HEART FAILUREHEART FAILURE

DEFINITION: A clinical syndrome DEFINITION: A clinical syndrome characterized by systemic perfusion characterized by systemic perfusion

inadequate to meet the body’s metabolic inadequate to meet the body’s metabolic demands as a result of impaired cardiac demands as a result of impaired cardiac

pump functionpump function

HEART FAILUREHEART FAILUREACC/AHAACC/AHA

• A COMPLEX CLINICAL SYNDROME THAT CAN RESULT FROM ANY STRUCTURAL OR FUNCTIONAL CARDIA DISORDER THAT IMPAIRS THE ABILITY OF THE VENTRICLE TO FILL OR EJECT BLOOD.

HAERT FAILUREHAERT FAILURE

• SYTOLIC HEART FAILURE ( 60% ):

REDUCED CARDIAC CONTRACTILITY AS IN CORONARY ARTERY DISEASE WITH MI OR CHRONIC ISCHEMIA, DILATED CARDIOMYOPATHY, VALVULAR HEART DISEASE, HYPERTENSIVE HEART DISEASE,TOXIN INDUCED CARDIOMYOPATHY ( DOXORUBICIN, HERCEPTIN, ALCOHOL) AND CONGENITAL HEART DISEASE.

DIASTOLIC HEART FAILUREDIASTOLIC HEART FAILURE

• IMPAIRED CARDIAC RELAXATION AND ABNORMAL VENTRICULAR FILLING

AS IN CHRONIC HT,IHD, RESTRICTIVE INFILTRATIVE AND HYPERTRPHIC CARDIOMYOPATHIES.

INADEQUATE RV FILLING FROM PERICARDIAL CONSTRICTION OR TAMPONADE

RIGHT VENTRICULAR SYSTOLIC DYSFUNCTIONRIGHT VENTRICULAR SYSTOLIC DYSFUNCTION

* CONSEQUNCE OF LV DYSFUNCTION.• OTHER CAUSES:VIZ. RV INFARCTION,

PAH,CHRONIC SEVERE TR, ARRHYTHMOGENIC RV DYSPLACIA

HIGH OUT PUT FAILUREHIGH OUT PUT FAILURE

• THYROTOXICOSIS.

• ARTRIOVENOUS FISTULAE

• PREGNANCY

• SEVERE ANEMIA

CLASSIFICATION OF HF( ACC/AHA)CLASSIFICATION OF HF( ACC/AHA)BASED ON STRUCTURAL ABNORMALITY OR BY SYMPTOMSBASED ON STRUCTURAL ABNORMALITY OR BY SYMPTOMS

Prevalence and Prevalence and magnitude of the problemmagnitude of the problem

• >5 million affected with HF in USA( 2% of population: 6-10% > 65 years age)

• 550,000 diagnosed each year

• Annual mortality 5 to 20 %

• 12.15 million office visits and 6.5 million hospital admission days.

• Total direct and indirect cost 27.9 billion US $ & Annual cost of drugs 2.9 Billion $.

NATURAL HISTORY OF HFNATURAL HISTORY OF HF

• PROGRESSIVE PUMP FAILURE AND DEATH• SCD 50%• END ORGAN FAILURE INDICATORS OF POOR PROGNOSIS: RENAL DYSFUNCTION,VALVULAR

REGURGITATION, VENTRICULAR ARRHYTHMIAS, HIGH NYHA CLASS, LOW EF, HIGH BNP AND CATECHOLAMINE LEVEL, LOW SODIUM, MARKED LV DILATATION, CACHEXIA AND COMBINED SYSTOLIC AND DIASTOLIC DYSFUNCTION.

PATHOPHYSIOLOGYPATHOPHYSIOLOGY LV DYSFUNCTION LV DYSFUNCTION * * LOW C.OLOW C.O * ELEVATED PA PRESSURES* ELEVATED PA PRESSURES * PULMONARY CONGESTION* PULMONARY CONGESTION * ACTIVATION OF NEUROHORMONAL PATHWAS TO INCREASE BLOOD * ACTIVATION OF NEUROHORMONAL PATHWAS TO INCREASE BLOOD

