Ischaemic heart disease is a condition in which inadequate blood supply to the myocardium, usually due to coronary artery atherosclerosis, results in myocardial ischaemia or infarction.

Exam domain	One-glance essentials
Definition / diagnosis	Myocardial ischaemia from insufficient coronary blood flow, usually atherosclerotic ^[1] Chronic coronary syndrome and acute coronary syndrome form a continuum ^[1]
Epidemiology / risks	Smoking, diabetes, hypertension and dyslipidaemia are major modifiable risks ^[1] Age, male sex and family history are non-modifiable risks ^[1]
Core mechanism	Plaque narrows arteries or ruptures with thrombosis ^[1] Demand-supply mismatch can cause ischaemia without acute plaque rupture ^[1]
Clinical picture	Pressure-like exertional chest pain radiating to arm/jaw with dyspnoea or diaphoresis ^[1] Women, older adults and diabetes may present atypically ^[1]
Investigations	Suspected ACS needs serial ECGs and high-sensitivity troponin ^[2] Stable disease uses risk-based coronary CT angiography or functional testing ^[2]
Management	ACS: antithrombotic therapy and timely reperfusion/revascularisation ^[3] Chronic disease: lifestyle, statin, antiplatelet when indicated and antianginal therapy ^[3]
Complications	Arrhythmia, heart failure, mechanical complications and sudden death ^[4] Recurrent infarction and bleeding from therapy require surveillance ^[4]
Prevention / follow-up	Stop smoking and control lipids, pressure, glucose, weight and activity ^[3] Cardiac rehabilitation and adherence reduce recurrent events ^[3]
Exam traps	*A normal initial ECG or troponin does not exclude ACS* ^[2] Give nitrates cautiously when hypotension, RV infarction or PDE5-inhibitor use is possible ^[3]

References

^[1] Senior notes: Maksim Medicine Notes.pdf (Section 1.3, Ischaemic Heart Disease, p.7)

^[2] Senior notes: Maksim Medicine Notes.pdf (Section 1.3, Ischaemic Heart Disease, p.7)

^[3] Senior notes: Maksim Medicine Notes.pdf (Sections 1.3, Stable Angina, ACS management, PCI, CABG, pp.7–13)

^[4] Senior notes: Maksim Medicine Notes.pdf (Sections 1.3, Complications of MI, PCI, CABG, pp.10–14)

Ischaemic Heart Disease (IHD)

Ischaemic heart disease (IHD) — also known as coronary artery disease (CAD) or coronary heart disease (CHD) — refers to the condition in which there is an imbalance between myocardial oxygen supply and demand, resulting in myocardial ischaemia and, if prolonged, myocardial necrosis (infarction) ^[1]^[2].

Breaking down the name:

"Ischaemic" → from Greek ischein (to hold back) + haima (blood) = restriction of blood supply
"Heart disease" → disease affecting the heart muscle

The overwhelming majority of cases are caused by coronary atherosclerosis — the progressive build-up of lipid-rich plaques within the coronary arteries that narrows the lumen and restricts blood flow to the myocardium ^[1]^[2].

IHD exists on a clinical spectrum:

Clinical Entity	Definition
Stable angina	Predictable chest pain on exertion, relieved by rest — caused by a fixed coronary stenosis ^[1]^[2]
Acute coronary syndrome (ACS)	Unstable angina, NSTEMI, or STEMI — caused by dynamic obstruction (usually plaque rupture + thrombus formation) ^[1]^[2]
Ischaemic cardiomyopathy	Chronic LV dysfunction secondary to prior MI or chronic ischaemia
Sudden cardiac death	Cardiac arrest from ischaemia-induced arrhythmia (VF/VT) ^[3]

Why is this distinction important? Stable angina implies a fixed stenosis where ischaemia only occurs when demand exceeds the limited supply (e.g. exercise). ACS implies an acute coronary event — often plaque rupture with superimposed thrombus — where ischaemia occurs even at rest, and there is imminent risk of myocardial necrosis ^[1]^[2].

Epidemiology

IHD is the leading cause of death worldwide, responsible for approximately 9 million deaths annually (WHO 2024).
It accounts for roughly 16% of all global deaths.
The burden is disproportionately high in low- and middle-income countries, where access to preventive care and acute revascularisation is limited.

IHD is consistently among the top 3 causes of death in Hong Kong (after cancer and pneumonia).
In 2023, diseases of the heart accounted for approximately 6,000+ deaths annually in Hong Kong (Centre for Health Protection data).
Hong Kong has a high prevalence of metabolic risk factors: diabetes mellitus prevalence ~10%, hypertension ~27%, dyslipidaemia, and increasing obesity rates, all of which drive CAD incidence.
Importantly, the Chinese population has certain epidemiological differences:
- Higher prevalence of single-vessel disease compared to multi-vessel disease relative to Western populations
- Possibly higher proportion of non-obstructive CAD and microvascular disease
- Historically lower rates than Western countries, but the gap has been narrowing with Westernisation of diet and sedentary lifestyles
- Atherosclerosis is a systemic disease ^[5] — patients with CAD in Hong Kong often have concurrent cerebrovascular or peripheral arterial disease

Risk rises sharply with age: men ≥ 45 years, women ≥ 55 years ^[4]
Pre-menopausal women are relatively protected (oestrogen has vasoprotective and lipid-modulating effects), but this advantage disappears post-menopause
Male-to-female ratio is approximately 2:1 before age 65, equalising thereafter

Risk Factors

Risk factors for IHD are essentially the risk factors for atherosclerosis — because coronary atherosclerosis is the underlying pathology in > 95% of cases ^[1]^[2]^[5].

Risk Factor	Explanation
Advanced age	Cumulative endothelial damage and plaque progression over decades. Atherosclerosis begins in childhood (fatty streaks) but becomes clinically significant in middle age ^[4]
Male sex	Oestrogen in pre-menopausal women promotes NO production (vasodilation), favourable lipid profile (↑HDL, ↓LDL), and reduces inflammatory markers. Loss of oestrogen at menopause → rapid rise in CVD risk
Family history of premature CAD	First-degree relative with CHD at < 55 years (male) or < 65 years (female) ^[4]. Suggests shared genetic susceptibility (e.g. familial hypercholesterolaemia, inherited propensity for endothelial dysfunction) + shared environmental exposures
Previous vascular event	Prior MI, stroke, or PVD indicates established systemic atherosclerosis ^[6]

Risk Factor	Pathophysiological Link to IHD
Smoking ^[5]	Endothelial injury by oxidative free radicals → ↑adhesion molecule expression → inflammatory cell recruitment. Also promotes thrombosis (↑fibrinogen, ↑platelet reactivity, ↓fibrinolysis), causes coronary vasospasm, and ↓HDL. Dose-dependent and partially reversible with cessation
Hypertension ^[5]	Mechanical shear stress damages endothelium → accelerated atherosclerosis. ↑Afterload → ↑myocardial O₂ demand. LVH → ↓coronary reserve. Target in stable CAD: < 140/90 mmHg ^[2]
Diabetes mellitus ^[5]	Multiple mechanisms: advanced glycation end-products (AGEs) damage endothelium, insulin resistance promotes dyslipidaemia (↑TG, ↓HDL, small dense LDL), pro-thrombotic state, pro-inflammatory state. DM is a coronary heart disease risk equivalent ^[4] — meaning a diabetic patient without known CAD has the same 10-year event risk as a non-diabetic patient with established CAD
Hyperlipidaemia ^[5]	↑LDL-C is the key driver. LDL enters the intima → oxidised → taken up by macrophages → foam cells → fatty streak → atherosclerotic plaque. ↓HDL is also an independent risk factor (HDL mediates reverse cholesterol transport). Target LDL-C in established CAD: < 1.4 mmol/L (ESC 2019/2021 guidelines) ^[4]
Obesity (especially abdominal/central)	Visceral adipocytes release excess free fatty acids → insulin resistance → metabolic syndrome. Also release pro-inflammatory adipokines (e.g. TNF-α, IL-6) → chronic low-grade inflammation → endothelial dysfunction ^[7]
Physical inactivity	↓AMPK activation → ↓glucose uptake, ↓fatty acid metabolism → contributes to obesity, insulin resistance, and dyslipidaemia ^[7]
Unhealthy diet	High saturated fat, trans fat, refined carbohydrate intake → dyslipidaemia and obesity. Low fruit/vegetable intake → ↓antioxidant protection

Metabolic Syndrome

Metabolic syndrome is a cluster of metabolic abnormalities driven primarily by central obesity and insulin resistance: hypertension, dyslipidaemia (↑TG, ↓HDL), hyperglycaemia, and central obesity ^[7]. These synergistically accelerate atherosclerosis. The concept is clinically useful because it identifies patients at multiplicatively higher risk who need aggressive multifactorial risk factor management.

Factor	Mechanism
Chronic kidney disease (CKD)	Independent CVD risk factor: ↑prevalence of traditional risk factors + medial vascular calcification (↑PO₄, ↑Ca balance) + uraemia-driven chronic inflammation → accelerated atherosclerosis ^[8]
Psychological stress / Depression	Chronic sympathetic activation → ↑HR, ↑BP, ↑cortisol → endothelial dysfunction, pro-thrombotic state
Obstructive sleep apnoea	Intermittent hypoxia → oxidative stress, sympathetic surges, endothelial dysfunction
Autoimmune/inflammatory diseases	RA, SLE — chronic systemic inflammation accelerates atherosclerosis
Cocaine use	Direct coronary vasospasm + accelerated atherosclerosis + pro-thrombotic
Oral contraceptive pills / HRT	↑thrombotic risk (especially when combined with smoking) ^[6]
Raised homocysteine	Endothelial toxicity, pro-thrombotic ^[6]
Polycythaemia	↑blood viscosity → ↓flow → ischaemia ^[6]

Formal risk assessment is critical to guide preventive therapy (especially lipid-lowering) ^[4]:

Indication: ≥ 40 years with ≥ 1 ASCVD risk factor (HK Consensus 2016) ^[4]
Not needed if patient already has overt ASCVD, DM, or ≥ 1 major risk factor (e.g. severe hypertension, severely elevated lipids) — these automatically meet treatment thresholds ^[4]
Tools available:
- Chinese Multiprovincial Cohort Study (CMCS) — validated for Chinese populations
- Framingham Risk Score
- ACC/AHA ASCVD Risk Calculator (Pooled Cohort Equations)
- SCORE/SCORE2 risk charts (ESC)
- JBS3 Risk Calculator ^[4]

The purpose of risk assessment is to determine whether a patient crosses the treatment threshold for lipid-lowering (statin) therapy and to set LDL-C targets. The higher the risk category, the more aggressive the LDL-C goal.

Anatomy of the Coronary Arteries

Understanding coronary artery anatomy is essential for correlating ECG changes, wall motion abnormalities, and clinical syndromes with the culprit vessel.

The left and right coronary arteries arise from the aortic root (from the left and right coronary sinuses of Valsalva, respectively), just above the aortic valve leaflets. They receive blood during diastole — this is critical because:

During systole, the contracting myocardium compresses intramural vessels → flow is impeded
Therefore, coronary perfusion is predominantly diastolic
Anything that ↓diastolic pressure (e.g. aortic regurgitation) or ↓diastolic time (e.g. tachycardia) will ↓coronary perfusion

The left main coronary artery (LMCA) is a short trunk (typically 1–2 cm) that bifurcates into:

Left anterior descending artery (LAD) — the "widow-maker"
- Runs in the anterior interventricular groove
- Gives off septal perforators (supply the anterior 2/3 of interventricular septum, including the bundle of His) and diagonal branches (supply anterolateral LV wall)
- Supplies: anterior wall of LV, anterior 2/3 of interventricular septum, apex ^[1]
- Clinical significance: LAD occlusion causes anterior STEMI — the most dangerous territory because it involves the largest area of myocardium. Leads V1-V4 (± V5-V6) on ECG
Left circumflex artery (LCx)
- Runs in the left atrioventricular groove
- Gives off obtuse marginal branches (supply lateral LV wall)
- Supplies: lateral and posterior wall of LV (depending on dominance) ^[1]
- Clinical significance: LCx occlusion causes lateral STEMI (leads I, aVL, V5-V6) or posterior MI. Can be electrocardiographically "silent" because standard leads do not face the posterior wall directly

Runs in the right atrioventricular groove
Gives off the posterior descending artery (PDA) in ~85% of people (= right-dominant circulation)
Also gives off the SA node artery (in 60%) and AV node artery (in 80%)
Supplies: right ventricle, inferior wall of LV, posterior 1/3 of interventricular septum, SA node (60%), AV node (80%) ^[1]
Clinical significance: RCA occlusion causes inferior STEMI (leads II, III, aVF) and may be associated with:
- Bradycardia / AV block (AV node ischaemia)
- Right ventricular infarction (hypotension, raised JVP, clear lungs — avoid nitrates and diuretics!)

Type	Definition	Prevalence
Right dominant	RCA gives off PDA	~85%
Left dominant	LCx gives off PDA	~8%
Co-dominant	Both contribute to PDA	~7%

Dominance determines who supplies the inferior wall and posterior septum. In a right-dominant system, RCA occlusion threatens the AV node.

Coronary Artery	Territory Supplied	ECG Leads	Wall Motion on Echo
LAD	Anterior LV wall, apex, anterior 2/3 septum	V1–V4 (± V5–V6)	Anterior, anteroseptal, apical
LCx	Lateral LV wall, ± posterior	I, aVL, V5–V6	Lateral, posterolateral
RCA	Inferior LV wall, RV, posterior 1/3 septum, conducting system	II, III, aVF	Inferior, RV

Why Does LAD Occlusion Cause the Worst MIs?

The LAD supplies the largest territory of the left ventricle — the entire anterior wall, the apex, and much of the septum. Occlusion here causes the greatest area of myocardial necrosis, the most severe LV dysfunction, and carries the highest mortality among all STEMIs. Hence its colloquial name: the "widow-maker".

Aetiology

This is overwhelmingly the dominant cause. The pathology is discussed in detail below.

These are less common but must not be missed, especially in younger patients without traditional risk factors:

Category	Examples	Mechanism
Vasospasm	Prinzmetal's (variant) angina, cocaine abuse ^[1]	Intense focal coronary artery spasm → transient transmural ischaemia. Prinzmetal's = spontaneous spasm, often at night, with transient ST elevation. Cocaine → sympathomimetic + direct smooth muscle contraction
Vasculitis	Takayasu arteritis, polyarteritis nodosa (PAN), Kawasaki disease, eosinophilic granulomatosis with polyangiitis (eGPA) ^[1]	Inflammation of coronary artery wall → stenosis, occlusion, or aneurysm formation. Kawasaki disease is the most important cause of acquired heart disease in children in developed countries — coronary artery aneurysms can thrombose or rupture
Embolism	Septic emboli (infective endocarditis), atrial myxoma, paradoxical embolism (PFO)	Embolic material lodges in coronary artery → acute occlusion
Dissection	Spontaneous coronary artery dissection (SCAD), retrograde extension of aortic dissection ^[1]	Intimal tear → blood tracks in arterial wall → false lumen compresses true lumen → ischaemia. SCAD is an important cause of MI in young women, especially peri-partum
Congenital anomalies	Anomalous origin (e.g. left coronary from pulmonary artery — ALCAPA), myocardial bridging	Abnormal anatomy → malperfusion or dynamic compression during systole
Microvascular disease	Cardiac syndrome X (microvascular angina)	Small vessel dysfunction → ischaemia despite angiographically normal epicardial coronary arteries. More common in women, diabetics
Others	Radiation-induced coronary artery disease, amyloidosis, hypercoagulable states	Various mechanisms of coronary compromise

Pathophysiology

A. Pathology of Atherosclerosis

Atherosclerosis is a chronic, progressive, inflammatory disease of medium and large arteries. Understanding its development is key to understanding the entire spectrum of IHD.

