Chronic Ischemic Heart Disease

Slide 1 · Chronic Ischemic

Heart Disease

Clinicopathologic mechanisms · Morphology · Heart failure

From ischemic injury to progressive ventricular dysfunction

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Learning outcomes

Define chronic ischemic heart disease (IHD) and its clinical context

Trace the transition from infarction or severe coronary disease to heart failure

Recognize the gross and microscopic morphologic constellation

Integrate structural lesions with ventricular dysfunction

Slide 3 · Where chronic IHD fits within IHD

Coronary ischemia

Chronic myocardial injury

Progressive heart failure

IHD encompasses several presentations of myocardial ischemia

Chronic IHD is the presentation associated with progressive heart failure

Angina, myocardial infarction, and sudden cardiac death are other IHD presentations

Slide 4 · Core pathologic definition

Progressive congestive heart failure follows accumulated ischemic myocardial damage

Compensatory responses may become inadequate to preserve function

The entity is defined by its ischemic substrate and functional course

Slide 5 · “Ischemic cardiomyopathy”: Clinical usage

Pathology term

Clinical usage

Chronic ischemic heart disease

Progressive heart failure

Ischemic cardiomyopathy

Ischemic ventricular dysfunction

Slide 6 · Two linked contributors to progression

Cumulative damage

Limited compensation

Progressive CHF

Cumulative ischemic damage reduces functioning myocardial tissue

Compensatory responses cannot indefinitely sustain cardiac performance

Either injury burden or inadequate adaptation can dominate an individual course

Slide 7 · The usual postinfarction pathway

Prior MI

Viable myocyte hypertrophy

Decompensation

Chronic CHF

Most chronic IHD cases have a preceding myocardial infarction

Noninfarcted tissue hypertrophies to compensate for loss of myocardium

Later functional decompensation of that hypertrophied tissue promotes CHF

Slide 8 · A prior infarction is common—not essential

Common pathway

Alternative pathway

Healed infarct

Compensatory hypertrophy

Progressive failure

Severe coronary obstruction

No prior infarction required

Chronic failure

Slide 9 · Coronary intervention in the history

Patients may have undergone coronary arterial interventions

Some have had coronary bypass surgery

Such a history can coexist with chronic ischemic dysfunction rather than excluding it

Slide 10 · Advanced clinical burden

~40%

The Robbins text associates chronic IHD with roughly 40% of cardiac transplant recipients

This statistic describes the transplant-recipient population, not the prevalence of IHD

Progression to advanced cardiac failure is a clinically important outcome

Slide 11 · The indispensable coronary substrate

Schematic — stenotic vessel

Some degree of stenotic coronary atherosclerosis is invariably present in the described morphology

Epicardial coronary atherosclerosis dominates the wider ischemic heart disease spectrum

The myocardium must therefore be interpreted together with its coronary arteries

Slide 12 · Less common routes to myocardial ischemia

Dominant cause

Less common causes

Coronary atherosclerosis

Vasospasm

Coronary embolism

Vasculitis

Slide 13 · Supply–demand imbalance: The central mechanism

Restricted perfusion

Supply–demand mismatch

Myocardial ischemia

Myocardial ischemia develops when coronary perfusion is insufficient for oxygen demand

Reduced delivery of oxygen and nutrients impairs ATP production

Underlying ischemia may intensify as myocardial workload increases

Slide 14 · Chronic coronary narrowing

Schematic — stenotic vessel

Chronic progressive atherosclerotic narrowing limits coronary blood flow

With advanced stenosis, compensatory dilation may not meet increased cardiac demand

Reduced flow reserve is more informative than stenosis severity alone in multifocal disease

Slide 15 · More than one coronary bed may be involved

Atherosclerosis can involve one, two, or all three major epicardial coronary vessels

Different territories may contribute to the viable but ischemia-prone ventricle

Widespread obstructive disease helps explain functional vulnerability beyond an old scar

Slide 16 · Collateral circulation: Partial protection

Slow coronary narrowing

Collateral enlargement

Partial tissue protection

Gradually narrowing coronary lesions can promote collateral channels

These channels may reduce ischemia in jeopardized myocardial regions

Protection is variable and does not erase the underlying obstructive coronary disease

Slide 17 · Why hypertrophy raises oxygen requirements

Loss of contractile mass

Viable myocyte hypertrophy

Higher oxygen demand

Surviving myocardium develops increased muscle mass after infarction

Greater tissue mass and heightened contractile work increase oxygen consumption

Compensatory enlargement therefore adds metabolic demand to a coronary-limited system