VOLUMEVOLUME * ENHANCED SYMPATHETIC ACTIVITY AND INREASED HR * ENHANCED SYMPATHETIC ACTIVITY AND INREASED HR

&CONTRACTILITY AND CATECHOLAMINE INDUCED &CONTRACTILITY AND CATECHOLAMINE INDUCED VASOCONSTRICTION OF VASCULAR BEDSVASOCONSTRICTION OF VASCULAR BEDS * RENIN SECRETION FROM JUXTAGLOMERULAR APPARATUS* RENIN SECRETION FROM JUXTAGLOMERULAR APPARATUS

CONSEQUENCES OF CONSEQUENCES OF COMPENSATORY MECHANISMS COMPENSATORY MECHANISMS

CATECHOLAMINES AGGRAVATE ISCHEMIA, CATECHOLAMINES AGGRAVATE ISCHEMIA, ARRHYTHMIA, INDUCE CARDIAC ARRHYTHMIA, INDUCE CARDIAC REMODELLING AND TOXIC TO MYOCYTES.REMODELLING AND TOXIC TO MYOCYTES.

STIMULATED RAA SYSTEM & SYMPATHETIC STIMULATED RAA SYSTEM & SYMPATHETIC STIMULATION > ARTERIOLAR STIMULATION > ARTERIOLAR CONSTRICTION, Na+ H2O CONSTRICTION, Na+ H2O RETENTION>ALDOSTERONE >Na+H2O> RETENTION>ALDOSTERONE >Na+H2O> ENDOTHELIAL DYSFUNCTION>FIBROSIS. ENDOTHELIAL DYSFUNCTION>FIBROSIS.

CONSEQUENCES OF CONSEQUENCES OF COMPENSATORY MECHANISMSCOMPENSATORY MECHANISMS

BARORECEPTOR AND OSMOTIC STIMULI> BARORECEPTOR AND OSMOTIC STIMULI> HYPOTHALAMIC VASOPRESSIN> H2O HYPOTHALAMIC VASOPRESSIN> H2O REABSORPTION IN COLLECTING DUCTREABSORPTION IN COLLECTING DUCT

^ENDOTHELIN.^ CYTOKINES.^ENDOTHELIN.^ CYTOKINES. CYTOKIES> CAHEXIA & APOTOSISCYTOKIES> CAHEXIA & APOTOSIS NATRIURETIC PEPTIDES FROM CARDIOMYOCYTES NATRIURETIC PEPTIDES FROM CARDIOMYOCYTES

> VASODILATATION> ENHANCED Na +H2O > VASODILATATION> ENHANCED Na +H2O EXCRETION & SUPRESS NEUROHORMONES.EXCRETION & SUPRESS NEUROHORMONES.

NEUROHORMONAL MODULATION IS THE BASIS OF NEUROHORMONAL MODULATION IS THE BASIS OF CURRENT TREATMENT OF HFCURRENT TREATMENT OF HF

InvestigationsInvestigations

• ECG, Chest X-ray.• ECHOCARDIOGRAM:

Systolic Vs Diastolic dysfunction, Valvular Heart disease, Tamponade, Constriction, restrictive/ infiltrative cardiomyopathy, LVH

• Cardiac catheterisation:Coronary angiography.• MRI in arrhythmogenic RV dysplasia, myocardial

viability assessment and infiltrative cardiomyopathy.

Echocardiography in HFEchocardiography in HF Plays major role in diagnosis of HF with preserved EF or Plays major role in diagnosis of HF with preserved EF or

mild LV systolic dysfunction mild LV systolic dysfunction ( LVEF 45-50 %)( LVEF 45-50 %)

Tissue Doppler imaging in assessment of diastolic Tissue Doppler imaging in assessment of diastolic dysfunction and in inter & intraventricular dyssynchrony dysfunction and in inter & intraventricular dyssynchrony

2 dimensional speckle tracking echo2 dimensional speckle tracking echo Calculation of myocardial velocities and deformation Calculation of myocardial velocities and deformation

parameters such as strain and strain rate.parameters such as strain and strain rate.

MRIMRI

• MRI and CT scan MRI accurate in assessment of LV and RV volumes,

global function, regional wall motion, myocardial thickness, thickening , mass, tumours, valves, pericardial disease CHD, ARVD, infiltrative myopathy And myocardial viability.

• MSCT,CT coronary angiography.

BNP in HFBNP in HF

Diagnosis of heart failure.Diagnosis of heart failure.BNP level correlates well with NYHA BNP level correlates well with NYHA

symptomatic class.symptomatic class.Useful in assessing response to therapyUseful in assessing response to therapyHelpful in discharge timing.Helpful in discharge timing.Useful in prognostication. Useful in prognostication.