The endothelium normally maintains a vasodilatory, anti-thrombotic, anti-inflammatory state via nitric oxide (NO) production.
Risk factors (smoking, hypertension, hyperglycaemia, oxidised LDL, etc.) cause endothelial injury and dysfunction:
- ↓NO production → loss of vasodilation and anti-thrombotic properties
- ↑expression of adhesion molecules (VCAM-1, ICAM-1, selectins) on endothelial surface
- ↑endothelial permeability to lipoproteins

Dysfunctional endothelium allows LDL particles to enter the subintimal space (intima)
LDL becomes oxidised (oxLDL) by reactive oxygen species — this is the critical step
oxLDL is:
- Chemotactic for monocytes → recruitment into intima
- Toxic to endothelium → further dysfunction
- Immunogenic → triggers inflammatory response
Monocytes differentiate into macrophages → express scavenger receptors (SR-A, CD36) → engulf oxLDL without negative feedback → become foam cells
Accumulation of foam cells = fatty streak — the earliest visible lesion ^[1]
- Slightly raised yellow deposits ^[1]
- Found in the aorta of virtually all people from childhood

Progressive lipid accumulation, smooth muscle cell migration from media to intima, and extracellular matrix deposition
Mature plaque structure = fibrous cap (smooth muscle cells + collagen + extracellular matrix) overlying a necrotic lipid core (dead foam cells, cholesterol crystals, debris) ^[1]
This is the atheromatous plaque ^[1]
The plaque progressively narrows the arterial lumen → when stenosis reaches > 70%, flow is significantly reduced during stress (exercise) → demand-supply mismatch → stable angina
At rest, flow is usually adequate until stenosis exceeds ~90%

The distinction between stable and unstable IHD lies in plaque biology:

Feature	Stable Plaque	Unstable (Vulnerable) Plaque
Fibrous cap	Thick, intact	Thinner fibrous cap ^[1]
Lipid core	Small, stable	Growing necrotic core ^[1]
Inflammation	Low-grade	Active inflammation with macrophages at plaque shoulder secreting matrix metalloproteinases (MMPs) that degrade collagen
Clinical consequence	Stable angina	Plaque rupture → thrombus formation → ACS ^[1]

What happens when a plaque ruptures?

Fibrous cap disruption (rupture or erosion) exposes the thrombogenic necrotic core (rich in tissue factor) to flowing blood
Platelet adhesion and activation → platelet plug
Coagulation cascade activation → fibrin mesh → thrombus formation
Thrombus can:
- Partially occlude the lumen → UA or NSTEMI
- Completely occlude the lumen → STEMI
- Embolise distally → microinfarcts
Vasospasm at the site (mediated by thromboxane A₂ and serotonin from activated platelets) further reduces flow

Other plaque complications ^[1]:

Aneurysm: pressure atrophy of the tunica media beneath a large plaque → weakening → aneurysmal dilation ^[1]
Atheroembolism: cholesterol crystal emboli from ulcerated plaques → distal end-organ damage ^[1]

The Central Concept

Stable angina = fixed plaque, stable cap, predictable symptoms on exertion. ACS = vulnerable plaque, cap rupture/erosion, thrombus, unpredictable symptoms at rest. The key determinant of clinical syndrome is plaque stability, NOT plaque size. A 40% stenosis with a thin cap and large lipid core is far more dangerous than an 80% stenosis with a thick, stable cap.

B. Mechanisms of Myocardial Ischaemia

Ischaemia = oxygen demand exceeds supply. Let's break down both sides:

Factor	Mechanism
Heart rate	↑HR → ↑number of contractions per minute → ↑ATP consumption. Also ↓diastolic time → ↓coronary perfusion time (double hit!)
Myocardial contractility	↑inotropy → ↑ATP use per contraction
Wall stress (= afterload)	By Laplace's law: wall stress ∝ (Pressure × radius) / (2 × wall thickness). ↑BP (HTN), ↑LV dilation → ↑wall stress → ↑O₂ demand. This is why hypertension and aortic stenosis exacerbate angina
Preload	↑preload → ↑LV volume → ↑wall stress

Factor	Mechanism
Coronary blood flow	Determined by coronary perfusion pressure (aortic diastolic pressure − LVEDP) and coronary vascular resistance. Stenosis ↑resistance → ↓flow
O₂ carrying capacity	Anaemia → ↓O₂ delivery even with normal flow. This is why anaemia exacerbates angina ^[2]
O₂ extraction	Already near-maximal at rest (~70–75%) → minimal reserve. Unlike skeletal muscle, the heart CANNOT compensate by simply extracting more O₂ — it is almost entirely dependent on increasing flow

Why does the heart rely so heavily on increasing flow rather than extraction? Because myocardial O₂ extraction is already ~75% at rest (compared to ~25% in skeletal muscle). There is almost no extraction reserve. The ONLY way to ↑O₂ supply to the myocardium is to ↑coronary blood flow — and this is exactly what is impaired in CAD.

Condition	Mechanism
Anaemia	↓O₂ carrying capacity → ↓supply
Thyrotoxicosis	↑HR, ↑contractility, ↑metabolic rate → ↑demand
Tachyarrhythmias	↑HR → ↑demand + ↓diastolic perfusion time → ↓supply
Aortic stenosis	↑afterload → ↑wall stress → ↑demand; also ↑LV mass outstrips coronary supply; ↓diastolic BP → ↓coronary perfusion
HCMP	↑LV mass → ↑demand; dynamic LVOT obstruction → ↑wall stress
Aortic regurgitation	↓diastolic aortic pressure → ↓coronary perfusion pressure
Hypertension	↑afterload → ↑demand; LVH → ↑demand
Fever / Sepsis	↑metabolic rate, ↑HR → ↑demand

When ischaemia occurs, events follow a predictable cascade called the "ischaemic cascade":

Coronary flow ↓
  → Metabolic abnormalities (↓ATP, lactic acidosis) [earliest]
    → Diastolic dysfunction (impaired relaxation)
      → Regional wall motion abnormality (RWMA)
        → ECG changes (ST depression/elevation, T wave changes)
          → Angina (chest pain) [latest]

Why do ECG changes appear BEFORE chest pain? Electrophysiological changes in ischaemic myocardium occur at a lower threshold than nociceptor activation. This is why some patients have "silent ischaemia" — detectable on Holter or stress testing without symptoms. This is particularly common in diabetic patients (autonomic neuropathy damages cardiac afferent nerves) and in complete infarcts > 6 hours ^[1].

Causes of painless ("silent") MI ^[1]:

Diabetes mellitus — cardiac autonomic neuropathy
Complete infarct (> 6h) — nerve destruction within the infarcted territory
Elderly patients — altered pain perception
Post-transplant hearts — denervated

If ischaemia is prolonged (typically > 20 minutes of complete occlusion), irreversible myocardial necrosis begins:

Subendocardial ischaemia begins first (the subendocardium is most vulnerable because it is furthest from the epicardial coronary supply, is subject to the highest wall stress, and has the highest O₂ demand)
With continued occlusion, the wavefront of necrosis extends from subendocardium → epicardium
By ~6 hours of total occlusion, transmural infarction is complete (though timing varies with collateral circulation)

This is the basis for the concept of "time is muscle" — early reperfusion salvages myocardium.

Classification of IHD

Category	Sub-type	Definition
Chronic coronary syndrome (CCS) / Stable IHD	Stable angina pectoris	Predictable chest pain with exertion, relieved by rest/nitrate ≤ 5 min ^[1]^[2]
	Ischaemic cardiomyopathy	Chronic LV dysfunction due to prior infarction or hibernating myocardium
	Silent ischaemia	Objective evidence of ischaemia without symptoms
Acute coronary syndrome (ACS)	Unstable angina (UA)	Any one of: (1) resting angina > 20 min, (2) new-onset angina that markedly limits normal activity, (3) increasing angina (more frequent/prolonged/less effort) ^[1]
	NSTEMI	Raised cardiac enzymes (troponin) WITHOUT ST elevation (may have ST depression or T wave inversion) ^[1]
	STEMI	Raised cardiac enzymes WITH ST elevation or new LBBB ^[1]
Sudden cardiac death		VF/pulseless VT from ischaemia — 85% of out-of-hospital cardiac arrests due to CAD ^[3]

The ACS Spectrum

A common mistake is thinking UA, NSTEMI, and STEMI are completely separate diseases. They are a continuum of the same pathology (plaque rupture + thrombosis). The difference lies in the degree and duration of coronary occlusion and whether there is myocardial necrosis:

UA: transient/partial occlusion, NO necrosis (normal troponin)
NSTEMI: partial/intermittent occlusion or distal embolisation, YES necrosis (↑troponin) but no complete transmural ischaemia (no ST elevation)
STEMI: complete occlusion of a major epicardial artery, transmural ischaemia (ST elevation), necrosis

This functional classification is widely used to grade the severity of stable angina:

CCS Grade	Description
I	Angina only with strenuous, rapid, or prolonged exertion
II	Slight limitation of ordinary activity — angina on walking > 2 blocks on level ground, climbing > 1 flight of stairs
III	Marked limitation of ordinary activity — angina on walking 1–2 blocks, climbing 1 flight
IV	Angina with any physical activity, or at rest

Type	Mechanism
Type 1	Spontaneous MI due to atherosclerotic plaque disruption (rupture, erosion, fissuring) → thrombus → ischaemia + necrosis. This is the "classic" MI
Type 2	MI secondary to supply-demand mismatch NOT from acute plaque disruption (e.g. coronary spasm, coronary embolism, anaemia, tachyarrhythmia, hypotension, respiratory failure). Troponin rises but the mechanism is different
Type 3	Cardiac death with symptoms suggestive of MI and presumed new ECG changes or VF, but death occurred before blood samples could be obtained
Type 4a	MI related to PCI (within 48 hours)
Type 4b	MI related to stent thrombosis
Type 5	MI related to CABG

Why is this classification important? Type 1 vs Type 2 MI has completely different management. Type 1 MI requires antiplatelet therapy, anticoagulation, and often revascularisation. Type 2 MI requires treatment of the underlying cause (e.g. transfusion for anaemia, rate control for tachycardia) — giving DAPT and rushing to the cath lab would be inappropriate and potentially harmful.

Clinical Features

A. Symptoms

Angina pectoris (Latin: angere = to choke, pectoris = of the chest) is the symptom complex caused by myocardial ischaemia ^[9].

Pathophysiology of anginal pain: Myocardial ischaemia → anaerobic metabolism → accumulation of metabolic byproducts (lactate, adenosine, bradykinin, hydrogen ions) → stimulation of cardiac sympathetic afferent nerve endings (unmyelinated C fibres) → signals travel via the sympathetic chain to spinal cord segments T1–T5 → referred pain perceived in the chest and along the C8–T5 dermatomes (arm, jaw, neck) ^[9].

Feature	Detail	Pathophysiological Basis
Quality	Dull, constricting, choking, "heavy". Described as squeezing, crushing, burning, or tightness. Patients often emphasize it is a discomfort, not a "pain" ^[2]^[9]. Levine's sign: patient places clenched fist on sternum when describing the sensation ^[9]	Visceral pain from the heart is transmitted via autonomic nerves → poorly localised, dull quality (unlike somatic pain which is sharp and well-localised)
Location	Retrosternal (behind the sternum), diffuse — patient cannot point to the pain with one finger ^[9]	Cardiac afferents converge on the same spinal cord segments (T1–T5) as somatic afferents from the chest wall → referred to a broad retrosternal area
Radiation	Arms (especially left), shoulders, jaw, neck, epigastrium ^[2]^[9]	Convergence of cardiac afferents with somatic afferents from C8–T5 dermatomes in the spinal cord → brain misinterprets visceral pain as originating from these somatic territories
Duration	Stable angina: typically < 30 minutes, usually 2–10 min ^[2]. ACS: often > 20 minutes and may last hours	Stable: ischaemia resolves with rest/reduced demand. ACS: ongoing ischaemia from persistent occlusion
Provocation	Exertion, emotional stress, cold weather, heavy meals ^[2]	All ↑myocardial O₂ demand: exercise ↑HR and contractility; emotion/cold → sympathetic activation → ↑HR, BP; post-prandial → ↑CO to splanchnic bed → ↑cardiac work
Relieving factors	Rest (within a few minutes) and sublingual GTN (within ≤ 5 min for stable angina) ^[2]	Rest → ↓HR, ↓BP → ↓demand → supply-demand balance restored. GTN → venodilation (↓preload → ↓wall stress → ↓demand) + some coronary vasodilation (↑supply)
Timing	May be worse in the morning (circadian variation in sympathetic tone, platelet aggregability, and fibrinolytic activity)	Cortisol and catecholamine peaks in early morning → ↑HR, ↑BP → ↑demand. Also ↑platelet reactivity → ↑thrombotic risk

Red flag features suggesting ACS rather than stable angina:

Pain at rest
New-onset angina (< 2 months) that markedly limits activity
Crescendo pattern (increasing frequency, severity, or occurring with less exertion)
Duration > 20 minutes
Not relieved by rest or GTN
Associated with autonomic symptoms (sweating, nausea, vomiting)

May be an angina equivalent ("anginal equivalent dyspnoea") — especially in elderly, diabetic, and female patients
Pathophysiology: ischaemia → diastolic dysfunction (impaired LV relaxation) → ↑LVEDP → ↑LA pressure → pulmonary congestion → dyspnoea
Can also indicate LV systolic dysfunction from prior infarction → chronic heart failure

Diaphoresis (sweating), nausea, vomiting, pallor
Pathophysiology: myocardial ischaemia activates cardiac sympathetic and vagal afferents → autonomic response. The inferior wall (RCA territory) is particularly vagally innervated → inferior MI often presents with bradycardia, nausea, and vomiting (vasovagal response)

Can occur if ischaemia causes significant ↓CO (large territory involvement or arrhythmia)
Pathophysiology: ↓CO → ↓cerebral perfusion. Or ischaemia-triggered VT/VF → cardiac arrest

Chronic fatigue may reflect chronic low cardiac output from ischaemic cardiomyopathy
Also an atypical angina equivalent in some patients

Atypical Presentations — Don't Miss These

IHD may present without classic chest pain in certain populations:

Women: more likely to have dyspnoea, fatigue, nausea, back/jaw pain rather than classic crushing chest pain
Elderly: dyspnoea, confusion, falls
Diabetic patients: silent ischaemia due to cardiac autonomic neuropathy ^[1]
Post-transplant: denervated heart → no pain Always maintain a high index of suspicion in patients with risk factors even without typical symptoms.

B. Signs

Physical examination in stable IHD is frequently unremarkable ^[2] — but there are several things to look for:

Sign	Finding	Pathophysiological Basis
Usually normal	Physical examination is frequently unremarkable in stable angina ^[2]	Fixed coronary stenosis causes symptoms only during increased demand; at rest, haemodynamics are normal
S4 gallop	Palpable or audible 4th heart sound	↑LVEDP from diastolic dysfunction (impaired relaxation of ischaemic myocardium) → atrial contraction against a stiff ventricle → S4
S3 gallop	Audible 3rd heart sound	Systolic dysfunction from prior MI → dilated LV → rapid early diastolic filling → S3. Indicates established LV failure
Dyskinetic apex beat	Sustained, displaced apex beat	Prior MI → scarred, akinetic or dyskinetic segment → adverse LV remodelling → dilation → displaced apex ^[2]
Mitral regurgitation murmur (transient)	Pansystolic murmur at apex	Ischaemia of papillary muscle → transient MR during episodes. Or chronic MR from papillary muscle dysfunction / LV remodelling post-MI
Pulmonary crepitations	Bilateral basal crepitations	LV dysfunction → ↑LVEDP → ↑pulmonary capillary pressure → transudation into alveoli
Signs of cardiogenic shock (in massive MI)	Hypotension, tachycardia, cold clammy peripheries, oliguria	Massive myocardial necrosis (> 40% of LV) → pump failure → ↓CO

Sign	What It Suggests
Xanthelasma (yellowish deposits around eyes)	Hyperlipidaemia — cholesterol deposition in the skin around the eyelids ^[4]
Corneal arcus (grey-white ring at corneal periphery)	Lipid deposition in the cornea. Non-specific in elderly, but suggestive of hyperlipidaemia if < 45 years ^[4]
Tendon xanthomas (Achilles, extensor tendons of hand)	Highly specific for familial hypercholesterolaemia (FH) — cholesterol deposition in tendons ^[10]
Nicotine-stained fingers	Active smoking
Hypertension (elevated BP)	Major modifiable risk factor
Signs of diabetes	Acanthosis nigricans, diabetic dermopathy, peripheral neuropathy
Central obesity	Component of metabolic syndrome

Sign	Location	Significance
Carotid bruit	Neck	Carotid artery stenosis — concurrent cerebrovascular disease ^[2]
Signs of peripheral vascular disease (PVD)	Lower limbs — absent/diminished peripheral pulses, hair loss, skin changes, ulcers, gangrene	Concurrent peripheral arterial disease. "Atherosclerosis is a systemic disease" ^[5] — if you find it in one bed, look for it in others
Abdominal aortic aneurysm	Pulsatile abdominal mass	Another manifestation of atherosclerosis

Sign	Condition
Ejection systolic murmur radiating to carotids	Aortic stenosis → ↑afterload, ↓coronary perfusion
Ejection systolic murmur ↑ with Valsalva	HOCM → dynamic LVOT obstruction ^[2]
Early diastolic murmur at left sternal edge	Aortic regurgitation → ↓diastolic coronary perfusion
Conjunctival pallor	Anaemia → ↓O₂ carrying capacity
Tremor, tachycardia, lid lag, thyroid enlargement	Thyrotoxicosis → ↑HR, ↑contractility, ↑metabolic demand ^[2]

The Exam-Ready Approach to P/E in IHD

When examining a patient with suspected IHD, systematically look for:

Signs of the disease itself: S3/S4 gallop, displaced apex, MR murmur, signs of HF
Signs of risk factors: xanthomas, xanthelasma, arcus, hypertension, obesity, DM features
Signs of systemic atherosclerosis: carotid bruits, absent peripheral pulses, AAA
Signs of conditions exacerbating angina: AS murmur, HOCM, anaemia, thyrotoxicosis

This framework ensures you don't miss anything on a ward round or in an OSCE.