Slide 18 · Hypertrophy is not matched by capillary growth

Growing demand

Limited supply

Larger myocytes

Higher myocardial workload

No proportional capillary increase

Stenotic coronaries

Slide 19 · Tachycardia is a double stressor

Increased demand

Reduced supply time

More contractions per minute

Greater oxygen consumption

Shorter relative diastole

Less time for coronary perfusion

Slide 20 · Systemic hypotension can worsen ischemia

Even moderate coronary disease may become consequential when systemic perfusion falls

Reduced coronary inflow adds to the pre-existing oxygen supply limitation

Perfusion pressure and coronary anatomy must be considered together

Slide 21 · Postinfarct tissue redistribution

Infarcted myocardium

Viable myocardium adapts

Compensatory hypertrophy

Infarction reduces functioning myocardial mass

Viable segments bear a greater compensatory workload

Work-related hypertrophy occurs in noninfarcted myocardium

Slide 22 · Ventricular remodeling: What the term covers

Tissue injury

Hypertrophy + dilation

Changed chamber geometry

After infarction, noninfarcted myocardium can hypertrophy and dilate

Changes in chamber shape and wall properties accumulate

Remodeling includes molecular, cellular, and structural adaptation to injury

Slide 23 · Compensation initially supports perfusion

Frank–Starling recruitment increases force as filling stretches myocytes

Neurohumoral responses can maintain pressure and perfusion initially

Hypertrophy increases contractile capacity in the early adaptive phase

Slide 24 · The Frank–Starling trade-off

Increased filling

Temporary output support

Progressive dilation may dominate

Greater filling can temporarily augment contraction

Persistent chamber dilation is not equivalent to preserved pump function

The compensatory effect may be overwhelmed as the ventricle remodels

Slide 25 · Adrenergic compensation

Norepinephrine increases heart rate and myocardial contractility

Vascular resistance also increases under adrenergic activation

These compensations alter the same demand–supply balance faced by ischemic myocardium

Slide 26 · RAAS: A volume-preserving response

Reduced effective perfusion

RAAS activation

Salt + water retention

Greater congestion

Renin–angiotensin–aldosterone activation retains salt and water

It also increases vascular tone

Persistent fluid retention can exacerbate the congestion of failing hearts

Slide 27 · Natriuretic counter-regulation

Volume-retaining response

Counter-response

RAAS

Salt and water retention

Increased vascular tone

Atrial natriuretic peptide

Diuresis

Vasorelaxation

Slide 28 · Why adaptation eventually fails

Persistent workload

Ischemic vulnerability

Remodeling

Cardiac failure

Surviving myocytes must sustain persistent mechanical work

Hypertrophy increases oxygen demand while coronary supply remains impaired

Dilation and fibrosis further compromise mechanical efficiency

Slide 29 · Dilation as a late dominant change

Increasing chamber size may overwhelm the initial benefit of hypertrophy

Altered ventricular shape contributes to depressed output

Dilation can occur with or without a discrete ventricular aneurysm

Slide 30 · Scar formation changes mechanics

Healed infarct scar

Wall stiffness + altered shape

Reduced function

Healed infarcts replace lost myocardium with scar

Scar formation can stiffen the ventricular wall

Stiffening and altered geometry further reduce effective cardiac output

Slide 31 · Interstitial fibrosis adds filling resistance

Workload + hypertrophy

Interstitial matrix deposition

Stiffer ventricle

Mechanical forces stimulating myocyte growth also activate fibroblast matrix synthesis

Interstitial collagen accumulation increases resistance to diastolic filling

This is a structural route from hypertrophy to functional impairment

Slide 32 · A self-reinforcing ischemic cycle

Ischemic myocardial injury

Compensatory hypertrophy

Higher oxygen demand

Worsening function

Coronary obstruction restricts myocardial perfusion

Compensatory hypertrophy elevates oxygen consumption

Progressive dysfunction increases the burden on remaining viable muscle

Slide 33 · Systolic dysfunction in the remodeled heart

Loss of viable muscle and adverse dilation can depress left ventricular contraction

