IDA 6 SEMINAR

ACUTE CORONARY SYNDROME &

HEART FAILURE

Syuraih Abdullah b. Abu Kassim

45244
Muhd. Haziq Qaiyum b. Roslan
45226
Bahiyah bt. Abdul Jabar
45245
Wan Nur Umirah bt. Wan Rusmi
45247

Epidemiology

Acute Coronary Syndrome

Acute coronary syndrome (ACS) is the leading cause of
death not only in Malaysia but also globally.
Estimated incidence =141/100,000 population per year
10% mortality rate for patients who were admitted to
hospital with STEMI in 2006-2008.
- The National Cardiovascular Disease (NCVD) ACS Registry -

Thrombolysis (for STEMI only) reduced in-hospital and

30-day mortality by nearly 50%.

Heart Failure
Estimated incidence = 3-20 per 1000 population.
Coronary Artery Disease & Hypertension
accounting for almost 70% of all cases.
The prognosis remains poor.
One year mortality rate = 5% to 52% depending on
the severity and the presence of co-morbidity.
In a study, about 40% of individuals with HF died
within a year of initial diagnosis.
About 25% of patients are readmitted within 30 days for
acute decompensation. (major health and economic
burden)

Case Study

Patients profile
Name
: Mr. C
Age
: 37 years old
Occupation : Army ranger
Home address : Kuching
Social
: Active smoker

History of Presenting Illness

Previously well. Had no history of being diagnosed with any kind of illnesses.

September 2014:
- Had sudden onset of central chest discomfort while resting and
smoking
cigarette at the army mess.
- The chest discomfort was described as dull in nature and radiates
to the left
arm and his jaw.
- Associated with sweating.
- Lasted for about 20 minutes.
- Went to hospital Ipoh by himself.
- Given treatment. Chest pain resolved.
- ECG was inconclusive. Some blood tests done.
- Was told that troponin was positive.
- Admitted for 6 days . Refused coronary angiogram even though
advised.
- Reason being he was still able to exercise and run as usual after

13th December 2014:

- Was on a mission at the Thai-Malaysian Border in the jungle.
- Had finished his medications for the past 2 weeks but did not
replenish his
supply from the hospital.
- Woke up suddenly at 8am with sudden onset of chest pain,
similar with the
previous one but more severe.
- Associated with shortness of breath, diaphoresis and nausea.
- Took some sublingual GTN but only improved slightly.
- Evacuated from the area via a helicopter. Subsequently admitted
to Hospital
Sultanah Bahiyah in Alor Setar.
- Not given thrombolysis because it was a late presentation.
- Coronary angiogram and PCI was done with a DES to the LAD.
(15/12/2015)
- Discharged well after admission for 1 week.

Late December, 2014 (*just around 2 weeks after PCI done):

- Started to have some mild shortness of breath on exertion but chose to
ignore the symptom.
Between late Feb and March, 2015:
- Stationed at Sematan, 100km from Kuching.
- Started to have pedal edema and reduced effort tolerance.
30th March 6th April, 2015 :
- Bilateral pedal edema up to thigh, mild orthopnea and NYHA III.
- Discharged after given diuretics and had good urine output.
- Started on warfarin after ECHO noted LV thrombus.

9th April 29th April, 2015:

- Worsening of pedal edema.
- Appeared jaundice.
- Claimed as compliant to medications but not to fluid
restrictions.
- Had no fever, no sputum and no dysuria to suggest any
infection.
- Had no malaena to suggest any upper GI bleeding.
- Had reduced urine output but had no uraemic symptoms.

Family History:
- Mother has diabetes mellitus, hypertension and dyslipidemia.
- All of his mothers male siblings have ischaemic heart disease.
- One had CABG. 2 had sudden death at an early age.
Social History:
- An army ranger.
- Smokes 2 packs per day for the past 19 years. Stopped in
December, 2014.
- Married. Has 3 children. 11 year-old daughter, 7 year-old and
1 year-old son.

Medications :
Rate control:
Carvedilol - 3.125mg
bd
Ivabradine - 5mg bd
Digoxin - 0.125mg od
Anti-coagulant:
Warfarin - 2mg
od

Diuretics:
Frusemide - 40mg bd
Spironolactone - 12.5mg
bd

Antidyslipidaemic:
Atorvastatin 40mg
noct

Anti-hypertensive:
Perindopril - 2mg od

Anti-platelet:
Aspirin - 75mg
bd
Clopidogrel 75mg
od

Proton-pump inhibitor:
Pantoprazole 40mg
bd

Clinical Examination:
- Raised JVP, pedal edema up to the knees.
- Displace apex beat. Soft systolic murmur at apical area

Tests

Results

Angiogram
(15/12/2014)

- Proximal to middle right coronary artery : 10 20%

stenosis.
- Distal circumflex artery
: Diffuse disease
- Middle left anterior descending artery
: 90% stenosis.
-

PCI done.