High Yield Summary

IHD = myocardial O₂ supply-demand mismatch, overwhelmingly due to coronary atherosclerosis (> 95%)
Risk factors = atherosclerotic risk factors: age, male, family Hx, smoking, HTN, DM, hyperlipidaemia, obesity, physical inactivity. Atherosclerosis is a systemic disease — always check for PVD, carotid disease
Coronary anatomy: LAD (anterior wall, septum, apex — "widow-maker"), LCx (lateral wall), RCA (inferior wall, RV, SA/AV nodes). Dominance determines posterior supply. Coronary perfusion is predominantly diastolic
Atherosclerosis pathology: endothelial dysfunction → LDL entry + oxidation → foam cells → fatty streak → atheromatous plaque (fibrous cap + necrotic core). Plaque rupture = ACS
Clinical spectrum: Stable angina (fixed stenosis, demand-driven) → ACS (UA, NSTEMI, STEMI — plaque rupture + thrombus, supply-driven)
Stable angina features: retrosternal, dull/constricting, exertional, < 30 min, relieved by rest/GTN ≤ 5 min
ACS features: rest pain > 20 min, new-onset limiting angina, crescendo pattern, ± autonomic symptoms
P/E often normal in stable IHD — look for S3/S4, displaced apex, MR murmur, risk factor signs (xanthomas, HTN), systemic atherosclerosis (carotid bruit, PVD), conditions exacerbating angina (AS, anaemia, thyrotoxicosis)
Silent MI: diabetes (autonomic neuropathy), elderly, post-transplant, complete infarct > 6h
Myocardial O₂ extraction is ~75% at rest — almost no extraction reserve — heart is entirely dependent on ↑flow to meet ↑demand. This is why coronary stenosis is so devastating

Active Recall - IHD Definition, Epidemiology, Risk Factors, Anatomy, Aetiology, Pathophysiology, Classification, Clinical Features

^[1] Senior notes: Maksim Medicine Notes.pdf (Section 1.3, Ischaemic Heart Disease, p.7) ^[2] Senior notes: Ryan Ho Cardiology.pdf (Section 3.2.1, Stable Angina and Ischaemic Heart Disease, pp.115–120) ^[3] Senior notes: Ryan Ho Critical Care.pdf (Section 1.5, Cardiac Arrest, p.28) ^[4] Senior notes: Ryan Ho Endocrine.pdf (Section 6.2.2, Approach to Abnormal Lipid Profile, pp.123–131) ^[5] Lecture slides: WCS 002 - Toe gangrene and leg ulcer - by Prof SWK Cheng.pdf (p.2) ^[6] Senior notes: Ryan Ho Neurology.pdf (Section on Risk Factors of Stroke, p.75) ^[7] Senior notes: Ryan Ho Endocrine.pdf (Type 2 DM and Obesity sections, pp.77, 117) ^[8] Senior notes: Ryan Ho Urogenital.pdf (Cardiovascular Morbidity in CKD, p.109) ^[9] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.1.1, Chest Pain and Angina Pectoris, pp.199–202) ^[10] Senior notes: Ryan Ho Chemical Path.pdf (Lipid Profile and Familial Hypercholesterolaemia, pp.46–48)

Differential Diagnosis of Ischaemic Heart Disease

When a patient presents with chest pain — or indeed dyspnoea, syncope, or fatigue — the clinician's first job is to decide where on the spectrum the symptom falls. The differential diagnosis of IHD is really two intertwined questions:

Is this chest pain cardiac or non-cardiac? (i.e. Is the symptom due to myocardial ischaemia at all?)
If cardiac, what is the specific aetiology? (i.e. Is it atherosclerotic CAD, vasospasm, myocarditis, pericarditis, aortic disease, etc.?)

The approach differs depending on whether the presentation is acute (ACS picture — pain at rest, haemodynamic instability) or chronic/stable (predictable exertional symptoms) ^[2]^[9].

The key teaching point: you must rule out life-threatening mimics before settling on a diagnosis of IHD. An aortic dissection misdiagnosed as ACS and treated with anticoagulation + antiplatelets is a catastrophe. A PE missed because "the ECG looks ischaemic" can be fatal. Always keep the differential broad initially, then narrow systematically.

A. Differential Diagnosis of Acute Chest Pain (ACS Mimics)

When a patient presents with acute chest pain, the differential must include all potentially life-threatening causes. These are the "big five" emergencies plus other important differentials ^[1]^[2]^[9]:

Diagnosis	Key Distinguishing Features	Why It Mimics ACS
Acute coronary syndrome	Dull/crushing central chest pain > 20 min, radiation to jaw/arm, ↑troponin, ECG changes (ST elevation/depression, T wave inversion) ^[2]	— (this IS the diagnosis being considered)
Aortic dissection	Sudden onset, maximal at onset "tearing" pain radiating to the back ^[1]^[9]. Asymmetric BP or pulses. Widened mediastinum on CXR. Often in setting of poorly controlled HTN, Marfan's, bicuspid aortic valve	Can cause ECG changes if dissection extends to involve coronary ostia (typically RCA → inferior ST elevation). Critical to exclude before giving antiplatelets/anticoagulants
Acute pulmonary embolism	Acute pleuritic chest pain, dyspnoea, haemoptysis, tachycardia. Risk factors: immobilisation, surgery, DVT, malignancy. ECG: sinus tachycardia, S1Q3T3, RBBB ^[11]. D-dimer, CTPA	Can cause troponin rise (RV strain), ST changes, chest pain — mimics NSTEMI. Massive PE causes crushing central chest pain and collapse, mimicking STEMI
Tension/massive pneumothorax	Sudden onset, pleuritic, unilateral. Tracheal deviation, absent breath sounds, hyperresonance. Young thin male (primary) or underlying lung disease (secondary)	Acute chest pain + dyspnoea + tachycardia can initially suggest ACS
Oesophageal rupture (Boerhaave's)	Severe retrosternal pain after forceful vomiting, subcutaneous emphysema, pneumomediastinum on CXR ^[1]	Retrosternal pain can mimic ACS, but history of vomiting and surgical emphysema are key

Aortic Dissection — The Most Dangerous Mimic

Target Hx and PE to rule out other life-threatening emergencies: aortic dissection, pulmonary embolism, tension pneumothorax, perforated peptic ulcer / esophagus ^[1]. Aortic dissection can produce ST elevation (when the dissection flap occludes a coronary ostium), elevated troponin, and haemodynamic instability — perfectly mimicking a STEMI. If you give thrombolysis, dual antiplatelets, or anticoagulation to a patient with aortic dissection, the bleeding is often fatal. Always ask about tearing/ripping pain maximal at onset radiating to the back, check for pulse/BP asymmetry, and look for a widened mediastinum on CXR before committing to an ACS pathway.

Diagnosis	Key Distinguishing Features	Why It Mimics IHD
Myopericarditis ± cardiac tamponade	Sharp, pleuritic chest pain better when sitting up and leaning forward, worse lying supine ^[1]. Diffuse concave ST elevation + PR depression on ECG (vs convex ST elevation in STEMI). Pericardial rub on auscultation. Recent viral illness. ± Tamponade (Beck's triad: hypotension, elevated JVP, muffled heart sounds) ^[1]	ST elevation can mimic STEMI. Troponin may rise if myocarditis is present. But the pattern of ST elevation is diffuse (not territorial), and PR depression is characteristic
Takotsubo cardiomyopathy ("stress cardiomyopathy")	Typically post-menopausal women after intense emotional or physical stress. ST elevation (often anterior leads), ↑troponin, apical ballooning on echo, but normal coronary arteries on angiography. Resolves spontaneously	Perfectly mimics anterior STEMI clinically and on ECG. Diagnosed only after coronary angiography shows patent arteries
Acute decompensated heart failure	Dyspnoea, orthopnoea, PND, ↑JVP, bilateral crepitations, S3 gallop. May be precipitated by ACS but also by many other causes. ↑BNP/NT-proBNP ^[1]	May coexist with ACS (ACS is a common precipitant of acute HF). Dyspnoea alone in an elderly patient could be ACS ("angina equivalent") or primary HF

Diagnosis	Key Distinguishing Features	Why It Mimics IHD
Pneumonia	Productive cough, fever, pleuritic pain, consolidation on CXR, ↑WCC/CRP	Chest pain + dyspnoea + tachycardia can suggest ACS, especially if ECG shows non-specific ST-T changes (type 2 MI can occur secondary to sepsis)
GERD / Oesophageal spasm	Retrosternal burning ^[9], a/w meals, relieved by antacids, ± dysphagia. Oesophageal spasm can respond to nitrates (confusing!) ^[1]	Retrosternal burning pain that responds to nitrates can be mistaken for angina. Key: oesophageal spasm is typically not exertion-related
Musculoskeletal pain / Costochondritis	Pain reproduced by palpation or specific movement ^[9], sharp, localised, a/w inspiration	Point tenderness and reproducibility with movement distinguishes it, but ACS can coexist with chest wall tenderness — don't be falsely reassured
Panic attack	Palpitations, sweating, tremor, chest tightness, SOB, paraesthesia (hyperventilation → respiratory alkalosis → ↓ionised Ca²⁺ → tingling), fear of dying ^[12]. Diagnosis of exclusion	Chest pain + palpitations + diaphoresis + fear of dying mimics ACS almost perfectly. Must always exclude organic causes first
Perforated peptic ulcer	Sudden-onset severe epigastric/abdominal pain, board-like rigidity, peritonism, free gas under diaphragm on erect CXR ^[1]	Epigastric pain can be referred upwards and confused with inferior MI. A perforated ulcer can cause vagal responses (bradycardia, sweating) that mimic inferior STEMI

For patients with recurrent, predictable chest discomfort, the differential is different ^[2]^[9]:

Category	Diagnoses	Key Distinguishing Features
Cardiac — Atherosclerotic	Stable angina from CAD	Reproducible exertional chest discomfort, relieved by rest/GTN ≤ 5 min, typical quality ^[2]
Cardiac — Non-atherosclerotic	Vasospastic (Prinzmetal's) angina	Rest angina (often nocturnal), transient ST elevation during pain, normal coronaries or non-critical stenosis. Responds dramatically to CCBs and nitrates. Cocaine-associated vasospasm similar mechanism ^[1]
	Microvascular angina (cardiac syndrome X)	Typical angina with evidence of ischaemia on stress testing but angiographically normal epicardial coronary arteries. More common in women. Thought to be due to endothelial dysfunction of small intramyocardial vessels
	Aortic stenosis / HCMP	Exertional angina due to ↑myocardial O₂ demand (↑wall stress, ↑LV mass) outstripping supply. Ejection systolic murmur. Echo confirms diagnosis ^[2]
Pulmonary	Subacute/chronic PE	Pleuritic pain, dyspnoea, risk factors for VTE. Sinus tachycardia ± S1Q3T3 on ECG ^[2]^[11]
	Pulmonary hypertension	Exertional chest pain (RV subendocardial ischaemia due to ↑RV wall stress) ^[13], exertional syncope, progressive dyspnoea, loud P2. RV heave
	Malignancy with chest wall/pleural involvement	Persistent, progressive pain, ± pleural effusion, weight loss, night sweats
GI	GERD	Retrosternal burning, worse after meals/lying down, relieved by antacids ^[1]^[9]
	Peptic ulcer disease	Epigastric pain related to meals, ± N/V, haematemesis, melaena ^[1]
Musculoskeletal	Costochondritis, rib trauma	Localised, sharp, reproducible with palpation or specific movement ^[1]
Neurological	Herpes zoster (shingles)	Dermatomal pain ± vesicular rash. Can cause severe unilateral chest wall pain before rash appears (pre-herpetic neuralgia) ^[2]
Psychological	Panic disorder / psychogenic chest pain	Chest tightness, palpitations, hyperventilation, paraesthesia. Diagnosis of exclusion ^[12]

This is a critical clinical concept. A raised troponin indicates myocardial injury but NOT necessarily acute plaque-related MI. Consider ^[2]:

Category	Conditions
Ischaemic (Type 1 MI)	ACS due to plaque rupture/erosion with thrombus
Ischaemic (Type 2 MI)	Supply-demand mismatch from tachyarrhythmia, severe anaemia, hypotension/shock, hypertensive crisis, respiratory failure, coronary spasm
Non-ischaemic myocardial injury	Myocarditis, takotsubo cardiomyopathy, heart failure, cardiac contusion, pulmonary embolism, aortic dissection, cardiotoxic drugs, post-PCI/CABG
Systemic	Renal failure (commonest non-cardiac cause — impaired clearance), sepsis/critical illness, stroke/SAH ^[2]

N.B. ↑cTn (troponin leak) in other conditions: Other ischaemia: tachycardia, coronary spasm, PCI or cardiothoracic surgery, hypoxia or hypotension. Other myocardial injury: myocarditis, heart failure, takotsubo cardiomyopathy, pulmonary embolism, aortic dissection, other cardiomyopathy (eg. infiltrative), cardiotoxins. Systemic diseases, eg. renal failure, sepsis, critical illness, stroke, SAH ^[2]

Troponin Is Not a Diagnosis

A common mistake is treating every raised troponin as ACS and rushing to the cath lab. Troponin is a marker of myocardial injury, not a specific marker of coronary thrombosis. You must integrate the troponin result with the clinical context (history, ECG, risk factors) to determine whether this is Type 1 MI (needs DAPT + possible PCI), Type 2 MI (needs treatment of the underlying cause), or non-ischaemic myocardial injury (needs disease-specific management). Giving dual antiplatelets to a patient with troponin rise from sepsis-related Type 2 MI is inappropriate and potentially harmful.

