2016 ESC Guidelines for the

diagnosis and treatment of

acute and chronic heart
failure
 2016 ESC Guidelines for the
diagnosis and treatment of chronic
heart failure
 Definition of heart failure

HF is a clinical syndrome characterized by:

**typical symptoms (e.g. breathlessness, ankle swelling and fatigue) that may be

**accompanied by signs (e.g. elevated jugular venous pressure, pulmonary crackles

and peripheral oedema) **caused by a structural and/or functional cardiac
abnormality,

**resulting in a reduced cardiac output and/or elevated intracardiac pressures at

rest or during stress.

The current definition of HF restricts itself to stages at which clinical symptoms are
apparent.
ACCF/AHA Stages of HF NYHA Functional Classification
At high risk for HF [Htn, atherosclerosis, DM, obesity, metabolic
syndrome, patients using cardio toxins, patients family history
of cardiomyopathy] but without structural heart disease or
A symptoms of HF. None
Goals: Treat HTn, lipid disorders & metabolic syndrome - stop
smoking & alcohol regular exercise. Drugs used: ACEIs/ARBs.
Structural heart disease [Previous MI - LV remodelling as LVH & No limitation of physical activity. Ordinary
I
low EF asymptomatic valve disease] but without signs or
B Asympt physical activity does not cause symptoms of
symptoms of HF
-omatic HF.
Goals & drugs: as A+ [BBs & ICD] if indicated
No limitation of physical activity. Ordinary
I
physical activity does not cause symptoms of HF.
Structural heart disease with prior or current symptoms of HF. Slight limitation of physical activity. Comfortable
Goals: as A & B + salt restriction II
Mild at rest, but ordinary physical activity results in
Drugs for routine use: Diuretics + ACEIs + BBs
symptoms of HF.
C Drugs for selected cases: Aldosterone Antagonists + ARBs +
Digitalis + Hydralazine III Marked limitation of physical activity.
Devices in selected cases: Bi-ventricular pacing & ICD. Moder Comfortable at rest, but less than ordinary
ate activity causes symptoms of HF.
IV Unable to carry on any physical activity without
Severe symptoms of HF, or symptoms of HF at rest.
Refractory HF : patients who have marked symptoms at rest
despite maximal medical therapy requiring specialized
Unable to carry on any physical activity without
D interventions. Goals: as A & B &C + more appropriate care. IV
symptoms of HF, or symptoms of HF at rest.
Special interventions: Heart transplant + Permanent
mechanical support + chronic use of Inotropes
Precursors of HF:

Before clinical symptoms become apparent, patients can present with:

** asymptomatic structural cardiac abnormalities [Previous MI - LV
remodelling as LVH asymptomatic valve disease]
or
** functional cardiac abnormalities [systolic or diastolic left ventricular
(LV) dysfunction].

but without signs or symptoms of HF

These precursors of HF are related to poor outcomes, and starting

treatment at the precursor stage may reduce mortality in patients with
asymptomatic systolic LV dysfunction.
Heart failure is a clinical syndrome characterised by:

Typical symptoms: breathlessness, fatigue, ankle swelling.

Typical signs: tachycardia, tachypnoea, pulmonary rales, pleural effusion, raised

jugular venous pressure (JVP), peripheral oedema, hepatomegaly.