Reduced ejection fraction reflects impaired systolic pump performance

Forward cardiac output can become inadequate for tissue needs

Slide 34 · Diastolic dysfunction from stiffness

Hypertrophy + fibrosis

Impaired relaxation

Elevated filling pressures

Hypertrophy and interstitial fibrosis limit ventricular relaxation and filling

Preserved contraction alone cannot guarantee normal filling

Higher filling pressures can contribute to pulmonary congestion

Slide 35 · Systolic and diastolic dysfunction

Systolic impairment

Diastolic impairment

Diminished contractile output

Reduced ejection fraction

Loss of viable myocardium / dilation

Stiff, poorly relaxing ventricle

Impaired diastolic filling

Hypertrophy / fibrosis

Slide 36 · Forward failure: Tissue hypoperfusion

Reduced cardiac output

Peripheral hypoperfusion

Organ consequences

Heart failure may prevent adequate tissue perfusion

Renal hypoperfusion stimulates fluid-retaining responses

Advanced hypoperfusion can compromise kidney and brain function

Slide 37 · Backward failure: Venous congestion

Elevated left-sided pressures

Pulmonary congestion

Dyspnea + edema

Raised filling pressures allow blood to pool upstream

Left-sided failure particularly causes pulmonary venous congestion

Pulmonary edema contributes substantially to the clinical syndrome

Slide 38 · Pulmonary consequences of left-sided failure

Pulmonary congestion progresses from interstitial edema to alveolar fluid

Chronic episodes can yield hemosiderin-laden alveolar macrophages

This lung morphology reflects failure of the left heart, not a new coronary lesion

Slide 39 · Dyspnea links myocardium to the lung

Exertional breathlessness can precede symptoms at rest

Orthopnea and paroxysmal nocturnal dyspnea emerge with worsening congestion

Fine basal rales correspond to reopening of fluid-affected alveoli

Slide 40 · Clinical signs related to remodeling

Cardiomegaly reflects cardiac enlargement

Tachycardia may accompany heart failure

S3 can reflect volume overload; S4 can reflect increased stiffness

Slide 41 · Dilation can contribute to mitral regurgitation

LV dilation

Papillary muscle displacement

Mitral regurgitation

Progressive left ventricular enlargement can displace papillary muscles

This may produce functional mitral regurgitation

The resultant volume burden can aggravate chamber remodeling

Slide 42 · Left-sided failure can burden the right heart

Left ventricular failure

Pulmonary vascular burden

Right ventricular failure

Elevated pulmonary circulatory pressure increases right ventricular workload

Persistent strain may contribute to right-sided failure

The clinical course can therefore progress to combined ventricular failure

Slide 43 · Gross morphology: Cardiomegaly

Chronic IHD hearts are enlarged

Myocardial hypertrophy and chamber dilation coexist

Gross enlargement is a structural signature but does not alone quantify dysfunction

Slide 44 · Left ventricular hypertrophy plus dilation

LV cavity

Schematic — not a specimen

Both thickened myocardium and an enlarged cavity may be present

In a dilated heart, wall thickness can be misleading as a measure of hypertrophy

Heart weight better reflects increased mass in markedly dilated ventricles

Slide 45 · The coronary arteries must be examined

Schematic — stenotic vessel

Stenosing coronary atherosclerosis is a constant feature in the chronic IHD morphology described

Severity and distribution of obstruction provide essential etiologic evidence

Coronary disease is interpreted alongside myocardial scars and remodeling

Slide 46 · Healed infarct scars: Discrete lesions

Conceptual tissue map — not histology

Discrete myocardial scars usually represent previous infarctions

They record earlier irreversible myocardial damage

The presence of a scar is compatible with later decompensation of surviving myocardium

Slide 47 · Absence of a visible scar does not exclude IHD

Evidence often present

Still compatible with chronic IHD

Healed infarct scars

LV hypertrophy and dilation

No documented earlier MI

Severe stenotic coronary disease

Slide 48 · Mural endocardial fibrous thickening

Conceptual tissue map — not histology

Patchy fibrosis of the mural endocardium is a recognized morphologic feature

This change to abnormal wall shear forces

The lesion reflects altered intracavitary mechanics accompanying remodeling

Slide 49 · Mural thrombi: A possible complication

Reduced wall motion + dilation

Stasis / endocardial injury

Mural thrombus

Mural thrombi may be found in chronic IHD

Postinfarct stasis, chamber dilation, and endocardial injury can favor thrombosis