DDx of ST elevation ^[1]:

Diagnosis	ECG Pattern	Key Distinguishing Feature
STEMI	Convex ST elevation, associated with Q waves, in a territorial distribution with reciprocal changes ^[1]	Clinical context: acute chest pain, ↑troponin
Acute pericarditis	Diffuse concave ST elevation and PR depression ^[1]	Diffuse (non-territorial), concave ("saddle-shaped"), PR depression (except aVR where PR is elevated), no reciprocal ST depression, no Q waves
LVH with strain pattern	Concave ST elevation in V1–V3, associated with LVH features (tall R in V5–V6, deep S in V1–V2) ^[1]	Chronic — does not change over time. No troponin rise
LBBB	Discordant ST changes (ST elevation in leads with predominantly negative QRS) ^[1]	Wide QRS > 120 ms, QS in V1, broad notched R in V5–V6. Apply Sgarbossa criteria to assess for acute MI in the setting of LBBB
Brugada syndrome	Coved or saddle-back ST elevation in V1–V3	No troponin rise, characteristic pattern, a/w syncope/SCD
Early repolarisation	Concave ST elevation, often with J-point elevation and "fish-hook" morphology	Common in young healthy individuals. No symptoms. Benign (usually)
Ventricular aneurysm	Persistent ST elevation in the territory of a prior MI	Persistently ↑ST segment after STEMI should raise suspicion for ventricular aneurysm ^[2]. Old pathological Q waves in the same leads

The mnemonic-driven history approach helps differentiate causes efficiently:

OPQRST Feature	Favours IHD	Favours Non-IHD
Onset	ACS: minutes to develop; Stable: gradual, proportional to exertion ^[9]	Sudden onset, maximal at onset → aortic dissection, PTX, massive PE ^[9]
Provocation	Exertion, emotion, cold, heavy meals ("4Es": Eating, Exertion, Emotion, Environment) ^[9]	Pain after exertion → musculoskeletal. A/w specific movement or palpation → MSK. A/w meals, lying down → GERD ^[9]
Quality	Dull, constricting, choking, "heavy" ^[9]	Sharp, stabbing, pleuritic → PE, PTX, pericarditis. Tearing → aortic dissection. Burning → GERD ^[9]
Radiation	Arms (esp left), jaw, neck ^[9]	Back (interscapular) → aortic dissection. Dermatomal → herpes zoster
Severity	Stable: moderate. ACS: more severe ^[9]	Very severe, "worst ever" → dissection, massive PE, PTX
Timing	Stable: < 2–10 min, relieved by rest/GTN ≤ 5 min ^[9]. ACS: > 30 min, not relieved by rest ^[9]	Sharp, "catching" a/w breathing, coughing → pleuritic/pericardial ^[9]. A/w specific movement → MSK ^[9]
Associated features	Autonomic features (diaphoresis, N/V) in ACS ^[9]. SOB, syncope, dizziness = angina equivalent esp in elderly and DM ^[9]	Cough, fever → pneumonia. Haemoptysis → PE. Dysphagia → oesophageal. Rash → herpes zoster

These are crucial to recognise because they require different management ^[1]:

Condition	Mechanism	Key Clinical Clue
Vasospastic (Prinzmetal's) angina	Focal coronary artery smooth muscle spasm → transient transmural ischaemia	Rest angina (often nocturnal, early morning), transient ST elevation during pain that resolves completely. Normal or non-critical stenosis on angiography. Responds to CCBs, not β-blockers (β-blockers may worsen vasospasm — unopposed α-receptor stimulation)
Cocaine-induced coronary vasospasm	Sympathomimetic → ↑HR, ↑BP, coronary vasoconstriction via α-adrenergic stimulation + direct smooth muscle toxicity + accelerated atherosclerosis	Young patient, recreational drug use history, may present with frank STEMI. Do NOT give β-blockers (unopposed α stimulation worsens vasospasm) — use benzodiazepines, nitrates, CCBs
Microvascular angina (syndrome X)	Endothelial dysfunction of small intramural coronary vessels	Typical angina + ischaemia on stress testing + normal epicardial arteries on angiography. More common in women, diabetics
SCAD (Spontaneous Coronary Artery Dissection)	Intimal tear → intramural haematoma → true lumen compression	Young women (often peri-partum), fibromuscular dysplasia. Presents as ACS. Diagnosed on angiography (characteristic smooth tapering/string of pearls appearance)
Takotsubo cardiomyopathy	Catecholamine-mediated myocardial stunning (apical ballooning)	Post-menopausal women, intense emotional/physical stress. Mimics anterior STEMI. Normal coronaries on angiography, classic apical ballooning on echo/ventriculography

When IHD presents with dyspnoea rather than chest pain (angina equivalent), the DDx of dyspnoea itself becomes important ^[1]:

Category	Differentials
Cardiac	CHF (from IHD or other cause), ACS, arrhythmia, valvular heart disease, pericardial disease
Respiratory — Acute	PE, pneumothorax, asthma exacerbation, AECOPD, acute pulmonary oedema
Respiratory — Subacute	Pneumonia, pleural effusion, TB
Respiratory — Chronic	COPD, ILD, malignancy
Metabolic	Anaemia, metabolic acidosis (e.g. DKA — Kussmaul breathing), thyrotoxicosis
Neuromuscular	Myasthenia gravis, GBS, stroke
Psychological	Panic disorder, hyperventilation syndrome

High Yield Summary — Differential Diagnosis of IHD

Acute chest pain DDx: The "big five" life-threatening causes = ACS, aortic dissection, PE, tension PTX, oesophageal rupture. Always rule these out before settling on a diagnosis
Aortic dissection is the most dangerous mimic — tearing pain maximal at onset, back radiation, BP/pulse asymmetry. Must exclude before giving antiplatelets or anticoagulation
PE can cause troponin rise (RV strain) and ECG changes (S1Q3T3, RBBB) mimicking ACS ^[11]
Stable chest pain DDx: IHD, chronic PE, pulmonary HTN, malignancy, GERD, MSK pain, psychogenic, herpes zoster ^[2]
Not all troponin rises = ACS: Type 2 MI (supply-demand mismatch), myocarditis, PE, HF, takotsubo, renal failure, sepsis all cause troponin elevation ^[2]
DDx of ST elevation: STEMI (convex, territorial, reciprocal changes), pericarditis (diffuse concave, PR depression), LVH strain (V1–V3, chronic), LBBB, Brugada, early repolarisation, ventricular aneurysm ^[1]
Non-atherosclerotic angina: Prinzmetal's vasospasm (rest, nocturnal, transient ST elevation), microvascular angina (normal coronaries), SCAD (young women), takotsubo (stress, post-menopausal), cocaine (young, illicit drug use) ^[1]
Angina equivalents: dyspnoea, syncope, fatigue — especially in elderly, diabetics, women — must prompt consideration of IHD even without classic chest pain ^[9]

Active Recall - Differential Diagnosis of IHD

References

^[1] Senior notes: Maksim Medicine Notes.pdf (Sections 1.1 and 1.3, Chest Pain DDx and IHD, pp.5, 7, 10) ^[2] Senior notes: Ryan Ho Cardiology.pdf (Sections 2.1, 3.2, Chest Pain, CAD, ACS approach, pp.54–58, 115, 128, 131) ^[9] Senior notes: Ryan Ho Fundamentals.pdf (Section 3.1.1, Chest Pain and Angina Pectoris, pp.199–203) ^[11] Senior notes: Ryan Ho Haemtology.pdf (VTE and PE, p.131) ^[12] Senior notes: Ryan Ho Psychiatry.pdf (Panic Disorder, p.179) ^[13] Senior notes: Ryan Ho Respiratory.pdf (Pulmonary Hypertension, p.138)

Diagnostic Criteria, Diagnostic Algorithm and Investigation Modalities for IHD

A. Diagnostic Criteria

The diagnostic framework for IHD depends on where on the clinical spectrum the patient sits: stable angina / chronic coronary syndrome vs acute coronary syndrome (ACS).

There is no single laboratory "diagnostic test" for stable angina in the way that troponin defines MI. Instead, the diagnosis is established by integrating:

Clinical assessment: history consistent with typical angina (retrosternal, dull/constricting, provoked by exertion/emotion, relieved by rest or GTN ≤ 5 min) ^[2]
Pre-test probability (PTP) of obstructive CAD based on age, sex, symptom type, and risk factors ^[2]
Objective demonstration of myocardial ischaemia or coronary stenosis by appropriate non-invasive or invasive testing ^[2]

The classic three-component definition of angina:

Component	Definition
1	Substernal chest discomfort with characteristic quality and duration
2	Provoked by exertion or emotional stress
3	Relieved by rest or nitrates within 5 minutes

Typical angina = all 3 features
Atypical angina = 2 of 3 features
Non-cardiac chest pain = 0–1 feature ^[2]^[9]

Why is there no single diagnostic criterion? Because stable angina is a clinical syndrome, not a pathological diagnosis. A patient can have significant coronary stenosis without angina (silent ischaemia), or can have angina without significant epicardial disease (microvascular angina). The diagnosis requires integrating symptoms with objective evidence of ischaemia.

This is the key exam-tested definition. The 4th Universal Definition of MI (building on the 3rd Universal Definition) ^[1]^[2]:

Universal Definition of Myocardial Infarction — Must Know

Detection of a rise and/or fall of cardiac biomarker (preferably cardiac troponin), with at least 1 value above the 99th percentile of the upper reference limit (URL) ^[1]

AND at least one of ^[1]:

Clinical: ischaemic symptoms (chest pain)
ECG: new significant ST segment / T wave changes, or new LBBB, or development of pathological Q waves
Imaging: new loss of viable myocardium or new regional wall motion abnormality (e.g. lateral wall hypokinesia)
Identification of an intracoronary thrombus by angiography or at autopsy (added in 4th definition)

Key points about this definition:

Both a rise and/or fall pattern AND ≥ 1 value above the 99th percentile are required — this distinguishes acute injury (dynamic change) from chronic elevation (e.g. in CKD where troponin may be chronically mildly elevated without a rise-and-fall pattern)
The rise/fall pattern distinguishes acute MI from chronic myocardial injury
Unstable angina is diagnosed when there are ischaemic symptoms ± ECG changes but NO troponin rise (i.e. no necrosis has occurred) ^[1]

Type	Description	Diagnostic Criteria
Type 1	Atherosclerotic plaque disruption (most common) ^[1]	Standard MI criteria above (rise/fall of troponin + ≥ 1 clinical/ECG/imaging criterion)
Type 2	Mismatch between O₂ supply and demand (e.g. vasospasm, anaemia, tachyarrhythmia, hypotension) — check CBC for anaemia, PR for GIB ^[1]	Same biomarker criteria, but mechanism is NOT primary plaque event. Context determines type
Type 3	Unexpected cardiac death before blood samples are drawn ^[1]	Symptoms of ischaemia + new ischaemic ECG changes or LBBB, but death before biomarkers available
Type 4a	PCI-associated ^[1]	↑cTn > 5× 99th percentile URL + ≥ 1 of: ischaemic symptoms, new ECG changes, angiographic complication, imaging of new wall motion abnormality ^[2]
Type 4b	Stent thrombosis ^[1]	Verified stent thrombosis on angiography or autopsy + rise/fall biomarker pattern ^[2]
Type 5	CABG-associated ^[1]	↑cTn > 10× 99th percentile URL + new pathological Q waves/LBBB, or angiographic new graft/artery occlusion, or imaging evidence ^[2]

ST elevation criteria for diagnosing STEMI (must be present in ≥ 2 anatomically contiguous leads) ^[1]:

Leads	Threshold
V2–V3 (males ≥ 40 years)	≥ 2 mm (0.2 mV)
V2–V3 (males < 40 years)	≥ 2.5 mm
V2–V3 (females)	≥ 1.5 mm
All other leads	≥ 1 mm (0.1 mV)

New LBBB in the setting of ischaemic symptoms is treated as STEMI equivalent ^[1].

STEMI Equivalents — Don't Miss These

Beyond classic ST elevation, there are STEMI equivalents that mandate emergent reperfusion:

New LBBB with ischaemic symptoms ^[1]
De Winter T waves: depressed ST take-off with hyperacute T waves in precordial leads → proximal LAD occlusion → treat as anterior STEMI ^[1]
Posterior MI: reciprocal changes in V1–V3 (ST depression, tall R waves, tall upright T waves) → place V7–V9 for confirmation ^[1]
ST elevation in aVR > 1 mm with diffuse ST depression → suggests left main or severe triple-vessel disease ^[1]
Isolated RV MI: ST elevation in V1 > V2, ST elevation in V3R–V4R (right-sided leads) ^[1]

B. Diagnostic Algorithm

The diagnostic approach is fundamentally different for stable presentations and acute presentations.

Roadmap to stable IHD (ESC 2019/2024, building on ESC 2013) ^[2]:

Step 1: Clinical Assessment

Clinical assessment for clinical presentation and risk factors for IHD ^[2]
Determine whether the chest pain is typical angina, atypical, or non-cardiac

Step 2: Baseline Evaluation

Basic blood tests, resting 12-lead ECG, ± echo/cardiac MRI ^[2]

Step 3: Estimate Pre-test Probability (PTP)

The test of choice depends on the clinical pre-test probability (PTP) of CAD ^[2]
Derived based on demographics, symptom profile and risk factor profile ^[2]
Updated ESC 2019 PTP tables use age, sex, and symptom type
Diagnostic testing is only useful for PTP between 15% and 85% ^[2]:
- If PTP > 85%, then assuming all to be diseased will be superior to performing testing → treat as CAD, consider direct invasive coronary angiography (ICA) ^[2]
- If PTP < 15%, then assuming all to be without disease will be superior → consider non-cardiac causes ^[2]

Step 4: Diagnostic Testing (based on PTP and clinical context)

Anatomical test: usually CT coronary angiography ^[2]
Functional test: exercise tolerance test (ETT), stress imaging (echo, MRI, SPECT, PET) ^[2]
Invasive coronary angiography for high-risk or when non-invasive tests are inconclusive ^[2]

Step 5: Prognostic Evaluation

Risk of all-cause mortality determines the need for revascularisation after institution of optimal medical therapy (OMT) ^[2]
Basis: (1) clinical evaluation (2) LVEF (3) stress testing response (4) coronary anatomy ^[2]

Step 6: Management Decision

Appropriate management (medical vs revascularisation) based on risk of event ^[2]

For acute chest pain, the approach is time-critical ^[1]^[2]^[9]:

Step 1: Immediate Actions

Admit CCU if high-risk (ongoing chest pain, ↓BP, APO, ventricular arrhythmia) ^[9]
Bed rest with continuous ECG monitoring ^[9]
12-lead ECG stat — ideally within 10 minutes of first medical contact ^[9]

Step 2: ECG Interpretation

If ST elevation or new LBBB → STEMI → emergent reperfusion (primary PCI or thrombolysis)
If ST depression, T wave inversion, or non-diagnostic → proceed to serial troponin

Step 3: Serial Biomarkers

Cardiac enzymes daily × 3d (repeat troponin 6–12h later if 1st Tn is normal) ^[9]
Diagnostic cut-off of hsTnT: positive if baseline > 14 and > 100% rise 3–6h later ^[1]

Step 4: Integrate for Diagnosis

STEMI: ST elevation + ischaemic symptoms ± troponin rise
NSTEMI: troponin rise/fall + ischaemic symptoms or ECG changes (ST depression/T inversion) but NO ST elevation
Unstable angina: ischaemic symptoms (± ECG changes) but NORMAL troponin

Step 5: Concurrent Workup

Basic bloods: CBC, L/RFT, lipid profile (≤ 24h), aPTT/INR (baseline for heparin) ^[9]
CXR: usually non-diagnostic in ACS, look for other causes (aortic dissection, PE, pneumonia, pneumothorax) ^[9]
Target Hx and PE to rule out other life-threatening emergencies ^[1]

C. Investigation Modalities — Detailed Breakdown

1. Baseline Investigations (All Suspected IHD — Stable and Acute)

Test	What to Look For	Why
CBC, ± TFT	Anaemia and thyrotoxicosis may exacerbate IHD ^[2]	Anaemia ↓O₂ supply; thyrotoxicosis ↑demand (↑HR, ↑contractility). Both are reversible causes of worsening angina. If you fix the precipitant, the angina may resolve
Fasting glucose, HbA1c, ± OGTT	Screen for potential T2DM ^[2]	DM is a coronary risk equivalent; identifying it changes management targets
Fasting lipid profile	Screen for hyperlipidaemia ^[2]	LDL-C level guides intensity of statin therapy and LDL target
RFT (U/Cr/eGFR)	Renal dysfunction has negative effect on prognosis of CAD ^[2]	CKD is an independent CVD risk factor; also affects drug dosing (e.g. LMWH, contrast use)
LFT, CK	Baseline before starting statin ^[2]	Statins can rarely cause hepatotoxicity (↑ALT) and rhabdomyolysis (↑CK). Baseline values allow monitoring

Every patient with suspected IHD needs a resting ECG. It may be normal, but look for:

Finding	Significance
Pathological Q waves	Evidence of previous MI ^[2] — Q waves develop 12–24h after transmural infarction and often persist indefinitely ^[1]
ST/T changes	Evidence of myocardial ischaemia: ST depression, T wave inversion, or reversible ST/T changes esp associated with symptoms ^[2]. In ACS: evolving ST elevation/depression
New LBBB	STEMI equivalent in the right clinical context ^[1]. LBBB always indicates heart disease ^[14] — acute or chronic LV pathology
LVH	↑voltage criteria suggest hypertensive heart disease or AS — both exacerbate IHD and reduce specificity of stress testing ^[2]
Arrhythmias	AF (cardioembolic risk, rate-related ischaemia), pre-excitation (WPW — affects stress test interpretation) ^[2]

In ACS: 12-lead ECG stat and repeat at least daily × 3d (more frequently in severe cases) ^[9]

Routine baseline echocardiography is recommended (ESC 2013) to evaluate for ^[2]:

Regional wall motion abnormalities (RWMA) — evidence of previous silent infarct or ongoing ischaemia
LVEF — important prognostic parameter in stable CAD. LVEF < 50% associated with ↑↑ event risk regardless of severity of ischaemia ^[2]
Other structural cardiac conditions, especially valvular heart disease (AS, AR, HOCM) that may exacerbate or cause angina ^[2]

In IHD, the ischaemic cardiomyopathy pattern may be seen — functional mitral regurgitation from papillary muscle displacement, LV dilation, chordae restriction, and annular dilation ^[15].