Objective evidence of a structural or functional abnormality of the

heart at rest: cardiomegaly, third heart sound, cardiac murmurs, echocardiogram
abnormalities, raised natriuretic peptide concentration.
 Classification
I] Acute and chronic
Heart failure has traditionally been described as acute or chronic but this can be
confusing and should be used to describe time, rather than severity.
Acute heart failure can present as new-onset heart failure in people without known
cardiac dysfunction, or as acute decompensation of chronic heart failure
II] Systolic and diastolic
many patients with heart failure have evidence of both.
Systolic : Left ventricular systolic dysfunction (LVSD) is usually defined as an LV
ejection fraction <40% on echocardiography.
Diastolic: Some symptomatic patients have a normal ejection fraction and no
obvious cause for increased myocardial demand. This condition has been variously
termed diastolic heart failure, heart failure with preserved LV function, heart failure
with a normal ejection fraction or heart failure with preserved systolic function
III] High and low output
High-output cardiac failure: Certain medical conditions are associated with high
cardiac output and cardiac demand, causing a clinical picture of heart failure. The
primary abnormality is not the heart and the heart failure is reversible with
treatment.
low-output failure: cardiac output is inadequate to perfuse the body (i.e. ejection
fraction <40%), or can only be adequate with high filling pressures.
 Aetiology
Coronary heart disease and hypertension are the most common causes of heart
failure.
I] Valve heart disease - approximately 10% of cases:
Aortic stenosis can cause left ventricular hypertrophy (LVH) due to chronic excessive afterload.
Aortic or mitral regurgitation, atrial septal defect (ASD), ventricular septal defect (VSD) and
tricuspid incompetence cause excessive preload.
II] Heart failure secondary to myocardial disease:
1. Coronary heart disease (myocardial infarction (MI) and ischemia, arrhythmias (e.g., atrial
fibrillation (AF), heart block).
2. Hypertension (increased vascular resistance, often with LVH but preserved ejection fraction).
3. Cardiomyopathies.
4. Drugs - e.g., beta-blockers, calcium antagonists, anti-arrhythmics, cytotoxics.
5. Toxins - e.g., alcohol, cocaine, mercury, cobalt, arsenic.
6. Endocrine - e.g., diabetes, hypothyroidism, hyperthyroidism, Cushing's syndrome, adrenal
insufficiency, excessive growth hormone, phaeochromocytoma.
7. Nutritional - e.g., deficiencies of thiamine, selenium, carnitine, and obesity, cachexia.
8. Infiltrative - e.g., sarcoidosis, amyloidosis, haemochromatosis, Lffler's eosinophilia,
connective tissue disease.
9. Infective - e.g., Chagas' disease, HIV.
III] High-output failure - this occurs when cardiac output is normal
or increased in the face of much increased needs. Causes include:
1. Anaemia.
2. Pregnancy.
3. Hyperthyroidism.
4. Paget's disease of bone.
5. Arteriovenous malformations.
6. Beriberi

Causes:
1] Coronary artery disease:
ischemia, or myocardial
infarction.
2] Chronic pressure overload:
hypertension, and obstructive
valvular lesions (MS, AS).
3] Chronic volume overload:
regurgitant valvular lesions (AR,
MR)or intracardiac left to right
shunt (ASD, VSD) or extra
cardiac shunting (PDA).
4] Dilated cardiomyopathy.
5] Chronic Brady or
tachyarrhythmia.
6] Chronic cor-pulmonale.
7] High output states (chronic
anemia, thyrotoxicosis, and
nutritional deficiencies as
beriberi).
Chronic heart failure
Precipitating factors:
1. Lack of compliance of patient: reduction of therapy
(most common), Intake of water & sodium.
2. Arrhythmia: (most common are AF, marked bradycardia).
3. High output states :( Anemia, thyrotoxicosis, pregnancy
..)
4. Pulmonary embolism.
5. Systemic infections or infective endocarditis.
6. Physical (severe, prolonged physical exertion),
Environmental (hot, humid environment), or emotional
stresses.
7. Cardiac depressant drugs: Large doses of BBs, CCBs.
Antiarrhythmics. NSAIDs.
8. Systemic diseases as renal failure, liver, disease, endocrinal
& metabolic diseases.
9. Peri-operative: over transfusion of fluids or toxic effects of
drugs or anaesthesia.
 Acute heart failure
Causes:
1] Acute coronary syndromes ( ACS):
a- AMI/UA. b- Mechanical complications of AMI. c-. Right ventricular infarction.

2] Valvular: acute valvular regurgitation. Endocarditis. Aortic dissection.