Intracardiac thrombus creates a potential embolic source

Slide 50 · Microscopy: Hypertrophied myocytes

Conceptual tissue map — not histology

Myocyte hypertrophy is a characteristic microscopic finding

It represents adaptation of viable tissue to persistent workload

It commonly coexists with interstitial fibrosis in failing hearts

Slide 51 · Subendocardial myocyte vacuolization

Conceptual tissue map — not histology

Diffuse vacuolization of subendocardial myocytes is specifically described

Its location links the finding to the ischemia-vulnerable subendocardial region

Do not mistake an abstract schematic for diagnostic histologic evidence

Slide 52 · Interstitial fibrosis: Between surviving myocytes

Conceptual tissue map — not histology

Fibrous matrix accumulates in myocardial interstitium

The change accompanies hypertrophy and raises myocardial stiffness

It is distinct from scars that replace infarcted tissue

Slide 53 · Replacement fibrosis: Loss followed by scar

Conceptual tissue map — not histology

Replacement fibrosis occupies regions of previous myocardial injury

Healed infarcts commonly leave discrete areas of scar

This reduces functioning muscle mass available to sustain contraction

Slide 54 · Fibrosis is not a single lesion

Interstitial fibrosis

Replacement fibrosis

Among surviving myocytes

Associated with stiffness

Within areas of tissue loss

Associated with old infarcts

Slide 55 · Integrated morphologic checklist

Compartment

Characteristic change

Coronary arteries

Stenotic atherosclerosis

Cardiac size

Cardiomegaly; LV hypertrophy and dilation

Myocardium

Healed scars; hypertrophied myocytes

Endocardium

Patchy fibrosis; possible mural thrombus

Microscopy

Subendocardial vacuoles and fibrosis

Slide 56 · Morphology and physiology are linked

Coronary stenosis

Scar + hypertrophy

Dilation + fibrosis

Functional failure

Coronary stenosis corresponds to constrained myocardial perfusion

Scar and hypertrophy alter ventricular work distribution

Dilation and fibrosis help explain impaired pumping and filling

Slide 57 · A late aneurysm differs from diffuse dilation

General ventricular dilation

Postinfarct aneurysm

Chamber enlargement

May occur without aneurysm

Localized thinned scarred wall

Late sequel of transmural MI

Slide 58 · Infarct characteristics shape later outcomes

Larger infarcts impair pump function to a greater extent

Transmural infarcts carry a greater likelihood of late CHF

Extent, location, and wall thickness of injury influence complications

Slide 59 · The surviving ventricle matters for prognosis

Cardiac functional reserve

Coronary supply to viable muscle

Residual LV function

Extent of loss from infarction

Remaining vascular obstructions

Risk to viable myocardium

Slide 60 · Prevention in the chronic ischemic course

Before any MI

After prior MI

Primary prevention

Avoid initial infarction

Secondary prevention

Avoid reinfarction

Slide 61 · Teaching case: Deterioration after infarction

Constructed teaching vignette

Hypothetical course: Remote infarction followed by progressive cardiac enlargement and CHF

Expected pathology: Coronary atherosclerosis with healed scar, hypertrophy, and dilation

Mechanistic question: Why did initially compensatory viable myocardium decompensate?

Interpretation is developed on the following slide.

Slide 62 · Case interpretation: Adaptation has limits

Old infarct

Compensatory hypertrophy

Ischemic vulnerability

CHF

Infarction permanently reduces myocardial mass

Noninfarcted myocardium hypertrophies and increases its oxygen requirement

Further dilation and stiffening can diminish output despite the earlier compensatory response

Slide 63 · Teaching case: CHF without a known infarct

Constructed teaching vignette

Hypothetical course: Progressive CHF with severe obstructive coronary artery disease

No previous MI needs to be assumed

Question: Is the absence of an infarct history sufficient to exclude chronic IHD?

Interpretation is developed on the following slide.

Slide 64 · Case interpretation: Stenotic CAD can suffice

Robbins explicitly describes severe obstructive CAD presenting as chronic CHF without prior infarction

The coronary substrate remains essential to the diagnosis

An infarct is usual but not required by this formulation

Slide 65 · Teaching case: Interpret combined pathology

Constructed teaching vignette

Hypothetical postmortem constellation: Cardiomegaly, severe coronary stenosis, patchy mural endocardial fibrosis

Microscopy: Hypertrophied myocytes, subendocardial vacuolization, and interstitial fibrosis

Question: What additional myocardial lesion is often present?

Interpretation is developed on the following slide.

Slide 66 · Case interpretation: Look for healed scars

Healed infarcts commonly appear as discrete myocardial scars

Replacement fibrosis can coexist with diffuse interstitial fibrosis

Mural thrombosis is possible, but is not required in every case

Slide 67 · Distinguish cause, response, and consequence

Coronary disease

Ischemic injury

Remodeling

Progressive CHF

Cause: Stenotic coronary disease limits myocardial supply

Response: Surviving myocardium undergoes hypertrophy and remodeling

Consequence: Accumulated injury and ineffective adaptation produce progressive CHF

Slide 68 · High-yield synthesis

Chronic IHD is an ischemic cause of progressive congestive heart failure

Usually postinfarction; Severe obstructive CAD may also cause it without prior infarct

Cardiomegaly, LV hypertrophy/dilation, scars, endocardial changes, and fibrosis form the pathologic pattern

The transition from adaptive hypertrophy to adverse remodeling explains progressive dysfunction

Slide 69 · Reference

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

The Heart — “Chronic Ischemic Heart Disease” and the parent ischemic heart disease section.

Related material: myocardial infarction, ventricular remodeling, and the pathophysiology of heart failure.