Ischemic Heart Disease

Dr. Nor Amzar Bin Md Noar

HKL
 OUTLINE
• Definition
• Pathophysiology
• Epidemiology
• Risk factors
• Differential diagnosis
• Investigations
• Diagnostic
• Management
• Case scenario
 DEFINITIONS
• Ischemic Heart Disease :  also called Coronary Heart Disease (CHD) or
Coronary Artery Disease (CAD), is the term given to heart problems
caused by narrowed coronary arteries that supply blood to the heart
muscle.

• Angina : chest pain / discomfort caused when the heart muscle doesn’t get
enough oxygen rich blood, typically induced by exertion / emotional stress.
 SPECTRUM OF IHD

Ischemic
Heart
Disease (IHD)

Acute Sudden
Stable coronary Cardiac
syndrome Death

Unstable
Stable Angina NSTEMI STEMI
angina
 PATHOPHYSIOLOGY
• For stable angina - myocardial ischemia that occur due to
imbalance between myocardial oxygen demand & supply, which is
transient & reversible .

• In acute MI – myocardial ischemia occur due to atherosclerotic

plaque rupture  thrombotic occlusion of coronary vessel  heart
muscle die / injured  MI
 EPIDEMIOLOGY
• In Malaysia, CVD has been the leading cause of morbidity and
mortality for more than a decade.
Health fact 2019 – the commonest cause of death in MoH hospital - disease of
circulatory system (22.27%), respiratory (21%) and infectious disease (12.4%).

• Data from the 2011-2013 registry indicated that Malaysians developed

ACS at a younger age than that seen in neighboring countries
Malaysia – mean age 58 (peak incidence 51-60)
Thai – 63years
Singapore 68 – 69 years

Source: world population review 2019

 CVD RISK FACTORS
Non Modifiable Risk Modifiable Risk Factors Targets of Individual Risk Factors
Factors Complete cessation
Smoking
Gender Min 30 mins / day, 5 days / week of moderate PA or
-Male (STEMI) Physical inactivity
15mins / day, 5 days / week of vigorous PA or
-Female (post menopausal) Combination of both
(NSTEMI , UA)
Very high risk – LDL <1.8mmol/L (or 50% from
Increase age Dyslipidemia baseline)
-female older – MI (63- High risk – LDL <2.6mmol/L (or 50% from baseline)
65y.o) UA (63y.o) Moderate & Low risk – LDL < 3.0mmol/L
-male –MI (55y.o) UA (59)
<140/90 mmHg in most individuals <80 yo
Family history - premature <150/90 mmHg in individuals >80 yo
CVD and sudden death Hypertension
-Male <55y.o FBS 4.4-7mmol/L
-Female <65y.o Post prandial (90-120mins) – 4.4-8.5mmol/L
Diabetes Melliatus HBA1C <6.5%
Past Hx of IHD BP <135/75 mmHg
LDL <2.6mmol/L or <1.8mmol/L in DM with CVD
Wt loss 5-10% in 6/12
Maintain wt in next 1-2 years, then further reduce
Overweight / obesity
 FRAMINGHAM SCORE
• The Framingham Risk Score (FRS) is a tool to assess future CV risk – in 10yrs
-patient age 30-79 years, with no prior hx IHD
 DIFFERENTIAL DIAGNOSIS

S –Retrosternal / Central / Left /Epigastric

O – Sudden / Gradual
C – Dull / Heavy / Burning / Pleuritic
R – Left arm/ Jaw / Back
A – Nausea / Vomiting/ Profuse sweating /
Palpitation / SOB / URTI / Fever / Water brash
sensation / Bloatedness
T – At rest / Exertion / Duration / Post Meal?
E – Relieving by GTN / rest /Meals / Position
S – Severity

Stable angina (definite angina)

-Atypical angina (probable) – if chest pain meets 2 out of the 3
-retrosternal chest discomfort with the following characteristics
and fulfilling these 3 criteria criteria.
I. predictable and with possible radiation to jaw, -Non angina – one or none of the criteria
shoulders, arms and/or back.
II. provoked by physical exertion and/or emotional stress.
III. relieved by rest and/or with glyceryl trinitrate (GTN)
 INVESTIGATIONS : STABLE CAD
Stable CAD

