Angina Pectoris

Slide 1 · Angina Pectoris

Transient myocardial ischemia: coronary pathology and clinical phenotypes

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning objectives

Explain why transient myocardial ischemia produces anginal symptoms without myocyte necrosis.

Relate coronary stenosis, plaque change, and arterial spasm to the three angina patterns.

Distinguish stable, variant, unstable, and silent ischemic presentations.

Apply clinicopathologic mechanisms to focused clinical vignettes.

Slide 3 · Angina within ischemic heart disease

Myocardial oxygen supply–demand imbalance

Transient ischemia

Anginal syndrome

Ischemic heart disease also includes myocardial infarction and chronic ischemic syndromes.

The defining lesion in angina is functional ischemia, not established necrosis.

Slide 4 · Angina: A clinicopathologic definition

Recurrent, paroxysmal substernal or precordial discomfort

Episodes reflect transient myocardial ischemia.

Duration in the text: Approximately 15 seconds to 15 minutes.

Ischemia is insufficient to cause myocyte necrosis.

Slide 5 · Ischemia is not synonymous with infarction

Angina pectoris

Myocardial infarction

Transient oxygen inadequacy

Prolonged ischemic injury

No myocyte necrosis by definition

Cardiomyocyte death occurs

Recurrent episodes can resolve

Irreversible tissue injury develops

Slide 6 · Transient ischemia as an episode

01

Coronary mismatch begins

02

Ischemic discomfort develops

03

Mismatch resolves

04

Symptoms abate

Conceptual sequence; The timing and severity vary between episodes.

Slide 7 · Why myocardial perfusion matters

Coronary perfusion

Oxygen delivery

Aerobic ATP generation

Mechanical function

Myocardium depends on an uninterrupted oxygen supply.

A supply–demand mismatch is the central mechanism of ischemic heart disease.

Slide 8 · Anginal pain: Biochemical mediators

Transient myocardial ischemia

Adenosine + bradykinin + other molecules

Activation of visceral afferents

Perceived discomfort

Adenosine and bradykinin as examples of ischemia-induced mediators.

Slide 9 · Autonomic afferents transmit the signal

Ischemic metabolites activate sympathetic and vagal afferent nerves.

The sensory signal is generated by viable, ischemic tissue.

Perceived pain intensity does not directly measure myocyte necrosis.

Neural activation explains symptoms; It is not evidence of infarction.

Slide 10 · The characteristic pain phenotype

Classically crushing or squeezing.

Usually substernal; It may be described as precordial pressure.

The episodic quality is an important clinical clue.

The pain description supports—but does not uniquely establish—ischemia.

Slide 11 · Referred pain from myocardial ischemia

Ischemic substernal discomfort

Left arm

Left jaw

These are classic referred-pain locations.

Slide 12 · Silent ischemia challenges symptom-based reasoning

Not all myocardial ischemic episodes are perceived as pain.

Some patients have non-pain symptoms; Others have no symptoms.

Absence of chest discomfort is not equivalent to absence of ischemia.

Symptoms and ischemia are related, but not identical.

Slide 13 · Symptoms of silent ischemia

Dyspnea

Breathlessness may replace chest pain.

Nausea / vomiting

Visceral symptoms can predominate.

Palpitations

An altered heartbeat may be noted.

Diaphoresis / fatigue

Autonomic or nonspecific manifestations.

Slide 14 · Who may experience silent ischemia?

Particularly common in older individuals.

Also important in patients with diabetic neuropathy.

Pain perception can be altered even when myocardial ischemia occurs.

An apparently “atypical” presentation may still reflect coronary disease.

Slide 15 · Three overlapping patterns of angina

Stable

Fixed coronary disease + increased demand

Variant

Episodic coronary spasm

Unstable

Acute plaque change ± thrombus / spasm

That these patterns may overlap.

Slide 16 · Oxygen supply versus myocardial demand

CORONARY SUPPLY

MYOCARDIAL DEMAND

Coronary perfusion

Vascular lumen

Vasomotor tone

Physical work

Emotional arousal

Psychological stress

Mismatch → ischemia

Ischemia develops when supply is inadequate for demand.

Slide 17 · Mechanisms that reduce myocardial supply

Fixed narrowing

Atherosclerotic lumen obstruction

Acute plaque change

Thrombotic reduction of perfusion

Vasospasm

Transient arterial constriction

All can alter perfusion, but their clinical patterns differ.