HEART FAILURE HEART FAILURE MANAGEMENTMANAGEMENTIdentification of precipitatingIdentification of precipitating factorsfactors

ACC/AHA stage ACC/AHA stage

CLASSIFICATION OF HF( ACC/AHA)CLASSIFICATION OF HF( ACC/AHA)BASED ON STRUCTURAL ABNORMALITY OR BY SYMPTOMSBASED ON STRUCTURAL ABNORMALITY OR BY SYMPTOMS

Management of HFManagement of HF

Modification of Life style-Cardiac Rehabilitation• 2 g sodium diet.• Weight monitoring daily• 2-L fluid restriction• Avoid cardiotoxic agents including alcohol and

tobacco• Monitoring BP, ideal weight, light aerobic

exercise, medications, follow-up, know whom to call SOS.

DiureticsDiuretics

• Loop diuretics :Furosemide,Torsemide. Bumetinide

• Thiazide:HTZ&Metolazone.

Seqential nephron blockade: Metolazone+ Loop diuretic

• K+ sparing agents.

I.V infusion of Furosemide

ACEIACEI Essential unless contraindicated.Essential unless contraindicated. Use regardless of EF esp. in DM &HT.Use regardless of EF esp. in DM &HT. Vasodilatation and neurohormonal modulation Vasodilatation and neurohormonal modulation

improves mortality, symptoms, effort tolerance, improves mortality, symptoms, effort tolerance, LVEF & visits to hospital.LVEF & visits to hospital.

Use maximum tolerated dose.Use maximum tolerated dose. 20 % intolerant.20 % intolerant. Problem: Angioedema and worsening of renal Problem: Angioedema and worsening of renal

function. function.

ARB AND RENIN INHIBITORARB AND RENIN INHIBITOR ARB no superior to ACEI in improving mortality.ARB no superior to ACEI in improving mortality. Improve morbidity when added to ACEIImprove morbidity when added to ACEI Recommended for those intolerant to ACEI.Recommended for those intolerant to ACEI. May have morbidity benefits in diastolic HF.May have morbidity benefits in diastolic HF. Addition of Renin inhibitor Alliskerin to standard Addition of Renin inhibitor Alliskerin to standard

therapy results in lower BNP levelstherapy results in lower BNP levels

Beta Blockers in HFBeta Blockers in HF Carvedilol,Metoprolol succinate and Bisoprolol Carvedilol,Metoprolol succinate and Bisoprolol

shown to improve survival.shown to improve survival. Nebivolol has some advantages over carvedilolNebivolol has some advantages over carvedilol (highly Beta 1 selective& enhances NO (highly Beta 1 selective& enhances NO

bioavailability)bioavailability) ? Benefit due to Antiarrhythmic, anti-ischemic, ? Benefit due to Antiarrhythmic, anti-ischemic,

antiremodelling and antiapototic properties and antiremodelling and antiapototic properties and reduced HR and MV O2.reduced HR and MV O2.

DM, COPD, PVD, euvolumic Class IV not DM, COPD, PVD, euvolumic Class IV not contraindicationscontraindications

Combine with ACEI Combine with ACEI

Digoxin in HFDigoxin in HF

• Neurohormonal modulating agent inhibiting enzyme Na+, K+-ATP ase and improves contractility, reduces CNS sympathetic outflow and inhibits renin release in Kidney.

Reduces rate of hospitalization for HF but not mortality

Esp. useful in AF with HF( Class I , level C)NSR, HF ,EF< 40 % ( Class II A, Level B) • Dose to maintain serum level < 1 ng/ml.

Hydralazine and NitratesHydralazine and Nitrates

• Hydralazine ( arterial dilator) and nitrate (venodilator) increase Nitric oxide bioavailability>

increased intracellular cGMP> vasodilatation.• Hydralazine prevents nitrate tachyphylaxis.Inferior to ACEI in improving survival

but better in improving hemodynamic.

Useful when ACEI/ARB cannot be used (Hyperkalemia or renal failure) . May be

added to ACEI if PAH is present.

Aldosterone antagonistsAldosterone antagonists

• 30 % reduction in mortality and hospitalizations when spironolactone is added to standard therapy for patients with advanced HF(NEJM 341:1999;709-717)

• 15 % reduction in risk in HF with EF<40 %

after MI when treated with eplerenone, a selective aldosterone blocker (EPHESUS study NEJM 348:2003;1309-1321)

Aldosterone blockersAldosterone blockers

• Use in moderate to severe HF and reduced LVEF.