Blood iX – FBC RP LFT FBS or HBA1c FLP

ECG – Baseline / upon chest pain - ? Pathological Q wave, LBBB, ST –

T abnormality, LVH

Diagnostic test: Functional VS Anatomical

1) Functional – EST , DSE

2) Anatomical – calcium score, CTA / MSCT/ coronary angiogram

LVH strain pattern
 When to decide for further diagnostic test?
• Depends on pre test probability (PTP) – likelihood of CAD
• Most valuable when PTP of CAD is intermediate.
 Low PTP of <15% - no significant obstructive CAD
Intermediate PTP (15 – 85%) – further non invasive testing
High PTP (>85%) – assumed to have significant obstructive CAD, may consider
coronary angiography
 INVESTIGATIONS : ACUTE
Diagnosis of Myocardial infarction:
-rise and/or fall in cardiac toponin, with at least one
Value above the 99th percentile of URL, accompanied with
At least one of the following :
1) Clinical hx consistent with CP of ischemic origin
2) New ischemic ECG changes / dvlpmnt pathological Q wave
3) Imaging – new loss of viable myocardium / RWMA
4) Angiogram / autopsy

ACS
Vitals sign : BP/HR/SPO2/Temp
ECG – repeat 15 mins interval , look for evidence of
ischemia (STE / ST-T changes?TWI, Q wave/ arrhytmia)

Cardiac Enzymes
FBC RP LFT
CXR

ECHO
-reciprocal changes at anterior
-inferior MI
 Do posterior ECG
 ECG CHANGES IN ACS

1. ONSET of CP – normal SR, ST isoelectric line

2. An HOUR after onset – ST elevate thrombolysis
3. DAYS -T wave inversion (reperfusion). Reduction of ST
4. WEEKS – Deepening T wave. Returning ST to isoelectric
5. & 6 – MONTHS .Deep Q wave – indicate myocardial tissue death
– will remain in ECG
CARDIAC BIOMAKERS CHANGES IN ACS
 DIAGNOSTIC TEST : FUNCTIONAL VS ANATOMICAL

Functional Anatomical

Exercise stress ECG (EST) – 1st line strategy - Coronary calcium score - more to risk stratification
than in the dx

Stress test + imaging in detection of myocardial Computed Tomography angiography (CTA) – visualize
ischemia and diagnosis of CAD coronary artery non invasively/ extent of coronary
Eg : stress –treadmill/pharmaco (dobutamin) calcification / degree of luminal stenosis
-MSCT

Invasive Coronary angiography – gold standard for

diagnosis CAD
 MANAGEMENT:
1. ACUTE MANAGEMENT
2. CHRONIC /STABLE CAD MANAGEMENT
MANAGEMENT : ACUTE
 MANAGEMENT : CHRONIC / STABLE CAD
Tx goals in stable CAD
1. Alleviate symptoms and improve QOL
2. Reduce risk of adverse CV outcomes and improve survival
3. Prevent progression of atherosclerotic disease
Behaviour modification tx (BMT) Pharmacological
Education – factor that provoke angina , urgent med attention, A. Prevent of future CV events
adhere to meds, Antiplatlet – aspirin, Plavic
-DAPT for 12 months
Diet –Mediterranean diet (reduce CV risk), DASH – reduce HTN Aim LDL < 1.8mmol/L – less progression of atherosclerotic
plaque
-statin , ezetimibe
Physical activity – at least 150 mins / week of moderate RAAS blocker – ACEi / ARB /MRA
intensity, or 75mins/week vigorous activity
Smoking cessation – important cause of plaque rupture that Depressed LVEF < 40% - ACEi/ ARB, B Blocker, MRA, ARNI
lead to ACS
Weight Mx – modest weight loss 5-10% - can reduce BP, B. Mx of ssx – Anti ischemic tx
improve glycemic control and QOL -decrease myocardial o2 consumption – lower HR, BP, cardiac
-goal – 5 – 10% weight loss, and to maintain over a period of 1 contractility OR increase myocardial o2 supply (increase
– 2 years b4 attempting further weight loss coronary blood flow)
B blocker, CCB, Ivabradine, Nitrates, vasteral
 CASE 1
En M, 37 yo, Malay, Male Brought to ED by his friends
Active smoker 15 pack years Arrived ED at 12am
No FHx of IHD Upon ED arrival, pt was alert conscious, GCS full,
Works as a Lorry driver however still in pain
Prev NKMI / NKDA Pink, cold peripheries, weak pulse vol,
BMI: 27.7 kg/m2 (WT : 80 kg, HT : 170cm)
BP 86/44
P/w HR 30 – 35
-sudden onset Left sided chest pain at 1130pm while SPO2 96% under RA
eating Temp 37
-sudden onset
-pain radiating to left UL, p/s 8, lasted more than 30 DXT 7
mins Lungs – clear
-A/w SOB, profuse sweating, nausea CVS DRNM
-no fever / urti ssx
Blood IX Pending

