Bd1e Management Of Heart Failure

Management of Management of Chronic Heart Chronic Heart

FailureFailureDR.SAMEER AMBARDR.SAMEER AMBAR

DEPT OF CARDIOLOGYDEPT OF CARDIOLOGY

JNMC BELGAUM, INDIAJNMC BELGAUM, INDIA

[email protected]@rediffmail.comom

Asses the functional classAsses the functional class BP <130/80 mm of HgBP <130/80 mm of Hg Good glycaemic controlGood glycaemic control LIPIDS LDL < 100 (IHD) <70 (DM)LIPIDS LDL < 100 (IHD) <70 (DM) Avoid smoking, alcoholAvoid smoking, alcohol Sodium restriction <2gms /daySodium restriction <2gms /day Fluid restriction ,2 Litres/dayFluid restriction ,2 Litres/day

ACEIACEIMECHANISM OF ACTIONMECHANISM OF ACTION

VASOCONSTRICTIONVASOCONSTRICTION VASODILATATION VASODILATATION

KininogenKininogen

KallikreinKallikrein

Inactive FragmentsInactive Fragments

AngiotensinogenAngiotensinogen

Angiotensin IAngiotensin I

RENINRENIN

Kininase IIKininase IIInhibitorInhibitor

ALDOSTERONEALDOSTERONE

SYMPATHETICSYMPATHETIC

VASOPRESSINVASOPRESSIN

PROSTAGLANDINSPROSTAGLANDINS

tPAtPA

ANGIOTENSIN IIANGIOTENSIN II

BRADYKININBRADYKININ

A.C.E.A.C.E.

SAVE (SAVE (NEJM 1992 327:669-677)NEJM 1992 327:669-677) 2231 pts EF<40%, 3-16d 2231 pts EF<40%, 3-16d post MIpost MI, , without sx of without sx of

heart failureheart failure, , Up to Up to 50 mg Captopril50 mg Captopril tid for 42 mo tid for 42 mo

AIRE AIRE (Lancet 1993:342:821)(Lancet 1993:342:821) 2006 patients 3-10 days 2006 patients 3-10 days post MIpost MI with with any any

evidence of post infarct clinical HF, evidence of post infarct clinical HF, Up to Up to 5 mg Ramipril bid5 mg Ramipril bid for 15 mos for 15 mos

TRACE TRACE (NEJM 1995; 333: 1670-1676)(NEJM 1995; 333: 1670-1676) 1749 pts 3-7 days 1749 pts 3-7 days post MIpost MI with EF<=35%, with EF<=35%, with with

or withoutor without symptomatic HF symptomatic HF trandolapril trandolapril for 24-50 mosfor 24-50 mos

ACEI IN POST MI HF

MortalityMortality SAVE: 25% (placebo) vs 20% (captopril) - 19% RRRSAVE: 25% (placebo) vs 20% (captopril) - 19% RRR AIRE: 23% (placebo) vs 17% (ramipril) - 27% RRRAIRE: 23% (placebo) vs 17% (ramipril) - 27% RRR TRACE: 42.3% (placebo) vs 34.7% (trandolapril)- 24% RRRTRACE: 42.3% (placebo) vs 34.7% (trandolapril)- 24% RRR

HFSA 2006 Practice Guideline (7.10)

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 for reasons other than hyperkalemia or renal insufficiency.

Strength of Evidence = A

Adams KF, Lindenfeld J, et al. HFSA 2006 Comprehensive Heart Failure Guideline. J Card Fail 2006;12:e1-e122.

