by DR NITESH

2.  Heart failure is a complex “clinical syndrome”
resulting from structural and functional
impairment of ventricular filling or ejection of
blood.

3.  HF affects 26 million (2.6 crore) people
worldwide and the burden of HF in India is about
1% of the population which comes to about 1
crore patients.
 The rural community has lower burden and
mortality is also high with almost 1/3 rd patients
getting readmitted or dying soon after an acute
HF event.
 Indian patients areYOUNGER, SICKER & get
LESS MEDICATIONS as compared to what is
recommended by the guidelines.

4.  The cardinal symptoms of HF are fatigue and
shortness of breath.
1. Fatigue- occurs due to low CO, anemia associated with
HF.
2. Dyspnea-cause is multifactorial- a) interstitial fluid
accumulation which activatesJ receptors, which in
turn stimulates rapid, shallow breathing characteristic
of cardiac dyspnea, b)reduction in pulmonary
compliance c) increased airway resistance
d)respiratory or diaphragmatic fatigue and e)anemia.

5. 3. Orthopnea-it results from redistribution of
fluid from the splanchnic and peripheral
circulation into the central circulation during
recumbency, with a resultant increase in
pulmonary capillary pressure.
It is a relatively specific symptom of HF, it may
also occur in patients with abdominal obesity or
ascites and patients with pulmonary disease.

6.  4.PND-It refers to acute episodes of severe shortness
of breath and coughing that generally occur at night
and awaken the patient from sleep, usually 1-3 h
after the a patient retires.
 It is not relieved by sitting upright with legs in a
dependent position.
 It occurs due to increased pressure in the bronchial
arteries leading to airway compression, along with
interstitial pulmonary edema that leads to increased
airway resistance.

7.  5. CHYNE-STOKES RESPIRATION- seen in 40%
patients with advanced heart failure and increases
with low CO.
 It occurs due to increased sensitivity of the respiratory
center to arterial pco2 and a lengthy circulation time.
There is an apneic phase, during which arterial po2 falls
and arterial pco2 rises.These changes in the arterial
blood gas content stimulates the respiratory center,
resulting in hyperventilation and hypocapnia, followed
by recurrence of apnea.

8.  6. OTHER SYMPTOMS-
 Anorexia, nausea and early satiety associated with
abdominal pain and fullness- related to gut wall edema
 Right upper quadrant pain due to liver congestion and
capsule stretching.
 Cerebral symptoms such as confusion, disorientation
and sleep and mood disturbances.
 Nocturia is common in early stages of HF as
recumbency reduces the deficit in CO in relation to
oxygen demand , renal vasoconstriction decreases and
urine formation increases and contributes to insomnia.

9.  5 main points to ask in history to find about
etiology of heart failure, one needs to ask is-
1. Cyanosis- (congenital heart disease)
2. Fever- eg-myocarditis, rheumatic fever
3. Chest pain- eg- CAD
4. Palpitations- eg-Volume overload
conditions, thyrocardiac disease, rhythm
disorders
5. Any past H/O hypertension- suggestive of
pressure overload condition eg- AS, CoA

10.  6. Family history of sudden cardiac death or
clinical heart failure, suggests Genetic or Familial
etiology. Eg- Brugada
 History should also include the identification of
risk factors (condition that puts the person at
risk) and both CVS and non-CVS precipitating
factors (event which triggers the onset) of heart
failure, in addition to the presence of co-
morbidities.

15. 2D ECHO CXR

20. ANTERIOR & ANTEROSEPTAL
SUBENDOCARDIAL LGE DISTRIBUTION
TYPICAL OF ANTEROSEPTALWALL MI
LVTHROMBI IDENTIFIED ON EARLY
GADOLINIUM ENHANCED IMAGES

21. EXTENSIVE MID-WALL LGE DISTRIBUTION
SEEN ON SHORTAXIS IMAGING IN DCMP
BASAL INFEROLATERAL LGE DISTRIBUTION
SEEN IN ANDERSON FABRY DISEASE

22.  Middle row: cardiac amyloidosis
on LGE imaging demonstrates
abnormal blood pool appearance
with “ZEBRA STRIPE
ENHANCEMENT” of and
difficulty nulling of myocardium
& there is diffuse increase in
myocardialT1 on nativeT1
mapping (right)
 Bottom row:acute myocarditis
demonstrating subepicardial
lateral wall enhancement on LGE
(left),diffusely increased signal
relative to skeletal muscle on t2-
STIR (middle) & increased lateral
wallT1 on native t1 mapping
(right)

23.  Left:Widespread
transmural distribution
of ATTR
 Right: Subendocardial
distribution in AL with
transmurality at the
base of LV

24.  Role in CAD, to
test for
myocardial
viability.
 Useful in
diagnosing
sarcoidosis
without
serologic signs
of
inflammmatory
activity

25.  Endomyocardial Biopsy remains the
gold standard investigation for
diagnosing many primary and
secondary cardiac conditions.
 It is widely used for surveillance of
cardiac allograft rejection and for
diagnosis of unexplained ventricular
dysfunction.
 In general, it is not routinely
recommended to diagnose other
cardiac disorders, unless dictated by
research protocols.
 It is associated with serious
complication rate of <1%.

