Hypertrophic Cardiomyopathy

Slide 1 · Hypertrophic Cardiomyopathy

Genetic pathogenesis • structural pathology • clinical consequences

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Objectives: Explain the HCM phenotype

Recognize myocardial hypertrophy that is not explained by loading conditions

Connect sarcomeric protein variants to ventricular thickening and abnormal function

Identify characteristic gross and microscopic pathology

Explain obstruction, clinical complications and treatment principles

Slide 3 · Cardiomyopathies: Primary myocardial disease

Cardiomyopathy denotes intrinsic myocardial dysfunction

Primary disorders principally affect myocardium; Systemic disorders may involve it secondarily

Coronary, hypertensive, valvular and congenital disorders must be considered separately

Pattern

Chamber

Principal defect

Dilated

Enlarged

Contractility

Hypertrophic

Thick-walled

Relaxation

Restrictive

Usually not dilated

Compliance

Schematic

Slide 4 · Three major morphofunctional patterns

Dilated cardiomyopathy: Chamber enlargement and reduced contraction

Hypertrophic cardiomyopathy: Myocardial thickening with poor compliance

Restrictive cardiomyopathy: Limited ventricular filling from stiffness

HCM

Marked wall thickening

Usually nondilated

Diastolic defect

DCM

Chamber dilatation

Poor contraction

Systolic defect

Schematic

Slide 5 · Hypertrophic cardiomyopathy: Defining phenotype

Common, clinically heterogeneous genetic myocardial disorder

Myocardial hypertrophy is disproportionate to other causes of ventricular thickening

The ventricle is heavy, thick-walled and often hypercontractile

The fundamental physiologic defect is impaired diastolic filling

Wall thickening

Reduced compliance

Outflow narrowing

(in some patients)

Symptoms and clinical risk

Schematic

Slide 6 · Thick wall does not imply poor systolic function

A hypertrophied ventricle can contract vigorously yet fill inadequately

Systolic function in typical HCM is usually preserved

A reduced ventricular chamber and poor compliance lower stroke volume

Contrast with DCM, where ineffective contraction is dominant

HCM

Thick wall; Smaller cavity

Reference LV

Thinner wall; Larger cavity

Schematic

Slide 7 · Prevalence and clinical heterogeneity

An HCM prevalence of approximately 1 in 500

Expression varies between families and among affected relatives

Severity of hypertrophy, obstruction and clinical events is heterogeneous

A single structural pattern does not determine an individual prognosis

HCM

Genotype

Morphology

Physiology

Clinical course

Schematic

Slide 8 · Autosomal dominant transmission

Most familial cases show autosomal dominant inheritance

An affected family can contain relatives with different degrees of expression

A family history supports suspicion but is not a morphology substitute

Variable penetrance complicates interpretation of screening results

Affected parent

Carrier

Possible

Carrier

Possible

Uncertain

Phenotype

Illustrates dominant transmission and variable expression; Not a pedigree prediction

Schematic

Slide 9 · Variable penetrance: A diagnostic limitation

Not all individuals carrying a disease-associated variant manifest the same phenotype

Age and family context can influence recognition of disease

Genotype and visible hypertrophy do not map one-to-one

Negative phenotype assessment at one time point does not resolve every inherited risk

Affected parent

Carrier

Possible

Carrier

Possible

Uncertain

Phenotype

Illustrates dominant transmission and variable expression; Not a pedigree prediction