Slide 18 · Why demand can trigger angina

Exertion or stress

Increased cardiac energy requirement

Fixed coronary supply limit

Transient ischemia

Stable angina is elicited when demand exceeds the attainable perfusion reserve.

Slide 19 · Chronic coronary atherosclerosis

CORONARY ARTERY (CROSS-SECTION)

Atherosclerotic plaques commonly involve epicardial coronary arteries.

The plaque reduces usable luminal cross-sectional area.

Chronic narrowing underlies the common stable-angina mechanism.

Slide 20 · Coronary vasodilator reserve

Rising myocardial demand

Compensatory coronary vasodilation

Additional blood delivery

With critical fixed stenosis, compensatory vasodilation cannot satisfy moderate extra demand.

Functional flow reserve matters more than local anatomy alone.

Slide 21 · Critical stenosis and exertional ischemia

Unrestricted reserve

Mild or no limitation

>70% area obstruction

Often symptomatic on exertion

≈90% area obstruction

Perfusion may fail at rest

Textbook cross-sectional area descriptions; Conceptual and not a stand-alone clinical test.

Slide 22 · Severe stenosis may compromise resting flow

CORONARY ARTERY (CROSS-SECTION)

Approximately 90% luminal-area obstruction as a level that can reduce resting flow.

Exertional and rest ischemia therefore reflect different degrees of reserve failure.

Anatomic narrowing and symptoms are not perfectly interchangeable.

Slide 23 · Which coronary arteries are affected?

LAD

Left anterior descending

LCX

Left circumflex

RCA

Right coronary artery

One, two, or all three epicardial vessels may have atherosclerosis.

Slide 24 · Proximal coronary distribution

Clinically important plaques often occur in the first several centimeters of the LAD or LCX.

Major branches can also be involved.

Penetrating intramyocardial branch atherosclerosis is described as uncommon.

Angina frequently reflects epicardial coronary disease.

Slide 25 · Multivessel stenosis and functional severity

Several arterial lesions

Combined resistance to flow

Reduced flow reserve

Demand-related ischemia

Multiple lesions may affect perfusion even when no one narrowing tells the entire story.

Slide 26 · Collateral circulation modifies ischemia

Slowly developing coronary obstruction

Collateral vessel formation

Alternative routes of perfusion

Collateralization may mitigate the consequences of even severe fixed narrowing.

Slide 27 · Stable angina: Core mechanism

Fixed coronary stenosis

Predictable rise in demand

Supply becomes insufficient

Transient ischemia

Typical stable angina is the most common pattern.

Slide 28 · Stable angina: Reproducible triggers

Physical activity

Increased workload

Emotional excitement

Higher myocardial requirements

Psychological stress

Demand can rise without exercise

Rest

Ordinarily does not provoke typical stable angina

Slide 29 · Exertion unmasks limited perfusion reserve

CORONARY SUPPLY

MYOCARDIAL DEMAND

Fixed stenosis

Limited extra flow

Walking uphill

Climbing stairs

Physical effort

Mismatch → ischemia

Conceptual mismatch during activity; Not a quantitative hemodynamic plot.

Slide 30 · Rest relieves demand-driven ischemia

Stop physical activity

Lower cardiac energy demand

Balance with available flow restored

Anginal discomfort resolves

Improvement with rest is characteristic of the typical stable pattern.

Slide 31 · Vasodilators and stable symptoms

Nitroglycerin / calcium channel blockers

Coronary vasodilation

Improved perfusion balance

Relief of angina

The Robbins passage cites vasodilators as a mechanism of symptomatic relief.

This is a pathophysiologic explanation, not a prescribing recommendation.

Slide 32 · Case: Reproducible exertional pain

A person develops squeezing substernal pressure each time they climb a steep staircase. The discomfort stops after resting.

Question 1: Which angina pattern best matches the symptom trigger?

Question 2: Which coronary mechanism produces the demand threshold?

Slide 33 · Case interpretation: Fixed coronary limitation

Best fit: Stable (typical) angina.

A chronic stenosing plaque constrains perfusion reserve.

Exercise raises myocardial demand; Rest lowers demand below the symptom threshold.

Slide 34 · Acute plaque change alters the clinical pattern

Previously existing atheroma

Sudden plaque disruption / erosion

Superimposed thrombosis

Abrupt decrease in coronary supply

This is a pathway to unstable angina and other acute coronary syndromes.

