This is a brief update on heart failure definition, prevalance, pathophysiology and management . THis is not an entry for any contest

1. HEART FAILUREHEART FAILURE
DEFINITION: A clinical syndromeDEFINITION: A clinical syndrome
characterized by systemic perfusioncharacterized by systemic perfusion
inadequate to meet the body’s metabolicinadequate to meet the body’s metabolic
demands as a result of impaired cardiacdemands as a result of impaired cardiac
pump functionpump function

2. HEART FAILUREHEART FAILURE
ACC/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.

3. 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.

4. 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

6. RIGHT VENTRICULAR SYSTOLIC DYSFUNCTIONRIGHT VENTRICULAR SYSTOLIC DYSFUNCTION
* CONSEQUNCE OF LV DYSFUNCTION.
• OTHER CAUSES:VIZ. RV INFARCTION,
PAH,CHRONIC SEVERE TR, ARRHYTHMOGENIC RV
DYSPLACIA

7. HIGH OUT PUT FAILUREHIGH OUT PUT FAILURE
• THYROTOXICOSIS.
• ARTRIOVENOUS FISTULAE
• PREGNANCY
• SEVERE ANEMIA

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

9. Prevalence andPrevalence 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 $.

10. 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.

11. PATHOPHYSIOLOGYPATHOPHYSIOLOGY
 LV DYSFUNCTIONLV 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

12. CONSEQUENCES OFCONSEQUENCES OF
COMPENSATORY MECHANISMSCOMPENSATORY MECHANISMS
 CATECHOLAMINES AGGRAVATE ISCHEMIA,CATECHOLAMINES AGGRAVATE ISCHEMIA,
ARRHYTHMIA, INDUCE CARDIACARRHYTHMIA, INDUCE CARDIAC
REMODELLING AND TOXIC TO MYOCYTES.REMODELLING AND TOXIC TO MYOCYTES.
 STIMULATED RAA SYSTEM & SYMPATHETICSTIMULATED RAA SYSTEM & SYMPATHETIC
STIMULATION > ARTERIOLARSTIMULATION > ARTERIOLAR
CONSTRICTION, Na+ H2OCONSTRICTION, Na+ H2O
RETENTION>ALDOSTERONE >Na+H2O>RETENTION>ALDOSTERONE >Na+H2O>
ENDOTHELIAL DYSFUNCTION>FIBROSIS.ENDOTHELIAL DYSFUNCTION>FIBROSIS.

13. CONSEQUENCES OFCONSEQUENCES OF
COMPENSATORY MECHANISMSCOMPENSATORY MECHANISMS
 BARORECEPTOR AND OSMOTIC STIMULI>BARORECEPTOR AND OSMOTIC STIMULI>
HYPOTHALAMIC VASOPRESSIN> H2OHYPOTHALAMIC VASOPRESSIN> H2O
REABSORPTION IN COLLECTING DUCTREABSORPTION IN COLLECTING DUCT
 ^ENDOTHELIN.^ CYTOKINES.^ENDOTHELIN.^ CYTOKINES.
 CYTOKIES> CAHEXIA & APOTOSISCYTOKIES> CAHEXIA & APOTOSIS
 NATRIURETIC PEPTIDES FROM CARDIOMYOCYTESNATRIURETIC PEPTIDES FROM CARDIOMYOCYTES
> VASODILATATION> ENHANCED Na +H2O> VASODILATATION> ENHANCED Na +H2O
EXCRETION & SUPRESS NEUROHORMONES.EXCRETION & SUPRESS NEUROHORMONES.
 NEUROHORMONAL MODULATION IS THE BASIS OFNEUROHORMONAL MODULATION IS THE BASIS OF
CURRENT TREATMENT OF HFCURRENT TREATMENT OF HF

14. 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.

15. Echocardiography in HFEchocardiography in HF
 Plays major role in diagnosis of HF with preserved EF orPlays major role in diagnosis of HF with preserved EF or
mild LV systolic dysfunctionmild LV systolic dysfunction
( LVEF 45-50 %)( LVEF 45-50 %)
 Tissue Doppler imaging in assessment of diastolicTissue Doppler imaging in assessment of diastolic
dysfunction and in inter & intraventricular dyssynchronydysfunction and in inter & intraventricular dyssynchrony
 2 dimensional speckle tracking echo2 dimensional speckle tracking echo
Calculation of myocardial velocities and deformationCalculation of myocardial velocities and deformation
parameters such as strain and strain rate.parameters such as strain and strain rate.

16. 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.