26. 1. Monitor cardiac transplant
rejection status.
2. Diagnose unexplained
cardiomyopathies like
myocarditis/ infiltrative
cmp’s
3. Diagnose cardiac tumors.
4. Detect suspected
anthracycline toxicity
5. Use in research

28.  For patients in Stage A, the specific aims are to
prevent the development of cardiovascular
disease by addressing risk factors, by providing
counseling for appropriate dietary and
exercise modifications, whereas patients in
stage B, the main aims are to prevent further
cardiac remodeling and symptomatic heart
failure through the appropriate initiation of
heart failure-specific therapies and
interventions when indicated.

29.  Heavy physical labor is not recommended but routine modest exercise has been
shown to be benificial in selected patients with NYHA class 1 to 3 HF.
 HF-ACTION trial failed to show a significant improvement in all cause mortality or
all-cause hospitalization in patients who received a 12 week exercise training
program.(HR 0.93[95%CI, 0.84-1.02];p=0.13).
 For euvolemic patients, regular isotonic exercises (walking, riding stationary
bicycle) are recommended.
 Exercise training is not recommended in- a)patients with HFrEf who have had a
major CV event or procedure in past 6 weeks ,b) in patients with cardiac devices
that limit the ability to achieve target heart rates c) patients with significant
arrhythmia or ischemia during baseline cardiopulmonary exercise testing.

30.  Dietary restriction of sodium to 2-3 g/d is
recommended in all patients with clinical syndrome of
heart failure and either preserved or depressed EF.
<2g/d can be considered in moderate to severe HF.
 Fluid restriction <2L/d is unnecessary except in the
setting of hyponatremia (Na<130 meq/L).
 Caloric supplementation is recommended for patients
with advanced HF and cardiac cachexia.
 Anabolic steroids, dietary supplements
(neutraceuticals) are not recommended.

31. DRUGS

32.  Although retrospective analysis of clinical trials suggest that
diuretic use is associated with worse clinical outcomes, a
meta-analysis (Cochrane Review) suggested that
treatment with diuretic therapy produced a significant
reduction in mortality and worsening HF.
 SOLUTE DIURETICS:Loop diuretics increase sodium
excretion by upto 20-25% of filtered sodium load while
thiazides increase by only 5-10%.
 WATER DIURETICS: “Aquaretics” , which inhibit ADH
action on collecting duct, thereby increasing free water
clearance. Eg;Vasopressin antagonists, lithium

34.  Torsemide has a better
oral bioavailability and
longer and sustained
duration of effect than
furosemide in HF.
 These pharmacokinetics
becomes more important
in HF because of hepatic
congestion, gut edema
and decreased gut blood
flow.

35.  DOSETrial- no significant difference in symptoms or renal function when patients
with ADHF were treated with iv bolus vs iv infusion of furosemide.
 RAPID-CHF trial- 8h ultrafiltration vs. usual care diuretics, n=40, showed that
fluid removal with UF was twice that of diuretics.
 UNLOADTrial-UF vs. iv diuretics, n=200, UF was associated with significantly
greater fluid loss over 48 h and a lower rate of rehospitalization during the next 90
days.
 CARRESSTrial-showed that UF resulted in similar weight loss but resulted in
increase in Creatinine levels, compared to standard of care and was associated with
more serious adverse events and iv catheter related complications.

37.  Indicated in HF with EF<35% with NYHA Class II to IV and who are
receiving standard therapy, including diuretics, ACEIs and Beta
blockers.
 Spironolactone should initated at dose of 12.5 to 25 mg daily and
uptitrated to 25 to 50 mg daily, wheras Eplerenone should be
initiated at doses of 25 mg/d and increased to 50 mg daily.
 Potassium levels and RFT should be rechecked within 3 days & again
at 1 week after initiation, subsequently monthly for first 6 months.
 S/E- a)life threatening hyperkalemia b) painful gynecomastia with
spironolactone in 10-15 % patients.
 Contraindications- include a)when creatine >2.5 mg/dl b)k>5.5
meq/L

44.  ACEIs, stabilizes LV remodeling , relieve patient symptoms,
prevent hospitalization and prolong life.
 Higher doses are more effective than lower doses.
 Titration generally is achieved by doubling doses every 3 to 5 days.
 It is acceptable to add therapy with beta blockers before full target
doses of ACEIs are reached in stable patients only.
 Rft/e should be evaluated within 1-2 weeks after initiating ACEIs.
 Abrupt withdrawal of treatment with an ACEI may lead to clinical
deterioration and should be avoided.