Schematic

Slide 10 · The sarcomere is the primary genetic target

HCM commonly arises from variants in genes encoding sarcomeric proteins

The involved machinery regulates myocardial force generation

Myosin-associated and thin-filament proteins are repeatedly implicated

Many genetic variants can converge on similar thick-walled morphology

Sarcomeric proteins

Myosin-binding

Protein C

β-myosin

Heavy chain

Troponins /

Tropomyosin

Schematic

Slide 11 · Myosin-binding protein C and β-myosin

Alterations involving myosin-binding protein C are prominent

β-myosin heavy chain, encoded by MYH7, is another major affected protein

Distinct mutations in one protein can produce the HCM phenotype

Clinical behavior cannot be deduced simply from the name of the protein

Sarcomeric proteins

Myosin-binding

Protein C

β-myosin

Heavy chain

Troponins /

Tropomyosin

Schematic

Slide 12 · Thin-filament genes contribute to HCM

Cardiac troponin I and troponin T are implicated in HCM

α-tropomyosin is another sarcomeric target account

These proteins participate in regulating contraction

The diversity of affected proteins explains genetic heterogeneity

Sarcomeric proteins

Myosin-binding

Protein C

β-myosin

Heavy chain

Troponins /

Tropomyosin

Schematic

Slide 13 · Allelic heterogeneity within a single gene

Different pathogenic variants in the same sarcomeric gene may cause HCM

Numerous distinct β-myosin heavy-chain variants

Morphologic similarity does not imply identical molecular etiology

Variant-level interpretation requires more than an abnormal gene label

One sarcomeric gene

Multiple possible variants

Related hypertrophic phenotype

Variable clinical behavior

Schematic

Slide 14 · Functional consequence: Hypercontractility

A unifying gain-of-function effect for the HCM-associated sarcomeric variants it discusses

Sarcomeric hypercontractility distinguishes typical HCM mechanisms from DCM

Increased force generation does not ensure effective ventricular filling

This mechanism informs myosin-directed therapeutic approaches

Sarcomeric variant

Increased contractile activity

Hypertrophic remodeling

Stiff ventricle / filling defect

Schematic

Slide 15 · One gene can contribute to contrasting cardiomyopathies

MYH7 variants are discussed in both HCM and DCM

The nature of functional disturbance, not merely the gene name, matters

HCM-associated hypercontractility with DCM-associated impaired function

Avoid assuming all variants in one gene lead to the same morphology

HCM

Sarcomere-associated

Hypercontractility

Thick myocardium

DCM

Multiple protein systems

Impaired force systems

Dilated chambers

Schematic

Slide 16 · From sarcomeric dysfunction to morphology

Abnormal force regulation is linked to hypertrophic remodeling

The ventricular wall increases in mass without proportionate chamber dilatation

Cellular disorganization and fibrosis compound functional impairment

The morphologic phenotype creates the substrate for impaired filling

Altered sarcomere function

Cardiomyocyte hypertrophy

Disarray + fibrosis

Decreased compliance

Schematic

Slide 17 · Genotype alone cannot establish prognosis

Many reported variants have uncertain significance

Clinical implications vary substantially across pathogenic variants

A variant must be interpreted alongside the phenotype and family history

Uncertain variants should not be equated with proven disease causation

Genetic finding

Phenotype and pedigree

Clinically contextualized interpretation

Schematic

Slide 18 · Family evaluation requires context

A genetic diagnosis can inform assessment of relatives

Variable penetrance limits predictions based on one family member

A variant of uncertain significance is not equivalent to a pathogenic mutation

Phenotypic assessment remains important within affected families

Affected parent

Carrier

Possible

Carrier

Possible

Uncertain

Phenotype

Illustrates dominant transmission and variable expression; Not a pedigree prediction

