Heart failure with preserved ejection fraction (HFpEF) accounts for nearly 50% of heart failure cases. It is more common in older patients and women. Survival rates for HFpEF have remained unchanged over time and are similar to those with reduced ejection fraction. The pathophysiology of HFpEF is heterogeneous and related to diastolic dysfunction from conditions like hypertension, diabetes and obesity. Diagnosis requires symptoms/signs of heart failure, preserved EF ≥50%, elevated natriuretic peptides and evidence of cardiac alterations on imaging like left atrial enlargement. Treatment focuses on controlling risk factors and relieving symptoms with diuretics, though no treatments have proven effective at reducing mortality.

1. Heart failure with preserved ejection fraction
Dr ODAY ABDOW

2. intoduction
The prevalence of heart failure is approximately 1-2%
of the addult population in developed countries raising
to ≥10% among people >70 years of age.
Epidemiological studies suggest that nearly 50% of
patients with heart failure have a preserved ejection
fraction.

3. mortality
The 5 year survival rate for all patients with heart
failure regardless of EF is less than 50%.
Although survival has improved over time for patients
with HFrEF it has not changed for patients with HFpEF
The survival of patients with HFpEFwas once thought
to be better than those with decreased EF, but current
evidence suggests similar mortality rates .

4. HFpEH survival rates are not improving

5. Defenition of heart failure
HF is a clinical syndrome caracterized by typical
symptoms(e.g. breathlessness, ankle swelling and
fatigue) that may be accompanied by signs(e.g. elevated
JVP,pulmonary crackles and peripheral edema) caused by
structural and/or functional cardiac abnormalities
resulting in reduced cardiac output and/or elevated
intracardiac pressures at rest or during exercise.

6. The current definition restricts itself to stages at which
clinical symptoms are apparent.
Before clinical symptoms become apparent,patients
can present with asymptomatic structural or
functional (systolic or diastolic LV dysfunction)which
are precusors of HF,these precusors are related to
poor outcomes,and starting treatment at the precusor
stage may reduce mortality in patients with
asymptomatic LV dysfunction.

7. ACC/AHA staging of heart failure
stageA At high risk for HF but without
structural heart disease or symptoms
of HF
Patients :
• HTN
• DM
• Obesity
• Using cardiotoxins
• Family history of
cardiomyopathy
stageB Stuctural heart disease but without
signs or symptoms of HF
- Previous MI
- LVH and low EF
- Asymptomatic VHD
stageC Structural heart disease with prior or
current symptoms of HF
- Known structurah heart
disease
- HF signs and symptoms
stageD Refractory HF requiring specialized
interventions
- Marked HF symptoms at rest
- Recurrent hospitalizations
despite GDMT

8. Definition of heart failure
Type of HF HFrEF HFmrEF HFpEF
criteria 1 Symptoms+
-signs
Symptoms+-signs Symptoms+-signs
2 LVEF<40% LVEF 40-49% LVEF ≥50%
3 1- elevated levels of
natriuretic peptides
2- at lest one criterion:
- relevant structural
heart disease(LVH/LAE)
- Diastolic dysfunction
1-elevated levels of
natriuretic peptides
2-at lest one criterion:
- relevant structural
heart disease(LVH/LAE)
- Diastolic dysfunction

9.  Differentiation of patients with HF based on LVEF is
important due to different underlying aetiologies,
demographic , co-morbidities,and response to therapies
 Most patients with HFrEF (previously referred to
systolic HF also have diastolic dysfunction, and subtle
abnormalities of systolic function have been shown in
patients with HFpEF(midwall and /or longitudinal systolic
dysfunction at rest and global systolic dysfunction during
exercise) ,hence the preference of stating preserved or
reduced LVEF over preserved or reduced systolic function.

10. Classic HFpEF is typically associated with one or more of
the following contributors:
• Hypertension
• Aging
• CAD
• Diabetes mellitus
• Obesity
• CKD
• Sleep disordered breathing
• anemia

11. Pathogenesis of HF
1- index event produces an
intial decline in pumping
capacity of the heart (this
index event may have an
abrupt onset like MI,or
gradual or insidious onset
as in hemodynamic
pressure or volume
overload)
2-compensatory
mechanisms are activated
to maintain CO:
Adrenergic nervous
system
RAS
Cytokine system
NP system

12. Pathogenesis of heart failure

13. disatvantages of chronic activation of compensatory
mechanisms without correcting the underlying cause:
1- chronic vasoconstriction>>> increased afterload
2- chronic salt and water retention >>>incresed preload
These chronic afterload and preload cause remodeling
of the heart

14. -Activation of SNS may contribute to the
pathophysiology of congestive HF by multiple
mechanisms involving cardiac,renal and vascular
function
-In the heart : increased SNS outflow may lead to
desensitization beta- adrenergic receptors,
Myocyte hypertrophy,necrosis,apoptosis and fibrosis