ARBs Clinical Study:ARBs Clinical Study:

1.Elite-II. Study:1.Elite-II. Study: Enrolled Target: CHF P’t Enrolled Target: CHF P’t Drug: losartan v.s. captoprilDrug: losartan v.s. captopril Primary Endpoint:CHF Improvement Primary Endpoint:CHF Improvement Result: losartan is not better than captoprilResult: losartan is not better than captopril 2.Va-HeFT Study: 2.Va-HeFT Study: Enrolled Target: CHF P’tEnrolled Target: CHF P’t Drug: valsartan + Usual Group v.s. Usual Drug: valsartan + Usual Group v.s. Usual

Group Group Primary Endpoint: CHF Event-Free Primary Endpoint: CHF Event-Free

Probability Probability Result: Reduce M/M by 13.3%Result: Reduce M/M by 13.3%

Granger CB, et al. Lancet. 2003;362:772-776.

CHARM-AlternativeCHARM-Alternative

Number at risk

Candesartan 1,013 929 831 434 122

Placebo 1,015 887 798 427 126

0 1 2 3

Years

0

10

20

30

40

50

Placebo

Candesartan

HR 0.77 (95% CI 0.67-0.89), P=.0004Adjusted HR 0.70, P<.0001

3.5

406 (40.0%)

334 (33.0%)

Pro

po

rtio

n W

ith

CV

Dea

th

or

CH

F H

osp

ital

izat

ion

(%

)Primary outcome of CV death or CHF hospitalization

www. Clinical trial results.org

CHARM Added Trial CHARM Added Trial CHARM Added Trial

CV Mortality orCHF hospitalization

HR 0.85p=0.011

37.9%

42.3%

0%

10%

20%

30%

40%

50%

Candesartan Placebo

37.9%

42.3%

0%

10%

20%

30%

40%

50%

Candesartan Placebo

23.7%

27.3%

0%

10%

20%

30%

Candesartan Placebo

23.7%

27.3%

0%

10%

20%

30%

Candesartan Placebo

European Society of Cardiology 2003European Society of Cardiology 2003

CV MortalityHR 0.84p=0.02

55% on BB

When to use Angiotensin receptor When to use Angiotensin receptor blockersblockers

1.1. There has been no definite There has been no definite mortality or morbility advantage of mortality or morbility advantage of ARBs over ACE inhibitors ARBs over ACE inhibitors demonstrateddemonstrated

2. Consider ARB in patient who is ACE 2. Consider ARB in patient who is ACE inhibitor eligible if the patient is inhibitor eligible if the patient is intolerant of ACE inhibitors because intolerant of ACE inhibitors because of cough, renal insufficiency, or of cough, renal insufficiency, or hyperkalemiahyperkalemia

When to use Angiotensin receptor When to use Angiotensin receptor blockersblockers

3. In the patient who is apparently ACE 3. In the patient who is apparently ACE inhibitor intolerant, rule out other causes of inhibitor intolerant, rule out other causes of presumed side effect:presumed side effect:

a. Cough-evaluate for pulmonary edemaa. Cough-evaluate for pulmonary edema b. Hyperkalemia-concurrent potassium b. Hyperkalemia-concurrent potassium

supplementation, potassium-sparing supplementation, potassium-sparing diuretic usediuretic use

c. renal insufficiency-evaluate for prerenal c. renal insufficiency-evaluate for prerenal azotemia, NSAID useazotemia, NSAID use

4. The incidence of cough and hyperkalemia 4. The incidence of cough and hyperkalemia is lower with ARBs versus ACE inhibitorsis lower with ARBs versus ACE inhibitors

There does not appear to be a significant There does not appear to be a significant difference in incidence of renal insufficiency difference in incidence of renal insufficiency

Beta blockade in Heart failureBeta blockade in Heart failure

Beta receptor levels in heart Beta receptor levels in heart failurefailure

Normal HeartNormal Heart B1 80 : B2 20B1 80 : B2 20 Severe Heart FailureSevere Heart Failure B1 60 : B2 40B1 60 : B2 40

B1 receptors to selectively down-regulate B1 receptors to selectively down-regulate secondary to high levels of catecholaminesecondary to high levels of catecholamine

B2 agonists retain full inotropic activity B2 agonists retain full inotropic activity mediated through a B2 population that is not mediated through a B2 population that is not significantly decreasedsignificantly decreased