Schematic

Slide 19 · Massive hypertrophy with little dilatation

A large cardiac mass accompanies marked myocardial wall thickening

The ventricular cavities are usually not dilated

These gross findings contrast with the flabby dilated heart in DCM

Thickness and stiffness together constrain effective filling

HCM

Thick wall; Smaller cavity

Reference LV

Thinner wall; Larger cavity

Schematic

Slide 20 · Asymmetric septal hypertrophy

The classic gross pattern disproportionately affects the ventricular septum

The septum is thicker than the left ventricular free wall

This pattern in roughly two-thirds of cases

A concentric symmetric pattern occurs in other patients

Simplified LV cross-section

Dark blue: Septal projection

White: Residual LV cavity

Schematic

Slide 21 · HCM is not always asymmetric

Concentric, relatively symmetrical hypertrophy can occur

Do not require a bulging septum in every HCM specimen

Gross distribution varies despite a related physiologic phenotype

Consider other causes of concentric thickening in the differential

HCM

Thick wall; Smaller cavity

Reference LV

Thinner wall; Larger cavity

Schematic

Slide 22 · The subaortic septum matters

Septal hypertrophy is often most pronounced in the subaortic region

The thickened septum projects toward the outflow channel

Regional anatomy sets up potential mitral–septal interaction

Septal geometry is central to obstructive HCM

Simplified LV cross-section

Dark blue: Septal projection

White: Residual LV cavity

Schematic

Slide 23 · Why the left ventricular cavity becomes narrow

Disproportionate myocardial growth encroaches on luminal space

In classic asymmetric disease, the cavity may become banana-like

A smaller chamber limits end-diastolic filling volume

A hypercontractile wall cannot compensate fully for poor filling

Simplified LV cross-section

Dark blue: Septal projection

White: Residual LV cavity

Schematic

Slide 24 · Two components of the obstructive phenotype

A prominent septum creates a reduced outflow passage

Systolic movement of the anterior mitral leaflet adds dynamic narrowing

Obstruction is functional and varies with systolic geometry

Not every patient has clinically important obstruction

Prominent septal muscle

Anterior mitral leaflet

Moves toward septum in systole

Leaflet–septum contact

Schematic

Slide 25 · Systolic anterior motion (SAM)

During systole, the anterior mitral leaflet can move toward the septum

The echocardiographic term is systolic anterior motion

Leaflet–septal contact can exacerbate outflow obstruction

The mechanism is dynamic rather than a fixed stenotic valve lesion

Prominent septal muscle

Anterior mitral leaflet

Moves toward septum in systole

Leaflet–septum contact

Schematic

Slide 26 · Why a fibrous endocardial plaque forms

Repeated mitral leaflet contact with the septum may injure endocardium

The contact region may develop a fibrous endocardial plaque

Thickening of the anterior mitral leaflet can also accompany contact

These findings anatomically corroborate the dynamic mechanism

Septal bulge

Geometric narrowing

Leaflet contact

Endocardial friction

Fibrous plaque

Repeated contact site

Schematic

Slide 27 · Gross pathology: An integrated inspection

Assess overall cardiac weight and ventricular wall thickness

Compare septal thickness with the LV free wall

Evaluate chamber size and the subaortic region

Look for a fibrous endocardial contact plaque

Septal bulge

Geometric narrowing

Leaflet contact

Endocardial friction

Fibrous plaque

Repeated contact site

Schematic

Slide 28 · Cardiomyocyte hypertrophy

Individual cardiomyocytes are conspicuously enlarged

Hypertrophy is a hallmark at the microscopic level

Large fibers alone do not define HCM without the broader phenotype

Interpret size changes together with disarray, fibrosis and clinical context

Aligned myocardium

Myofiber disarray

Conceptual fiber organization — not histology

Schematic

Slide 29 · Myofiber disarray

Bundles of myocytes run in haphazard rather than parallel directions

Disorganization may affect individual cells and intracellular myofibrils

Architectural disarray is a classic histologic hallmark

It should be interpreted alongside the full pattern of myocardial findings

Aligned myocardium

Myofiber disarray

Conceptual fiber organization — not histology

Schematic

Slide 30 · Interstitial and replacement fibrosis

Interstitial collagen accumulates among cardiomyocytes

Replacement fibrosis marks loss and substitution of myocardial tissue

Fibrosis contributes to increased stiffness and electric heterogeneity

The distribution and extent can vary between affected hearts

Interstitial collagen

Replacement scar

Collagen between cells

Cell-free fibrotic region

Schematic

Slide 31 · Fibrotic narrowing of intramural arteries

Small intramural coronary vessels may have thickened, fibrotic walls

A reduced vascular lumen can compromise myocardial perfusion

Small-vessel changes help explain ischemia without epicardial CAD

Vascular and interstitial abnormalities coexist with myocyte changes

Narrowed lumen

Thickened vascular wall (schematic)