3] Myopathies: Postpartum cardiomyopathy. Acute myocarditis.

4] Hypertensive crisis.

5] Acute arrhythmia (VT, VF, AF, SVT). 6] Acute severe myocarditis.

7- Cardiac tamponade. 8] Acute Pulmonary embolism.
9] Circulatory Failure: Septicemia. .

10] Acute Decompensation of Pre-existing Chronic HF: (precipitating factors):

Lack of adherence Volume overload
Pulmonary emboli
Infections, especially pneumonia
Cerebrovascular insult
Surgery
Renal dysfunction
Asthmas, chronic obstructive pulmonary disease
Drug abuse
Alcohol abuse
Precipitants and causes of acute heart failure:
Events usually leading to less rapid
deterioration
Infection (including infective
endocarditis)
Exacerbation of COPD/asthma
Anaemia
Kidney dysfunction
Non-adherence to diet/drug therapy
Iatrogenic causes (e.g. prescription of
an NSAID or corticosteroid; drug
interactions)
Arrhythmias, bradycardia, and
conduction disturbances not leading to
sudden, severe change in heart rate
Uncontrolled hypertension
Hypothyroidism or hyperthyroidism
Alcohol and drug abuse
Events usually leading to rapid
deterioration
Rapid arrhythmia or severe
bradycardia/conduction
disturbance
Acute coronary syndrome
Mechanical complication of
acute coronary syndrome (e.g.
rupture of
interventricular septum, mitral
valve chordal rupture, right
ventricular
infarction)
Acute pulmonary embolism
Hypertensive crisis
Cardiac tamponade
Aortic dissection
Surgery and perioperative
problems
Peripartum cardiomyopathy
Aetiologies of heart failure
Aetiologies of heart failure (continue)
 HF With Preserved EF

The criteria that define the syndrome of HFpEF include:

a) clinical signs or symptoms of HF;
b) evidence of preserved or normal LVEF; and
c) evidence of abnormal LV diastolic dysfunction that can be determined by Doppler
echocardiography or cardiac catheterization.

Patients with HFpEF are usually:

*older women with a history of hypertension.
*Obesity, CAD, diabetes mellitus, atrial fibrillation (AF), and hyperlipidemia are also
highly prevalent in HFpEF.
*Hypertension remains the most important cause of HFpEF, with a prevalence of
60% to 89% from large controlled trials.
Pathophysiology of HFpEF
 Pathophysiology of HFpEF
A] HF is explained by diastolic LV dysfunction, which consisted of:
1. prolonged isovolumic LV relaxation,
2. slow LV filling, and
3. increased diastolic LV stiffness.

B] Other mechanisms include:

1. resting and exercise-exacerbated systolic dysfunction,
2. impaired ventricularvascular coupling,
3. Vascular dysfunction: abnormal exercise-induced and flow mediated vasodilation,
4. chronotropic incompetence, and
5. Systolic and diastolic Cardiovascular Reserve Dysfunction.
 A] Diastolic Left Ventricular Dysfunction
In the absence of endocardial or pericardial disease,
diastolic LV dysfunction results from:
increasedmyocardial stiffness.
Determinants of myocardium stiffness
are:
1. the extracellular matrix and
2. the cardiomyocytes.
3. matricellular proteins.

1. Stiffness of the extracellular matrix: due to excessive collagen type I deposition [ due to exaggerated synthesis
and a depressed degradation]. The depressed degradation is due to downregulation of matrix metalloproteinases (MMPs)
and upregulation of tissue inhibitors of matrix metalloproteinases .
2. Intrinsic cardiomyocyte stiffness is related to the cytoskeletal protein titin [a giant elastic protein expressed in
cardiomyocytes].
3. Matricellular Proteins: A stiffness change is transmitted from one compartment to the other compartment via
matricellular proteins.
By binding to collagen, cell surface receptors, and MMPs, matricellular proteins improve both matrix quality and
cardiomyocyte function. Their role in HFpEF remains unexplored.
 B.1] Systolic dysfunction
Ejection fraction is preserved in HFpEF, but EF is more accurately regarded as a measure of ventriculararterial
coupling than contractility alone.