16. Pathophysiology of HFpEF
The pathophysiology underlying HFpEF is
heterogenous ,and associated with cardiovascular
diseases(eg AF,CAD,arterial
hypertension,pulmonary hypertension)and
noncardiovascular diseases(e.g
diabetes,CKD,anemia,iron deficiency,COPD,obesity

17. Most pathophysiologic abnormalities in patients with
HFpEF are related to diastolic dysfunction
The two major determinants of diastolic function are:
 LV relaxation
(relates to cellular mechanisms ,an -ATP dependent
process )
 LV stiffness
(relates to compliance of myocardial tissue,like increased
fibrosis and collagen deposition in the extracellular matrix
eg. Hypertensive heart disease)

18. Diastolic dysfunction and HFpEF are not
synonymous,diastolic dysfunction indicates a
functional abnormalities of diastolic
relaxation,filling,or ditensibility of the LV regardless
whether the LVEF is normal or not and whether the
patient is symptomatic or not .
Diastolic dysfunction alone is essentially part of
human aging and is seen in many peoplethat do not
have HFpEF

19. Other mechanisms in the pathogenesis of HFpEF
- Longitudinal systolic dysfunction
- Endothelial dysfunction
- Chronotropic incompetence
- Pulmonary hypertension and RV dysfunction
- Atrial fibrillation ,atrial dilatation and remodeling
- Abnormalities in the skeletal muscles and peripheral
vasculature
Proinflammatory miliue created by comorbid
conditions that may lead to hypertrophy of the ventricle

20. Chamber remodeling
 Many HFpEF patients exhibit concentric remodeling of
LV with:
- Normal end diastolic volume
- Increased wall thickness/ LV mass and Increased RWT
- (increased cardiomyocytes diameter with little or no
change in length)
 By contrast HFrEFpatients exhibit eccentric remodeling
with :
- Increase end diastolic volume
- Increased LV mass
- Little increase in LV wall thickness and decreased RWT
(in HFrEF cardiomyocytes are elongated withlittle or no
change in diameter)

21. (Adapted from Katz AM. Physiology of the Heart. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2001])

23. The diagnosis of HFpEF requires the following to
be fulfilled:
1- the presence of symptoms and signs of HF
2- preserved EF ≥50%
3- elevated levels of NPs (BNP>35pg/ml and/or NT pro-
BNP>125pg/ml)
4- objective evidence of other cardiac functional and
structural alterations underlying HF
Key structual alterations are:
LAVI >34ml/m2 or LVMI ≥115g/m2 for males and
≥95g/m2 for females
Key functional alterations are:
an elevated e/é and mean septal and lateral e’ <9cm/s

24. • Patients with HFpEF may have several comorbidities(
obesity,pulmonary disease, CKD, etc…) that can mimic
symptoms of HFpEF such as dyspnea on exertion or
fatigue.
• To further confound the diagnosis it is not
uncommon for patients with HFpEFto have normal
BNP levels particulary in obese patients

25. Clinical presentation
Clinical manifestations of HFpEF are indistinguishable
from those of HFrEF
When compared with patients with HFrEF those with
HFpEF tend to be older and more likely to be female
associated comorbiditis include hypertension,diabetes
and chronic kidny disease ..

26. Symptoms and signs
Symptoms are often nonspecific,and do not therefor
desccriminate between HF and other problems.
Symptoms and signs due to fluid retention may
resolve quickly with diuretic therapy. Signs such as
elevated JVP, apical impulse displacement may be
more specific but are harder to detect and have poor
reproducibility.

27. Some patients present with only fatigue or exertional
dyspnea,
Others experince overt symptoms and signs of :
left sidedHF
(orthopenia, paroxysmal nocturnal dyspnea, pulmonary
rales and effusion ) or
right sided HF
(elevated JVP, hepatic congestion, ascitis,lower extremity
edema )

28. Symptoms and signs typical of heart failure
Symptoms signs
typical More specific
Breathlessness
Orthopnoea
Paroxysmal nocturnal
dyspnoea
Reduce exercise tolerance
Fatigue , increased time to
recover after exercise
Ankle swelling
Elevated jugular venous
pressure
Hepatojugular reflux
Third heart sound(gallop
rhythm)
Laterally displaced apical
impulse

29. Symptoms and signs of heart failure
Less typical Less specific
Nocturnal cough Weight gain (>2kg/week)
Wheezing Weight loss (in advanced HF)
Bloated feeling Cachexia (tissue wasting)
Loss of appetite Cardiac murmur
Confusion especially in elderly Peripheral edema(ankle,sacral,scrotal)
depression Pulmonary crepitations
palpitations Pleural effusion
dizziness Tachycardia, irregular pulse ,narrow pulse
pressure
syncope Hepatomegaly,ascites,cold extremities
Bendopnea Oliguria
Tachypnoea
Cheyne stokes respiration

30. NYHA classification of heart failure

31. ECG
- An abnormal ecg increases the likelihood of the
diagnosisi og HF but has low specifity
- HF is unlikely in patients presenting with a completely
normal ECG
 The most important finding is the amplitude of QRS
voltage :
Presence of high voltage (LVH criteria ) can suggest
possible etioilogy e.g Hypertensive heart disease
Conversly in a patient who has low voltage or
pseudoinfarction pattern on ECG and increased wall
thickness identified by echocardiography infiltrative
cardiomyopathy should be considered
 Atrial fibrillation is common