Full Blood
count

- Haemoglobin
- Total white cell
- Platelet

BUSE &
Creatinine

- Sodium
- Potassium
- Urea
- Creatinine

INR

Liver Function
Test

: 12.5 g/dL
: 10.5
: 263

130
3.8
5.0
93

1.8
Total bilirubin 58.2
AST
243
ALT
200
Protein
74
Albumin
22
Globulin
52
ALP
246

Direct bilirubin

42.5

201
4
Late
Dec.

Sept.
First
heart
attack

Second
heart
attack

Mid
Dec.
Medicati
on only

201
5

Stenting
done

Onset of
HF
sympto
ms

??
?

Feb-MarchApril
Worsening of HF
symptoms

Right
heart
failure +
renal sx

MidLate,
April
HF
medicatio
ns

??

Summary
A 37-year-old male, army, active smoker, with history of
being diagnosed with ischaemic heart disease, on
medications and stenting done 5 months ago,
complicated with heart failure and on medications,
currently presenting with worsening of pedal edema,
and jaundice. Physical examination also revealed pedal
edema up till knee level and jaundice plus raised JVP,
displaced apex beat and soft systolic murmur at the
apical area.

What are the issues?

Why did the patient develop heart failure despite PCI
was done?
Why he needs warfarin?
What are the precipitating and perpetuating factors that
pose high risks in this patient?
What are the next options that this patient has for
treatment?

Acute Coronary
Syndrome

 RCA and its branches

supplies the RA, RV
& inferoposterior
aspects of the LV.
RCA supplies the SA
node in 60% of
individuals and the AV
node in 90% of
individuals.
Sinus bradycardia and
AV nodal block.
Occlusion:
- RCA Right-sided and
inferior infarct.
- LAD, CX Left-sided
infarct

ACS

Myocardi
al
infarctio
n
Unstable
angina

NSTEMI
STEMI

Etiology of ACS
Atheroscler
otic plaque
***

Coronary
artery
dissection

Coronary
emboli

Coronary
arteritis

Coronary
spasm

Excess LDL accumulates in intima

Macrophage ingest the cholesterol

Macrophage becomes lipid laden foam cells

Foam cells die and release fatty content

Lipid pool formation

Smooth muscle cells (SMC) moves to intima from

media (chemotatic cytokines from foam cells)

SMC proliferates, produces collagen and elastin,

thus form fibrous cap

Stimulated by LDL and atherogenic cytokines, SMC

produces matrix metalloproteinases (MMP)

MMP degrades the fibrous cap

Lower SMC:lipid ratio, increasing lipids and cellular debris

in lipid core, higher plaque vulnerability

Plaque rupture

Activation of platelet aggregation, coagulation pathway

and vasoconstriction

Partial or total occlusion of coronal artery

Ischemia of cardiac muscles leads to myonecrosis

Risk factors
NON MODIFIABLE
Age (55 years old)
Gender (Male > Female)
Family history of coronary
heart disease

MODIFIABLE
Smoking
Hypertension
Diabetes mellitus
Obesity
Dyslipidemia

Symptoms and Signs

Symptoms

Signs

Chest pain
Nausea & vomiting
Sweating
Shortness of breath
Palpitation
Syncope
Atypical chest pain

Diaphoresis
Hypotension

How to diagnose?

Investigations
ECG

Cardiac
Markers

Angiogram

Echocardiogra
m

MRI

Electrocardiogram (ECG)
UNSTABLE
ANGINA

MYOCARDIAL
INFARCTION
NSTEMI

STEMI

ST depression

ST elevation

T wave inversion

Diminution of R wave

Loss of R wave

Q wave

Absent Q waves

T wave inversion

ST depression
T wave inversion

Cardiac markers
CARDIAC
ENZYMES

Rise

Peak

Falls

Creatinine
Kinase
(CKMB)

4-6 hours

12 hours

48-72 hours

Troponin T
&I

3-4 hours

18-36 hours

After 2
weeks

Echocardiography: Assess ventricular function

& complication
Findings: Left ventricle thrombus

Angiogram: Blockage of the vessels

Findings:
Proximal to middle right coronary artery : 10 to
20% stenosis.
Distal circumflex artery : Diffuse disease
Middle left anterior descending artery : 90%
stenosis.