Slide 35 · Plaque rupture and plaque erosion

Plaque rupture

Plaque erosion

Fibrous cap disruption

Loss / injury of luminal endothelium

Thrombogenic plaque contents exposed

Subendothelial structures exposed

Thrombosis may follow

Thrombosis may follow

Slide 36 · Why plaque disruption is thrombogenic

Endothelial barrier lost

Collagen / plaque contents exposed

Platelet and coagulation activation

Coronary thrombus

Plaque disruption or erosion to acute thrombosis.

Slide 37 · Thrombus size determines flow limitation

Thrombus on disrupted plaque

Partial obstruction → ischemia

Complete obstruction → often infarction

A nonocclusive thrombus can still cause substantial ischemia.

Slide 38 · Distal thromboembolization

Mural coronary thrombus

Embolic fragments enter distal branches

Downstream microvascular compromise

Distal thromboemboli and microinfarcts in the setting of unstable angina.

Focal microinfarction is not the defining lesion of angina itself.

Slide 39 · A culprit plaque need not be critically stenotic

Some plaques provoke few symptoms before disruption.

Acute change—not only the pre-existing luminal narrowing—determines sudden coronary events.

A stable symptom history cannot rule out a future acute plaque event.

Plaque stability and stenosis severity describe different properties.

Slide 40 · Vulnerable plaque: Structural attributes

CORONARY ARTERY (CROSS-SECTION)

Large lipid-rich atheromatous core.

Thin overlying fibrous cap.

Mechanical disruption exposes thrombogenic plaque material.

Slide 41 · Cap strength depends on matrix balance

CORONARY SUPPLY

MYOCARDIAL DEMAND

Smooth muscle cells

Collagen synthesis

Macrophages

Matrix metalloproteinases

Mismatch → ischemia

Plaque stability depends on synthesis versus breakdown of fibrous-cap matrix.

Slide 42 · Inflammation promotes plaque vulnerability

Inflammatory macrophages

Matrix degradation

Cap thinning / weakening

Greater rupture susceptibility

The source identifies inflamed, smooth-muscle-poor plaques as especially vulnerable.

Slide 43 · Vasospasm can accompany acute plaque change

Dynamic coronary constriction

Further perfusion reduction

Transient ischemia

Spasm may contribute alone or superimpose on plaque-related disease.

Plaque rupture, thrombosis and vasospasm are not mutually exclusive.

Slide 44 · Unstable angina: Crescendo symptoms

Increasing frequency, duration, or severity of attacks

Provoked by progressively less physical activity.

May develop during rest.

The Robbins text describes prolonged episodes, often >20 minutes.

Slide 45 · Unstable angina: A falling exertional threshold

01

Earlier: Substantial activity

02

Later: Minor activity

03

More severe: At rest

Qualitative clinical progression characteristic of a crescendo pattern.

Slide 46 · Rest pain changes the clinical concern

Unstable angina can occur without a rise in physical demand.

A new perfusion limitation may result from plaque disruption, thrombus, or spasm.

The pattern is a warning of possible progression to infarction.

A changing symptom threshold is more alarming than a reproducible stable threshold.

Slide 47 · Unstable angina is an acute coronary warning

Plaque disruption

Thrombus ± vasospasm

Increasing ischemia

Risk of complete occlusion / MI

Robbins explicitly characterizes unstable angina as a harbinger of myocardial infarction.

Slide 48 · Case: Angina becoming more frequent

Over several days, a patient’s exertional substernal discomfort becomes more intense, occurs during shorter walks, and finally appears while seated.

Question 1: Which new descriptor matters most?

Question 2: What underlying coronary change should be considered?

Slide 49 · Case interpretation: Unstable angina

The escalating, lower-threshold pattern is crescendo angina.

Think of acute plaque alteration, mural thrombosis, and/or vasospasm.

The risk of complete occlusion distinguishes this pattern from uncomplicated stable angina.

Slide 50 · Variant angina: Dynamic coronary spasm

CORONARY ARTERY (CROSS-SECTION)

Prinzmetal variant angina reflects transient coronary arterial spasm.

The ischemia is episodic rather than predictably demand-triggered.

Attacks can occur at rest.

Slide 51 · Variant angina is not exertion-dependent

Stable angina

Prinzmetal variant angina

Predictable with increased demand

Unrelated to exertion

Chronic stenosing atherosclerosis

Episodic coronary spasm

Typically absent at rest

May appear at rest

Slide 52 · Spasm and atherosclerosis can coexist

Variant angina episode

Coronary spasm

May coexist with atheromatous plaque

The presence of fixed coronary disease does not exclude the variant mechanism.