Usually non-diagnostic in ACS ^[9]
Look for alternative diagnoses (widened mediastinum for aortic dissection, PTX, consolidation)
In chronic IHD: cardiomegaly (LV dilation from ischaemic cardiomyopathy), signs of heart failure (ABCDE: Alveolar oedema, Kerley B lines, Cardiomegaly, Dilated upper lobe vessels, pleural Effusion) ^[1]

2. Cardiac Biomarkers [1][2]

Cardiac troponins: gold standard for myocardial ischaemia ^[1]

Property	Detail
What are they?	Regulatory proteins of the cardiac sarcomere (troponin T, I, C). Troponin T and I are specific to cardiac muscle (unlike CK which is also in skeletal muscle)
Why do they rise in MI?	Myocardial necrosis → disruption of sarcolemma → release of intracellular troponin into bloodstream
Rise time	Rise at 4–6h after onset ^[2], detectable earlier with high-sensitivity assays (hsTn can detect at 1–3h)
Peak	Peak at 24–48h ^[1]
Duration of elevation	Return to baseline over 5–14 days ^[1] (TnT > TnI for duration)
Diagnostic cut-off of hsTnT	Positive if baseline > 14 ng/L and > 100% rise 3–6h later ^[1]
High-sensitivity troponin (hsTn) rapid rule-out protocols	0h/1h algorithm (ESC 2020): Rule-out if hsTnT < 5 at 0h, or < 12 at 0h with delta < 3 at 1h. Rule-in if ≥ 52 at 0h, or delta ≥ 5 at 1h

Other causes of elevated troponins (non-ACS) — troponin leak ^[2]:

Other ischaemia: tachycardia, coronary spasm, PCI or cardiothoracic surgery, hypoxia or hypotension
Other myocardial injury: myocarditis, heart failure, takotsubo cardiomyopathy, pulmonary embolism, aortic dissection, other cardiomyopathy (e.g. infiltrative), cardiotoxins
Systemic diseases: renal failure, sepsis, critical illness, stroke, SAH ^[2]

Interpreting Troponin — The Rise-and-Fall Pattern

A single troponin value is NOT diagnostic. What matters is the dynamic rise and/or fall pattern. A chronically elevated but stable troponin (e.g. in CKD) does not indicate acute MI. A patient with hsTnT of 20 at 0h and 85 at 3h has a delta > 100% — this is diagnostic of acute myocardial injury. Always compare serial values.

Cardiac-specific (cf. CK-MM for skeletal muscle, CK-BB for brain/GI) ^[1]
Rise at 4–6h, peak at 12h, normalize at 48–72h ^[2]
Caveat: not sensitive or specific (skeletal muscle damage, e.g. IM injection, causes false positives) ^[2]
Use: mainly to detect early re-stenosis — because cTn stays elevated for up to 10–14 days, a new CK-MB rise can identify re-infarction within this window ^[2]

Myoglobin: first marker to rise ^[1]^[2] (within 1–2h) but very non-specific (also rises in skeletal muscle injury)
LDH, AST: historical markers, rarely used now. LDH peaks at 3–5 days ^[1]

Biomarker	Rise	Peak	Normalisation	Best Use
Myoglobin	1–2h	6–8h	24h	Very early detection (largely superseded by hsTn)
CK-MB	4–6h	12h	48–72h	Detect re-infarction within 14 days
cTnT/cTnI	4–6h (hsTn: 1–3h)	24–48h	5–14 days	Gold standard for initial diagnosis

3. Non-Invasive Diagnostic Testing for CAD

Choice of investigation is generally dependent on pre-test probability of CAD ^[2]^[9]. The fundamental principle: different tests have different sensitivity and specificity → suitable for different groups of patients ^[2].

The simplest and most widely available functional test.

Property	Detail
Principle	Progressively increasing cardiac workload → provoke ischaemia in territories supplied by stenosed coronary arteries → detect by ECG changes, symptoms, or haemodynamic response
Protocol	Bruce protocol (7-stage test with treadmill increasing speed and grade) ^[1]
Target HR	Exercise until target HR reached: HR = (220 − age) × 0.8, or symptomatic, or ST-T changes ^[1]
Pre-test preparation	Stop antihypertensive on the day of test ^[1] (β-blockers should be withheld 48h before if assessing for diagnosis — they blunt HR response)
Positive test	Horizontal or downsloping ST depression ≥ 0.1 mV (1 mm) 80 ms after J point during exercise ^[2]

Useful in: Low-intermediate PTP (15–65%), normal baseline ECG, not on anti-ischaemic drugs ^[2]

Not suitable for ^[2]:

Abnormal baseline ECG (LBBB, paced rhythm, WPW, AF, LVH, digoxin) — these make ST interpretation unreliable
Limited exercise tolerance (unable to reach 85% max HR) due to non-cardiac disease

Duke Treadmill Score ^[1]: prognostic tool = Exercise time (min) − (5 × max ST deviation in mm) − (4 × angina index: 0 = none, 1 = non-limiting, 2 = exercise-limiting)

≥ 5: low risk (annual mortality < 1%)
−10 to +4: intermediate risk
≤ −11: high risk (annual mortality ≥ 5%)

Alternatives to exercise (for patients who cannot exercise) ^[1]:

Dobutamine (β₁ agonist → ↑HR, ↑contractility → ↑O₂ demand) — C/I: recent MI ^[1]
Adenosine / dipyridamole (coronary vasodilator → coronary steal phenomenon) — C/I: asthma ^[1] (adenosine can cause bronchospasm via A₁ receptor stimulation)

Alternatives to ECG (when ECG is uninterpretable) ^[1]:

Stress echocardiogram
Radionuclide myocardial perfusion imaging (rMPI) (thallium / technetium-99m) ^[1]

An anatomical test that directly visualises the coronary artery lumen.

Property	Detail
Principle	ECG-gated multi-detector CT with IV contrast to obtain high-resolution images of coronary arteries
Use	Non-invasive alternative for invasive coronary angiogram; significant stenosis defined as ≥ 70% stenosis ^[2]. To assess coronary artery anatomy in a non-invasive means ^[1]
Best for	Low-intermediate PTP (15–50%) due to excellent NPV (99–100%) ^[2] — superb at ruling out CAD
Advantages	↑↑NPV (a normal CTCA essentially excludes obstructive CAD), rapid, non-invasive
Limitations	Requires adequate breath-holding, HR ≤ 65 bpm (may need pre-treatment with β-blocker), not ideal in severe obesity, CKD (contrast nephropathy), prior CABG, prior stenting (metal artefact) ^[2]

CT Calcium Scoring (Agatston Score) ^[2]^[16]:

Non-contrast CT used to quantify coronary artery calcification
Coronary calcium content is exclusively due to coronary atherosclerosis except in renal failure patients (associated with medial calcification) ^[2]
Quantification: > 130 HU pixels regarded as calcium; Agatston score > 100 generally correlated with significant risk of CAD ^[2]
Caveat: poor correlation with degree of luminal stenosis → zero calcium score cannot be used to rule out coronary artery stenoses in symptomatic individuals ^[2]
Role: ↑Ca score associated with ↓specificity of CTA → NOT interpret CTA with Agatston > 400 ^[2]

Why can a calcium score of zero still miss significant stenosis? Because the vulnerable (unstable) plaque that causes ACS is often a non-calcified, lipid-rich plaque with a thin fibrous cap. Calcium is a marker of plaque burden and atherosclerosis, but not all plaques are calcified. A young patient with a soft, non-calcified culprit lesion can have a calcium score of zero and still have a critical stenosis.

Property	Detail
Principle	Echocardiography performed at rest and during stress (exercise or dobutamine). Ischaemic segments show new regional wall motion abnormalities (RWMA) under stress
Advantages	No radiation, widely available, provides additional structural information (VHD, LVEF), can assess viability (dobutamine low-dose protocol)
Limitations	Operator-dependent, poor acoustic windows in some patients (obesity, lung disease)
Interpretation	Normal segments become hyperkinetic with stress. Ischaemic segments become hypokinetic/akinetic. Scarred segments are akinetic at rest and remain so

A functional test that directly assesses myocardial blood flow.

Property	Detail
Radiopharmaceuticals	Thallium-201 (²⁰¹Tl) or technetium-99m sestamibi (⁹⁹ᵐTc-sestamibi) ^[1]^[16]
Principle	Coronary steal phenomenon ^[16]: at rest, flow to ischaemic territory maintained by compensatory vasodilation + collaterals. With stress (exercise or pharmacological vasodilation with adenosine/dipyridamole), normal vessels dilate maximally → blood "stolen" to normal myocardium → ↓↓ perfusion of affected myocardium → appears as "cold spots" ^[16]
Interpretation ^[16]	Normal → homogeneous perfusion
	Ischaemia → cold spots under stress only (reversible defect)
	Infarct → cold spots at rest AND under stress (fixed defect)
Main uses ^[16]	Determine adequacy of blood flow ± stress (functional → detects haemodynamically significant stenosis defined by ≥ 50% diameter stenosis) ^[16]
	Determine viability of myocardium → decide whether to perform PCI or CABG ^[16]

This is important because compensatory vasodilation in response to hypoxaemia means that significant ischaemia will not set in with < 50% stenosis despite presence of structural lesions detected in anatomical imaging. This gives an advantage to MPI as a functional test over anatomical tests such as cardiac MRI, CT coronary angiography or calcium score. ^[16]

Prognostic value of stress imaging ^[2]:

High risk = area of ischaemia > 10% (> 10% for SPECT, ≥ 3 LV segments for echo)
Intermediate risk = area of ischaemia 1–10%
Low risk = no ischaemia ^[2]

Property	Detail
Principle	Multimodal cardiac assessment: structure, function, perfusion, and viability, all without radiation
Use	To assess both structure + function ^[1]. Resting cardiac MRI as alternative to echo at rest ^[2]
Stress CMR	Adenosine or do

Management of Ischaemic Heart Disease

The management of IHD rests on two pillars ^[2]:

Improve quality of life → symptomatic relief (anti-anginal therapy)
Improve life expectancy → prognostic therapy (prevent MI, death, heart failure)

The approach differs fundamentally between stable IHD (chronic coronary syndrome) and acute coronary syndrome (ACS = UA/NSTEMI/STEMI). In stable disease, you have time to optimise medical therapy and decide on revascularisation electively. In ACS, the immediate priorities are to restore coronary flow, limit infarct size, prevent death, and treat complications ^[1]^[2]^[9].

PART I: MANAGEMENT OF STABLE IHD

Measure	Detail	Rationale
Lifestyle: stop smoking, regular exercise (but not beyond point of discomfort) ^[2]	Smoking cessation drastically ↓MI risk after just 1 year ^[2]. Moderate exercise 30 min × 5/week	Smoking causes endothelial injury, ↑thrombosis, ↑vasospasm. Exercise ↑HDL, ↓insulin resistance, improves endothelial function
Treat precipitating factors: thyrotoxicosis, anaemia ^[2]	Check TFT and CBC in all patients with angina ^[2]	Thyrotoxicosis ↑O₂ demand (↑HR, ↑contractility). Anaemia ↓O₂ supply. Correcting these may abolish angina entirely without need for further intervention
DM: aim A1c < 7%, consider SGLT2i or GLP-1a ^[2]	SGLT2i (empagliflozin, dapagliflozin) and GLP-1 RA (semaglutide, liraglutide) have proven cardiovascular outcome benefits	DM accelerates atherosclerosis via multiple mechanisms. SGLT2i/GLP-1 RA independently reduce MACE (major adverse cardiovascular events)
HTN: aim < 140/90, use BB if indicated ^[2]	β-blocker preferred if coexistent angina; otherwise ACEI/ARB	HTN ↑afterload → ↑wall stress → ↑O₂ demand. Also accelerates endothelial dysfunction
Lipids: ↓LDL to < 1.8 mmol/L with lifestyle and drug ^[2]	ESC 2019/2021: very high risk = LDL < 1.4 mmol/L AND ≥ 50% reduction ^[17]	LDL is the primary driver of atherosclerosis; aggressive lowering stabilises plaques and reduces events

B. Pharmacological Therapy — Prognostic Treatment [2]

These drugs reduce the risk of MI and death and should be given to all patients with established CAD unless contraindicated.

Drug	Mechanism	Regimen	Key Points
Aspirin	Irreversible COX-1 inhibition → ↓thromboxane A₂ (TXA₂) synthesis → ↓platelet aggregation	Low-dose (75–325 mg daily) prescribed for all patients with CAD indefinitely ^[2]	First-line antiplatelet. S/E: GI bleeding, peptic ulcer → consider PPI cover
Clopidogrel (Plavix)	Irreversible P2Y₁₂ ADP receptor antagonist on platelets → ↓ADP-mediated platelet activation	75 mg daily	Equally/more effective; used as alternative to aspirin if intolerant (↑cost) ^[2]. Combination therapy (DAPT): standard of care post-ACS/PCI, but not associated with benefit in stable CAD ^[2]

Why is DAPT not used in stable CAD alone? In stable disease, the plaque surface is intact with no acute thrombus. Single antiplatelet (aspirin) provides adequate protection. Adding a second antiplatelet increases bleeding risk without proportionate benefit. The exception is post-PCI, where the denuded stent surface is thrombogenic.

Statins: recommended in all patients ^[2]

Property	Detail
MoA	Inhibit HMG-CoA reductase → ↓intracellular cholesterol synthesis → ↑LDL receptor expression → ↑LDL-C clearance from blood. Also: plaque stabilisation, ↓inflammation, reversal of endothelial dysfunction, ↓thrombogenicity ^[17] — "pleiotropic effects"
Target	LDL < 1.8 mmol/L and/or > 50% reduction if goal cannot be achieved ^[2]. Updated ESC 2019: < 1.4 mmol/L for very high-risk patients
Choice	High-intensity: atorvastatin 40–80 mg or rosuvastatin 20–40 mg ^[17]. Generally more conservative dosing in Asians (higher plasma concentrations at same dose) ^[17]
S/E	Generally very well-tolerated (serious S/E < 2%) ^[17]. Myopathy (myalgia → myositis → rhabdomyolysis), hepatotoxicity (↑ALT), ↑diabetes risk
Monitoring	Baseline LFT and CK before starting ^[2]. Repeat LFT at 3 months, then periodically

If LDL target not achieved on maximum tolerated statin ^[17]:

Add ezetimibe (blocks intestinal cholesterol absorption via NPC1L1 transporter) — typically ↓LDL by further 15–20%
Add PCSK9 inhibitor (evolocumab, alirocumab — monoclonal antibodies that ↑LDL receptor recycling → ↑LDL clearance) — can ↓LDL by 50–60% on top of statin. Reserved for very high-risk patients not at target on statin + ezetimibe

Property	Detail
MoA	ACEI: inhibits ACE → ↓angiotensin II → ↓vasoconstriction, ↓aldosterone → ↓preload/afterload, ↓cardiac remodelling, ↓endothelial dysfunction. ARB: blocks AT₁ receptor directly
Indication	Evidence unclear in stable CAD alone without comorbidities ^[2]. Indications: when comorbidities are present, e.g. DM, HTN, LV HF where otherwise indicated ^[2]
Regimen	Ramipril, perindopril, or enalapril (ACEI); valsartan, losartan (ARB). Use one, not both — combination associated with ↑adverse events without ↑benefits ^[2]
C/I	Bilateral renal artery stenosis, hyperkalaemia, pregnancy, angioedema (ACEI)

C. Pharmacological Therapy — Anti-Anginal (Symptomatic) Treatment [1][2]

These drugs relieve angina symptoms but have limited or no proven effect on mortality (except β-blockers post-MI).