Schematic

Slide 32 · Four microscopic elements in HCM

Marked myocyte hypertrophy

Haphazard myofiber disarray

Fibrotic thickening of small intramural arteries

Interstitial and replacement myocardial fibrosis

Myocyte

Vessel

Interstitium

Hypertrophy

Wall fibrosis

Fibrosis

Disarray

Lumen narrowing

Replacement scar

Abnormal topology

Ischemic substrate

Stiffness

Schematic

Slide 33 · Structural remodeling creates functional stiffness

Hypertrophied cells increase myocardial mass

Fibrotic interstitium resists ventricular expansion

A reduced chamber further limits filling

These combined changes underlie a major diastolic defect

Hypertrophied myocardium

Smaller, stiff LV chamber

Higher filling pressure

Reduced stroke volume

Schematic

Slide 34 · Diastolic dysfunction is central

The LV is poorly compliant and requires more pressure to fill

Thick walls reduce the effective filling capacity

Even preserved contractile function may coexist with reduced stroke volume

The result is impaired cardiac performance during demand

Thick and fibrotic myocardium

Reduced ventricular compliance

Impaired diastolic filling

Reduced stroke volume

Schematic

Slide 35 · Reduced stroke volume despite hypercontraction

The amount ejected depends on the amount entering during diastole

A hypercontracting, small cavity can still deliver inadequate forward output

Exercise increases the demand for cardiac flow

Symptoms may arise despite preserved conventional systolic measures

Small LV chamber

Restricted diastolic filling

Low filling volume

Limited forward output

Schematic

Slide 36 · Why pulmonary venous pressure rises

Poor LV filling produces higher pressure upstream

The left atrium and pulmonary veins face increased filling pressure

This contributes to exertional dyspnea

Clinical symptoms link diastolic mechanics with pulmonary congestion

Poor LV compliance

Elevated LV filling pressure

Pulmonary venous pressure

Exertional dyspnea

Schematic

Slide 37 · Dynamic obstruction compounds impaired output

Outflow narrowing occurs during ventricular systole

Mitral–septal interaction adds to reduced forward flow

Obstruction can coexist with the primary filling abnormality

Its presence and magnitude contribute to heterogeneity

Diastole

Systole

Impaired filling

Dynamic LVOT

Obstruction

Reduced forward flow on exertion

Schematic

Slide 38 · Exertional dyspnea: Two mechanisms

A stiff ventricle restricts end-diastolic filling

Pulmonary venous pressure rises as LV filling pressure increases

Dynamic obstruction can further compromise forward cardiac output

The combination helps explain symptoms with activity

Diastole

Systole

Impaired filling

Dynamic LVOT

Obstruction

Reduced forward flow on exertion

Schematic

Slide 39 · The systolic ejection murmur

Dynamic LV outflow obstruction produces a harsh systolic ejection murmur

The audible finding reflects disturbed systolic outflow

A murmur is not required in nonobstructive HCM

Interpret auscultation with structural and functional assessment

Prominent septal muscle

Anterior mitral leaflet

Moves toward septum in systole

Leaflet–septum contact

Schematic

Slide 40 · Myocardial ischemia without epicardial stenosis

Massive ventricular hypertrophy raises myocardial oxygen demand

High intracavitary pressures increase wall stress

Fibrotic small intramural vessels impair microvascular supply

Focal ischemia may occur even without obstructive epicardial CAD

Narrowed lumen

Thickened vascular wall (schematic)

Schematic

Slide 41 · Ischemic substrate: Demand and supply

Greater muscle mass increases perfusion requirements

Small-vessel narrowing limits local blood delivery

The net supply–demand imbalance produces focal myocardial ischemia

Ischemia may add to scarring and functional deterioration

Marked hypertrophy

High pressure + microvascular disease

Perfusion-demand mismatch

Focal ischemia

Schematic

Slide 42 · Atrial fibrillation: A major complication

Altered filling and atrial pressure create a clinically important atrial burden

Atrial fibrillation is a major problem in HCM

Loss of coordinated atrial activity can worsen diastolic filling

Rhythm disturbance can initiate a thromboembolic sequence

Atrial fibrillation

Ineffective atrial emptying

Intracardiac thrombus

Systemic embolization / stroke

Schematic

Slide 43 · From atrial arrhythmia to embolic stroke

Atrial fibrillation can be associated with intracardiac thrombus formation

Thrombus may embolize from the heart

Systemic arterial embolization can involve cerebral circulation

Stroke prevention is therefore clinically important in affected patients

Atrial fibrillation

Ineffective atrial emptying

Intracardiac thrombus

Systemic embolization / stroke

Schematic

Slide 44 · Ventricular arrhythmias and sudden death

Ventricular arrhythmias are a major complication

Hypertrophied, disarrayed, ischemic and fibrotic myocardium provides an arrhythmogenic substrate