33. LVH
Cornell criteria :
R avl+ Sv3 >28mm
(20mm in females)
Sokolow- lyon criteria:
S v1 + R v5 or v6 >35 mm
St depresion 1-avl v5-v6
( strain pattern)

34. Chest x ray
 P-A CXR may reveal normal sized heart
otherwise the findings are the same in HFrEF
( Pulmonary edema,Pulmonary vascular
redistribution .Pleural effusion,….)
 CXR may identify other pulmonary disease

35. Natriuretic peptides
- Patients with normal plasma Np concentrations are unlikely
to have HF
- Patients with values below the cut point for exclusion of
important cardiac dysfunction do not require
echocardiography
-The use of NPs is recommended for ruling- out HF but not to
establish the diagnosis
- NP levels may be disproportionally low in obese patients
-The upper limit of normal in nona-cute setting :
For BNP is 35pg/ml
For NT-pro BNP is 125pg/ml

36. Causes of elevated concentrations of natriuretic peptides
cardiac Non-cardiac
Heart failure Advanced age
ACS Ischaemic stroke
Pulmonary embolism Renal dysfunction
myocarditis Liver dysfunction mainly cirrhosis
LVH Paraneoplastic syndromes
HCM,RCM COPD
Valvular heart disease Sever infections
Congenital heart disease Sever burns
Atrial and ventricular tachyrrhythmia anemia
Cardioversion, ICDshock Sever metabolic /hormon abnormalities
ex thyrotoxicosis,diabetic ketoacedosis
Surgical procedures involving the heart
Cardiac contusion
Pulmonary hypertension

37. echocardiogram

39. Grades of diastolic dysfunction

40. Diagnosis of diastolic dysfunction

41. Progression of LVH and diastolic dysfunction

42. 70 years old ,history of longstanding
HTN ,obesity,OSA
In 2010:
He was in sinus rhythm
LVH with septal wall thickness 1.3 cm
impaired relaxation
normal EF
patient was asymptomatic
7 years later:
•He developed overt ( HFpEF) NYHA
classIV
•LVH with septal wall measuring 2cm
•High LV filling pressure e/é =22
•Atrial fibrillation
•Pulmonary hypertension
This case highlights th importance of
early recignition of diastolic dysfunction
and prevention of future HF byaggresive
risk factor control
From AJGP

44. ECG: poor R progression
with out typical LVH
pattern
Concentric LVH by echo
septal thichness 1.7cm and
posterior wall
thichness1.6cm
Restrictive pattern
E/A>3
e/é =18
Global longitudinal strain
showing apical sparing
highly suggestive of
Amyloid heart disease
AJGP

45. Differential diagnosis
- Restrictive cardiomyopathies
- Hypertrophic cardiomyopathy
- Constrictive pericarditis
- Valvular heart disease
- Right heart failure not due to HFpEF including RV
infarction ,ARVD,pulmonary hypertension not due to
left heart disease…however many patient with
advanced HFpEF also display substantial RV
dysfunction,TV insufeciency and RV failure and
associated with worse outcome

46. In patients presenting primarily with exercise intolerance
or exertional dyspnea HFpEF should be considered in
addition to CAD ,primary lung disease ,anemia, etc

47. Treatment of HFpEF
No treatment has yet been shown convincingly
to reduce mortality or morbidity in patients with
HFpEF

48. Trials of ACEIs,ARBs, beta blockers , MRAs have all
failed to reduce mortality in patients with HFpEF

49. Treatment is directed toward:
1-relief symptoms and congestion
2- tretment of associated conditions like
hypertension,CAD,AF,diabetes,CKD,COPD,
anemia,etc..)

50. 1- Diuretics usually improve congestion and improve
symptoms and signs of HFpEF
The evidence that diuretics improve symptoms is
similar across the spectrum of LVEF
2- Sodium restriction to less than 2 g/day is
recommended

51. Managing comorbid conditions is importana
1-Managing hypertension
2-Controlling diabetes offer an adjunctive
target for reduction systymic inflammation
3-Atrial fibrillation is common in patients with
HFpEF and increases hospitaliations, AF
management is important

52. - Avoidance and reversal of obesity
- Obesity itself impairs exercise intolerance but also
contributes to the development of
hypertension,diabetes and sleep apnea
- BMI is an important predictor of outcome in patients
with HFpEF
- Weight loss produced by caloric
reduction,exercise,appetite suppressants,bariatric
surgery may represent an important management
strategy in patients with HFpEF

53. References:
-ESC guidelines
-AHA/ACC guideline
- EACVI textbook of echocardiography second
edition
-Braunwald’s heart disease eleventh edition
-Manual of cardiovascular medicine fifth edition
Medscape
-Uptodate
-Australian journal of general practice