Effect of Sympathetic Effect of Sympathetic Activation in Heart Activation in Heart

FailureFailureCNS Sympathetic Outflow

Sympathetic activity to kidneys & blood vessels

Activation of RAS

VasoconstrictionSodium retention

Disease Progression

Cardiac sympathetic Activity

1 Receptors

2 Receptors

1Receptors

Myocyte deathIncreased arrhythmias

Benefit Of Beta BlockersBenefit Of Beta Blockers

Improve symptoms and clinical Improve symptoms and clinical statusstatus

Increase LV ejection fractionIncrease LV ejection fraction Little effect on exercise toleranceLittle effect on exercise tolerance Reduce frequency of Reduce frequency of

hospitalizations for heart failurehospitalizations for heart failure Decrease mortalityDecrease mortality

ActionAction

Time dependant improvement in LV Time dependant improvement in LV remodellingremodelling

Reduce cetecholamine myocyte Reduce cetecholamine myocyte toxicitytoxicity

Improved B1 signalingImproved B1 signaling AntiapoptosisAntiapoptosis antiarrthymicantiarrthymic RAAS inhibitionRAAS inhibition

Sympathetic ActivationSympathetic Activation

B1 Receptors

B2 Receptors

A1Receptors

CardiotoxicityCarvedilol

Metoprolol

Propranolol

Clinical TrialsClinical Trials

Prospective Randomized Evaluation of Carvedilol on Prospective Randomized Evaluation of Carvedilol on Symptoms and Exercise (PRECISE)Symptoms and Exercise (PRECISE) 278 patients with chronic stable symptomatic 278 patients with chronic stable symptomatic

heart failure EF<35% despite diuretics and ACE heart failure EF<35% despite diuretics and ACE Carvedilol group was associated with greater Carvedilol group was associated with greater

improvement in NYHA Classimprovement in NYHA Class 39% reduction in combined risk of 39% reduction in combined risk of

death/hospitalization for any reasondeath/hospitalization for any reason 46% reduction in risk of46% reduction in risk of hospitalization for hospitalization for

cardiovascular reasoncardiovascular reason

Circulation 1996;94:2793-2799

Clinical TrialsClinical Trials

Merit-HF Trial( metaprolol randomised Merit-HF Trial( metaprolol randomised interventional trial in CHF)interventional trial in CHF) 3991 patients with an ischemic or 3991 patients with an ischemic or

nonischemic cardiomyopathy (NYHA nonischemic cardiomyopathy (NYHA Class II or III) randomized to either Class II or III) randomized to either Metoprolol XL up to 200mg/day or Metoprolol XL up to 200mg/day or placebo. placebo.

Metoprolol XL was associated with a Metoprolol XL was associated with a 35% reduction in mortality35% reduction in mortality

Amer J Cardiol 1997;80:54J-58J

MERIT-HFMERIT-HFMETOPROL-XL: Mortality and MorbidityMETOPROL-XL: Mortality and Morbidity

MERIT-HF Study Group. Lancet. 1999;353:2001-2007

NYHA III/IVNYHA III/IV

EF <0.25EF <0.25

Post-MI Patients with Post-MI Patients with Severe Heart Failure (n= 384)Severe Heart Failure (n= 384)