Sudden death can occur, including in young individuals

Risk varies and must not be assigned from wall thickness alone

Myocardium

Disarray

Fibrosis

Ischemia

Arrhythmia

Schematic

Slide 45 · HCM and sudden death in young athletes

HCM as an important cause of sudden death in young athletes

An apparently healthy or highly active individual may have unrecognized disease

A single exercise-related event should not be generalized to all patients

The natural history remains highly variable

HCM

Occult disease

Ventricular rhythm risk

Sudden death

Variable course

Schematic

Slide 46 · Other major clinical consequences

Reduced filling and outflow obstruction may impair exertional tolerance

Atrial fibrillation can worsen symptoms and predispose to thrombus

Progressive cardiac failure can occur

Arrhythmia, embolization and sudden death are distinct clinical hazards

HCM

Dyspnea

Atrial fibrillation

Heart failure

Embolism

Schematic

Slide 47 · Natural history is highly variable

Some individuals have an indolent or minimally symptomatic course

Others develop obstruction, arrhythmias or cardiac failure

Different mutations and myocardial phenotypes contribute to variability

Clinical assessment must integrate structure, function and symptoms

Inherited variant

Hypertrophy

Diastolic dysfunction

Variable outcomes

Schematic

Slide 48 · Clinical identification starts with a pattern

Recognize otherwise unexplained LV hypertrophy

Establish whether the dominant physiology is impaired filling

Assess for septal thickening and systolic anterior mitral motion

Exclude conditions that cause similar wall thickening

Phenotype recognition

Exclude mimicking causes

Relate structure to symptoms

Schematic

Slide 49 · Cardiac imaging and the morphologic phenotype

Imaging can assess ventricular wall distribution and chamber dimensions

A thickened septum and reduced chamber can support the phenotype

Echocardiographic SAM documents leaflet movement toward the septum

Morphology must still be interpreted with competing etiologies in mind

Wall distribution and cavity

LV outflow / leaflet motion

Contextual differential diagnosis

Schematic

Slide 50 · Mimic 1: Deposition-related myocardial disease

Amyloidosis and Fabry disease as important HCM mimics

Myocardial thickening may arise from accumulation rather than sarcomeric hypertrophy

The mechanism and associated pathology differ

A thick ventricular wall is therefore a phenotype, not the complete diagnosis

Apparent LV wall thickening

Sarcomeric HCM

Amyloid deposition

Fabry disease

Schematic

Slide 51 · Mimic 2: Hypertensive heart disease

Longstanding hypertension can cause LV hypertrophy

Age-related subaortic septal hypertrophy can add to the resemblance

Clinical pressure-loading context is diagnostically important

Do not label any prominent septum as genetically mediated HCM

Septal or LV thickening

Primary HCM

Hypertensive LVH

Age-related septal change

Schematic

Slide 52 · Mimic 3: Fixed outflow stenosis

Valvular aortic stenosis is an important alternative explanation

Congenital subvalvular aortic stenosis can also mimic obstruction

Fixed valvular/subvalvular lesions differ from dynamic mitral–septal contact

Correct diagnosis requires attention to obstructive anatomy

Dynamic HCM

Septal thickening

Systolic mitral motion

Variable obstruction

Fixed stenosis

Valve/subvalvular lesion

Fixed narrowing

Alternative cause of LVH

Schematic

Slide 53 · HCM, DCM and restrictive disease compared

HCM is typically thick-walled and nondilated

DCM predominantly has a dilated, poorly contracting ventricle

Restrictive cardiomyopathy has impaired filling, often without striking hypertrophy