Slide 53 · Vasodilator response in variant angina

Transient vasospasm

Reduced regional blood delivery

Vasodilator administration

Prompt symptom relief

A generally prompt response to vasodilators.

Slide 54 · Case: Episodic pain at rest

A person has abrupt episodes of chest discomfort while resting. The attacks do not track physical activity or changes in heart rate.

Question 1: What mechanism best explains the episodes?

Question 2: Would known atherosclerosis exclude that mechanism?

Slide 55 · Case interpretation: Prinzmetal angina

Pattern: Variant (Prinzmetal) angina.

Transient coronary spasm explains ischemia independent of exertion.

Coexisting atherosclerosis does not rule out vasospastic episodes.

Slide 56 · Three syndromes: Mechanistic comparison

Feature

Stable

Variant

Unstable

Dominant mechanism

Fixed stenosis

Coronary spasm

Acute plaque change ± thrombus

Typical trigger

Exertion / stress

Not activity-linked

Lower effort / rest

Pattern over time

Reproducible

Episodic

Crescendo

Rest attacks

Not typical

Can occur

Can occur

Clinical implication

Demand limit

Dynamic constriction

Threat of infarction

Slide 57 · Anginal syndromes can overlap

Stenosis

Chronic plaque reduces reserve

Spasm

Dynamic constriction lowers flow

Thrombosis

Acute plaque change abruptly lowers flow

The same patient may have more than one coronary mechanism.

Slide 58 · Anatomic plaque ≠ symptoms ≠ tissue death

What is observed?

What it establishes

Coronary atheroma

A structural coronary lesion

Chest discomfort

A potential ischemic symptom

Transient ischemia without necrosis

Angina pectoris

Myocyte necrosis

Myocardial infarction, not angina alone

Slide 59 · Angina has no defining myocyte necrosis

Myocardial ischemia can be severe enough to activate pain pathways.

The defining anginal episode does not progress to myocyte death.

The underlying coronary vessel may nevertheless contain severe atherosclerotic pathology.

Do not equate a vascular plaque with myocardial infarction.

Slide 60 · Morphology: Identify the relevant tissue

Arterial wall

Atherosclerosis / cap structure

Arterial lumen

Fixed narrowing, thrombus or spasm

Myocardium

Transient ischemia; No defining necrosis

Interpret the coronary lesion and its myocardial consequence separately.

Slide 61 · How to reason from an anginal history

1

Is there predictable demand-triggered discomfort?

2

Are episodes independent of exertion?

3

Is the frequency, duration, or severity worsening?

4

Could ischemia be silent or present atypically?

A mechanistic interpretation framework, not a validated diagnostic algorithm.

Slide 62 · Pitfall: Pain characteristics alone are insufficient

Symptoms are the perceived output of an ischemic process.

Some episodes are silent or manifest through dyspnea or autonomic symptoms.

Overlapping mechanisms prevent a simple one-symptom/one-lesion correspondence.

Clinical patterns raise mechanistic hypotheses; They do not anatomically prove the culprit lesion.

Slide 63 · Pitfall: Fixed stenosis does not predict plaque rupture

Chronic stenosis determines perfusion reserve.

Cap composition and inflammation influence plaque rupture susceptibility.

Some culprit plaques were not critically narrowing the lumen before disruption.

Ischemia risk and acute thrombosis risk require distinct pathological reasoning.

Slide 64 · Integrated pathologic model

Fixed stenosis / spasm / plaque change

Myocardial supply–demand mismatch

Transient ischemia

Symptoms—or silent ischemia

Unstable plaque change adds a clinically important risk of coronary occlusion.

Slide 65 · Four conclusions to retain

Angina is transient myocardial ischemia without myocyte necrosis.

Stable angina tracks limited flow reserve under increased demand.

Prinzmetal angina reflects episodic coronary spasm; Unstable angina reflects acute plaque-related flow compromise.

Silent ischemia and overlapping mechanisms limit symptom-only interpretation.

Slide 66 · Reference and scope

Robbins, Cotran & Kumar. Pathologic Basis of Disease. 11th ed. (2026).

Chapter 12, The Heart — Ischemic Heart Disease; Chronic Arterial Occlusion; Acute Plaque Change; Angina Pectoris.

Source pages: 492–494.

All vascular drawings are original editable schematics; not scale drawings, photographs, or patient-specific images.