Systolic functions , assessed by Tissue Doppler imaging, are impaired (longitudinal and radial systolic
function) in HFpEF, despite a normal global measures of systolic function (Normal EF).

The extent of myocardial contractile dysfunction in HFpEF was associated with increased mortality,
suggesting that it may be a mediator or nominally a marker of more severe disease.

End-systolic elastance (Ees), defined by the slope and intercept of the end-systolic pressurevolume
relationship, is a gold standard measure of chamber contractility that, in contrast to other measures, is elevated in
HFpEF despite depressed contractility.

Ees is also influenced by chamber geometrybeing increased with concentric remodelling and passive ventricular
stiffeningprocesses commonly observed in HFpEF.

It is speculated that the same processes that promote diastolic ventricular stiffening in HFpEF also increase systolic
stiffening (Ees) and contribute to reduced myocardial contractility and limited systolic reserve.
 B.2] Ventricular-arterial Coupling [VAC]: Ees/Ea
Ventricular and vascular stiffening increase with ageing, hypertension,
and diabetes, and are abnormally elevated in patients with HFpEF.

Both arterial elastance (Ea) and End-systolic elastance (Ees) are elevated in HFpEF,
explaining the labile blood pressure swings commonly seen in HFpEF. Combined
ventricular-arterial stiffening leads to greater blood pressure lability.

Systemic vasorelaxation with exercise is attenuated in HFpEF, promoting

impaired delivery of blood flow to skeletal muscle.

B.3] Vascular Dysfunction

Vascular dysfunction in HFpEF may be due in part to endothelial dysfunction

[abnormal exercise-induced and flow-mediated vasodilation (a biomarker of
endothelial function)] .

Vascular dysfunction is not confined to the systemic circulation in HFpEF, as pulmonary

hypertension is frequently observed as well.
Arterial elastance EA = ESP / SV (SV stroke volume)

Higher elastance = greater sensitivity to volume change, more

variable pressure

Ventricular elastance (Ees) ELV = ESP / ESV (ESV LV end-systolic

volume) Net arterial load exerted on the ventricle

Ventricular - Arterial Coupling (VAC) = EA / ELV

= ESP / SV ESP / ESV
= ESP / SV 1 / (ESP / ESV)
= ESP / SV ESV / ESP
= ESV/SV

SV = VTI x CSA
 Fig 4. Summary results figure.

the torsion to shortening ratio (TSR),

Parikh JD, Hollingsworth KG, Wallace D, Blamire AM, MacGowan GA (2017) Left ventricular functional, structural and energetic effects of normal aging:
Comparison with hypertension. PLOS ONE 12(5): e0177404. https://doi.org/10.1371/journal.pone.0177404
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0177404
 B.4] Chronotropic Incompetence

During physical exertion in normal subjects , cardiac output increases through integrated enhancements in venous
return, contractility, heart rate, and peripheral vasodilation.

Chronotropic reserve is depressed in HFpEF, independent of rate-slowing medication use. This is

likely related to downstream deficits in -adrenergic stimulation.

B.5] Systolic and diastolic Cardiovascular Reserve Dysfunction

B.5.1] Diastolic Cardiovascular Reserve Dysfunction: Diastolic reserve is also reduced with
exertion in HFpEF, Just as impairment of diastolic function [patients display blunted increases in preload
volume with exercise, despite marked elevations in filling pressure]. This is likely related to increased chamber
stiffness and inadequate enhancement of early relaxation.

B.5.2] Systolic Cardiovascular Reserve Dysfunction: Systolic reserve with exertion is also impaired
in HFpEF [patients display blunted increases in EF, contractility, and longitudinal systolic shortening
velocities during exercise]. Exercise stress may 'unmask' mild deficits in resting systolic function, and the
inability to reduce end-systolic volume, combined with less increase in end-diastolic volume, greatly limits
stroke volume responses during exercise.