17. BNP in HFBNP in HF
Diagnosis of heart failure.Diagnosis of heart failure.
BNP level correlates well with NYHABNP level correlates well with NYHA
symptomatic class.symptomatic class.
Useful in assessing response to therapyUseful in assessing response to therapy
Helpful in discharge timing.Helpful in discharge timing.
Useful in prognostication.Useful in prognostication.

18. HEART FAILUREHEART FAILURE
MANAGEMENTMANAGEMENT
Identification of precipitatingIdentification of precipitating factorsfactors
ACC/AHA stageACC/AHA stage

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

20. 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.

21. DiureticsDiuretics
• Loop diuretics :Furosemide,Torsemide.
Bumetinide
• Thiazide:HTZ&Metolazone.
Seqential nephron blockade:
Metolazone+ Loop diuretic
• K+ sparing agents.
I.V infusion of Furosemide

22. 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 modulationVasodilatation 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 renalProblem: Angioedema and worsening of renal
function.function.

23. 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 standardAddition of Renin inhibitor Alliskerin to standard
therapy results in lower BNP levelstherapy results in lower BNP levels

24. Beta Blockers in HFBeta Blockers in HF
 Carvedilol,Metoprolol succinate and BisoprololCarvedilol,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 andantiremodelling and antiapototic properties and
reduced HR and MV O2.reduced HR and MV O2.
 DM, COPD, PVD, euvolumic Class IV notDM, COPD, PVD, euvolumic Class IV not
contraindicationscontraindications
 Combine with ACEICombine with ACEI

25. 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.

26. 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.

27. 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)

28. 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

29. 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]

30. 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.

31. 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

32. 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

33. LEVOSIMENDANLEVOSIMENDAN
• Total 3500 patients in trials
• Initial BNP reduction
• No reduction in mortality at 6 months
Superior to Dopamine in acutely
decompensated HF on B blocker
Reduces troponin leak after cardiac
surgery when used perioperatively

34. AQUARETICSAQUARETICS
Up regulated Arginine VasopressinUp regulated Arginine Vasopressin
stimulation represents a maladaptivestimulation represents a maladaptive
neurohormonal response in HF.neurohormonal response in HF.
AVP increases blood volume by waterAVP increases blood volume by water
retention via V2 receptors in collectingretention via V2 receptors in collecting
ducts.ducts.
VasoconstrictiveVasoconstrictive
Causes cardiac HypertrophyCauses cardiac Hypertrophy
V1a receptors mediate vasoconstrictionV1a receptors mediate vasoconstriction

35. TOLVAPTANTOLVAPTAN
 Selective oral V2 Vasopressin receptorSelective oral V2 Vasopressin receptor
antagonist.antagonist.
 Conivaptan is dual V1a/V2 receptor antagonistConivaptan is dual V1a/V2 receptor antagonist
– I.V– I.V
 Sodium free diuresis.Sodium free diuresis.
 Weight reduction, Decreases edema andWeight reduction, Decreases edema and
dyspnoea, corrects hyponatremia and nodyspnoea, corrects hyponatremia and no
worsening of renal failureworsening of renal failure
 No reduction in number of hospitalizations andNo reduction in number of hospitalizations and
long term mortality.long term mortality.

36. 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

37. PHOSPHODIESTERASE INHIBITORSPHOSPHODIESTERASE INHIBITORS
AND ENDOTHELIN RECEPTORAND ENDOTHELIN RECEPTOR
BLOCKERS.BLOCKERS.
 Sildenafil ( PDE 5 inhibitor), improves effortSildenafil ( PDE 5 inhibitor), improves effort
tolerance and symptoms on 6 minute walk test intolerance 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 sildenafilreceptor blocker may be combined with sildenafil
to reduce PA pressure in idiopathic PAH andto 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.

38. HF WITH AF/SVTHF WITH AF/SVT
• 10-30 % of HF.
• Decreased atrial support
• Reduced filling time
• Decresed contraction and relaxation
• Embolism
Tachycardiomyopathy
• Rate control

39. 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

40. CARDIAC RESYNCHRONYSATION THERAPYCARDIAC RESYNCHRONYSATION THERAPY
CRT recommended to reduce morbidityCRT recommended to reduce morbidity
and mortality ( Class 1,Level A) inand mortality ( Class 1,Level A) in
NYHA III-IV symptoms despite optimalNYHA III-IV symptoms despite optimal
medical therapymedical therapy
LVEF=< 35 %LVEF=< 35 %
QRSD => 120 msec with ventricularQRSD => 120 msec with ventricular
dyssynchronydyssynchrony
CRTD in resuscitated cardiac arrest,CRTD in resuscitated cardiac arrest,
Ischemic aeteology,complex VTIschemic aeteology,complex VT

41. IABPIABP
• Diastolic augmentation
• Reduces after load
• Improves coronary perfusion
• Valuable in unstable ACS peri PCI
• Frequently used peri-operatively
• Short term measure

42. 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

43. 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.