Breaking down the mechanism from first principles:

Nitrates release nitric oxide (NO) → activates guanylate cyclase → ↑cGMP → smooth muscle relaxation
Venodilation (major effect) → ↓venous return → ↓preload → ↓LVEDV → ↓wall stress → ↓O₂ demand
Arteriodilation (modest) → ↓afterload → ↓O₂ demand
Coronary vasodilation → ↑supply, especially to ischaemic zones by redistributing perfusion from epicardial to endocardial sites ^[2]

Form	Drug	Use	Notes
Short-acting	Sublingual nitroglycerin (GTN) 0.3–0.6 mg Q5min, max 1.2 mg within 15 min ^[2]	For ALL patients with symptomatic stable CAD — acute effort angina or prophylactically before exertion ^[2]	Should rest sitting while taking nitrates (standing → syncope from ↓BP; supine → ↑VR → ↑preload → negates the effect) ^[2]
Long-acting	Isosorbide mononitrate (ISMN) 20–60 mg daily	Usually as 2nd line if BB/CCB are ineffective ^[2]	Must have nitrate-free or nitrate-low interval of 8–10h to avoid tolerance ^[2]. Risk of worsening endothelial dysfunction with long-term use ^[2]

S/E: headache, dizziness, flushing, hypotension ^[1]

C/I: HOCM (↓preload → ↓LV cavity size → ↑LVOT obstruction), PDE5 inhibitors (e.g. Viagra within 24h, tadalafil within 48h ^[1]) — both cause vasodilation → combined use → severe life-threatening hypotension

Beta-blocker (cardio-selective): proven survival benefit [in post-MI patients], ↓HR/BP/contractility and improve coronary perfusion ^[1]

Property	Detail
MoA	Block β₁-adrenoceptors → ↓HR (negative chronotropy) → ↓myocardial O₂ demand AND ↑diastolic filling time → ↑coronary perfusion. ↓Contractility (negative inotropy) → ↓O₂ demand. ↓BP → ↓afterload
Role	1st line anti-anginal treatment in patients without C/I ^[2]. Clearly effective in ↓exercise-induced angina, ↑exercise tolerance, limit ischaemic episodes ^[2]. Definitely prognostic in post-MI, but effect unclear in stable CAD only ^[2]
Choice	β₁-selective: metoprolol (Betaloc), bisoprolol (Zebeta); α₁β-selective: carvedilol ^[2]
Target	Titrate to HR < 70 ^[1]
S/E	Precipitates ADHF, bronchospasm, exacerbate PAD, fatigue, sexual dysfunction, hypoglycaemia masking, hyperkalaemia ^[2]

Contraindications of beta-blockers ^[1]:

Poor ventricular function (in acute decompensation — but NOT in stable, compensated HF where BB improve survival)
Acute pulmonary oedema
Heart block (2nd / 3rd degree)
Asthma / COPD (severe obstructive airways disease — β₂ blockade → bronchospasm)

BB in Heart Failure — A Common Confusion

β-blockers are contraindicated in acute decompensated heart failure (they worsen pump function acutely). However, in stable, compensated HFrEF, specific β-blockers (bisoprolol, carvedilol, metoprolol succinate) are life-saving — they reverse maladaptive sympathetic activation and reduce mortality. The key is to start low and go slow, only when the patient is euvolaemic and stable. BB is NOT C/I in stable HF, COPD, or peripheral vascular disease ^[2].

CCBs block L-type calcium channels. There are two functionally distinct classes:

Class	Drugs	Effects	Use in IHD	C/I
Dihydropyridine (DHP)	Amlodipine, nifedipine, felodipine	Mainly vascular: vasodilation with little cardiac effect ^[2]. Reflex tachycardia possible	Usually combined with BB ^[2] (BB counteracts reflex tachycardia). Safe in patients with poor cardiac function ^[2]	Severe AS, HOCM (↓PVR → ↓↓BP due to fixed ↓SV) ^[2]
Non-DHP	Diltiazem, verapamil	Vascular + cardiac: ↓HR, ↓contractility, ↓AVN conduction ^[2]	Alternative to BB in those who cannot take BB ^[2]. Anti-anginal properties similar to BB	C/I: HFrEF (negative inotropy worsens pump failure) ^[2]. NOT combined with BB → 3rd degree HB risk ^[2]

Alternative: rate-limiting CCB (diltiazem / verapamil) used if BB contraindicated ^[1]

Usually used as 2nd line to BB/CCB combination ^[2]:

Drug	Mechanism	Key Notes
Ranolazine	Inhibits late inward Na⁺ channel → ↓Na/Ca exchange → ↓intracellular Ca²⁺ → ↓contractility → ↓angina ^[2]	Also ↓recurrent ischaemia, possible ↓arrhythmia but associated with ↑QTc ^[2]
Trimetazidine (Vastarel)	↓Fatty acid oxidation → protect myocardium from ischaemic injury ^[2]	Metabolic modulator — shifts energy substrate from FA to glucose (more O₂-efficient)
Nicorandil	Opens K⁺ channel → arteriovenous + coronary dilatation ^[2]	Dual mechanism: K⁺ channel opening + nitrate-like effect
Ivabradine	Blocks HCN channel → ↓If → ↓HR ^[2]	Used if sinus rhythm ≥ 70 bpm. Should be limited to HF patients as latest trials showed possible ↑CVD death and non-fatal MI ^[2]

Revascularisation = restoring coronary blood flow, either by PCI or CABG.

Indications for revascularisation ^[2]:

Group	Purpose	When
High-risk anatomy	Improve prognosis	Left main stem disease (≥ 50% stenosis), proximal LAD disease (≥ 70%), 3-vessel disease (≥ 70%) ^[1]^[2] — these carry high mortality on OMT alone
Symptomatic despite OMT	Improve symptoms	Medically refractory angina ^[1] — persistent symptoms despite maximal tolerated anti-anginal therapy
Large area of ischaemia	Both	> 10% ischaemic myocardium on functional testing

PART II: MANAGEMENT OF ACUTE CORONARY SYNDROME

This is extremely high-yield for exams. The initial approach applies to all ACS (STEMI, NSTEMI, UA):

Admit CCU for high-risk cases ^[1] Complete bed rest + NPO for first 12h ^[1] Close monitoring: BP/P, IO Q1h, cardiac monitoring with defibrillator standby ^[1] Target Hx and PE to rule out other life-threatening emergencies: aortic dissection, pulmonary embolism, tension pneumothorax, perforated peptic ulcer / esophagus ^[1]

Acute pharmacological therapy — the mnemonic "MONA-B" (Morphine, Oxygen, Nitrates, Aspirin, Beta-blocker) is a useful framework:

Agent	Detail	Rationale
Oxygen	Supplement to keep SaO₂ > 90% and pO₂ > 60 mmHg ^[2]. Do NOT give routinely if SpO₂ > 94% (DETO₂X-AMI trial)	↑O₂ delivery to ischaemic myocardium. But hyperoxia → coronary vasoconstriction → potentially harmful
Nitrates	IV GTN infusion, titrated to pain relief and BP (avoid if SBP < 90)	↓Preload (venodilation) → ↓O₂ demand. Some coronary vasodilation → ↑supply
Aspirin	Aspirin at/suspect diagnosis ^[2]. Loading dose 300 mg PO stat, then 80–100 mg daily indefinitely	Irreversible COX-1 inhibition → ↓TXA₂ → ↓platelet aggregation on the acute thrombus. Mortality benefit proven (ISIS-2 trial)
P2Y₁₂ blocker	P2Y₁₂ blocker at diagnosis or at PCI ^[2]. Ticagrelor 180 mg loading then 90 mg BD (preferred for ACS — faster onset, reversible). Clopidogrel 300–600 mg loading then 75 mg daily (if ticagrelor C/I or patient needs OAC). Prasugrel 60 mg loading then 10 mg daily (if going for PCI, no prior stroke)	Blocks ADP-mediated platelet activation via P2Y₁₂ receptor → more complete platelet inhibition when combined with aspirin (DAPT)
Beta-blocker	Metoprolol 25 mg BD oral, titrate to HR < 70 ^[1]. Give within 24h if no C/I	↓HR → ↓O₂ demand + ↑diastolic perfusion time. ↓Risk of arrhythmia. Mortality benefit in post-MI (COMMIT, CAPRICORN)
Heparin	LMWH (enoxaparin 1 mg/kg SC Q12h) or UFH ^[1]. Choice: UFH if primary PCI (faster onset), LMWH if thrombolysis, UFH/LMWH if not for reperfusion ^[1]	Anticoagulation prevents propagation of the coronary thrombus and reduces re-occlusion risk
Statin	High-intensity statin always (≤ 24h) ^[2]. Atorvastatin 80 mg stat	Early pleiotropic effects: plaque stabilisation, ↓inflammation, ↓endothelial dysfunction. Late: lipid-lowering
ACEI/ARB	ACEI/ARB always (≤ 24h) ^[2]. Ramipril or perindopril	↓Ventricular remodelling, ↓afterload, ↓neurohormonal activation. Mortality benefit especially if ↓LVEF or anterior MI
MRA	MRA if LVEF ≤ 40% + HF/DM ^[2]. Eplerenone 25–50 mg	Blocks aldosterone → ↓fibrosis, ↓remodelling. Mortality benefit (EPHESUS trial)
Morphine	IV morphine ^[2] if nitrates insufficient. IV Maxolon 5–10 mg antiemetic ± sedation ^[2]	↓Distress → ↓adrenergic drive → ↓SVR, ↓BP, ↓risk of ventricular arrhythmia ^[2]. Use cautiously — delays absorption of oral P2Y₁₂ inhibitors

S/E of LMWH/UFH: heparin-induced thrombocytopenia (HIT), osteoporosis, hyperkalaemia ^[1]

B. Reperfusion Therapy in STEMI [1][2]

"Time is muscle" — the earlier reperfusion occurs, the more myocardium is salvaged. The two strategies are primary PCI (preferred) and thrombolysis (if PCI unavailable).

Indications in STEMI ^[1]:

Primary PCI (aim door-to-balloon time ≤ 90 minutes):
- Present < 12 hours after onset of chest pain
- Clinical and/or ECG evidence of ongoing ischaemia between 12–24 hours of onset
- Cardiogenic shock / severe acute HF (irrespective of onset time) ^[1]
Rescue PCI: within 3 hours after failed thrombolysis ^[1]
Post-thrombolytic PCI: within 24 hours after successful thrombolysis to reduce re-infarction rate ^[1]

PCI Procedure ^[1]:

Pre-med: DAPT ^[1]
Vascular access: femoral artery vs radial artery (preferred due to lower bleeding risk: radial artery is paired with ulnar artery, and can be compressed easily against radius) ^[1]
Coronary angiography: inject contrast at mouth of coronary artery ^[1]
PTCA: balloon + stent placement ^[1]

Stent types ^[1]:

Type	Detail	DAPT Duration
Drug-eluting stent (DES)	Drugs reduce neointimal proliferation → reduce in-stent restenosis. Drugs: paclitaxel (antiproliferative), sirolimus ^[1]. Standard of care	12 months ± extra 18 months if no S/E (late stent thrombosis risk) ^[1]
Bare metal stent (BMS)	30% risk of re-stenosis ^[1]	4–6 weeks ^[1]

BMS used if: high bleeding risk / cannot take DAPT (e.g. anticipated surgery within 12 months) ^[1]

Pre-PCI: DAPT (aspirin + ticagrelor) ± heparin ± GPIIb/IIIa inhibitors (only in STEMI) ^[1]

GPIIb/IIIa inhibitor (IV abciximab / eptifibatide): if heavy clot load ^[1]. Mechanism: blocks the final common pathway of platelet aggregation (glycoprotein IIb/IIIa receptor mediates fibrinogen cross-linking between platelets)

Post-PCI (with stent) ^[1]:

DAPT (aspirin + ticagrelor) for 12 months (DES)
Lifelong aspirin 80 mg/day ^[1]

PCI Complications ^[1]:

Overall mortality < 0.5% ^[1]
Puncture: pseudoaneurysm, aortic dissection, coronary artery dissection, myocardial infarction
Balloon: in-stent restenosis (15%) — due to elastic recoil and neointimal hyperplasia
Stenting: stent thrombosis (1–2%), stent infection (rare)

Indications: STEMI with symptom onset within 12h + PCI not available within 2h from diagnosis ^[1] NOT used in NSTEMI/UA ^[1] — because there is no complete thrombotic occlusion; the thrombus is platelet-rich, non-occlusive, and thrombolysis may paradoxically worsen things

Choice of agent ^[1]:

Agent	Type	Notes
Tenecteplase (TNK-tPA)	Fibrin-specific	Single bolus (weight-adjusted). Need LMWH cover ^[1]. Most commonly used
Alteplase (tPA)	Fibrin-specific	Infusion protocol. Need LMWH cover ^[1]
Reteplase (rPA)	Fibrin-specific	Double bolus protocol. Need LMWH cover ^[1]
Streptokinase	Fibrin non-specific	Cheaper. Cannot give with IV heparin (long half-life: combined use = bleeding risk) ^[1]. Cannot be re-used within 6 months (antigenic)

Signs of successful reperfusion ^[1]^[2]:

Clinical: chest pain subsides
Biochemical: early CPK peak ^[1]
ECG: accelerated nodal/idioventricular rhythm (AIVR), resolution of ST elevation of ≥ 50% in the worst ECG lead 90 min post-fibrinolytic ^[1]^[2]

S/E: allergy/anaphylaxis (2%), haemorrhagic stroke (1%) ^[1]

Post-thrombolysis pathway ^[1]:

Successful reperfusion → routine PCI in 2–24h
Failure → rescue PCI stat

Thrombolysis Contraindications — Must Know

Absolute C/I ^[2]:

Previous haemorrhagic stroke at any time
Other strokes/CVA within 3 months (except acute ischaemic stroke within 4.5h)
Known malignant intracranial neoplasm
Known structural cerebrovascular lesion (e.g. AVM)
Active bleeding or bleeding diathesis (does not include menses)
Suspected aortic dissection
Significant closed head/facial trauma within 3 months
Intracranial/intraspinal surgery within 2 months
Severe uncontrolled HTN unresponsive to emergency therapy
For streptokinase: prior treatment within 6 months

Relative C/I ^[2]:

Severe uncontrolled HTN on presentation (BP > 180/110)
History of chronic severe poorly controlled HTN
Prior ischaemic stroke > 3 months or known intracerebral pathology
Traumatic or prolonged (> 10 min) CPR
Oral anticoagulant therapy
Major surgery < 3 weeks
Non-compressible vascular punctures
Recent internal bleeding (within 2–4 weeks)
Pregnancy
Active peptic ulcer

Thrombolysis is NOT indicated in NSTEMI/UA — no benefit, may even be harmful (not thrombotic occlusion → no benefit at all) ^[2].

The key decision is timing of invasive strategy based on risk stratification:

High-risk features requiring invasive treatment ^[1]:

Refractory angina
Cardiogenic shock
Acute pulmonary oedema
Ventricular arrhythmia
ST segment changes ≥ 0.1 mV
New bundle branch block
Elevated troponin > 0.1 mg/mL
High risk score (TIMI ≥ 3, GRACE > 140) ^[1]

NSTEMI note: ST elevation (> 1 mm) in aVR suggests left main / severe triple vessel disease → directly go for CABG ^[1]

CABG indications for NSTEMI/STEMI ^[1]:

Anatomical considerations (can apply SYNTAX score ≥ 23 → favours CABG) ^[1]:
- Triple vessel disease (≥ 70% stenosis)
- Proximal LAD disease (≥ 70% stenosis)
- Left main disease (≥ 50% stenosis) or left main-equivalent disease (proximal LAD + proximal LCx) ^[1]
Post-MI mechanical complications ^[1]:
- Ventricular septal rupture (VSR)
- LV free wall rupture / aneurysm

Mortality: number of vessels — 1VD < 2VD < 3VD < LMS disease ^[2]

Aspect	CABG	PCI
Best for	3VD, LMS, proximal LAD, DM, LV dysfunction	1–2 VD, non-proximal LAD, surgical high risk
SYNTAX score	≥ 23 favours CABG	< 23 favours PCI
Graft conduit	LIMA-to-LAD (gold standard: 90% 10y patency), saphenous vein grafts (60–70% 10y patency)	Drug-eluting stent
DAPT duration	Aspirin lifelong, no mandatory P2Y₁₂ inhibitor long-term (unless stented)	DAPT for 12 months (DES), then aspirin lifelong
Advantages	More complete revascularisation, better long-term survival in complex disease	Less invasive, shorter recovery, lower procedural risk
Disadvantages	Major surgery (sternotomy, CPB), longer recovery, higher procedural risk (stroke 1–2%)	In-stent restenosis, stent thrombosis, incomplete revascularisation in complex anatomy

IHD is a common cause of functional mitral regurgitation — papillary muscle displacement, restricted leaflet closure, annular dilation from LV remodelling post-MI ^[15]. Significant MR may require concurrent mitral valve repair at CABG.

