Contents

 Definition
 Incidence
 Pathophysiology
 Classification
 Causes
 Diagnosis
 Assessing cardiovascular disability
 Treatment
 Messages
 Definition

•A state in which the heart cannot

provide sufficient cardiac output to
satisfy the metabolic needs of the body.

• It is a common end point for many

diseases of cardiovascular system.
 The burden of heart failure
NUMBER of PATIENTS ECONOMIC BURDEN
21 MILLION adults worldwide are In 2012, the overall worldwide
living with heart failure cost of heart failure was nearly
This number is expected to rise. $108 BILLION.

MORTALITY
50% of heart failure patients die
within 5 years from diagnosis.

REHOSPITALISATION COMORBIDITIES: The vast

Heart failure is the NUMBER 1 majority of HF patients has 3 or
cause of hospitalisation for more comorbidities
patients aged >65 years.
 Pathophysiology
Injury to myocytes
due to myocardial ELECTRICAL INSTABILITY
VENTRICULAR
infarction or other REMODELING
cause
REDUCTION of EF

NEUROHUMORAL
IMBALANCE

An imbalance occurs in three key neurohumoral systems:

• The renin–angiotensin–aldosterone system
• The sympathetic nervous system
• The natriuretic peptide system

The systemic responses in the renin–angiotensin–aldosterone and sympathetic nervous systems

cause further myocardial injury, and have detrimental effects on the blood vessels, and various organs,
thereby creating a pathophysiological ‘vicious cycle’. The natriuretic peptide system has a protective
function, which can counterbalance these detrimental effects.
 Classification of Heart Failure
• Systolic & Diastolic
• High Output Failure:
– Pregnancy, anemia, thyrotoxisis, A/V fistula,
Beriberi, Pagets disease
• Low Output Failure:
– Systolic heart failure

• Acute:
– large or complicated MI, acute decompensated chronic HF
• Chronic:

•Right sided heart failure :

– Most common cause is * left sided failure
– Other causes included : all causes of pulmonary htn.
( chest causes, pulm. Embolism)
– RV infarction
– Usually presents with:
LL edema, gastropathy, ascites
hepatic congestion
cardiac cirrhosis (on the long run)
 Causes
 The performance of the heart depends in four
essential components :
- Contractility of the muscle
- Preload
- Afterload
- Heart rate
Diagnosis
 Laboratory findings
• Natriuretic peptides:
• The plasma concentration of natriuretic peptides (NPs) can be used as an initial
diagnostic test, especially in the non-acute setting when echocardiography is not
immediately available.

• Patients with normal plasma NP concentrations are unlikely to have HF.

•The upper limit of normal in the non-acute setting for B-type natriuretic peptide (BNP) is
35 pg/mL and for N-terminal pro-BNP (NT-proBNP) it is 125 pg/mL.

• In the acute setting, higher values should be used [BNP , 100 pg/mL, NT-proBNP , 300
pg/mL and mid-regional pro A-type natriuretic peptide (MR-proANP), 120 pmol/L].
 • other lab:
 Haemoglobin and WBC
 Sodium, potassium, urea, creatinine (with estimated
GFR)
 Liver function tests (bilirubin, AST, ALT, GGTP)
 Lipid profile
 Glucose, HbA1c
 TSH
 Ferritin, TSAT = TIBC
 CARDIAC IMAGING
1. Electrocardiogram (ECG):
• Has low specificity.

• But An abnormal electrocardiogram (ECG) increases the

likelihood of the diagnosis of HF.

• Therefore, the routine use of an ECG is mainly recommended to

rule out HF.
2. Chest X-ray:

* Is of limited use in the diagnostic work-up of patients

with suspected HF.

* It is probably most useful in identifying an alternative,

pulmonary explanation for a patient’s symptoms and signs,
i.e. pulmonary malignancy and interstitial pulmonary disease,
3. Transthoracic echocardiography

• Echocardiography is the most useful, widely available test in

patients with suspected HF to establish the diagnosis.

•It provides immediate information on chamber volumes,

ventricular systolic and diastolic function, wall thickness, valve
function and pulmonary hypertension.

•This information is crucial in establishing the diagnosis and in

determining appropriate treatment.
• Othertests are generally required only if the diagnosis remains
uncertain (e.g. if echocardiographic images are suboptimal or an
unusual cause of HF is suspected)
4. Transoesophageal echocardiography
•Not needed in the routine diagnostic assessment of HF.