Jánosi A et al, Am Heart J 2003;146:721-8

MERIT-HFMERIT-HF

Total MortalityTotal Mortality

Months of follow-upMonths of follow-up

Pe

r ce

ntP

er

cent

2020

1515

1010

55

00

PlaceboPlacebo

Metoprolol CR/XLMetoprolol CR/XL

p = 0.0004p = 0.0004

Risk reduction = 40%Risk reduction = 40%

00 33 66 99 1212 1515 1818


MERIT-HFMERIT-HF

Post-MI PatientsPost-MI Patients

Pe

r c e

ntP

er

cen t

1212

99

66

33

00


Sudden Death

PlaceboPlacebo


p = 0.0004p = 0.0004

00 33 66 99 1212 1515 1818


MERIT-HFMERIT-HF



Pe

r ce

ntP

er

cent

55

44

33

11

00


Death from Worsening Heart FailureDeath from Worsening Heart Failure

PlaceboPlacebo


p = 0.021p = 0.021

22

00 33 66 99 1212 1515 1818


MERIT-HFMERIT-HF



Total Number of HospitalizationsTotal Number of Hospitalizations

Heart failure

p=0.006

-32%

All-cause

ns-8%

CV cause

p=0.037-17%

MERIT-HFMERIT-HF



Post-MI severe CHFPost-MI severe CHF

Total mortalityTotal mortality

Cardiac death/nonfatal MICardiac death/nonfatal MI

History of revasc. History of revasc. (PTCA or CABG)(PTCA or CABG)

40%

45%

Risk Risk reductionreduction

EventsEventsPlac/BetaPlac/Beta

122/74

44/2444/24

37/2637/26

132/74

46/2246/22

42/2742/27

All Post-MI patientsAll Post-MI patients

Post-MI severe CHFPost-MI severe CHF

All Post-MI patientsAll Post-MI patients

Relative risk and 95% CIRelative risk and 95% CI0.00.0 1.01.0

History of revasc. History of revasc. (PTCA or CABG)(PTCA or CABG)


MERIT-HFMERIT-HF


Effect of metoprolol and placebo Effect of metoprolol and placebo treatment on survival and treatment on survival and

hospitalization risk in class III and IV hospitalization risk in class III and IV HFHF

MERIT-HF

Goldstein S et al. J Am Coll Cardiol 2001; 38(4):932-8

Endpoint Endpoint MetoprolMetoprolol (N)ol (N)

PlacebPlacebo (N)o (N)

Risk Risk reductioreductio

n (%)n (%)

p valuep value

Total mortalityTotal mortality 4545 7272 39%39% 0.00860.0086

CV mortalityCV mortality 4040 7070 44%44% 0.0028 0.0028

Sudden deathSudden death 2222 3939 45%45% 0.0240.024

Death from worsening Death from worsening HFHF

1313 2828 55%55% 0.0150.015

Total hospitalizationsTotal hospitalizations 273273 363363 27%27% 0.0037 0.0037

Total hospitalizations Total hospitalizations due to worsening HFdue to worsening HF

105105 187187 45%45% <0.000<0.00011

Comparison of findings in Comparison of findings in subanalysis and entire MERIT-subanalysis and entire MERIT-

HF cohort HF cohort

MERIT-HF

Goldstein S et al. J Am Coll Cardiol 2001; 38(4):932-8

EndpointEndpoint Reductions in Reductions in entire MERIT-entire MERIT-

HF cohortHF cohort

Reductions in Reductions in class III and IV class III and IV

MERIT-HF MERIT-HF subsetsubset

Total mortalityTotal mortality -34% -34% -39%-39%

Sudden deathSudden death -41%-41% -45%-45%

Death due to worsening Death due to worsening HFHF

-49%-49% -55%-55%

40% reduction in Total Mortality40% reduction in Total Mortality

50% reduction in Sudden Death50% reduction in Sudden Death

32% reduction in number of hospitalizations for 32% reduction in number of hospitalizations for Worsening Heart Failure Worsening Heart Failure


MERIT-HFMERIT-HF


Mortality/HospitalizationsMortality/HospitalizationsSummarySummary

• Enrolled 2289 patients with severe HF (LVEF <25%)• Randomized to carvedilol in a target dose of 25 mg bid for up to 29 months

Carvedilol Prospective Randomized Cumulative Survival Trial

(COPERNICUS)