A. Secondary Prevention [2]

This is the lifelong pharmacological and lifestyle strategy after any ACS event.

Long-Term Drug Therapy [2]

Drug	Regimen	Notes
DAPT = Aspirin + P2Y₁₂ inhibitor	Aspirin: administered indefinitely ^[2]. P2Y₁₂ blocker: administered for ≥ 12 mo if any stent used (mandatory), 1–12 mo even if no PCI done ^[2]	Clopidogrel 75 mg QD, prasugrel 10 mg QD, or ticagrelor 90 mg BD ^[2]. Caveat: clopidogrel interacts with PPI → inhibit CYP2C19/3A4 activation of clopidogrel prodrug → treatment failure ^[2]
β-blockers	Given to all stable patients if no C/I ^[2]. C/I: bradycardia, AVB, ↓BP, asthma ^[2]	NOT C/I in HF, COPD, peripheral vascular disease ^[2]
ACEI/ARB	Given to all post-ACS patients, especially if ↓LVEF, anterior MI, DM, HTN	↓Ventricular remodelling, ↓mortality
High-intensity statin	Statin always, regardless of serum cholesterol level ^[2]	Target LDL < 1.4 mmol/L (ESC 2019)
MRA	If LVEF ≤ 40% + HF/DM ^[2]. Eplerenone	Monitor K⁺ and renal function
Anticoagulation	Warfarin if ↑embolic risk (e.g. LV thrombus, AF) ^[2]. Consider DOAC for AF	"Triple therapy" (DAPT + OAC) for limited period if concomitant AF, then step down

Risk Factor Modification [2]

Smoking: drastic ↓MI risk after just 1 year of smoking cessation, doubles 5-year mortality ^[2]
Hyperlipidaemia: high-dose statins for aggressive ↓lipid (regardless of serum cholesterol level) → ↓mortality ^[2]
Lifestyle: regular exercise, maintain ideal body weight, Mediterranean diet ^[2]
Other co-morbidities: good control of HTN and DM ^[2]

Mobilisation and Rehabilitation [2]

Takes 4–6 weeks to replace necrotic tissue by fibrotic tissue → restrict physical activities until then, offer cardiovascular rehabilitation ^[2]
Usually: mobilise in 2d, discharge in 3–5d, resume work in 4–6w ^[2]

Post-MI Risk Stratification [2]

LVEF by echo → guide further management to ↓LV remodelling + ↓arrhythmia risk ^[2]
Residual ischaemia → stress test: pre-discharge or symptom-limited stress 2–3w post-MI ^[2]
Arrhythmia during convalescent phase by 24h ECG for VT/frequent ventricular arrhythmia ^[2]

ICD indications post-MI ^[2]:

LVEF ≤ 30–35%, ≥ 40 days post-MI, on optimal medical therapy, NYHA II-III, good functional status with expected survival > 1 year

Modality	Stable IHD	NSTEMI/UA	STEMI
Aspirin	Lifelong	Loading + lifelong	Loading + lifelong
P2Y₁₂ inhibitor	Only if post-PCI or intolerant to aspirin	Loading + 12 months	Loading + 12 months
Anticoagulation	Not routine	LMWH or UFH acutely	UFH if PCI, LMWH if lysis
β-blocker	1st line anti-anginal; prognostic post-MI	Always if no C/I	Always if no C/I
Nitrates	PRN (short-acting) ± long-acting	IV acutely	IV acutely
CCB	If BB C/I or added to BB	If ongoing symptoms	Not 1st line
Statin	All patients	High-intensity ≤ 24h	High-intensity ≤ 24h
ACEI/ARB	If comorbidities	All patients	All patients
MRA	Not routine	If LVEF ≤ 40% + HF/DM	If LVEF ≤ 40% + HF/DM
Reperfusion	Elective if refractory / high-risk anatomy	Risk-stratified invasive approach	Primary PCI or thrombolysis

High Yield Summary — Management of IHD

Stable IHD: Prognostic (aspirin + statin ± ACEI/ARB) + Symptomatic (GTN PRN + BB 1st line ± CCB ± 2nd line agents). Revascularise if high-risk anatomy (LMS, 3VD, proximal LAD) or refractory symptoms
ACS Initial Mx (SAQ!!): Admit CCU, bed rest, monitoring, rule out DDx. MONA-B + heparin + statin + ACEI/ARB
STEMI reperfusion: Primary PCI (door-to-balloon ≤ 90 min) preferred. Thrombolysis if PCI unavailable within 120 min and onset < 12h. Rescue PCI if lysis fails. Routine PCI 2–24h after successful lysis
Thrombolysis NOT for NSTEMI/UA — no complete occlusion, no benefit, may be harmful
NSTEMI/UA: Risk-stratify (GRACE/TIMI) → immediate/early/delayed invasive vs ischaemia-guided conservative
PCI: DES preferred (DAPT 12 months + lifelong aspirin). BMS only if high bleeding risk / anticipated surgery
CABG: LMS ≥ 50%, 3VD, proximal LAD, SYNTAX ≥ 23, DM with multi-vessel disease, mechanical complications
Secondary prevention post-ACS: DAPT (aspirin + P2Y₁₂) ≥ 12 months → lifelong aspirin. BB, ACEI/ARB, high-intensity statin for ALL. MRA if LVEF ≤ 40%. ICD if LVEF ≤ 30–35% ≥ 40d post-MI
Nitrate C/I: HOCM, PDE5 inhibitors. BB C/I: acute pulm oedema, 2nd/3rd degree HB, asthma, acute HF decompensation
Clopidogrel + PPI interaction: PPI inhibits CYP2C19 → ↓clopidogrel activation → treatment failure. Use pantoprazole (less interaction) or switch to ticagrelor

Active Recall - Management of IHD

References

^[1] Senior notes: Maksim Medicine Notes.pdf (Sections 1.3, Stable Angina, ACS management, PCI, CABG, pp.7–13) ^[2] Senior notes: Ryan Ho Cardiology.pdf (Sections 3.2, CAD management, ACS approach, long-term management, pp.115–145) ^[9] Senior notes: Ryan Ho Fundamentals.pdf (Sections 3.1.1, Chest Pain approach, HF management, pp.202–219) ^[15] Lecture slides: Cardiac Surgery Tutorial_Prof. D Chan.pdf (p.43, Ischaemic heart disease and functional MR) ^[17] Senior notes: Ryan Ho Endocrine.pdf (Section 6.2.3.2, Management of Dyslipidaemia, pp.125–128)

Complications of Ischaemic Heart Disease

The complications of IHD — particularly of acute myocardial infarction — are a high-yield SAQ/OSCE topic. Understanding when and why each complication occurs is far more useful than rote memorisation.

The key principle: once myocardial necrosis occurs, the infarcted tissue undergoes a predictable sequence:

Minutes to hours: electrically unstable (→ arrhythmias)
Hours to days: necrotic tissue is soft, weak, and infiltrated by inflammatory cells (→ mechanical rupture, pericarditis)
Days to weeks: granulation tissue replaces necrotic myocardium (→ ongoing weakness, risk of aneurysm)
Weeks to months: fibrotic scar formation (→ remodelling, heart failure, chronic arrhythmias)
Long-term: adverse ventricular remodelling, ischaemic cardiomyopathy, recurrent events

Complications of MI — Timeline Framework

Timing	Complications
Immediate (min–hours)	Arrhythmias (VF, VT, AV block), sudden cardiac death, cardiogenic shock
Early (hours–days)	Pump failure/APO, peri-infarction pericarditis, acute MR, IV septal rupture, free wall rupture
Subacute (days–weeks)	Dressler syndrome, LV aneurysm, mural thrombus + embolism
Late (weeks–months+)	Ventricular remodelling, ischaemic cardiomyopathy, chronic HF, recurrent ischaemia

I. Arrhythmic Complications

Arrhythmia: usually due to scar tissue after MI ^[1]

During the acute phase (first hours), the ischaemic/infarcted myocardium is electrically unstable because:

Anaerobic metabolism → intracellular acidosis → K⁺ efflux from damaged cells + Ca²⁺ influx ^[2] → altered resting membrane potential and action potential duration
This creates electrical heterogeneity between healthy and injured tissue → re-entrant circuits → VT/VF
Autonomic imbalance: ↑sympathetic activation (pain, anxiety) promotes ectopy; vagal activation (especially in inferior MI) promotes bradycardia

During the chronic phase, the scar tissue from healed MI forms a fixed substrate for re-entry → risk of late VT/VF and sudden cardiac death.

Arrhythmia	Mechanism	Management
Ventricular ectopics (most common) ^[1]	Electrical instability of ischaemic myocardium → premature depolarisations from irritable foci	Usually benign, no specific Rx unless frequent/sustained. Correct electrolytes (K⁺, Mg²⁺)
VT/VF (15%) ^[1]	Re-entrant circuit involving border zone between infarct and normal myocardium. VF is the most common cause of death in the first hour after MI	VF: Prompt defibrillation with reference to ACLS algorithm ^[2]. Stable sustained monomorphic VT: Amiodarone 150 mg IV over 10 min ^[2], lignocaine, or synchronised cardioversion if haemodynamically unstable. Sustained polymorphic VT: Unsynchronised cardioversion starting with 200 J ^[2]
AF/AFlutter	Common and frequently transient, can be a sign of impending or overt LVF ^[2]. Atrial stretch from ↑LA pressure (LV failure) → triggers AF	Digoxin, diltiazem, or amiodarone for rate/rhythm control ^[2]. Cardioversion if haemodynamic compromise
Sinus bradycardia	Vagal activation (Bezold-Jarisch reflex), especially in inferior MI (RCA supplies SA node in 60%)	Atropine 0.3–0.6 mg IV bolus. Pacing if unresponsive to atropine ^[2]
AV block	Inferior MI: AV node ischaemia (RCA supplies AV node in 80%) → usually transient, narrow QRS escape. Anterior MI: extensive septal necrosis (LAD supplies His bundle/bundle branches) → usually permanent, wide QRS escape, poor prognosis	Conservative if 1° or Mobitz type I 2° HB. Pacing if Mobitz type II 2° HB or complete HB ^[2]. Conservative under careful monitoring as alternative if inferior MI with narrow QRS escape rhythm and adequate rate ^[2]
PSVT	Re-entry involving AV node	Cardioversion if severe haemodynamic compromise. ATP 10–20 mg IV bolus → verapamil ^[2]

Why is AV block in inferior MI more benign than in anterior MI? In inferior MI, the block is at the AV node level (RCA territory) → the escape rhythm arises from the bundle of His (narrow QRS, rate 40-60, relatively reliable). The ischaemia is often transient and the block resolves. In anterior MI, the block is below the His (bilateral bundle branch necrosis from LAD occlusion) → the escape rhythm arises from the ventricles (wide QRS, rate 20-40, unreliable, may fail completely → asystole). This carries a far worse prognosis and almost always requires pacing.

Other indications for temporary pacing ^[2]:

Bifascicular block + 1° AVB
Alternating BBB/RBBB + alternating LAHB/LPHB
(Anterior infarct → ↑risk of sudden asystole) ^[2]

II. Pump Failure and Cardiogenic Shock

Pump failure represents a downward spiral exacerbating myocardial ischaemia ^[2]:

↓Systolic function → ↓coronary perfusion → ↓supply → ischaemia ^[2]
↓Diastolic function → ↑pulmonary congestion → hypoxaemia → ischaemia ^[2]

This is a vicious cycle: ischaemia → ↓contractility → ↓CO → ↓coronary perfusion → more ischaemia → further ↓contractility → cardiogenic shock.

Indicates extensive myocardial damage → poor prognosis ^[2]

Killip Class	Signs	Implications
I	No rales or S3	No clinical signs of HF
II	Rales < 50% lung field or S3, ↑JVP	Pulmonary congestion
III	Rales > 50% lung field	Pulmonary oedema
IV	SBP < 90 mmHg + peripheral vasoconstriction (oliguria, cyanosis, sweating)	Cardiogenic shock

Cardiogenic shock occurs when ≥ 40% of the LV myocardium is non-functional (from current infarct + prior damage) ^[15]. Mortality is extremely high (≥ 50%) even with aggressive treatment.

Type	Characteristics	Management
LV dysfunction (95%)	Normal or ↓CO with APO	Vasodilators (esp ACEI) if BP stable. Inotropes (dopamine → dobutamine) if ↓BP. IABP with view for catheterisation ± revascularisation ^[2]
RV dysfunction (5%)	↓CO without APO, usually in inferior MI	Bedside echo: non-compressible IVC. Swan-Ganz catheter for PCWP monitoring. Volume expansion with colloids/crystalloids if low or normal PCWP ^[2]

RV Infarction — A Unique Haemodynamic Trap

In RV infarction, the RV cannot pump blood into the pulmonary circulation → ↓LV preload → ↓CO and hypotension with clear lungs (no pulmonary oedema because the problem is upstream). The JVP is elevated (backed up venous return). Nitrates, diuretics, and other preload-reducing agents are CONTRAINDICATED — they will further reduce the already inadequate LV filling and cause catastrophic hypotension. Treatment is IV fluid resuscitation to increase RV preload and force blood through the failing RV.

III. Mechanical Complications

Acute mechanical complications from MI ^[15]:

Shock — Large area (~40%) myocardium involved
VSD — Transmural infarct and rupture of muscular septum
MR — Rupture of papillary head
Tamponade — Free wall rupture, myocarditis, pericarditis, iatrogenic

Anyone of this is high risk for mortality ^[15]

Occurs in 0.3% of all MI patients, majority occurring in STEMI due to ↑myocardial damage. Associated with high in-hospital mortality (accounts for 10–15% of in-hospital deaths from AMI) ^[2]

Property	Detail
Mechanism	Causes: papillary muscle dysfunction or rupture, chordae rupture, or acute LV dilation or aneurysm ^[2]. In IHD, functional MR results from papillary muscle displacement, restricted leaflet closure, and annular dilation from LV remodelling ^[15]
Timing	Papillary muscle rupture: occurs 2–7 days after infarct ^[2]
Which papillary muscle?	Most commonly posteromedial (6–12× more common) due to single blood supply by posterior descending artery (PDA — from RCA). The anterolateral papillary muscle has dual supply from LAD and LCx, so is relatively protected ^[2]
Clinical features	Often poorly tolerated with APO and shock (but may be silent). Pansystolic murmur (PSM) with S3 on auscultation. Murmur may be absent if MR too severe ^[2] — because when MR is massive, the pressure gradient between LV and LA equalises rapidly → low-velocity regurgitant jet → quiet murmur
Diagnosis	By echo (to confirm papillary muscle disease) ^[2]
Management	Observe if stable (may be transient if only dysfunction). Emergency MVR with papillary muscle repair if severe ^[2]

Why is the posteromedial papillary muscle so much more vulnerable? It has a single blood supply (from the PDA, usually a branch of the RCA). If the RCA or PDA occludes, the entire papillary muscle becomes ischaemic and may rupture. The anterolateral papillary muscle has a dual blood supply (diagonal branches from LAD + obtuse marginal from LCx), providing a safety net.