45.  ARBs blocks action of angiotensin II on
angiotensin type I receptor, which is responsible
for all the adverse effects.
 The general consensus is that ACEIs remain the
first line agents for the treatment of heart
failure, whereas ARBs are recommended for
ACE-intolerant patients.

46.  It combines valsartan (AT1 receptor antagonist) with sacubitril (a neprilysin inhibitor) in a 1:1 ratio.
 It slows down the degradation of natriuretic peptides,bradykinin and adrenomedullin , thereby enhancing diuresis,
natriuresis and myocardial relaxation.
 It also inhibits renin and aldosterone secretion
 It selectively blocks AT1 receptors, thereby reducing vasoconstriction, sodium, water retention and myocardial
hypertrophy.
 RECOMMENDATION: in patients with HFrEf NYHA II or III who are tolerating an
ACEI or ARB, ARNIs are recommended as a replacement for ACE/ARB to furthur
reduce morbidity and mortality

47.  PARAGON-HF [Prospective comparison of ARNI with
ARB global outcomes in HF with preserved ejection
fraction ] trial failed to show the desired results in
patients of HFpEF tried on ARNI in comparison to
patients of HFrEF .
 Womens showed mild improvements over men but does
not lead to desired outcomes.

50. 3 βeta blockers reduced mortality in HF-
1)Bisoprolol 2)Metoprolol succinate and 3)Carvedilol
Bucindolol-(BEST trial) is a completely non-selective β1 & β2 blocker
with some α1 blockade properties, showed statistically significant
mortality reduction in whites only and was secondary to polymorphism
(Arg 389) in β1 receptors that is more prevalent in whites.
Nebivolol- (SENIORS Trial) is a selective β1 anatgonist with
vasodilatory properties due to NO release.This drug significantly
reduced the composite outcome of death or CV hospitalizations but did
not reduce mortality. So, it is not FDA approved for treatment of HF.

51. COMET Study-
carvedilol 25 mg bd was compared with
immediate release metoprolol tartarte 50 mg
bd with respect to all-cause mortality.
Carvedilol was associated wit 33% reduction
in all cause mortality compred with
metoprolol tartarate . Based on these results,
short-acting metoprolol tartarate is not
recommended in the treatment of HF.

54.  It blocks If (“funny”) current that controls the spontaneous
diastolic depolarization of the sinoatrial node.
 It blocks in a concentration dependent manner and is most
effective at higher heart rates.
 SHIFTTRIAL enrolled patients of HFrEF in sinus rhythm
with HR>70bpm and showed that ivabradine uptitrated to
maximal dose of 7.5 mg BD reduced primary outcome of CVS
death and HF hospitalization by 18%.
 BEAUTIFULTRIAL- in patients with CAD & LV dysfunction
EF<40% ,10000 patients were enrolled & treated with
ivabradine but it didn’t show any mortality benefit.

55.  FAIR-HF, CONFIRM-HF &
EFFECT-HF trials showed
statistically significant
benefit effect of ferric
carboxymaltose vs.
placebo on symptoms,
functional capacity and
oxygen consumption.
 Results of morbidity,
mortality trials are
awaited.

57.  TRIAL- DAPA-HF concluded that dapagliflozin reduced
the composite end-point of CV death and worsening HF
event in HFrEF patients with and without diabetes in
comparision to placebo.
 Mechanism-
1. Reduction in preload due to natriuresis and osmotic
diuresis
2. Improvement in cardiac metabolism and bioenergetics
3. Myocardial Na/H exchange inibition
 Dose: Dapagliflozin 5-10 mg/d, Canagliflozin 100-300
mg/d & Empagliflozin 10-25 mg/d

58.  Na/H exchanger is the
common link between
T2DM & HF.
 NHE 3 in glomeruli & NHE
1 in cardiomyocytes
causes renal sodium
retention and cardiac
hypertrophy, injury,
fibrosis, impaired insulin
sensitivity and micro-
macrovascular
complications.