Cardiac MRI

Define cardiac anatomy

Quantify right & left ventricular function
Assess myocardial perfusion
Quantify blood flow
Assess myocardial scar & viability

EARLY HOSPITAL CARE

Arrived at
hospital
Medication
s:
-B blocker
Nitroglyceri
n
-Morphine
Test for
-Aspirin cardiac
biomarkers

ECG

Outline Treatment of Acute

Coronary Syndromes
ST-Elevation
(STEMI)

Non-ST-Elevation
(UA and NSTEMI)

Emergent PCI available

within 90 min?

No

Yes

Risk Assessment
(e.g., TIMI Score)

Low

Fibrinolytic Primary PCI

Conservative
Therapy
Strategy
(e.g., tPA)
(Proceed to cardiac cath
only if recurrent angina
or predischarge
stress test is markedly
positive)

High

Invasive
Strategy
(Cardiac cath
leading to
PCI or CABG)

Coronary Artery Bypass Graft Surgery

(CABG)

Percutaneous Coronary Intervention

INDICATIONS OF PCI:
-Have frequent or severe anginathat is not responding to medicine
and lifestyle changes.
-Have evidence of severely reduced blood flow (ischemia) to an
area of heart muscle caused by one or more narrowed coronary
arteries.
-Have a narrowed or blocked artery that is likely to be
treated successfully with angioplasty.
-Are in good enough health to have the procedure.

Back to our case:

Fibrinolytic therapy: was not given due to late
presentation
PCI and stenting: done after 2 days from the onset of
symptoms
DELAY IN TREATMENT!

COMPLICATION OF ACS

Arrhythm
ias
Cardioge
nic shock

Mitral
valve
regurgita
tion

Pericardi
tis

Complicati
ons
Of
ACS

Heart
Failure

Ventricul
ar
aneurys
m

Myocardi
al
rupture
Cardiac
tamponat
e

Heart Failure
HF is an abnormality of cardiac structure or
function leading to an impairment of
ventricular filling or ejection of blood. It is a
clinical syndrome in which patients have
typical symptoms and signs.
Management of Heart Failure 3rdEd CPG
2014

Right,
Left,
biventricul
ar

Practical
purpose

Acute,
Chronic

Classificati
ons

High
Output
Failure

Systolic,
Diastolic

Orthopnoea
Paroxysmal nocturnal
dyspnoea (PND)
Reduced exercise tolerance
Ankle swelling

Clinic
al

Diagno
sis
Exercise capacity
1 year mortality

NYHA
Functiona
l
Classifica
tion

Elevated jugular venous

pressure
Ankle edema
Pulmonary crackles
Laterally displaced apex
beat
Third heart sound
Peripheral edema
Tachycardia
Narrow pulse pressure
Hepatomegaly
Ascites

Objecti
ve
eviden
ce

Reduced LVEF
Normal, non-dilated LV

The New York Heart Association

Functional Classification
Class

1 Year
mortality

CLASS
I

No limitation. Ordinary physical activity

does not cause undue fatique, dyspnoea or
palpitation.

5 - 10%

CLASS
II

Slight limitation of physical activity. Such

patients are comfortable at rest. Ordinary
physical activity results in fatique,
palpitation, dyspnoea or angina.

10 - 15%

CLASS
III

Marked limitation of physical activity.

Although patients are comfortable at rest,
less than ordinary activity will lead to
symptoms.

15 - 20%

CLASS
IV

Inability to carry on any physical activity

without discomfort. Symptoms of congestive
failure is present at rest. With any physical
activity, increased discomfort is
experienced.

20 - 50%

Pathophysiological Classification
Pathophysiological Classification of Heart Failure (HF)
Classification
I. Heart Failure with Reduced Ejection Fraction (HFrEF)
II. Heart Failure with Preserved Ejection Fraction
(HFpEF), borderline
III. Heart Failure with Preserved Ejection 50%Fraction
(HFpEF)

LVEF (%)
40%
41-49%
50%

Factors Contributing to Decompensation in a

Patient with stable HF
Patient
factors

Non compliance to medications

Dietary indiscretion especially salt and fluid intake
Inappropriate medications e.g. NSAIDS and COX-2
inhibitors
Alcohol consumption
Superimposed myocardial ischaemia or infarction (often

Cardiac
causes
Systemi
c
conditio
ns

asymptomatic)
Uncontrolled hypertension
Arrhythmias
Pulmonary embolism
Secondary mitral or tricuspid regurgitation

Superimposed infections
Anemia
Thyroid disease
Electrolyte disturbances
Worsening renal disease

Investigations for
Heart Failure

53

Investigations

Confirm
diagnosi
s

Underlyi
ng
causes

Assess
severity

55

1) Electrocardiography (ECG)

heart rate
heart rhythm
QRS morphology
QRS duration

QRS voltage

evidence of ischaemia

LV hypertrophy

arrhythmias

2) Chest Radiograph

ABCDE

Alveolar oedema (bats

wings)
kerley B lines (interstitial
oedema)
Cardiomegaly
Dilated prominent upper
lobe vessels
Effusion (pleural)
57

Signs of heart failure

Cardiomegaly CTR = 18/30
(1)Upper zone vessel
enlargement - a sign of
pulmonary venous
hypertension
(2) Pulmonary oedema bilateral
increased lung
markings (classically perihilar and shaped like bats
wings)
(3) Septal (Kerley B) lines
(4) Pleural effusions

Septal lines (Kerley B lines)

Costophrenic angle
Horizontal lines reaching
the lung edge

3) Echocardiography

To identify structural abnormalities and assess systolic and

diastolic function

61

4) B type natriuretic peptide (BNP) assay and N terminal pro BNP (NT- pro BNP)

Hormones secreted by ventricles in response to wall

stress.
Emergency setting, as a rule out test - acute heart
failure
Levels increase with age, reduced in obesity.
Level correlate with severity of heart failure
62

Blood tests

Full blood count: anemia, infection

Renal profile: deteriorating renal function
Liver function test: elevated liver enzymes
Thyroid function test: thyrotoxicosis
D-dimer: risk for thrombosis
Cardiac markers: myocardial infarction
Arterial blood gas: hypoxia, pulmonary diseases

Test for myocardial ischaemia and/ or viability

Cardiac MRI: Assess myocardial perfusion and viability, infiltrative cardiomyopathy,
congenital, anatomy vessels, gold standard for RV function
Stress Echocardiography: examine viability in impaired LV function
Myocardial perfusion scanning: SPECT (single photon emitting CT): detect inducible
ischaemia and hibernating myocardium
Exercise (stress) ECG
Underlying CAD may be diagnosed
Prognostic aid-following myocardial infarction
Distinguish between CAD and pulmonary causes

Invasive
Coronary angiography- assess extent and
severity of stenoses, thrombus and calcification,
PCI and CABG planning

Others
Urinalysis
Proteinuria, Glycosuria
24 hour Holter monitoring
Detects arrhythmias
Lung function tests
FVC and FEV1 reduced in HF
Reversibility testing may be useful to decide use of
beta blocker

Management

66

Acute Decompensation of Chronic

Heart Failure
Principles of management:

Rapid recognition of the condition

Stabilization of haemodynamics
Improvement in clinical symptoms and signs
Identification and treatment of the
Underlying cause
Precipitating / aggravating factors

67

Initial management
Sit patient upright
Maintain oxygenation
5 to 6 liters/ minute
keep SaO2>95%
mechanical ventilation is indicated if hypercapnia co-exist or
oxygenation is inadequate
Non-invasive positive pressure ventilation (NIPPV) if patient alert &
coorperative

correct severe metabolic acidosis (pH<7.2) to prevent

negative inotropic and pro-arrhythmic effects
68

Insert IV cannula:
Frusemide
I.V frusemide 40 mg- 100 mg depend on the severity of the clinical
condition (renal function)

Nitrate
Morphine sulphate
I.V Morphine 2.5- 5 mg
Reduces pulmonary venous congestion and sympathetic drive

Further treatment based on systolic pressure:

SBP 100 mmHg

SBP 100 mmHg

Frusemide
Inotropes (dopamine,
dobutamine)
Vasodilators

Noradrenaline
Dopamine
Intubation and mechanical
ventilation
Correct acidosis
Invasive haemodynamic
monitoring
Intra-aortic balloon

69

70

Chronic Heart Failure Management

71

Non- Pharmacological

Low salt and low

fat diet

Ideal Body Weight

Smoking and
Alcohol Cessation

Exercise

72

Pharmacological
1. Diuretics

73

2. Vasodilators

74

3. Inotropic agents

75

4. Anticoagulants
Types: Warfarin / Heparin
Indications: atrial fibrillation, intracardiac thrombus
(except for organized mural thrombus), past
history of thromboembolic episode(s)
Side effects: bleeding

5. Antiarrhythmic agents
Type: Amiodarone
Side effects: Photosensitivity, hepatitis, lung
fibrosis

Device Therapy
Cardiac Resynchronisation Therapy (CRT)

77

 Implantable Cardioverter Defibrillator (ICD)

Combined Biventricular Pacing with ICD Capabilities

78

Parachute

79

80

Surgery
Revascularisation Procedures
PCI
Coronary artery bypass surgery
(CABG)

Valve surgery
LV Reduction Surgery
Patients with a large discrete LV
aneurysm

LV Assist Devices
For patients awaiting for heart
transplantation
81

82

Heart Transplantation
Treatment of refractory end stage HF but it
is limited by lack of donor organs

83