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Ischemic

Heart
Disease
(IHD)

Definition
(Davidson's Essentials of Medicine 2e)
Ischemic heart disease is also known as coronary artery disease
Disease of the coronary arteries is almost always due to
atherosclerosis and its complications, particularly thrombosis.
(Goldman Cecil's Medicine 25e 2016)
Ischemic heart disease is most commonly caused by
obstruction or stenosis of one or more of the epicardial
coronary arteries by atheromatous plaque.
Obstruction can result in myocardial ischemia and may
culminate in infarction with associated symptoms of angina,
dyspnea, heart failure arrhythmic complications ,and ultimately
death.

CORONARY ARTERY DISEASE


Stable Angina
Acute Coronary Syndrome (UA, STEMI, NSTEMI)
Heart Failure
Cardiac Arrhythmias
Sudden Cardiac Death

Acute Coronary Syndrome


ACS is a term that encompasses both unstable angina
and myocardial infarction.
May present as new phenomenon or worsening/ chronic
stable angina

Predisposing factors/Risk factors


(Davidson's priciples and practice of Medicine 22e)

Age and sex:


Age is the most powerful independent risk factor for
atherosclerosis. Pre-menopausal women have lower rates of
disease than men but thereafter risk is similar. Elder people
have higher chance of developing CAD.

Family history:
A positive family history is present when clinical problems
occur in first-degree relatives aged < 50 yrs (male) or < 55 yrs
(female). Increased risk reflects a combination of shared
genetic and environmental (e.g. smoking, exercise, diet)
factors.

Hypertension:
The incidence of atherosclerosis increases as BP
(systolic and diastolic) rises. Antihypertensive therapy
reduces cardiovascular mortality and stroke

Hypercholesterolaemia:
Risk rises with plasma cholesterol concentration.
Lowering low-density lipoprotein (LDL) and total
cholesterol reduces the risk of cardiovascular events
(death, MI, stroke).

Diabetes mellitus:
This is a potent risk factor for all forms of
atherosclerosis and is often associated with diffuse
disease. Insulin resistance (normal glucose homeostasis
with high levels of insulin) is also a risk factor for CAD.

Lifestyle factors:
There is a strong, dose-linked relationship between
cigarette smoking and CAD.
Alcohol is associated with reduced rates of coronary
disease, but alcohol excess is associated with
hypertension and cerebrovascular disease.
Physical inactivity and obesity are independent risk
factors for atherosclerosis; regular exercise appears to
have a protective effect.
Diets deficient in fresh fruit, vegetables and
polyunsaturated fatty acids are associated with an
increased risk of vascular disease.

Risk Factors
Modifiable
Dyslipidemia
Raised LDL
Low HDL
Raised TGs
Smoking
Hypertension
Haemostatic factors
Diabetes mellitus
Obesity
Dietary factors
Sedentary lifestyle

Non-modifiable
Family history
Age
Sex

Coronary Artery Disease


Clinical Problem
Stable Angina
Unstable Angina

Myocardial Infarction

Heart Failure
Arrhythmia
Sudden death

Pathology
Fixed artheromatous stenosis of one or more
coronary arteries Ischaemia
Plaque rupture or erosion with superimposed
thrombosis Dynamic obstruction of a coronary
artery Ischaemia
Plaque rupture / erosion with superimposed
thrombosis acute occlusion of a coronary artery
Myocardial necrosis
Infarction / Ischaemia Myocardial dysfunction
Ischaemia / Infarction Altered conduction
Ventricular arrhythmia, asystole or massive
myocardial infarction

Pathogenesis

Ischaemic Heart Disease


a consequence of reduced blood flow in
coronary arteries, due to a combination of fixed
vessel narrowing and abnormal vascular
tone as a result of atherosclerosis and
endothelial dysfunction.
Imbalance between supply and demand

Ischaemia of myocardial tissue

Atherosclerotic Process
Response to Injury Hypothesis
Inflammatory response proliferation of tissue
within the arterial wall obstruction of blood flow
Causes:
1. Elevated levels of cholesterol and
triglyceride in the blood
2. High blood pressure turbulent blood flow
3. Tobacco smoke
4. Glycosylated substances

Response to Injury Hypothesis


1. Injury to endothelium causing to platelets adhere to

endothelium then release of growth factors


2. Monocytes attach to endothelium and penetrate

(also LDL receptor activation) monocytes become


macrophages and take up LDL and SMCs
3. Smooth muscle cell proliferation and migrate from

medial to intimal layer


4. Foam cells are formed - migration to the intima

smooth muscles with lipids form fatty streaks


5. Fibromuscular plaque fibromuscular layer with

cholesterol core

Non-atherosclerotic Causes of Ischemia


1. Decreased coronary perfusion pressure due to hypotension
(hypovolemia, septic shock)
2. Decreased blood oxygen content (marked anemia, pulmonary
disease)
3. Significant increase in myocardial oxygen demand (e.g. rapid
tachycardias, acute hypertension, severe aortic stenosis)
4. Coronary emboli from endocarditis or artificial heart valves
5. Inflammation of the coronary arteries from vasculitic syndromes
6. Severe transient coronary spasm, either primary/ induced by
cocaine abuse
7. Congenital abnormalities, trauma or aneurysm of the coronary
arteries

Clinical features

Ischemic Heart Disease : Clinical


Manifestations
a) Stable angina
b) Unstable angina
Acute Coronary
Syndrome
c) Myocardical infarction

Stable Angina
-Pathology: Ischaemia due to fixed atheromatous
stenosis of one or more coronory
arteries
-Symptoms: Central chest pain/discomfort
Breathlessness
-Precipitated by physical exertion, heavy meals, cold
exposure and intense emotion

Signs: -Unremarkable; otherwise should include a careful


search for evidence of valve disease.
-Risk factors: Diabetes mellitus and hypertension
-Gallop rhythm and cardiomegaly indicating left
ventricular dysfunction
-Other manifestations: Carotid bruits, peripheral vascular disease, or
due to anaemia, tyrotoxicosis

Risk Stratification in Stable Angina


HIGH RISK

LOW RISK

Post-infarct angina

Predictable exertional angina

Poor effort tolerance

Good effort tolerance

Ischaemia at low workload

Ischaemia only at high workload

Left main or three-vessel disease

Single-vessel or two-vessel disease

Poor LV function

Good LV function

Canadian Cardiovascular Society: Functional


Classification of Stable Angina
Grade 1 No angina with ordinary activity such as walking or
climbing stairs. Occurs only with strenuous or rapid and
prolonged activity
Grade 2 - Slight limitation of ordinary activities, eg. Walking
uphill, walking rapidly upstairs, in cold, in wind
Grade 3 Marked restriction of ordinary physical activities,
angina with low levels of activity, eg: walking up 1 flight of
stairs, walking 1-2 blocks on the level
Grade 4 Angina at rest or any level of exercise

Acute Coronary Syndrome


Unstable angina: Ischaemia caused by dynamic
obstruction of a coronary
artery due to plaque rupture
or erosion with superimposed
thrombosis

Myocardial infarction: Myocardial necrosis


caused by acute occlusion
of a coronary artery due to
plaque rupture or erosion
with superimposed
thrombosis.

Symptoms: - Chest pain which may travel to


the right shoulder, arm, back, neck,
or jaw.
-Anxiety and fear of impending
death (angor animi)
-Nausea and vomiting.
-Breathlessness
- Collapse/syncope.

Signs: - Pallor, sweating, tachycardia (Sympathetic


activation)
-Vomiting, bradycardia (Vagal activation)
-Hypotension, oliguria, cold peripheries
-Narrow pulse pressure, raised JVP
-Quiet first heart sound is auscultated
-Third heart sound is present
-Diffuse apical impulse
-Lung crepitations

Risk Stratification in the Acute Coronary Syndrome: The GRACE Score

Investigations

1. ECG in STEMI
ECG is central to conforming the
diagnosis
The presence of ST elevation in two contiguous leads in
patients with symptoms of ischaemia is the cardinal feature of
STEMI.
Earliest ECG change is usually ST-segment deviation.
With proximal occlusion of a major coronary artery, STsegment elevation is seen initially.
With later diminution in the size of the R wave
In transmural (full-thickness) infarction, development of a Q
wave.
Subsequently, the T wave becomes inverted because of a
change in ventricular repolarisation
This change persists after the ST segment has returned to
normal.

ECG changes in transmural MI

A. Normal ECG complex


B. Acute ST elevation ( the current of injury) (appears
within minutes )
C. Progressive loss of the R wave , developing Q wave ,
resolution of the ST elevation and terminal T-wave
inversion (appears within hours)
D. Deep Q wave and T wave inversion(appears within
days )
E. Old or established infarct pattern : the Q wave tends
to persist but the T-wave changes become less
marked .(appears after several weeks or months )

ECG in Non-STEMI/UA
In non-ST segment elevation acute coronary
syndrome, there is partial occlusion of a major
vessel or complete occlusion of a minor
vessel, causing unstable angina or partialthickness (subendocardial) MI.
Features suggestive of UA/NSTEMI are:
Dynamic ST/T changes
ST depression > 0.5 mm in 2 or more contiguous
leads
T-wave inversion deep symmetrical T-wave
inversion
However, a completely normal ECG does not
exclude the diagnosis of UA/NSTEMI. Serial ECGs
should be done as the ST changes may evolve.

ECG In Stable Angina


A full 12-lead ECG may show some ischaemic changes
but a normal ECG does not rule out a diagnosis of angina.
Changes on a resting 12-lead ECG that shows CAD
include:
Pathological Q waves.
ST-segment and T-wave abnormalities (eg, flattening or
inversion).

2. Cardiac
Biomarkers
Creatine Kinase
30-200 U/L
Aspartate
Transaminase
Lactate
Dehydrogenase
Troponin I
Troponin T

5-34 U/L
125-243 U/L
<10 g/L.
00.1 g/L.

1. In unstable angina there is no detectable


rise in cardiac biomarkers or enzymes
2. In myocardial infarction there is a rise in
the plasma concentration of enzymes and
protein that are normally concentrated
within cardiac cell .

Changes in plasma cardiac biomarkers


concentrations after MI

1. Creatine kinase (CK) and troponin I (Tn1)


are the first to rise.
2. CK starts to rise at 46 hours, peaks at
about 12 hours and falls to normal within
4872 hours.
3. Cardiac troponins T and I, which are
released within 46 hours and remain
elevated for up to 2 weeks
4. Followed by aspartate aminotransferase
(AST) and lactate dehydrogenase (LDH)
5. In patient treated with reperfusion
therapy , a rapid rise in plasma creatine
kinase (curve CK (R) occurs due to a
washout effect.

The troponin level may not be elevated if the test is


done early (<6 hours). To confidently exclude
myocardial necrosis (infarction), a repeat test needs
to be done 612 hours after admission.
The absence of ST elevation on the resting ECG
and elevated troponin levels indicates NSTEMI.
CK and CKMB have a shorter half life and hence
are more useful than troponins when diagnosing
reinfarction.

3. Chest X- Ray
Usually the heart size is normal but there
may be cardiomegaly due to pre-existing
myocardial damage
4.Echocardiography
To assess ventricular function and for
detecting important complications of MI
such as mural thrombus , cardiac rupture ,
ventricular septal defect , mitral
regurgitation.

5.Other Tests available


1. Full blood count - leucocytosis is usually at peak on
the first day
2. Erythrocyte sedimentation rate elevated
3. Urine and electrolytes Renal Function
4. Lipid Profile Hyperlipidaemia

MANAGEMENT

Stable angina : Treatment


GOALS :
Prevents MI and death
Minimize symptoms and improve QOL

Stable angina : Treatment


1. Lifestyle modification
- Smoking cessation : Nicotine gum / patch /
Varenicline tartrate
- Dietary control : healthy diet ; ideal BMI ; ideal waist
circumference
- Alcohol restriction
- Physical activity : 30min 3-4 times per week

Stable angina : Treatment


2. Well control of underlying comorbidities
- HTN : BP <130 /80 mmHg
- DM : HbA1c < 6.5%
- Hypercholesterolemia :
LDL < 2.6mmol/l
HDL >1 mmol /l (male) ; > 1.2 mmol /l (female)
TAG <1.7 mmol /l

Stable angina : Treatment


3. Acute symptoms :
- Advice to rest
- Sublingual / buccal GTN adr
- Seek for medical attention if symptoms persist >10min
after resting and/or is not relieved by 3 GTN

Stable angina : Treatment


4. Long term management
- Low dose aspirin : 75 150 mg OD

Alternative : clopidogrel 75mg OD ; Ticlopidine 250mg BD adr


- Beta blocker : Bisoprolol , Carvedilol , Metoprolol

Alternative : non-dihydropyridine CCB ; LA-nitrates


- Calcium channel blocker : Amlopidine ; Nifedipine ; Verapamil
; Diltiazam

+ ACEIs if pts having LVEF <40% , DM , HTN, CKD Alternative :


ARB

Stable angina : Treatment


5. Myocardial revascularization
- Percutaneous coronary intervention (PCI)
- Coronary artery bypass grafting (CABGs)

ACS - Management
Is this ACS ?
UA / NSTEMI or STEMI ?
Risk stratification
If STEMI , how long is onset and is revascularization
facilities available ?

ACS Initial management


Aspirin 300 mg crushed stat ( regular > enteric coated for faster onset of
action)
Sublingual GTN
Do 12 lead ECG and cardiac biomarkers
Suggestive clopidogrel 300 mg 600 mg stat
Inconclusive risk stratification

Set up IV access
O2 therapy SpO2 > 95%
Pain relief : IV morphine 3-5mg slowly
IV antiemetic : metoclopramide 10mg or Promethazine 25mg 8hrly
Referral to nearest healthcare facilities

Risk stratification UA / NSTEMI

ACS management
1. Antiplatelet :
Oral
Aspirin maintenance 75-150 mg daily
ADP receptor antagonist
+ Clopidogrel maintainence 75 mg/day OR
Ticlopidine 250 mg BD
Ticagrelor loading 180 mg, maintenance 90mg BD ----better efficacy than clopidogrel + short acting not
increasing bleeding for pts planning for PCI ADR SOB,
transient ventricular pause

IV --- high risk pts awaiting to PCI facility


GP IIb/IIIa inhibitor
Abciximab
Tirofiban

2. Anti-coagulant
UFH 60 IU/kg followed by 12IU/kg/hr adjusted to maintain
aPTT 1.5-2 times normal for 2-8 days
LMWH enoxaparin 30mg IV bolus sc 1mg/kg/12 hour
for 2-8days
Anti Xa-inhibitor fondaparinux 2.5 mg sc daily for 8days
or duration of hospitalization

3. Anti-ischemic
Nitrates
-blocker CI : 1st degree AV block >0.24s or 2nd-3rd AV block ;
AEBA ; severe peripheral arterial disease ; cardiogenic shock
CCB for those CI to (b)

4. Revascularization strategies PCI


IND :
Urgent : ST deviation, heart failure, life threatening
arrhythmias and /or hemodynamic instability
Early (<72hrs) : high risk group according TIMI scale or
equivalent

Management of STEMI

STEMI : Risk stratification

Reperfusion strategies [STEMI]


Time lost = Myocardium lost
2 methods :
i. Primary PCI >>
ii. Fibrinolytic

[DBT : 90min]
[DNT : 30min]

Which to choose ?
Early presentation (<3hr) : equally effective
Late presentation (3-12hr) : Primary PCI better
Very late (>12 hrs) : not recommended if asymptomatic and
hemodynamically stable.

Fibrinolytic
When given within 2hr from time of onset, reduce
motality up to 50%
DOC :
Streptokinase : 1.5 mega unit in 100 ml normal saline or 5%
DXT over 1 hr
Tenecteplase (TNT-tPA) weight regime

Fibrinolytic Contraindication
Absolute
Risk of ICH ---- history o ICH , history of ischemic
stroke within 3months ; AV malformation ; intracranial
neoplasm
Risk of bleeding --- active bleeding , head trauma
within 3months ; suspecting aortic aneurysm

Relative
ICH : severe HTN >180/110 , ischemic stroke more than
3months
Bleeding --- anticoagulant , major surgery <3wks,
prolonged CPR>10min, recent internal bleed within 4
wks, active peptic ulcer
Pregnancy
Prior exposure to streptokinase ( >5 days and within
12months of first usage)

Primary PCI
Ischemic symptoms <12hrs
IND :
- Fibrinolytic is contraindicated or failed
- Cardiogenic shock
- Association with acute HF

Take home
Stable angina= symptomatic/prophylatic management
+ Antiplatelet
UA / NSTEMI = above + anticoagulant +- PCI
STEMI = above + reperfusion strategies