59.  ALOFT & ASTRONAUTTRIAL- No significant
difference in primary outcome was observed in
aliskerin treated group (300mg/d)and rates of
hyperkalemia, hypotension & renal impairment
were higher.
 ATMOSPHERETRIAL- In patients with CHF ,
aliskerin/enalapril combination led to more
adverse events without an increase in
benefit.Non-inferiority was not shown for
aliskerin as compared with enalapril.

60.  It is recommended for blacks with NYHA
III/IV HFrEf who remain symptomatic despite
concomitant use of ACEIs, beta blockers and
aldosterone antagonists.
 It shows mortality benefit.
 Drug: BIDIL (trade name)
 Initial dose: Hydralazine 37.5 mg- Isosorbide
20 mgTDS
 Maximum dose: Hydralazine 75 mg-
Isosorbide 40mgTDS

61.  It is recommended in patients with symptomatic LV systolic dysfunction
who have concomitant atrial fibrillation and should be considered for
patients who have signs or symptoms of HF while receiving standard
therapy, including ACE inhibitors and beta blockers.
 RADIANCE & PROVED Studies showed that increased HF
hospitalizations were more with patients whose digoxin was
withdrawn.
 DIGTRIAL- showed that a strong trend towards a decrease in deaths
secondary to pump failure but an increase in sudden and other non-
pump failure deaths.
 This trial also showed that mortality was directly related to serum
digoxin levels. In men, it showed decreased mortality with levels
between 0.5-0.8 ng/ml.
 There is evidence of more potential harm in women with digoxin use.

62.  They have favorable effects on inflammation
including a reduction in endothelial activation
and production of inflammatory cytokines,
platelet aggregation ,BP,HR & LV function.
 GISSI-HFTrial- sowed that long term
administration of omega acids resulted in
significant redution in both all cause mortality
and cvs admissions.
 ASCENDTrial- No role in HF.

64.  Depressed LV function is believed to promote relative stasis of
blood in dilated cardiac chambers with increased risk of
thrombus formation.
 Treatment with warfarin is recommended for: a) all patients with
history of systemic or pulmonary emboli including stroke orTIAs, b)
patients with asymptomatic or symptomatic ICMP & documented
large anterior MI or recent MI with documented LV thrombus.
 WARCEFTRIAL- showed that warfarin did not reduce time to
ischemic stroke, ICH and death from any cause; although it did
reduce rates of ischemic stroke but this benefit was offset by increase
in major hemorrhage. SO, ASPRIN should be used in patients with
HFrEf who are in sinus rhythm.

65.  AF is the MC arrhythmia in HF.
 Rhythm control strategy is not superior to rate
control strategy in terms of mortality.
 Rhythm control strategy is useful in- a)patients
with reversible secondary cause of AF b)intolerant
symptoms
 For rate control, Beta blockers preferred over
digoxin.
 The short term use of iv amiodarone can be used
for acute treatment of patients of AF with FVR.
AMIODARONE & DOFETILIDE LACK NEGATIVE
INOTROPIC EFFECT.

66.  ANDROMEDATRIAL- Dronedarone treated
patients showed increased mortality and is
contraindicated in patients with heart failure.
 AF-CHFTRIAL- It did not show a difference in
composite outcome when a strategy of strict
rate control (<80 bpm at rest & <110 bpm during
6MWT) was compared with lenient rate control.
 GOAL OF RATE CONTROL STRATEGY- resting
ventricular rate of 60-80 bpm and between 90-
115 bpm during moderate exercise.

68.  CRT when combined with optimal medical
therapy, it leads to reversal of LV remodelling,
improved quality of life and exercise capacity.
 CRT should be considered for patients with NYHA
class II-IV HFrEF (<35%) & a wide QRS, who
have been on OMT for several months & maybe
considered in patients with NYHA I HF with a wide
QRS.
 For eligible patients, consideration should be given
for CRT with an ICD (CRT-ICD).

69.  Implantation of ICD should be considered for patients
with NYHA II or III HF (ischemic or non-ischemic
cardiomyopathy ) with depressed EF<35% who are
already on optimal medical therapy and who have a
reasonable life expectancy > 1 year.
 Prophylactic implantation of ICDs in patients with mid
to moderate HF NYHA II/ III has been shown to reduce
the incidence of sudden cardiac death in patients with
ICMP or NICMP.
 CRT-ICD should considered for NYHA IV patients.

70. 1. Medical Management
2. Mechanical Circulatory Support
3. HeartTransplantation
4. Continous Iv inotrope infusions for
palliation
5. Hospice Care

73.  It is a mechanical circulatory device used to
partially or completely replace the function of
either the left ventricle (LVAD); the right
ventricle (RVAD); or both ventricles (BiVAD).
 They can be used for short term and long term
for months to years.

79. THANKS