• Prevent sodium and water retention, endothelial dysfunction and myocardial fibrosis.

• Avoid if S.Creatinine > 2.5 mg/dl.

• No gynecomastia or menstrual irregularity with eplerenone

IVABRADINEIVABRADINE

• Acts on If ion current and reduces sinus rate : Beneficial in angina 36 % reduction in fatal and non fatal MI ( BEAUTIFUL study ).

Chronic heart failure• In the SHIFT study, ivabradine significantly reduced the risk of the primary

composite endpoint of hospitalization for worsening heart failure or cardiovascular death by 18% (P<0.0001) compared with placebo on top of optimal therapy. These benefits were observed after 3 months of treatment. SHIFT also showed that administration of ivabradine to heart failure patients significantly reduced the risk of death from heart failure by 26% (P=0.014) and hospitalization for heart failure by 26% (P<0.0001). The improvements in outcomes were observed throughout all prespecified subgroups: female and male, with or without beta-blockers at randomization, patients below and over 65 years of age, with heart failure of ischemic or non-ischemic etiology, NYHA class II or class III, IV, with or without diabetes, and with or without hypertension.[8]

I.V ionotropes and vasodilators.I.V ionotropes and vasodilators.

• Dobutamine : Cardiac B1 receptor stimulation to improve contractility in acute hypotensive HF. Long term use only in those with ICD awaiting transplant.

Useful in acute decompensated heart failure• Milrinone: Phosphodiesterase inhibitor: vasodilator: May

improve PAH: useful in those on B-blocker> proarrhythmic.

• NTG Anti ischemic vasodilator.• Nitroprusside : Vasodilator; may provoke ischemia by

steal: Thyocynate accumulation in renal failure.

NesiritideNesiritide

• Nesiritide ( recombinant synthetic BNP) : vasodilation in arteries and veins: promotes diuresis, lowers PAW pressure: useful in “up-front” care of decompensated HF.

No increase in HR or MVO2. No tolerance and not proarrhythmic

No mortality benefit

LEVOSIMENDANLEVOSIMENDAN

• Calcium sensitizer.

• Increases contractility without rise in intracellular Ca.

• Binds to troponin-c of myocytes

• Vasodilatory effect by opening ATP sensitive K channels in vascular SMC

• Decreases preload and after load

LEVOSIMENDANLEVOSIMENDAN

• Total 3500 patients in trials

• Initial BNP reduction

• No reduction in mortality at 6 monthsSuperior to Dopamine in acutely

decompensated HF on B blockerReduces troponin leak after cardiac

surgery when used perioperatively

AQUARETICSAQUARETICSUp regulated Arginine Vasopressin Up regulated Arginine Vasopressin

stimulation represents a maladaptive stimulation represents a maladaptive neurohormonal response in HF.neurohormonal response in HF.

AVP increases blood volume by water AVP increases blood volume by water retention via V2 receptors in collecting retention via V2 receptors in collecting ducts.ducts.

VasoconstrictiveVasoconstrictiveCauses cardiac HypertrophyCauses cardiac HypertrophyV1a receptors mediate vasoconstrictionV1a receptors mediate vasoconstriction

TOLVAPTANTOLVAPTAN Selective oral V2 Vasopressin receptor Selective oral V2 Vasopressin receptor

antagonist.antagonist. Conivaptan is dual V1a/V2 receptor antagonist Conivaptan is dual V1a/V2 receptor antagonist

– I.V – I.V Sodium free diuresis.Sodium free diuresis. Weight reduction, Decreases edema and Weight reduction, Decreases edema and

dyspnoea, corrects hyponatremia and no dyspnoea, corrects hyponatremia and no worsening of renal failureworsening of renal failure

No reduction in number of hospitalizations and No reduction in number of hospitalizations and long term mortality.long term mortality.

AQUAPHARESISAQUAPHARESIS

• Ultrafiltration to remove excess fluid without sodium through a filter.