The causes of systolic and diastolic reserve dysfunction in HFpEF remain unclear, but
may be related to myocardial ischaemia (epicardial/microvascular coronary disease or vascular
rarefaction), impaired -adrenergic signalling, myocardial energetics, or abnormal calcium handling.
Chronotropic incompetence is defined as lesser HR rise with exercise & is common, an important
cause of exercise intolerance, and an independent predictor of major adverse cardiovascular events
and mortality.
It is present in up to 1/3 of patients with HF and contributes to their prominent exertional
symptoms and reduced quality-of-life. Although the underlying mechanisms for CI in HF are
incompletely understood, available data suggest roles for reduced beta-receptor density and/or
sensitivity secondary to increased sympathetic drive.

Mechanisms of chronotropic incompetence in heart failure

CI in HF is associated with a 50% reduction in -adrenergic receptor density in the left ventricular
myocardium, downregulation of -receptors, and desensitization assessed by decreased
responsiveness to norepinephrine infusion and exercise.36 HF patients also have significant sinus
node remodelling.

Diagnosis of chronotropic incompetence in heart failure

Chronotropic incompetence (CI) is most commonly diagnosed when HR fails to reach an arbitrary
percentage (either 85%, 80%, or less commonly, 70%) of the APMHR (usually based on the 220 age
equation described earlier) obtained during an incremental dynamic exercise test.

Effect of exercise training on chrotropic incompetence in heart failure

While exercise training and rate-adaptive pacing have been shown to improve chronotropic
responses and exercise capacity in HF, clearly more research is needed to fully evaluate the impact
of these therapies on key clinical outcomes.
 Presentation
I] Symptoms
Patients do not necessarily have all and some may be predominant at times.

1. Dyspnoea and fatigue (may limit exercise tolerance).

2. Fluid retention (may cause pulmonary or peripheral oedema).
3. Orthopnoea.
4. Paroxysmal nocturnal dyspnoea (PND).
5. Nocturnal cough ( pink frothy sputum) or wheeze.
6. Nocturia, cold peripheries, weight loss and muscle wasting.
7. Right ventricular failure (RVF): peripheral oedema (up to thighs, sacrum,
abdominal wall), abdominal distension (ascites), nausea, anorexia, facial
engorgement, pulsation in the neck and face (tricuspid regurgitation), epistaxis.
II] Signs
1. The patient may look ill and exhausted, with tachypnoea, cool peripheries,
peripheral central cyanosis.
2. There may be a tachycardia at rest, low systolic blood pressure (BP), a displaced
apex (LV dilatation) or RV heave (pulmonary hypertension), a narrow pulse
pressure or pulsus alternans (alternating large and small pulse pressures) and a
raised JVP.
3. There may be a gallop rhythm due to presence of S3 or murmurs of mitral or
aortic valve disease.
4. Bilateral basal end-inspiratory crackles wheeze ('cardiac asthma').
5. Pleural effusions.
6. Tender hepatomegaly - pulsatile in tricuspid regurgitation, with ascites.
7. Often extensive peripheral oedema.

The peak expiratory flow rate may be reduced but, if it is <150 litres/minute,
suspect chronic obstructive pulmonary disease (COPD) or asthma.
Symptoms and signs typical of heart failure
III] Investigations
A] If there has been a previous MI
The patient should be referred for Doppler echocardiography. It enables an assessment of:
1. Overall LV systolic function.
2. Diastolic function (necessary to diagnose heart failure with preserved ejection fraction).
3. LV wall thickness.
4. Valvular disease.
5. Estimation of pulmonary artery systolic pressure.

If an abnormality is found consistent with heart failure, the severity, aetiology, precipitating
factors, type of cardiac dysfunction and treatable causes are assessed.