Given fluid resus, BP not responding ,started on Ivi

norad
T Aspirin 300mg , T Palvix 300mg
 Posterior ECG

ECG x1

Right sided ECG

Given IV Metalyse 8000U

Followed with Ivi Heparin 5000u stat and 1000u/hr

ECG x2
O minit 60 minit

30 minit
Subsequently p/s reduce from 10 2
RP/ LFT/ FBC normal
CXR : clear, no cardiomegaly, no overload features

IMP : Acute Inferior posterior MI Killip 4 with resolved CHB, successfully thrombolysis

Plan
1. Admit CCU
2. Cont Ivi Heparin
3. IVD 3 pint NS/24 Hr
4. Strict I/O charting
5. Taper down Ivi norad
6. For pharmacoinvasive cm
Pharmacoinvasive finding : 2VD,PCI to RCA
(Drug Eluting Stent (DES))
• LM : normal
• LAD : mid 30 – 40%
• LCX : proximal mild disease
• RCA : dominant, Prox 80%, Mid 30%,
Distal normal

Done PCI to RCA with DES

 LAD

LCX
RCA
-prox 80%
-mid 30%
-distal normal
RCA
RCA-
Stented
with DES
BLOOD IX

• TC : 5.24
• HDL: 1.14
• LDL: 3.54
• FBS: 5.5
• TG : 1.2
ECG PRIOR TO DISCHAGRE
 PROGRESS IN CCU
ECHO – EF 50 – 55%, good LV contractility, hypokinesia at Inferiorseptal wall
Patient was discharge at day 3 of admission
Diagnosis:
1. Acute Inferior posterior MI Killip 4
2. 2VD successful PCI to RCA
3. Dyslipidemia

PLAN:
4. DAPT 1 year
5. T.Peridopril 2mg OD , T. Atorvastatin 40mg ON
6. TCA cardio 3/12 – for CV risk optimization
• Aim: BP: < 140/90 mmHg. 
• Lipids: LDL-C < 1.8 mmol/L
7. Non-pharmacological mx
• Smoking cessation –quit smoking clinic
• Aim wt 72kg (5 – 10% wt loss in 6/12)
• Refer dietitian
HYPERLIPIDEMIA
 ROLE IN PRIMARY
CARE
- Early screening in DM/HTN (30 years old), early
diagnosis  early treatment
> reduce CVD risk
- Routine annual assessment- annual ECG
in DM/HTN
- Optimisation risk factor in primary care
- Offer quit smoking clinic
- Offer obesity clinic
- Dietician for healthy diet
 REFERENCE
CPG: Stable Coronary Artery Disease 2018
CPG: Primary and Secondary Prevention of Cardiovascular Disease 2017
CPG: Management of Acute ST segment Myocardial Infarction (4th
Edition)
Oxford Handbook of Clinical Medicine 8th Edition
Health Facts 2020 – reference data for year 2019