• Upto 500 ml fluid removed/ hour

• Reduces hospitalizations

• Avoids problems with over diuresis

• No large scale studies

PHOSPHODIESTERASE INHIBITORS PHOSPHODIESTERASE INHIBITORS AND ENDOTHELIN RECEPTOR AND ENDOTHELIN RECEPTOR

BLOCKERS.BLOCKERS. Sildenafil ( PDE 5 inhibitor), improves effort Sildenafil ( PDE 5 inhibitor), improves effort

tolerance and symptoms on 6 minute walk test in tolerance and symptoms on 6 minute walk test in Idiopathic PAH and PAH secondary to CHD.Idiopathic PAH and PAH secondary to CHD.

Endothelin receptor blockers Bosentan ( non –Endothelin receptor blockers Bosentan ( non –selective ) and Sitaxentan ( selective ET- A) selective ) and Sitaxentan ( selective ET- A) receptor blocker may be combined with sildenafil receptor blocker may be combined with sildenafil to reduce PA pressure in idiopathic PAH and to reduce PA pressure in idiopathic PAH and shunt dependent PAH with high PVR. shunt dependent PAH with high PVR.

No proven benefit in LV dysfunction.No proven benefit in LV dysfunction.

HF WITH AF/SVTHF WITH AF/SVT

• 10-30 % of HF.

• Decreased atrial support

• Reduced filling time

• Decresed contraction and relaxation

• EmbolismTachycardiomyopathy

• Rate control

Other medical therapiesOther medical therapies

• Aspirin,statin to lower LDL < 70 mg/dL, Amlodipine, warfarin in AF, Thrombii, LV aneurysm, sleep apnoea and anemia management, Thyroid disease management.

Hepatitis C viral infection can cause cardiomyopathy/myocarditis and respond to prednisolone + azathioprine/?Interferon

HIV associated DCM difficult to treat.Zidovudine may induce cardiomyopathy

CARDIAC RESYNCHRONYSATION THERAPYCARDIAC RESYNCHRONYSATION THERAPY

CRT recommended to reduce morbidity CRT recommended to reduce morbidity and mortality ( Class 1,Level A) inand mortality ( Class 1,Level A) in

NYHA III-IV symptoms despite optimal NYHA III-IV symptoms despite optimal medical therapymedical therapy

LVEF=< 35 %LVEF=< 35 %QRSD => 120 msec with ventricular QRSD => 120 msec with ventricular

dyssynchronydyssynchronyCRTD in resuscitated cardiac arrest, CRTD in resuscitated cardiac arrest,

Ischemic aeteology,complex VT Ischemic aeteology,complex VT

IABPIABP

• Diastolic augmentation

• Reduces after load

• Improves coronary perfusion

• Valuable in unstable ACS peri PCI

• Frequently used peri-operatively

• Short term measure

EXTERNAL COUNTER PULSATIONEXTERNAL COUNTER PULSATION

• Use of device applied to lower limbs to inflate and deflate synchronous with cardiac cycle.

• Reduces frequency and severity of angina • May be employed for intermediate term use in

HF

LVADLVAD

• Implantable devices with inflow cannula at LV apex, an impeller and outflow cannula connected to aorta.

• Used as a bridge to transplant.( Destination therapy survival 58 % at 2 years with Heartmate II)

• May be useful in conditions likely to improve like peripartum cardiomyopathy.

• Complications like infection, thromboembolism, coagulopathy etc. common.

Other optionsOther options

• Ventricular reconstruction surgery ( DOR procedure/ Batista)

• Mitral valve repair

• Transmyocardial Laser revascularisationStem cell therapy.Cardiac transplantation for End Stage

Heart Failure without PAH, infection psychosocial contraindication

CARDIAC TRANSPLANTATIONCARDIAC TRANSPLANTATION

• SURVIVAL AFTER TRANSPANT 85% AT 1 YEAR

• DECLINES 4 % ANNULALY THEREAFTER• COMPLICATIONS: REJECTION, INFECTION,

TRANSPLANT CORONARY VASCULOPATHY, MALIGNANY.