• But may be valuable in some clinical scenarios of patients with

valve disease, suspected aortic dissection, suspected
endocarditis or congenital heart diseases.

5.Stress echocardiography
• May
be used for the assessment of inducible ischaemia ,
myocardium viability and low-flow–low-gradient aortic stenosis
6. Cardiac magnetic resonance
• CMR is the gold standard for the measurements of volumes,
mass and EF of both the left and right ventricles.

• It is the best alternative cardiac imaging modality for patients

with :
- Nondiagnostic echocardiographic studies (particularly for
imaging of the right heart)
- The method of choice in patients with complex congenital
heart diseases
- Allows the characterization of myocardial tissue of
myocarditis, amyloidosis, sarcoidosis, Chagas disease, non-
compaction cardiomyopathy and haemochromatosis
7. Single-photon emission computed
tomography and radionuclide
ventriculography

• (SPECT) May be useful in assessing ischaemia and myocardial

viability.

8. Positron emission tomography

•(PET) (alone or with CT) may be used to assess ischaemia and
viability.
9. Coronary angiography
• Coronary angiography should be considered in patients
with HF and intermediate to high pre-test probability of CAD
and the presence of ischaemia in non-invasive stress tests
in order to establish the ischaemic aetiology and CAD
severity

10. Cardiac computed tomography

• Cardiac CT in patients with HF with Low to intermediate pre-
test probability of CAD to exclude the diagnosis of
CAD.
Assessing cardiovascular
disability
 ACC/AHA stages of HF NYHA functional classification
(based on structure and damage to heart) (based on symptoms or physical activity

Stage A At high risk for HF, but without structural or Class I No limitation of physical activity. Ordinary physical
functional abnormality activity does not cause undue fatigue, palpitation or
No signs or symptoms dyspnoea

Stage B Developed structural heart disease strongly Class II Slight limitation of physical activity. Comfortable at
associated with development of HF, but without rest, but ordinary physical activity results in HF
signs or symptoms symptoms

Stage C Symptomatic HF associated with underlying Class III Marked limitation of physical activity. Comfortable at
structural heart disease rest, but less than ordinary activity results in HF
symptoms

Stage D Advanced structural heart disease and marked Class IV Symptoms of HF present at rest. If any physical
symptoms of HF at rest, despite maximal medical activity is undertaken, discomfort is increased
therapy
Treatment
1. Treatment of chronic heart
failure with reduced systolic
function
 Goals of therapy:

* Relieving symptoms and improving functional capacity

* Delaying progression of reversing remodeling and myocardial

dysfunction

* Reducing mortality

These objectives are attained by general , pharmacological and

non-pharmacological measures
 General therapeutic measures
 Preventive measures:
- by detecting and controlling risk factors befor affect
ventricular function
 Correction of precpitating factors and reversable
causes:
- eg: aneamia - chest infection – immunization
: correct valvular lesion and congenital defects
 Diet and changes in activity:
- Na , fluid , caloric, physical activity and emotional
stress
 Pharmacological treatment
 Medications recommended includes:
Non pharmacological measures
 Implantable cardioverter-defibrillator
(ICD): for
• Cardiac resynchronization therapy:
2. Treatment of heart failure
with
preserved ejection fraction
• The
guidance in this section applies to patients with both
HFmrEF and HFpEF

• As Patients with HFmrEF have generally been included in

trials of HFpEF.
3. Treatment of acute heart
failure
•AHF refers to rapid onset or worsening of
symptoms and/or signs of HF.

• It is a life-threatening medical condition requiring

urgent evaluation and treatment, typically leading
to urgent hospital admission.

•AHF may present as a first occurrence (de novo)

or, more frequently, as a consequence of acute
decompensation of chronic HF
Applied diagnostic measurements
Continue..,
Continue..,
Messages
 References
 Mozaffarian D et al. Circulation. 2015;131(4):e29-e322.
 Mosterd A et al. Heart. 2007;93(9):1137-1146.
 http://www.cms.gov/Research-Statistics-Data-and-Systems/Statistics-Trends-and-
Reports/Chronic-Conditions/Downloads/2012Chartbook.pdf
 Cowie MR et al. Oxford PharmaGenesis; 2014.
http://www.oxfordhealthpolicyforum.org/AHFreport. Accessed February 18, 2015.
 Fauci AS et al. Harrison's Principles of Internal Medicine. 17th ed. New York: McGraw-
Hill; 2008.
 Cook C et al. Int J Cardiol. 2014;171(3):368-376.
 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure.