Heart Failure Therapy

8/16/2019 Heart Failure Therapy

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Heart

Failure


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Heart failure (HF)

A pathological condition in which heart isunable to pump enough blood to the restof the body

-unable to ll with a sucient volume ofblood

-unable to generate sucient force to

pump out enough blood


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“Ejection Fraction refers to the fraction ofblood the heart pumps out with each beat


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RA LA

RVLVH

!oss of elasticity

"ecline in pumping action

IVC

SVC

Aorta

PV

LUNGS

PALUNGS

LV


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MyocardialIscheia

Cardioyo!athy

Val"ular Heart#isease

#ecreased Cardiac

$ut!ut

Hy!erte%sio%

Carotid &arorece!tor Stiulatio% #ecreasesRe%al Perfusio% #ecreases

Acti"atio% of SNS a%dRAAS

I%crease Heart Rate a%dI%otro!y

Myocardial 'oicity

Vasoco%strictio% I%creases afterloadHeody%aic alteratio%s I%creases

!reload

Ne*ati"e Reodeli%*+orse%ed LV Fu%ctio%

Sy!tos of HF

'hus, - a.or co!e%satory systes are acti"ated i% the/ody012 Sy!athetic Ner"ous Syste (SNS)-2 Re%i% a%*iote%si% aldostero%e syste (RAAS)


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#hat are the cardinal symptomsof HF$

"yspnea

Fatigue


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Classi3catio%

ACCF4AHA Sta*es of HF

A At high ris% for HF but without

structural heart disease or

symptoms of HF

& &tructural heart disease but

without signs or symptoms of HF

C &tructural heart disease with

prior or current symptoms of HF

# 'efractory HF re(uiring

speciali)ed interventions

N5HA Fu%ctio%al Classi3catio%

I *o limitation of physical activity+

,rdinary physical activity does

not cause symptoms of HF+

II &light limitation of physical

activity+ omfortable at rest. butordinary physical activity results

in symptoms of HF+

III /ar%ed limitation of physical

activity+ omfortable at rest. but

less than ordinary activity

causes symptoms of HF+

IV 0nable to carry on any physical

activity without symptoms of HF.

or symptoms of HF at rest+


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&ased o% Left Ve%tricular 6.ectio% Fractio%(LV6F)0

12Systolic HF or Systolic dysfu%ctio%• "efect in ventricular contraction

• !eft ventricle loses ability to generate enough pressure toeject blood forward into the aorta

• "ecreased !1EF 234 or 567

-2 #iastolic HF or #iastolic dysfu%ctio%

• 8mpaired ability of ventricles to ll

• 9atients have symptoms and:or signs of HF

• 9reserved or abnormal !1EF ;56-467

Soe !atie%ts 7ith systolic HF ha"e associateddiastolic dysfu%ctio% therefore, i% ost cases,diastolic 8 systolic HF are %ot co%sidered as

se!arate e%tities


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&ased o% Mai% Site of Co%*estio%0

12 Left9sided HF0 Most coo%

•


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-2 Ri*ht9sided HF

• 0nresolved left-sided HF eventually leads to right sided HF

• ow of blood into the right atrium and venouscirculation

• 'esult= &ystemic edema

?ugular vein distention

9edal edema Ascites Hepatomegaly #eight gain


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!eft Heart Failure'ight Heart Failure

9eripheral >uid overload 9ulmonary >uid overload

http://www.netterimages.com/image/808.htmhttp://www.netterimages.com/image/808.htm


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Ho7 to dia*%ose HF:

o History and physical e@aminationo -"imenional doppler echocardiography

o hest B-ray

o

E@ercise testo Electrocardiography CED or ED

o !aboratory tests - omplete blood count. &erumelectrolytes Csodium and potassium.


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&ioar;ers

• Natriuretic !e!tides


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Ho7 to a%a*e HF:

• 'elief from signs and symptoms

• 8mprove survival

AE8: A'


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"iuretics• 8nhibits reabsorption of sodium or chloride at specic sites in

renal tubulesJ improves dyspnea and peripheral edema

• 0sed in conjunction with AE8. beta-bloc%er and analdosterone antagonist

• Gherapy is commonly initiated at low doses and dose isincreased until urine output increases and weight decreasesC6+4-K %g daily

• Hypovolemia. Hyponatremia. Hypo%alemia 8ncrease ris% ofhypotension and renal dysfunction

• 9referred diuretics - !oop diuretics Ctorsemide. furosemide

• Ghia)ide diuretics Chydrochlorthia)ide. chlorthalidone Hypertensive patients with HF and mild >uid retention

• ombination can be used in patients with resistant edema


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&eta9/loc;ers

• 'ecommended in all stable HF patients with reduced EFClass 8. !,E AJ reduce ris% of death and hospitali)ation

• !essen the symptoms. improve patientLs clinical status.and enhance overall well-being

•


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A%*iote%si% co%"erti%*e%=ye i%hi/itors (AC6Is)• 'educes ris% of death and hospitali)ation

•


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A%*iote%si% rece!tor/loc;ers (AR&s)

• 'ecommended in patients

- as an alternative who are intolerant to AE8s Class 8. !,EA

- as an alternative to AE8s as a rst-line therapy in

patients already ta%ing A'


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Aldostero%e a%ta*o%ists

• Aldosterone promotes sodium retention. electrolyteimbalanced. vascular remodeling and myocardialhypertrophy

• 0sed in patients with !1EF O347 and severe HF to reducemortality and morbidity Class 8. !,E AJ

• &hould be added to all patients on AE8s Cor A'


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I"a/radi%e

• 8nhibits 8f channel in the sinus node

• &lows the heart rate in patients in sinusrhythm Cdoes not slow the heart rate inAF


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"igo@in

• /ild inotropic eMect

• 8mproves symptoms. (uality of life and e@ercisetolerance in mild to moderate HF but not survival

•Added in case of persistent symptoms

• *ot recommended as a rst line therapy. used in HFpatients with AF but beta-bloc%ers are usually moreeMective

• /ajor side eMects include cardiac arrhythmias. D8

symptoms Canore@ia. nausea. vomiting and neurologiccomplaints


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Hydrala=i%e a%disosor/ide %itrate

• Hydrala)ine produces arterial vasodilation and reductionin systemic vascular resistance

• *itrates produce arterial and venous vasodilation

• onsidered in patients with EF O547 despite treatment

with a beta-bloc%er. AE8 Cor A'


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Anticoagulants

• 9latelet activation and hypercoagulability in HF

• #arfarin therapy has shown to reduce ris% of stro%e

• However. available data suggests that the ris% of bleeding

overshadows its benet in HF patients with sinus rhythm• !arge trials are needed to establish the role of anti-

thrombotics in HF patients with sinus rhythm


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8notropes

• 'eserved for patients with HF refractory to othertherapies

• &hould be considered in systolic dysfunction who havelow cardiac inde@ and evidence of systemic hypoperfusion

and: or congestion• /ay increase ris% of morality because of increased

myocardial o@ygen consumption and increasedtachycardia eMect

• !ower doses are preferred

• E+g+ intravenous dopamine. dobutamine. milrinone andlevosimendan


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*on-pharmacologicalmanagement

o 8mplantable cardioverter debrillator C8"

o ardiac resynchroi)ation therapy C'G

o 1alvular surgery

o oronary revasculari)ation

o !eft ventricular assist device

o Heart transplantation


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I!la%ta/le cardio"erterde3/rillator

• 'educes ris% of serious rhythm problems in ventricles. theprimary cause of sudden cardiac death C&"

• 'ecommended as a primary prevention to reduce mortalityin patients with !1 dysfunction. !1EF O347. *PHA class 88or 888. &tage HFrEF Class 8. !,E A

• *ot warranted in stage " or class 81 patients


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Cardiac resy%chro%i=atio%thera!y (CR')

• Also called as Qbiventricular pacingL

• 8t not only functions as a pacema%er but it re co-ordinatesCresynchroni)es the beating of the two ventricles bypacing both simultaneously and specically improving the

contraction of left ventricle• Ghus. improving symptoms of heart failure and prolongs

survival

• 'ecommended for *PHA class 888 or 81J &tage


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Coro%aryre"asculari=atio%

• A


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Val"ular sur*ery

• 1alvular disease may cause or aggravate HF

• &urgical aortic valve replacement

• Granscatheter aortic valve replacement

• Granscatheter mitral valve repair or mitral valvesurgery


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Heart transplantation

• 8ndicated for stage " HF patients despite device adsurgical management Class 8. !,E


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Articial Hearts

• Gypically used to bridge the time to heart transplantation.or to permanently replace the heart in casetransplantation is impossible

• an dramatically improve symptoms of late-stage HF. andsometimes even provide long-term treatment


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Mecha%ical circulatoryde"ices (MCS)

• &tage " patients

• 1entricular assist devices

• !ong term strategies bridge to transplantation. bridge tocandidacy and destination therapy

• /& facilitates !1 reverse remodelling


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!STUT

• ,rally active angiotensin receptor neprilysin inhibitorCA'*8

• 8ntended as rst line treatment for patients with chronicHF C*PHA stage 88-81 and reduced !1EFJ administered 66mg twice daily

• !STUT enhances myocardial rela@ation V reduced

ventricular hypertrophy

J Am Coll Cardiol HF. 2013;1:1–20

9A'A"8D/ HF di l " th H t


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0

16

32

40

24

8

Enalapril(n=4212)

360 720 10800 180 540 00 1260

Days After Randomization

4187

4212

322

3883

3663

357

3018

222

2257

2123

1544

1488

86

853

24

236

!C"66

#nala$ril

%a&i'n& a& i*

1117

K a p l a n - M e i e r E s t i m a t e o f

C u m u l a t i v e R a t e s ( % )

14

LCZ!(n=4187)

"R # $%&$ ($%'-$%&')

# $%$$$$$$*

+um,er needed to treat # *

9A'A"8D/-HF= ardiovascular "eath or HeartFailure Hospitali)ation C9rimary Endpoint

+ #n,l J -'d 2014; 371:31004


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LC>?@?(%B1

D)

6%ala!ril(%B-1-

)

Ha=ardRatio

(@E CI)

PValue

ardiovasculardeath 44WCK3+37 TU3CKT+47

6+W6

C6+XK-6+WU

6+66665

Hospitali)ationfor heartfailure

43XCK+W7

T4WCK4+T7

6+XUC6+XK-6+WU

6+66665

All-causemortality

XKKCKT+U7

W34CKU+W7

6+W5C6+XT-6+U3

2 6+666K

9A'A"8D/-HF= EMect of !STUT vs Enalapril on,ther Endpoints

+ #n,l J -'d 2014; 371:31004


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&erala@in

• A recombinant form of the human hormonerela@in

• 'E!AB-AHF trial

• /ay be potentially a attractive option forpatients with acute HF


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ardiac myosin activators

• ,mecamtiv mecarbil

• 8ncreases cardiac output and stro%e volume

• &uggest a new therapeutic target in HFrEF


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&tem cell therapy

•


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Dene Gherapy

• 'eplacing a faulty gene with anormal one

• 1iral vectors carrying the

correct gene bind to a receptoron the cardiac myocytes.travel to the nucleus where thegene is incorporated into thegenome V transcription occurs

• an be used along with stemcell therapy to increasebenets

Heart Failure Therapy

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