Functional overlap makes morphologic interpretation necessary

Attribute

HCM

Restrictive

LV wall

Marked thickening

Often not marked

Diastole

Abnormal

Abnormal

LV cavity

Usually not dilated

Not dilated

Myocyte disarray

Characteristic

Not defining

Schematic

Slide 54 · Therapeutic principle: Reduce cardiac work

β-adrenergic blockade as beneficial for many patients

Lower heart rate allows more time for ventricular filling

Reduced contractility can attenuate hyperdynamic physiology

Treatment details require patient-specific specialist assessment

Lower heart rate

Reduce excessive contractility

Improve functional filling conditions

Schematic

Slide 55 · Myosin-directed treatment follows mechanism

Sarcomeric hypercontractility is a mechanistic drug target

Newer therapies based on inhibiting myosin activity

The therapeutic logic is to modify excessive contractile activity

This mechanistic concept is separate from prescribing criteria

HCM-associated hypercontractility

Myosin activity as target

Reduced excessive force

Physiologic treatment strategy

Schematic

Slide 56 · Implantable defibrillator: A distinct objective

Some HCM patients are at risk for life-threatening ventricular arrhythmias

An implantable cardioverter-defibrillator addresses selected arrhythmic risk

An ICD does not remove myocardial hypertrophy or septal anatomy

Indication requires individualized clinical risk assessment

Arrhythmic risk assessment

Selected ICD implantation

Prevention of fatal ventricular rhythm outcome

Schematic

Slide 57 · Septal myectomy: Mechanical relief

Surgical excision can reduce the mass of an obstructing septum

The aim is to widen the LV outflow region

This approach addresses a geometric component of obstruction

It does not reverse the underlying inherited sarcomeric abnormality

Prominent septal muscle

Anterior mitral leaflet

Moves toward septum in systole

Leaflet–septum contact

Schematic

Slide 58 · Alcohol septal ablation: Another strategy

Catheter-delivered alcohol can create a carefully controlled septal infarction

The subsequent reduction of septal muscle mass mitigates outflow obstruction

This is an anatomically targeted therapy for selected patients

It differs mechanistically from surgery but shares the obstruction-relief objective

Target obstructing septum

Controlled septal infarction

Reduction in obstructing muscle mass

Schematic

Slide 59 · Matching treatment to pathophysiology

Filling impairment suggests a role for reducing heart rate/contractility

Ventricular rhythm risk is a separate reason to consider an ICD

Severe obstructive anatomy may warrant septal reduction

These treatments address distinct physiologic or clinical problems

Problem

Intervention

Goal

Rapid/hyperdynamic

β-blockade

Slow / reduce force

VT/VF risk

ICD

Arrhythmia rescue

Septal obstruction

Septal reduction

Improve outflow

Schematic

Slide 60 · Case: Exertional dyspnea and septal thickening

A patient develops exertional dyspnea and a systolic ejection murmur

Imaging demonstrates marked asymmetric septal hypertrophy

The anterior mitral leaflet approaches the septum during systole

Question: Which two processes most directly impair forward output?

Septal hypertrophy + SAM

Reduced compliance / filling

Dynamic systolic outflow obstruction

Schematic

Slide 61 · Case reasoning: Integrate physiology

Diastolic filling falls because the LV is small and poorly compliant

The anterior mitral leaflet can narrow outflow during systole

Raised filling pressure contributes to exertional dyspnea

The combination is characteristic of obstructive HCM

Diastole

Systole

Impaired filling

Dynamic LVOT

Obstruction

Reduced forward flow on exertion

Schematic

Slide 62 · Case: Hypertrophy with no obvious obstruction

A second patient has a thick left ventricular wall but no documented SAM

Question: Does absence of obstruction exclude HCM?

No: Symmetric or nonobstructive HCM phenotypes occur

The differential must also address hypertension and infiltrative disorders

LV hypertrophy without SAM

Nonobstructive HCM

Pressure load

Deposit disease

Schematic

Slide 63 · Pathology synthesis: Molecules to events

Sarcomeric variation alters contraction and leads to hypertrophic remodeling

Disarray, intramural arterial disease and fibrosis alter the tissue substrate

Reduced compliance and sometimes outflow obstruction diminish effective output

Arrhythmias, embolism, failure and sudden death define major clinical risks

Sarcomeric disease

Hypertrophy / disarray / fibrosis

Filling defect ± obstruction

Clinical complications

Schematic

Slide 64 · Four findings to recognize at autopsy

A thick and heavy ventricular myocardium

Septal-predominant thickening with small LV cavity when classic

Endocardial plaque at the mitral–septal contact zone in obstructive cases

Microscopic hypertrophy, disarray, microvascular changes and fibrosis

Simplified LV cross-section

Dark blue: Septal projection

White: Residual LV cavity

Schematic

Slide 65 · Three distinctions to retain

HCM is principally a filling disorder; DCM is principally a contractile disorder

Hypertrophic wall thickness is not synonymous with sarcomeric HCM

Dynamic outflow obstruction is clinically important but not universal

A genetic result must be interpreted in phenotypic and family context

Underlying disease

Sarcomeric dysfunction

Myocyte enlargement

Disarray and fibrosis

Clinical phenotype

Diastolic impairment

± LVOT obstruction

Arrhythmic / embolic risk

Schematic

Slide 66 · Primary reference and scope

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

Chapter 12, The Heart — Cardiomyopathies; Hypertrophic Cardiomyopathy

Teaching text and schematic concepts derived from the verified printed pp. 520–521

All diagrams in this deck are original editable schematics; no diagnostic specimen images are reproduced