Property	Detail
Incidence	~0.1% of MI ^[2]
Timing	Usually occurs in ~24h from MI but may occur in up to 2 weeks ^[2]
Mechanism	Usually complicates anterior MI (LAD) especially if extensive MI with poor collateral. Rupture occurs at margin of necrotic and non-necrotic myocardium ^[2]
Consequence	L-to-R shunting → sudden haemodynamic deterioration + new onset pansystolic murmur (PSM) radiating to the right lower sternal border (RLSB) ^[2]. Usually develops RV failure ^[2]
DDx	Differentiate from LVF leading to APO in acute MR — also with new PSM ^[2]. Key: in VSR the murmur is loudest at the RLSB and there is a "step-up" in O₂ saturation on right heart catheterisation (oxygenated blood shunting from LV → RV). In acute MR, the murmur is loudest at the apex and radiates to the axilla
Diagnosis	Echo, right heart catheterisation ^[2] (O₂ saturation step-up in RV/PA confirms L-to-R shunt)
Management	Observe with delayed surgery if stable. Emergency cardiac catheterisation followed by repair if unstable ^[2]. Note that surgical repair of MI-related VSD is associated with relatively high mortality ^[2] — the friable necrotic tissue makes sutures unreliable

Property	Detail
Incidence	< 1% (uncommon), 50% occurs ≤ 5 days, > 90% occurs ≤ 2 weeks ^[2]
Mechanism	Transmural necrosis → weakening of the full-thickness ventricular wall → rupture, often at the junction of infarcted and viable myocardium
Consequence — Complete rupture	Blood pumped into pericardial cavity → cardiac tamponade. Usually presents with sudden profound right HF + shock followed by PEA and death ^[2]
Consequence — Incomplete rupture	Ventricular defect sealed by pericardial tissue and thrombus → presents with persistent/recurrent pleuritic chest pain ^[2]. This is called a "pseudoaneurysm" — the contained rupture is sealed only by pericardium (vs true aneurysm which is contained by thinned myocardial wall). Pseudoaneurysms have a high risk of subsequent complete rupture
Diagnosis	Should be made clinically, supported by ECG/CXR/echo features of cardiac tamponade ^[2]
Management	Emergency percutaneous pericardiocentesis → surgical repair if blood aspirated ^[2]

Differentiating Mechanical Complications by Murmur and Haemodynamics

Complication	Murmur	Location	Haemodynamic Pattern
Acute MR	PSM	Apex → axilla	APO (pulmonary oedema), ↑↑LA pressure, ↑PCWP with tall V waves
VSD	PSM	RLSB	RV failure predominant, O₂ step-up on RHC
Free wall rupture	None (tamponade)	—	PEA, Beck's triad (hypotension, ↑JVP, muffled heart sounds)

IV. Pericardial Complications [2]

Property	Detail
Timing	Common on 2nd/3rd day post-MI, occurs in 1.2% of MI patients ^[2]
Mechanism	Transmural infarction → inflammation extends to the overlying epicardium and pericardium
Clinical features	Development of a different pain: positional, sharp pleuritic, especially at trapezius ridge. Pericardial rub (diagnostic) ^[2]
ECG	New widespread ↑ST or ↓PR beyond typically anatomic regional boundary ^[2] — this helps differentiate from ongoing/recurrent ischaemia which would be territorial
Management	Panadol ± aspirin (650 mg Q6–8h) ± opiate-based analgesia (usually self-limited). Avoid NSAIDs/steroids 7–10 days after acute MI due to ↑risk of aneurysm/rupture ^[2]

Why avoid NSAIDs/steroids early after MI? NSAIDs (except aspirin) inhibit prostaglandin-mediated healing of the infarcted myocardium and may impair scar formation → ↑risk of thinning, aneurysm formation, and myocardial rupture. Corticosteroids also impair wound healing.

Common, occurs in ~1/3 of acute STEMI, often minimal ^[2]

Usually asymptomatic and detected incidentally ^[2]
Management: none except if tamponade → drainage ^[2]

Property	Detail
Timing	In weeks/months post-MI, usually subsides in a few days ^[2]
Mechanism	Probably autoimmunity due to release of cardiac antigens into pericardial space ^[2] — exposed intracellular myocardial proteins (e.g. myosin) trigger an autoimmune inflammatory reaction
Clinical features	Persistent fever, pericarditis, pleurisy with compatible history of prior cardiac injury ^[2]
Investigations	Often associated with ↑inflammatory markers (↑WCC, CRP/ESR) with pericardial ± pleural effusion ^[2]
Management	High-dose aspirin/NSAID (e.g. indomethacin 25–50 mg TDS × 1–2 days), colchicine ± steroid ^[2] — note that by this time (weeks post-MI), the scar has matured and NSAIDs are safer to use than in the acute phase

Property	Detail
Risk factors	Most common in (1) anterior STEMI (2) LAD infarct (3) large infarct with EF < 30% ^[2]
Mechanism	Ventricular thrombus due to wall motion abnormality/aneurysm ^[2] — akinetic or dyskinetic segments create stasis zones where thrombus forms on the damaged endocardium. Atrial thrombus due to AF ^[2] — another mechanism
Risk of embolisation	Risk of embolisation in non-anticoagulated documented LV thrombus is 10–15% ^[2]
Prevention	Usually indicated to start anticoagulation to prevent systemic embolisation ^[2] — therapeutic anticoagulation (typically with heparin then warfarin/DOAC) for ≥ 3–6 months if LV thrombus documented
Consequences	Stroke, ischaemic limb... classically occurring in 1–3 weeks after MI ^[2]

Why is anterior MI the highest risk for LV thrombus? The LAD supplies the apex and anterior wall — these are the regions most likely to become akinetic or dyskinetic after infarction. The apex is also a "stagnation point" where blood flow velocity is lowest, creating ideal conditions for thrombus formation (Virchow's triad: stasis + endothelial injury + hypercoagulability).

VI. Ventricular Remodelling and Aneurysm

After MI, the heart undergoes structural changes to compensate for the loss of functioning myocardium. This process, called ventricular remodelling, is initially adaptive but ultimately maladaptive:

Acute phase: infarcted segment thins and may expand (infarct expansion)
Subacute phase: non-infarcted segments undergo compensatory hypertrophy (Frank-Starling mechanism attempts to maintain CO). Neurohormonal activation (RAAS, sympathetic nervous system) → volume retention, vasoconstriction
Chronic phase: progressive LV dilation, eccentric hypertrophy, spherical shape → ↑wall stress (Laplace's law) → further dilation → functional MR → heart failure

This is why ACEI/ARB + β-blockers + MRA are given post-MI — they counteract neurohormonal activation and slow/prevent adverse remodelling.

Property	Detail
Definition	A localised outpouching of the LV wall composed of thinned, scarred (fibrotic) myocardium
Timing	Develops weeks to months after transmural MI
Mechanism	Transmural scar replaces normal myocardium → thinning → paradoxical expansion (dyskinesis) during systole → aneurysm
Clinical features	Persistent HF symptoms, recurrent arrhythmias (the scar border zone is arrhythmogenic), persistent ST elevation on ECG (does not evolve further — "frozen" ST elevation), mural thrombus with embolic risk
ECG clue	Persistently ↑ST segment after STEMI should raise suspicion for ventricular aneurysm ^[2]
Diagnosis	Echocardiography (dyskinetic, thinned segment with aneurysmal outpouching), cardiac MRI
Management	Medical (ACEI/ARB, BB, anticoagulation if thrombus). Surgical aneurysmectomy (Dor procedure) if refractory HF or recurrent VT

Feature	True Aneurysm	Pseudoaneurysm
Wall	Composed of thinned, scarred myocardium	Contained by pericardium only (wall ruptured)
Neck	Wide neck	Narrow neck
Rupture risk	Low	High — requires urgent surgical repair

Indicated by symptoms/ECG changes + new rise in cTn > 20% or to > 5× ULN (if normal baseline) ^[2]

Cause	Detail
Post-PCI MI	Side branch occlusion (60%), stent complications, microembolisation ^[2]
Post-thrombolysis	Up to 50% have post-infarct angina (due to residual stenosis) ^[2]. Should consider early (6–24h) coro/PCI in all thrombolysis patients ^[2]

Management: High risk → prompt coro/PCI + IV GPIIb/IIIa inhibitor (if dynamic ECG changes) ^[2]

Coronary artery disease accounts for 85% of cardiac arrests ^[3]:

Myocardial ischaemia, AMI, prior MI with myocardial scarring ^[3]
Most common rhythm: VF (80% can be reversed by defibrillation, but 10% ↓survival per minute delay) ^[3]

Prevention in survivors of MI:

ICD implantation if LVEF ≤ 30–35%, ≥ 40 days post-MI, on optimal medical therapy, NYHA II-III, expected survival > 1 year ^[2]
β-blockers (↓arrhythmia risk), ACEI/ARB (↓remodelling), revascularisation of residual ischaemia

The end-stage of chronic IHD — progressive LV dysfunction from cumulative ischaemic damage and adverse remodelling.

Feature	Detail
Mechanism	Repeated ischaemic insults + chronic remodelling → global LV systolic dysfunction → HFrEF. May also have "hibernating myocardium" (chronically underperfused but viable tissue that could recover with revascularisation)
Clinical features	Symptoms and signs of chronic biventricular heart failure: dyspnoea, orthopnoea, PND, peripheral oedema, hepatomegaly, S3 gallop ^[1]
Functional MR	IHD causes functional mitral regurgitation through papillary muscle displacement, restricted leaflet closure, and annular dilation ^[15] — this worsens HF in a vicious cycle
Management	Guideline-directed medical therapy for HFrEF (ACEI/ARNI + BB + MRA + SGLT2i + diuretics). Assess for viable myocardium → consider revascularisation if significant viability and operable anatomy. ICD/CRT if indicated. Cardiac transplantation for end-stage — IHD is the 2nd commonest indication for cardiac transplantation in HK ^[2]

X. PCI and CABG Complications

Category	Complications
Coronary artery related	Dissection, intramural haematoma, perforation, side branch occlusion ^[2]. ALL can lead to myocardial ischaemia or infarction ^[2]
Stent-related	Stent thrombosis (1–2%): acute event, usually presents with severe STEMI or cardiac death ^[2]. In-stent restenosis (ISR): chronic event, usually presents with recurrent stable angina, usually ≥ 6–9 months after stenting ^[2]
Access-related	Pseudoaneurysm, bleeding, infection, atheroembolism ^[1]^[2]
Systemic	AKI (contrast, haemodynamic instability, atheroembolism), stroke, bacteraemia ^[2]

Complication	Detail
Mortality 1–2% ^[1]
AF 30% in first week ^[1]	Most common arrhythmia post-CABG (pericardial inflammation, atrial stretch)
Peri-operative stroke 2.5%	Microembolisation of gaseous and particulate matter ^[1]
Peri-operative MI ^[1]	Graft occlusion or incomplete revascularisation
Post-op low cardiac output syndrome (LCOS)	Due to ventricular dysfunction ^[1]
Graft occlusion	May require PCI to graft / re-CABG ^[1]. Vein grafts: ~5–10% fail within 30 days, then ~1–2%/year for 6 years, then ~5%/year ^[2]
Wound infection / mediastinitis ^[1]	Especially in diabetics, obese patients

High Yield Summary — Complications of IHD

Arrhythmias are the most common early complication. VF is the #1 cause of death in the first hour. AV block in inferior MI is usually transient; in anterior MI it is ominous
Pump failure creates a vicious cycle: ↓CO → ↓coronary perfusion → more ischaemia → ↓CO. Killip class IV = cardiogenic shock (SBP < 90, peripheral vasoconstriction)
Acute mechanical complications (VSD, papillary muscle rupture, free wall rupture) are rare but lethal — anyone of these is high risk for mortality ^[15]. They occur in STEMI, typically days 2–7
Papillary muscle rupture: posteromedial > anterolateral (6–12×) because of single blood supply from PDA. Causes acute severe MR → APO
VSR: anterior MI > inferior MI. New PSM at RLSB + RV failure. DDx from acute MR by murmur location and O₂ step-up on RHC
Free wall rupture: PEA + tamponade = sudden death. Incomplete rupture → pseudoaneurysm (narrow neck, high rupture risk)
Pericardial complications: PIP (day 2–3, pericardial rub, avoid NSAIDs early), Dressler (weeks later, autoimmune, treat with aspirin/NSAID/colchicine)
LV thrombus: most common in anterior MI with EF < 30%. Risk of systemic embolism 10–15% if not anticoagulated
Persistent ST elevation after STEMI → suspect LV aneurysm
Ischaemic cardiomyopathy: end-stage of chronic IHD with HFrEF, functional MR, and risk of sudden death. IHD causes functional MR through papillary muscle displacement, restricted leaflet closure, and annular dilation ^[15]

Active Recall - Complications of IHD

References

^[1] Senior notes: Maksim Medicine Notes.pdf (Sections 1.3, Complications of MI, PCI, CABG, pp.10–14) ^[2] Senior notes: Ryan Ho Cardiology.pdf (Sections 3.2, Complications of MI, PCI and CABG complications, pp.124–144) ^[3] Senior notes: Ryan Ho Critical Care.pdf (Section 1.5, Cardiac Arrest, p.28) ^[9] Senior notes: Ryan Ho Fundamentals.pdf (HF diagnosis and staging, Killip class, p.217) ^[15] Lecture slides: Cardiac Surgery Tutorial_Prof. D Chan.pdf (pp.31, 43 — Mechanical complications of MI, functional MR)

Ischaemic Heart Disease

Definition

Epidemiology

Global Burden

Hong Kong Context

Age and Sex Distribution

Risk Factors

Non-modifiable Risk Factors

Modifiable Risk Factors

Other Risk Factors and Associations

ASCVD Risk Assessment

Anatomy of the Coronary Arteries

Origin and Major Branches

Left Coronary Artery (LCA)

Right Coronary Artery (RCA)

Coronary Dominance

Coronary Artery Territory Summary

Aetiology

1. Coronary Atherosclerosis (Most Common — > 95% of IHD)

2. Non-Atherosclerotic Causes of IHD [1]

Pathophysiology

A. Pathology of Atherosclerosis

Stage 1: Endothelial Dysfunction (The Initiating Event)

Stage 2: Fatty Streak Formation

Stage 3: Atherosclerotic Plaque Formation

Stage 4: Plaque Complications (Why ACS Happens)

B. Mechanisms of Myocardial Ischaemia

Determinants of Myocardial O₂ Demand

Determinants of Myocardial O₂ Supply

Conditions That Exacerbate Angina (by Worsening the Supply-Demand Balance) [2]

C. Consequences of Ischaemia

D. Progression of Ischaemia to Infarction

Classification of IHD

By Clinical Presentation

By Canadian Cardiovascular Society (CCS) Grading of Angina Severity

Universal Classification of MI (5th Definition, 2018)

Clinical Features

A. Symptoms

1. Angina Pectoris (The Cardinal Symptom)

2. Dyspnoea

3. Autonomic Symptoms

4. Lightheadedness / Syncope

5. Fatigue

B. Signs

Signs Related to IHD Itself

Signs of Risk Factors and Comorbidities [2]

Signs of Other Arterial Disease (Systemic Atherosclerosis) [2]

Signs of Conditions That May Exacerbate Angina [2]

Key Pathophysiological Concepts — Summary Diagram

Active Recall - IHD Definition, Epidemiology, Risk Factors, Anatomy, Aetiology, Pathophysiology, Classification, Clinical Features

References

The Core Problem: "Is This Chest Pain From IHD?"

A. Differential Diagnosis of Acute Chest Pain (ACS Mimics)

Life-Threatening Differentials

Other Cardiac Differentials

Non-Cardiac Differentials of Acute Chest Pain

B. Differential Diagnosis of Stable/Chronic Chest Pain

C. Differential Diagnosis of Raised Troponin (Not All Troponin = ACS!)

D. Differential Diagnosis of ST Elevation on ECG

E. Systematic Approach to the Differential Diagnosis — Clinical Algorithm

F. How to Differentiate — Key Discriminating Features by History

G. Special Differential: Cardiac Causes of Angina Without Coronary Atherosclerosis

H. Differential Diagnosis of Dyspnoea as an IHD Presentation

Active Recall - Differential Diagnosis of IHD

A. Diagnostic Criteria

1. Diagnostic Criteria for Stable Angina (Chronic Coronary Syndrome)

2. Diagnostic Criteria for Myocardial Infarction (Universal Definition — 4th, ESC/AHA 2018)

Types of AMI (Universal Classification) [1][2]

3. ECG Criteria for STEMI [1]

B. Diagnostic Algorithm

1. Diagnostic Algorithm for Suspected Stable IHD

2. Diagnostic Algorithm for Suspected ACS

C. Investigation Modalities — Detailed Breakdown

1. Baseline Investigations (All Suspected IHD — Stable and Acute)

a. Blood Tests [2][9]

b. Resting 12-Lead ECG [2][9]

c. Resting Echocardiography [2]

d. CXR

2. Cardiac Biomarkers [1][2]

a. Cardiac Troponins (cTnT, cTnI) — Gold Standard