• LIFELONG IMMUNOSUIPPRESSION

HEART FAILURE WITH HEART FAILURE WITH PRESERVED LV FUNCTIONPRESERVED LV FUNCTION

• Diagnostic challenge. Doppler & BNP useful.• No evidence based treatment effective in

reducing morbidity and mortality.• Diuretics offer symptomatic improvement.• Adequate control of BP, myocardial ischemia,

ventricular rate important.• Verapamil improves exercise capacity and

symptoms• (CHARM)- preserved & PEP-CHF trials showed

reduced number of hospitalization

SUMMARYSUMMARY

• ALL HF PATIENTS SHOULD RECEIVE AN ACEI/ARB AND A BETA BLOCKER

• DIURETICS REQUIRED IN MOST PATIENTS TO MANAGE FLUID RETENTION

• DIGOXIN RESERVED FOR THOSE WITH SIGNS AND SYMPTOMS OF HF/ AF

• ALDOSTERONE ANTAGONIST USED FOR CLASS III OR IV HF OR HF POST MI

• ARB OR HYDRALAZINE+NITRATE MAY BE ADDED FOR ADDITIONAL BENIFIT

o We have been able to add some Life to We have been able to add some Life to YearsYears

However, it is doubtful whether we have However, it is doubtful whether we have been successful in adding Years to Life.been successful in adding Years to Life.

DIASTOLIC DYSFUNCTIONDIASTOLIC DYSFUNCTION(Heart failure with preserved LV function)(Heart failure with preserved LV function)

• Impaired LV relaxation> high diastolic pressures > poor ventricular filling.

• Compensatory LA pressure increases >

hydrostatic and oncotic pressure in pulm capillaries > pulmonary edema.

Increased HR shortens filling time and catecholamines worsen diastolic dysfunction.

• With special thanks to Dr.Tarig Ali

For the Special effects

BRAIN NATRIURETIC PEPTIDE BRAIN NATRIURETIC PEPTIDE IN HFIN HF

• BNP- 32 amino acid polypeptide secreted by ventricles in response to excess stretching of myocytes

• NT ProBNP 76 amino acid polypeptide co secreted and inactive- longer half life

• BNP binds to and activates ANP receptors

- short half life

Biologic actions of BNPBiologic actions of BNP

• Decreases SVR

• Decreases CVP

• Increases natriuresis

• Decreases blood volumePlasma conc. of both BNP and NT-Pro

BNP elevated in asymptomatic and symptomatic heart failure

•

•

•

Risk factors for developing HFRisk factors for developing HF

• Hypertension

• CAD

• Diabetes Mellitus

• Familial history of cardiomyopathy

• Use of cardiotoxins

• obesity

HIGH OUT PUT FAILUREHIGH OUT PUT FAILURE

• THYROTOXICOSIS.

• ARTRIOVENOUS FISTULAE

• PREGNANCY

• SEVERE ANEMIA

ProblemsProblems

• Advancing age of population

• Advances in treatment improving survival

• Decision making on appropriateness of initiation of treatment and use of combinations.

• Clinical Heart failure with normal EF- limitation of evidence based treatment

HEART FAILUREHEART FAILUREPATHOPHYSIOLOGYPATHOPHYSIOLOGY

• BARORECEPTOR AND OSMOTIC STIMULI> HYPOTHALAMIC VASOPRESSIN> H2O REABSORPTION

• ^ENDOTHELIN.^ CYTOKINES.• APOTOSIS• NATRIURETIC PEPTIDES FROM

CARDIOMYOCYTES > VASODILATATION> ENHANCED Na +H2O EXCRETION & SUPRESS NEUROHORMONES.

PATHOPHYSIOLOGYPATHOPHYSIOLOGY

• NEUROHORMONAL STIMULATION• MYOCYTE HYPERTROPHY AND

ELONGATION , LV HYPERTROHY AND DILATION(REMODELLING) , INCREASED WALL TENSION, DECREASED SUBENDOCARDIAL PERFUSION & MR DUE TO DILATION

• APTOSIS AND WORSENING OF CONTRACTILITY.

New approach to classification of New approach to classification of Heart failure Heart failure

ACC/AHA STAGING OF HEART ACC/AHA STAGING OF HEART FAILUREFAILURE

• Stage A : Patients at risk of HF but have no structural heart disease.

Management: Prevention of heart failure

• Stage B : Structural heart disease without symptoms.

Management goal: Prevention of LV remodeling leading to HF.

ACC/AHA STAGING OF HEART ACC/AHA STAGING OF HEART FAILUREFAILURE

• Stage C : Structural heart disease with current or prior symptomatic HF

Management: Diuretics, digoxin, aldosterone antagonists, ACEI/ARB,betablockers and CRT SOS

• Stage D: Severe refractory heart failure

Management : Cardiac transplant or

End of life care.

Heart failureHeart failure

• Stage A: High risk of HF Hypertension,Diabetes,CAD, Family H/O cardiomyopathy.