44. 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

45. CARDIAC TRANSPLANTATIONCARDIAC TRANSPLANTATION
• SURVIVAL AFTER TRANSPANT 85% AT 1
YEAR
• DECLINES 4 % ANNULALY THEREAFTER
• COMPLICATIONS: REJECTION, INFECTION,
TRANSPLANT CORONARY VASCULOPATHY,
MALIGNANY.
• LIFELONG IMMUNOSUIPPRESSION

46. HEART FAILURE WITHHEART 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

47. 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

48. o We have been able to add some Life toWe have been able to add some Life to
YearsYears
However, it is doubtful whether we haveHowever, it is doubtful whether we have
been successful in adding Years to Life.been successful in adding Years to Life.

50. 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.

51. • With special thanks to Dr.Tarig Ali
For the Special effects

52. BRAIN NATRIURETIC PEPTIDEBRAIN 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

53. Biologic actions of BNPBiologic actions of BNP
• Decreases SVR
• Decreases CVP
• Increases natriuresis
• Decreases blood volume
Plasma conc. of both BNP and NT-Pro
BNP elevated in asymptomatic and
symptomatic heart failure

56. •

58. •

59. •

60. Risk factors for developing HFRisk factors for developing HF
• Hypertension
• CAD
• Diabetes Mellitus
• Familial history of cardiomyopathy
• Use of cardiotoxins
• obesity

61. HIGH OUT PUT FAILUREHIGH OUT PUT FAILURE
• THYROTOXICOSIS.
• ARTRIOVENOUS FISTULAE
• PREGNANCY
• SEVERE ANEMIA

62. 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

63. HEART FAILUREHEART FAILURE
PATHOPHYSIOLOGYPATHOPHYSIOLOGY
• BARORECEPTOR AND OSMOTIC STIMULI>
HYPOTHALAMIC VASOPRESSIN> H2O
REABSORPTION
• ^ENDOTHELIN.^ CYTOKINES.
• APOTOSIS
• NATRIURETIC PEPTIDES FROM
CARDIOMYOCYTES > VASODILATATION>
ENHANCED Na +H2O EXCRETION &
SUPRESS NEUROHORMONES.

64. 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.

65. New approach to classification ofNew approach to classification of
Heart failureHeart failure

66. ACC/AHA STAGING OF HEARTACC/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.

67. ACC/AHA STAGING OF HEARTACC/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.

68. 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.

69. 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

70. NYHA HF symptoms ClassificationNYHA HF symptoms Classification
based 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

71. 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

72. 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.

73. 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.

74. 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.

75. 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

76. 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.

77. 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

78. Biologic actions of BNPBiologic actions of BNP
• Decreases SVR
• Decreases CVP
• Increases natriuresis
• Decreases blood volume
Plasma conc. of both BNP and NT-
ProBNP elevated in asymptomatic and
symptomatic heart failure

79. 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/ml
BNP elevated in LVH,Tachycardia, RV overload,
Myocardial ischemia, hypoxemia, renal
dysfunction, advanced age, cirrhosis,sepsis and
infection.
Decreased in obesity

80. 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.

81. 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.

82. 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

83. PHOSPHODIESTERASE INHIBITORS ANDPHOSPHODIESTERASE 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.

84. 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

85. IABPIABP
• Diastolic augmentation
• Reduces after load
• Improves coronary perfusion
• Valuable in unstable ACS peri PCI
• Frequently used peri-operatively
• Short term measure

86. 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.

87. 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

88. CARDIAC TRANSPLANTATIONCARDIAC TRANSPLANTATION
• SURVIVAL AFTER TRANSPANT 85% AT
1 YEAR
• DECLINES 4 % ANNULALY
THEREAFTER
• COMPLICATIONS: REJECTION,
INFECTION, TRANSPLANT CORONARY
VASCULOPATHY, MALIGNANY.
• LIFELONG IMMUNOSUIPPRESSION

89. 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

90. HEART FAILURE WITHHEART 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

92. Definition of heart failureDefinition of heart failure
ESC 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)