35% reduction in the risk of all-cause mortality among patients with severe congestive heart failure (CHF) treated

with carvedilol compared to placebo

COPERNICUS: Effect of COPERNICUS: Effect of carvedilol on the combined risk carvedilol on the combined risk

of morbidity and mortalityof morbidity and mortality

Death or Death or hospitalization hospitalization for HFfor HF

0.000000.0000044

p valuep valueEndpointEndpoint

COPERNICUS and CAPRICORN

0.000040.00004

3131%%

Death orDeath or hospitalization hospitalization for a CV for a CV reasonreason

0.760.76

Death or Death or hospitalizatiohospitalization for any n for any reasonreason

Relative risk reduction

24%

0.00002

Odds ratio

27% 0.73

0.69

Beta BlockersBeta BlockersPost MI LV dysfunctionPost MI LV dysfunction

CAPRICORN( carvedilol post CAPRICORN( carvedilol post infarct survival control in LVD)infarct survival control in LVD) 1959 pts post MI LVEF<40%1959 pts post MI LVEF<40% Randomized to carvedilol or placeboRandomized to carvedilol or placebo Results: Results:

Lower all cause mortality (12% vs. 15%)Lower all cause mortality (12% vs. 15%) Lower non-fatal MILower non-fatal MI

Lancet 2001; 357: 1385–90

CAPRICORN All-Cause MortalityCAPRICORN All-Cause Mortality

0 0.5 1 1.5 2 2.5

Carvedilol n=975

Placebo n=984

Years

Pro

po

rtio

n E

ven

t-fr

ee

23%(2%, 40%)

Risk reduction

0

0.90

0.70

0.60

0.80

The CAPRICORN Investigators. Lancet. 2001;357:1385-1390.

Mortality Rates: Placebo 15%; Carvedilol 12%

Carvedilol Post-Infarct Survival Control in LV Dysfunction

1.00

Clinical Use Of Beta Clinical Use Of Beta Blockers Blockers

Recommended for patients with NYHA class Recommended for patients with NYHA class II-IVII-IV

General contraindications:General contraindications: Decompensated heart failureDecompensated heart failure Severe claudicationSevere claudication BronchospasmBronchospasm Advanced heart blockAdvanced heart block Use with caution if patient requires Use with caution if patient requires

inotropes for support of circulatory inotropes for support of circulatory functionfunction

Beta-Blockade

Cardiac Output

RenalBlood Flow

SodiumRetention

Worsening Heart Failure

Considerations in selecting a Considerations in selecting a beta-blockerbeta-blocker

1.1. Patients should be clinically stable Patients should be clinically stable and euvolemic before initiating and euvolemic before initiating beta-blocker therapybeta-blocker therapy

2.2. Start at low doses and titrate Start at low doses and titrate upward gradually upward gradually (doubling every (doubling every 2-4 weeks)2-4 weeks)

3.3. Patients may experience an initial Patients may experience an initial exacerbation of heart failure exacerbation of heart failure symptoms because of transient symptoms because of transient worsening of cardiac outputworsening of cardiac output

Clinical Use Cont . . .Clinical Use Cont . . .

Clinical response may not be seen Clinical response may not be seen until 2 to 3 months after initiation of until 2 to 3 months after initiation of therapytherapy

Abrupt withdrawal can lead to Abrupt withdrawal can lead to dramatic deteriorationdramatic deterioration

Patient education paramountPatient education paramount

Outcome in Post-MI Patients with Heart FailureOutcome in Post-MI Patients with Heart Failure

CAPRICORN and MERIT-HFCAPRICORN and MERIT-HF

11Time to first eventTime to first event

CAPRICORNCAPRICORNAll-cause mortalityAll-cause mortality

All-cause mortality/CV hosp.All-cause mortality/CV hosp.11

MERIT-HF MERIT-HF

23%

8%

Risk Risk reductionreduction

p-p-valuevalue

p=0.03

Plac/BetaPlac/Beta

151/116151/116

122/74122/74 40% p=0.0004

CAPRICORNCAPRICORN

MERIT-HF MERIT-HF

367/340367/340

326/258326/258

ns

22% p=0.002

The CAPRICORN Investigators, Lancet 2001;357:1385-90Jánosi A et al, Am Heart J 2003;146:721-8