• Stage B: Asymptomatic HF Previous MI,LV dysfunction, , Valvular heart disease

• Stage C: Symptomatic HF Structural heart disease, Dyspnoea and fatigue and impaired exercise tolerance.

• Stage D:Refractory end-stage HF Marked symptoms at rest despite maximal medical therapy.

Signs and Symptoms of HFSigns and Symptoms of HF

• Due to fluid overload and pulmonary congestion:Dyspnoea, Orthopnoea,PND

• Due to RVF: Elevated JVP, Oedema, Hepatosplenomegaly and ascitis.

• No congestive symptoms

low C.O: Fatigue, effrot intolerance, renal hypoperfusion,Cachexia

NYHA HF symptoms ClassificationNYHA HF symptoms Classificationbased on level of impairment.based on level of impairment.

• Class I : No symptom limitation with ordinary physical activity

• Class II: Ordinary physical activity somewhat limited by dyspnoea ( climbing two flights of stairs)

• Class III: Exercise limited by dyspnoea with moderate work load ( short distance walk< one flight of stairs)

• Class IV: Dyspnoea at rest or with very little exertion

Physical ExaminationPhysical Examination

• Decompensated HF Diaphoretic,pale,Tachycardia, Tachypnoea, Raised JVP, Rales,edema, Cardiomegaly,Soft S1, Wide or paradoxic split S2, S3, S4 & Murmur of MR/TR

InvestigationsInvestigations

• ECG, Chest Xray.• ECHOCARDIOGRAM:

Systolic Vs Diastolic dysfunction, Valvular Heart disease, Tamponade, Constriction, restrictive/ infiltrative cardiomyopathy, LVH

• Cardiac catheterisation:Coronary angiography.• MRI in arrhythmogenic RV dysplasia,myocardial

viability assesment and infiltrative cardiomyopathy.

Echocardiography in HFEchocardiography in HF

• Plays major role in diagnosis of HF with preserved EF or mild LV systolic dysfunction

( LVEF 45-50 %)

• Tissue Doppler imaging in assessment of diastolic dysfunction and in inter & intraventricular dyssynchrony

• 2 dimensional speckle tracking echo Calculation of myocardial velocities and deformation

parameters such as strain and strain rate.

MRI and CT scanMRI and CT scan

• MRI accurate in assesment of LV and RV volumes, global function, regional wall motion, myocardial thickness, thickening , mass, tumours, valves, pericardial disease CHD, ARVD, inflitrative myopathy And myocardial viability.

• MSCT,CT coronary angiogarphy.

Aldosterone blockersAldosterone blockers

• Use in moderate to severe HF and reduced LVEF.

• Prevent sodium and water retention, endothelial dysfunction and myocardial fibrosis.

• Avoid if S.Creatinie > 2.5 mg/dl.

• No gynecomastia with eplerenone

Investigations in HFInvestigations in HF

• Metabolic ( Cardiopulmonary ) exercise testing. – Peak VO2 > 25 ml/Kg./ Min normal for middle aged adults. < 14 ml/Kg./Min indicates severe cardiac limitation and poor prognosis.

BNP in HFBNP in HF

• BNP- 32 amino acid polypeptide secreted by ventricles in response to excess stretching of myocytes

• NT ProBNP 76 amino acid polypeptide co secreted and inactive- longer half life

• BNP binds to and activates ANP receptors

- short half life

Biologic actions of BNPBiologic actions of BNP

• Decreases SVR

• Decreases CVP

• Increases natriuresis

• Decreases blood volumePlasma conc. of both BNP and NT-

ProBNP elevated in asymptomatic and symptomatic heart failure

BNP in HFBNP in HF• BNP > 100 pg/ml

Sensitivity 90%; Specificity 76 %• BNP > 50 pg/ml

Sensitivity > 97 %: Specificity 62 %

Grey area 100-500 pg/mlBNP elevated in LVH,Tachycardia, RV overload,

Myocardial ischemia, hypoxemia, renal dysfunction, advanced age, cirrhosis,sepsis and infection.

Decreased in obesity

BNP in HFBNP in HF

• Diagnosis of heart failure.

• BNP level correlates well with NYHA symptomatic class.

• Useful in assessing response to therapy

• Helpful in discharge timing.

• Useful in prognostication.

Other medical therapiesOther medical therapies

• Aspirin,statin to lower LDL < 70 mg/dL, Amlodipine, warfarin in AF, Thrombii, LV anerysm, sleep apnoea and anemia mangement, Thyroid disease management.

AQUAPHERESISAQUAPHERESIS

• Ultrafiltration to remove excess fluid without sodium through a filter.

• Upto 500 ml fluid removed/ hour

• Reduces hospitalizations

• Avoids problems with over diuresis

• No large scale studies

PHOSPHODIESTERASE INHIBITORS AND PHOSPHODIESTERASE INHIBITORS AND ENDOTHELIN RECEPTOR BLOCKERS.ENDOTHELIN RECEPTOR BLOCKERS.

• Sildenafil ( PDE 5 inhibitor), improves effort tolerance and symptoms on 6 minute walk test in Idiopathic PAH and PAH secondary to CHD.

• Endothelin receptor blockers Bosentan ( non –selective ) and Sitaxentan ( selective ET- A) receptor blocker may be combined with sildenaphil to reduce PA pressure in idiopathic PAH and shunt dependent PAH with high PVR.

• No proven benefit in LV dysfunction.

CARDIAC RESYNCHRONYSATION THERAPYCARDIAC RESYNCHRONYSATION THERAPY

• CRT recommended to reduce morbidity and mortality ( Class 1,Level A) in

NYHA III-IV symptoms despite optimal medical therapy

• LVEF=< 35 %• QRSD => 120 msec with ventricular

dyssynchrony• CRTD in resuscitated cardiac arrest,

Ischemic aeteology,complex VT

IABPIABP

• Diastolic augmentation

• Reduces after load

• Improves coronary perfusion

• Valuable in unstable ACS peri PCI

• Frequently used peri-operatively

• Short term measure

LVADLVAD

• Implantable devices with inflow cannula at LV apex, an impeller and outflow cannula connected to aorta.

• Used as a bridge to transplant.• May be useful in conditions likely to

improve like peripartum cardiomyopathy.• Complications like infection,

thromboembolism, coagulopathy etc.common.

Other optionsOther options

• Ventricular reconstruction surgery ( DOR procedure/ Batista)

• Mitral valve repair

• Transmyocardial Laser revascularisation

• Stem cell therapy.Cardiac transplantation for End Stage

Heart Failure without PAH, infection psychosocial contraindication

CARDIAC TRANSPLANTATIONCARDIAC TRANSPLANTATION

• SURVIVAL AFTER TRANSPANT 85% AT 1 YEAR

• DECLINES 4 % ANNULALY THEREAFTER

• COMPLICATIONS: REJECTION, INFECTION, TRANSPLANT CORONARY VASCULOPATHY, MALIGNANY.

• LIFELONG IMMUNOSUIPPRESSION

SUMMARYSUMMARY

• ALL HF PATIENTS SHOULD TRECEIVE AN ACEI/ARB AND A BETA BLOCKER

• DIURETICS REQUIRED IN MOST PATIENTS TO MANAGE FLUID RETENTION

• DIGOXIN RESERVED FOR THOSE WITH SIGNS AND SYMPTOMS OF HF/ AF

• ALDOSTERONE ANTAGONIST USED FOR CLASS III OR IV HF OR HF POST MI

• ARB OR HYDRALAZINE+NITRATE MAY BE ADDED FOR ADDITIONAL BENIFIT

HEART FAILURE WITH HEART FAILURE WITH PRESERVED LV FUNCTIONPRESERVED LV FUNCTION

• Diagnostic challenge. Doppler & BNP useful.• No evidence based treatment effective in

reducing morbidity and mortality.• Diuretics offer symptomatic improvement.• Adequate control of BP,myocardial ischemia,

ventricular rate important.• Verapamil improves exercise capacity and

symptoms• (CHARM)- preserved & PEP-CHF trials showed

reduced number of hospitalization

Definition of heart failureDefinition of heart failureESC GuidelinesESC Guidelines

Heart failure is a clinical syndrome in which patients have the following features:• † Symptoms typical of heart failure (breathlessness at rest or on exercise, fatigue, tiredness, ankle swelling) and• † Signs typical of heart failure (tachycardia, tachypnoea, pulmonary rales, pleural effusion, raised jugular venous pressure, peripheral oedema, hepatomegaly) and• † Objective evidence of a structural or functional abnormality of the heart at rest (cardiomegaly, third heart sound, cardiac murmurs, abnormality on the echocardiogram, raised natriuretic peptide concentration)