If there is no obvious abnormality, consider measuring serum natriuretic peptides (if

not already done). *If the levels are raised, there may be heart failure with a preserved ejection
fraction or another diagnosis. *If the levels are normal, the diagnosis is unlikely to be heart
failure.
B] No previous MI
Measure serum natriuretic peptides:
*If levels are high (BNP 400 pg./ml), the patient should be referred for specialist assessment
and Doppler echocardiography within two weeks .
*If (BNP 100-400 pg./ml), the referral and assessment may be made within six weeks.
*If the levels are normal (BNP 100 pg./ml), heart failure is unlikely and other diagnoses should
be considered.
Very high levels of serum natriuretic peptides (400 pg/ml) carry a poor prognosis.

Natriuretic peptide levels may also be elevated in other conditions such as chronic hypoxemia, renal
dysfunction, advanced age, liver cirrhosis and sepsis.
Causes of elevated concentrations of natriuretic peptides
The European Society of Cardiology (ESC) guidelines place almost
equal emphasis on the role of the 12-lead ECG.

This not only identifies potential aetiological factors but is also

necessary for treatment decisions - e.g., rate control and
anticoagulation for AF or pacing for bradycardia.

A normal ECG makes LVSD unlikely (negative predictive value of 98%).

Echocardiography is recommended in patients with suspected heart

failure who have either a raised BNP or NT-pro BNP level or abnormal
ECG, in order to confirm the diagnosis and establish the underlying
cause.
Recommendations for cardiac imaging in patients with
suspected or established heart failure
Recommendations for diagnostic tests in patients with heart failure
Recommendations for diagnostic tests in patients with heart failure
Thank you
Recommendations to prevent or delay the development of overt heart
failure or prevent death before the onset of symptoms [Stage A & B]
Evidence-based doses of disease-modifying drugs in randomized trials in HF with reduced EF (or after MI)

If (f is for "funny",
because it had unusual
properties current
system. If is a mixed
Na+K+ inward current
system channel)

ARNI = angiotensin
receptor neprilysin
inhibitor
 Empagliflozin

Treating type 2 diabetes in certain patients. It is used along with diet and exercise.

Empagliflozin is a sodium-glucose cotransporter 2 (SGLT2) inhibitor. Increase sugar in the urine.

Do NOT use empagliflozin if:

allergy to empagliflozin type 1 diabetes diabetic ketoacidosis. severe kidney problems or are
on dialysis

Some MEDICINES MAY INTERACT with empagliflozin: especially any of the following:
Insulin or oral (e.g., repaglinide, glipizide)hypoglycaemia. Antihypertensive: (e.g., diuretics)
hypotension.
 Angiotensin Receptor Neprilysin Inhibition (ARNI)

Neprilysin is an enzyme that contributes to the breakdown of the biologically active natriuretic peptides
and several other vasoactive compounds.

Inhibiting neprilysin has been a therapeutic target for several compounds that have been tested in
cardiovascular disease. Both ANP and BNP have multiple mechanisms of actions, including vasodilation,
natriuresis, and diuresis.

Neprilysin inhibition represents a potential alternative strategy to exogenous BNP administration

(nesiritide, a synthetic BNP drug) by preventing the breakdown of endogenous NPs.
Angiotensin Receptor Neprilysin Inhibition (ARNI)
LCZ696 (sacubitril valsartan) is a first-in-class angiotensin receptor neprilysin inhibitor. LCZ696 is a novel,
dual-acting crystalline complex composed of the neprilysin inhibitor sacubitril and the angiotensin receptor
blocker valsartan in their anionic forms, sodium cations, and water molecules. Soon after oral ingestion,
LCZ696 dissociates into sacubitril (a neprilysin inhibitor prodrug, AHU-377, which is enzymatically cleaved
to the active form, LBQ657) and valsartan. LCZ696 was designed to have a reduced risk for angioedema
because it inhibits only one of the enzymes responsible for bradykinin breakdown.

The PARAMOUNT (Prospective Comparison of ARNI With ARB on Management of Heart Failure With
Preserved Ejection Fraction) trial assessed the efficacy of LCZ696 in patients with HFpEF. patients in the
LCZ696 arm had greater improvements in left atrial size and greater improvements in New York Heart
Association (NYHA) class. BP was lowered to a greater extent in the LCZ696 arm. Nevertheless, subsequent
analyses have shown that the effects on reduction in NT-proBNP and improvements in left atrial size and
NYHA class were independent of the BP-lowering effect (23). Moreover, despite the substantial reduction in
BP in the LCZ696 arm, estimated glomerular filtration rate was not reduced in patients receiving LCZ696 and
was significantly higher than in those receiving valsartan. LCZ696 was well tolerated in these patients, with
no significant differences in adverse events between groups.

Dual inhibition of the renin-angiotensin-aldosterone system and neprilysin inhibition represent a novel
approach to treating patients with HF. The results of PARADIGM-HF, showing significant reductions in the
primary composite endpoint, cardiovascular death, and all-cause mortality in patients receiving LCZ696 in
comparison with those receiving enalapril, suggest that this drug could replace ACE inhibitors and ARBs as
first-line therapy in the treatment of patients with HFrEF, once regulatory approval is obtained.
 Other pharmacological treatments recommended in selected patients with symptomatic (NYHA
Class II-IV) = (Stage C & D) heart failure with reduced ejection fraction

Omega-3 fatty
acids = -3 fatty
acids = n-3 PUFA =
n-3 polyunsaturated
fatty acids
Recommendations for implantable cardioverter-defibrillator in patients with
heart failure
Recommendations for cardiac resynchronization therapy implantation in
patients with heart failure
 Recommendations for the prevention of thrombo-embolism in patients with
symptomatic heart failure (NYHA Class IIIV) and paroxysmal or
persistent/permanent atrial fibrillation

AF = atrial fibrillation; CHA2DS2-VASc = Congestive heart failure or left ventricular dysfunction,

Hypertension, Age 75 (doubled = 2 points), Diabetes, Stroke (doubled= 2 points)-Vascular disease, Age 6574,
Sex category (female); HAS-BLED = Hypertension, Abnormal renal/liver function, Stroke, Bleeding history or
predisposition, Labile international normalized ratio, Elderly (>65 years), Drugs/alcohol concomitantly (1 point
each); HF = heart failure; LMWH = low molecular weight heparin; NOAC = non-vitamin K antagonist oral
anticoagulant; NYHA = New York Heart Association; TOE = transoesophageal echocardiography.
Considered score of:

0 to be low risk for TE events (none seen in cohort at one year),

score of 1 intermediate risk (0.6% rate at 1 year), and

greater than 1 high risk (3% rate at 1 year).

 What Are the Available Non-vitamin K antagonist
Oral Anti-Coagulants (NOACs)?
There are currently 4 NOACs available for healthcare providers to prescribe for patients with atrial :
dabigatran (Pradaxa), rivaroxaban (Xarelto), apixaban (Eliquis), and edoxaban (Lixiana/Savaysa).
Recommendations for the treatment of stable angina pectoris with symptomatic
(NYHA Class II-IV) heart failure with reduced ejection fraction

Ranolazine, = trade name Ranexa. It is inhibitor of late Na channel

Recommendations for the treatment of hypertension in patients with
symptomatic (NYHA Class II-IV) heart failure with reduced ejection fraction
Recommendations for treatment of valvular diseases in patients with heart
failure
 2016 ESC Guidelines for the
diagnosis and treatment of acute
heart failure
Factors triggering acute heart failure
Definitions
Recommendations for the management of patients with acute heart failure:
oxygen therapy and ventilatory support
Recommendations for the management of patients with acute heart failure:
pharmacotherapy
Recommendations for the management of patients with acute heart failure:
pharmacotherapy (continue)
Intravenous vasodilators used to treat acute heart failure
Positive inotropes and/or vasopressors used to treat acute heart
failure
Recommendations regarding management of patients with cardiogenic
shock

IABP = intra-aortic balloon pump

Patients potentially eligible for implantation of a left ventricular assist
device

CI = cardiac index; HF = heart failure; i.v. = intravenous; LVEF =

left ventricular ejection fraction; PCWP = pulmonary capillary
wedge pressure; SBP = systolic blood pressure; VO2 = oxygen
consumption.
Heart transplantation: indications and contra-indications
Messages from the Guidelines
Messages from the Guidelines
 Recommendations in treatment of
asymptomatic Systolic CHF

1- All pts should be treated with ACEIs indefinitely unless

intolerant.
2- Anti-hypertensive therapy should be used to prevent
subsequent CHF in pts with Htn.
3- Preventive treatment with ACEIs may be considered in pts at
high risk of LV dysfunction.
4- BBs should be started early after AMI whether or not pt has
LV systolic dysfunction.
5- Statins should be used as part of risk management strategy
to prevent ischaemic events and subsequent CHF.

Recommendations in treatment of
symptomatic CHF
1-ACEIs unless not tolerated or contraindicated are
recommended for all pts with systolic CHF (all classes).
2-Every effort should be made to increase dose of ACEIs to
beneficial doses in major trials.
3-Diuretics should be used ,if necessary, to achieve euvolaemia in
fluid-overloaded pts. They are never used alone but should always
be combined with ACEIs to maintain euvolaemia.
4-BBs are recommended, unless not tolerated or
contraindicated for all pts with symptomatic HF even in
advanced cases after being euvolemic.
5-Add aldosterone antagonists ( Spironolactone ) is
recommended for pts who remain severely
symptomatic.Eplerenone is recommended in early post MI pts
with LV syst dysfunction.(aldosterone
fibrosis,hypertrophy&arrhythmogenesis).
 MOA of ACEIs

ACEIs block the conversion of A-I to A-II leading to

A-II, and Aldosterone arteriolar resistance.
venous capacity.
cardiac output, cardiac index, stroke work, and
volume.
Reno vascular resistance; and lead to increased
natriuresis.

Bradykinin will increase due to less inactivation that

is done by ACE enzyme.

Clinical uses of ACEIs

[1] ACEIs are used primarily to treat hypertension.

[2] They may also be used for:

cardiac failure.
renal disease.
systemic sclerosis.
diabetic nephropathy.
left- ventricular hypertrophy.
 HOPE (Heart Outcomes
Prevention Evaluation)
Trial
Conclusions:
*There is overwhelming evidence that, in a broad
range of high-risk patients, ramipril prevents:
1. cardiovascular death, stroke, and MI
2. heart failure, revascularization
3. development of diabetes
4. diabetic micro vascular complications including
nephropathy
*The benefits of ramipril are incremental to existing
therapy.
The beneficial effects of ramipril are independent of
blood pressure lowering.

AIRE trial

2006 patients with acute myocardial infarction,

complicated at any time by left ventricular failure,
were randomised to:
ramipril, an ACE-inhibitor, 5 mg twice daily & placebo
Randomisation took place 3-10 days post-MI (mean 5
days).
Treatment with ramipril resulted in:
an absolute reduction in mortality of 6%
an odds reduction for death of 26%
the prevention of 45 premature deaths per 1000
patient years
Are all ACEIs the same:
Survival post-MI by ACEI at
discharge
N = 7512
100

90
Unadjusted
cumulative Ramipril n = 905
survival Perindopriln = 243
(%)
Lisinopril n = 2201
80
Enalapril n = 2577

Quinapril n = 276

Fosinopril n = 889

Captopril n = 421
P < 0.001 log-rank

70
0 2 4 6 8 10 12
Months
Pilote L et al. Ann Intern Med.
2004;141:102-12.