Relative risk and 95% CIRelative risk and 95% CI0.00.0 1.01.0

Metoprolol CR/XL 1

Metoprolol CR/XL 1

Carvedilol 1 2 (1)

Carvedilol 1 2 (1)

LVEF: Change From BaselineLVEF: Change From BaselineWithin Treatment-arm Within Treatment-arm

ComparisonComparison

* P < 0.05; ** P < 0.01; *** P < 0.001

EnalaprilCarvedilol &Enalapril

Carvedilol

-1-1

00

11

22

33

44

55

L

VE

F (

%)

****** ****** ******

****** ****** ****

**

M6 M12 M18 M6 M18M12 M6 M12 M18

Diuretics Diuretics

HFSA 2006 Practice Guideline (7.14-7.15)

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) due to LV systolic dysfunction (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 an ARB. Strength of Evidence = A

Adapted from: Adams KF, Lindenfeld J, et al. HFSA 2006 Comprehensive Heart Failure Guideline. J Card Fail 2006;12:e1-e122.

RALES(randomised RALES(randomised aldactone evaluation study)aldactone evaluation study)

1663 patients Class 1663 patients Class 3-4 CHF, LVEF<35% 3-4 CHF, LVEF<35% on on ACE-inhibitor/diuretiACE-inhibitor/diuretic/dig c/dig

randomized to randomized to 25 25 mg spironolactonemg spironolactone vs. placebovs. placebo

issues: issues: only 10% of only 10% of

patients on beta patients on beta blockersblockers

NEJM 1999:341:709-17

RALESRALES Results: 46% mortality Results: 46% mortality

placebo vs 35% placebo vs 35% spironolactone (30% spironolactone (30% RRR)RRR)

adverse effects: adverse effects: 10% of pts in 10% of pts in

spironolactone group spironolactone group developed developed gynecomastia.gynecomastia.

-serious hyperkalemia -serious hyperkalemia (K>6) 14% vs 10% (not (K>6) 14% vs 10% (not statist sig)statist sig)

EPHESUS(eplerenone post EPHESUS(eplerenone post AMI HF efficacy and AMI HF efficacy and

survival study)survival study) 6642 patients:6642 patients: a) 3-14 days a) 3-14 days post MIpost MI, , b) EF<40, b) EF<40, c) CHF (rales, pulm venous congestion c) CHF (rales, pulm venous congestion

seen on CXR, 3rd heart sound) seen on CXR, 3rd heart sound) OROR DiabetesDiabetes

randomized to randomized to 25 mg eplerenone25 mg eplerenone titrated titrated up to 50 mg po qdup to 50 mg po qd

NEJM 2003;348:1309-21

Results:Results: One year mortality: 15% risk reduction (11.8% vs One year mortality: 15% risk reduction (11.8% vs

13.6%)13.6%) CV death or cardiovascular hospitalizations (26% vs CV death or cardiovascular hospitalizations (26% vs

30.0%)30.0%)

(75% of patients on beta blockers)(75% of patients on beta blockers)

adverse effects: adverse effects: serious hyperkalemia (K>6) Epler- 5.5% vs plac- serious hyperkalemia (K>6) Epler- 5.5% vs plac-

3.9% (p=.002)3.9% (p=.002) serious hypokalemia (K<3.5) Epler- 8.4% plac- serious hypokalemia (K<3.5) Epler- 8.4% plac-

13.1% (p<.001)13.1% (p<.001) gynecomastia- 0.5% vs 0.6%gynecomastia- 0.5% vs 0.6%

EPHESUSEPHESUS

Criteria for treatment with Criteria for treatment with spironolactonespironolactone

New York heart Association class 3-4New York heart Association class 3-4 Left ventricular ejection fraction Left ventricular ejection fraction

