discontinuedy Check potassium level within 3-7 days of initiating therapy y Check potassium level within 3-4 days for patients withrenal insufficiency or borderline hyperkalemiay Gynecomastia is a problematic side effect (10%)


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Evidence-b a sed P h a rm a ceutic a l Ca reD igoxin

y DIG:y Neutral effect on mortality y

R educe hospitalizationsy Optimal concentration of digoxin 0.5-1 ug/Ly Death from other cardiovascular causes was slightly

higher for the digoxin groupy

It is no longer a first-line therapy for heart failurey For patients who remain symptomatic despite ACE

inhibitors, F-Blockers, and diuretics


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Evidence-b a sed P h a rm a ceutic a l Ca reD iuretics

y R elief of congestive symptomsy Neurohormonal activationy H igh dose of diuretics are related to a higher

mortality (uncontrolled, retrospective datat)y The lowest dose of a diuretic that maintains

a euvolemic or near euvolemic state shouldbe used


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Evidence-b a sed P h a rm a ceutic a l Ca reCa lcium Ch a nnel Blockers

y Do not play a role in treating heart failurey PR AISE

y No differences in mortality (Amlodipine)y PR AISE II

y No difference in all-cause mortality y Amlodipine appears to be a safe drug to use in treating

heart failure patients with ischemic heart disease andhypertension

y Amlodipine may be useful to treat concomitant illnesses if treatment with ACE inhibitors and F-Blockers have notadequately controlled the patient s blood pressure oranginal symptoms


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Evidence-b a sed P h a rm a ceutic a l Ca reAntithrombotic Str a tegies

y Anticoagulation has been widely debated inmanaging heart failure

y H FSA:y Warfarin is recommended in all patients with heart failure and atrial fibrillation

y Warfarin may be considered in patients with LVEF


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Evidence-b a sed P h a rm a ceutic a l Ca reInotro p es

y Is not recommened as standard care for heart failure, as all clinicaltrials to date using chronic inotropic therapy have demonstrated alower survival rate

y Inotropes are often required in acute exacerbations of chronic heartfailure

y Dobutamine increases myocardial oxygen consumption and may worsen ischemia in patients with ischemic cardiomyopathy

y OPTIME-CH F (Milrinone)y Total mortality rates were not significantly different between the

two groupsy H igher incidence of treatment-related new AF and sustained

hypotensiony Trend toward more MIs and ventricular tachyarrhymias


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Evidence-b a sed P h a rm a ceutic a l Ca reCost-effecti ve An a lysis

y Therapy proven to reduce morbidity andmortality (ACE inhibitors and F-Blockers )are cost-effective and should beimplemented in patients with heart failure

y Focus should be placed on implementing

strategies that decrease rehospitalization inheart failure patients


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Tre a tment Go a lsy The ultimate treatment goal for heart failure is to prolong survival

y Quality of lifey Decrease morbidity (rehospitalization)y Decrease health care costsy End-of-life issues: comfort measures

y All patients with symptomatic or asymptomatic LVD should receive ACE inhibitor, unless the patients has an absolute contraindication or asignificant relative contraindication such that the patients is intolerantof the therapy

y Appropriate patient evaluation is key to initiating these therapies andensuring that patients are maintained on them

y ACE inhibitors should form the basis for all treatment of heart failure


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M ultidisci p lina ry M a n a gement A pp ro a chy Physiciansy Nursesy Dietitiansy Social workersy Pharmacists are an important component of the team

duringy Patient assessmenty

Development of the therapeutic plany Patient education: purpose and importance of each drugy Follow-upy Costy Noncompliance


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Conclusiony Both Pharmacological and non-pharmacological strategies

to optimize patient outcomes should be exploredy H eart failure patients benefit from close monitoring and

follow-upy The importance of incorporating a pharmacist in the care

of these patients has been documentedy H eart failure patients often have concomitant illness that

must be treated without worsening the heart failurecondition

y Incorporate evidence-based pharmacological and non-pharmacological strategies into patient care

management heart failure (papros)

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