<35%<35% Serum creatinine <2.5 mg/dLSerum creatinine <2.5 mg/dL Serum potassium <5 mmol/LSerum potassium <5 mmol/L Baseline treatment with ACE inhibitor Baseline treatment with ACE inhibitor

(or other vasodilator if ACE inhibitor (or other vasodilator if ACE inhibitor intolerance), loop diuretic, and intolerance), loop diuretic, and digoxin as indicateddigoxin as indicated

DigoxinDigoxin

Digoxin has a significant role in Digoxin has a significant role in improving symptoms and improving symptoms and rehospitalization raterehospitalization rate

No impact on the total and No impact on the total and cardiovascular mortalitycardiovascular mortality

Usually used only in severe CHF or in Usually used only in severe CHF or in patients who remain symptomatic patients who remain symptomatic with optimal treatmentwith optimal treatment

Digoxin is useful in CHF with atrial Digoxin is useful in CHF with atrial fibrillationfibrillation

DigoxinDigoxin

DIG trial DIG trial 6800 pts EF <45%6800 pts EF <45% 0.25 mg/day0.25 mg/day 22% reduction in hospitalisation22% reduction in hospitalisation No mortlity benefitNo mortlity benefit 28% RRR of death in post hoc 28% RRR of death in post hoc

analysisanalysis

NesiritideNesiritide

Identical to human BNPIdentical to human BNP Causing vasodilation and decrease Causing vasodilation and decrease

LV filling pressureLV filling pressure Decrease pulmonary capillary wedge Decrease pulmonary capillary wedge

pressurepressure Improves patients’ symptomsImproves patients’ symptoms Improvement in hemodynamics Improvement in hemodynamics

VMAC trial 5.8 mm of hg decrease on VMAC trial 5.8 mm of hg decrease on PCWPCW

NesiritideNesiritide

2 mcg/kg bolus infusion 0.01-0.03 2 mcg/kg bolus infusion 0.01-0.03 mcg/kg/min for 3 hrsmcg/kg/min for 3 hrs

Improved safety profile compared Improved safety profile compared with dobutamine with fewer with dobutamine with fewer arrhythmias and better outcomesarrhythmias and better outcomes

It should not be used in patients who It should not be used in patients who are overdiuresed, hypotensive, or are overdiuresed, hypotensive, or present with other signs of present with other signs of inadequate perfusion -inadequate perfusion -Worsening of Worsening of renal failure (45%)renal failure (45%)

InotropesInotropes

Inotropes: direct adrenergic agonists, Inotropes: direct adrenergic agonists, phosphodiesterase inhibitors, and phosphodiesterase inhibitors, and dopaminergic agonistsdopaminergic agonists

Inotropes improve short term Inotropes improve short term hemodynamics, they do not improve hemodynamics, they do not improve and in several cases may worsen long-and in several cases may worsen long-term survival term survival

Oral inotropic agents have resulted in Oral inotropic agents have resulted in excess mortality in patients with HFexcess mortality in patients with HF

AmiodaroneAmiodarone

Antiarrhythmic effectAntiarrhythmic effect Low dose amiodarone was safe and Low dose amiodarone was safe and

significantly reduced 2-year mortality significantly reduced 2-year mortality (33.5% vs 41.4%, p=0.02)(33.5% vs 41.4%, p=0.02)

in patients with moderate to severe HF in patients with moderate to severe HF (GESICA trial)(GESICA trial)

Another trial did not demonstrate Another trial did not demonstrate mortality benefit, either all-cause or mortality benefit, either all-cause or sudden death sudden death

AnticoagulationAnticoagulation

LVEF < 30%LVEF < 30% LV thrombusLV thrombus Atrial fibrillationAtrial fibrillation INR 2-3INR 2-3

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Bd1e Management Of Heart Failure

Health & Medicine

Transcript of Bd1e Management Of Heart Failure