Cardiomyopathy

10/17/2024 1
Definition
Cardiomyopathies are diseases that affect the
structure and function of the heart muscle
(myocardium) in the absence of secondary
causes (e.g., coronary artery
disease, hypertension, valvular disease,
and congenital heart disease).

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Epidemiology
Incidence and prevalence difficult to estimate
due to inconsistent reporting
Second most common cause of sudden death
after ischemic heart disease
Both sporadic and familial forms exist.
No clear gender or racial predominance

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Etiology
Causes vary: Genetic neurologic and
Infectious diseases neuromuscular disorders
Inflammatory/ Hematologic/oncologic
autoimmune conditions disorders
Endocrinologic disorders Cardiovascular disorders
Toxins Endomyocardial
Medications diseases
Nutritional deficiencies Genetic (gene
Deposition diseases  mutations)
Familial storage diseases Approximately ⅓ of
cases have a genetic
cause.
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Classification
 By morphology:
 Dilated cardiomyopathy (DCM):
 Heart appears enlarged.
 Muscle is thinned.
 Restrictive cardiomyopathy (RCM):
 Heart is normal size (or smaller).
 Muscle is stiffened.
 Hypertrophic cardiomyopathy (HCM)
 Heart is enlarged.
 Muscle is thickened.
 Arrhythmogenic right ventricular
cardiomyopathy/dysplasia
 Unclassified cardiomyopathy
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10/17/2024 6
Classification
 By etiology:  Secondary: caused by or
associated with a known
 Primary: arises from underlying systemic
condition
an exclusively  Disorders of connective tissue
cardiac issue  Muscular dystrophies
 Genetic  Autoimmune disease
 Infections of the heart muscle
 Mixed
 Infiltrative diseases
(nongenetic/geneti (hemochromatosis, sarcoidosi
c) s, or amyloidosis)
 Endocrine disorders
 Acquired (thyroid conditions, diabetes)
 Chronic substance abuse
(especially alcohol or cocaine)
 Pregnancy
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 Comparison of the Cardiomyopathies
Dilated Restrictive Hypertrophic Arrhythmogenic
right ventricular CM

Etiology •Idiopathic •Amyloidosis •Genetic •Idiopathic

•Genetic •Sarcoidosis •Chronic hype •Genetic
•Alcohol abuse •Hemosiderosi rtension
•Postpartum s
•Medication •Post radiation
• therapy
•Postsurgical
•Diabetes

Clinical •Fatigue •Dyspnea •Asymptomati •Sudden

presentation •Dyspnea •Exercise c cardiac death
•Dizziness intolerance •First •Syncope
•Exercise •Lower- symptom may •Palpitations
intolerance extremity ede be sudden •Dyspnea
ma cardiac death •Chest pain
•Weight gain •.Syncope
•Cough •Exercise
•Fatigue intolerance
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 Dilated Restrictive Hypertrophic Arrhythmogenic
right ventricular
CM
Physical exam •S3 gallop •S3 •May be normal. •Often normal
findings •Systolic • gallop •S3 •S3 or S4 gallop
regurgitant •Systolic heart • or S4 •Wide
murmur murmur (from • gallop split S2 sound
•Jugular venous mitral or tricuspid •Split S2 may be present.
distention regurgitation) •Harsh •Peripheral edema
•Ascites •Kussmaul’s crescendo/decresc •Tachycardia
sign (jugular endo systolic
distention murmur
on inspiration) •Pansystolic
murmur
• of mitral
regurgitation
•Systolic thrill at
the apex
•Palpable left
ventricular heave

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 Ejection ↓ ↓ or ↑ or ↓
fraction normal normal

L ↑ ↑ ↓ Normal
ventricular
diastolic
dimension

Left ↓ Normal or ↑↑ Normal

ventricular ↑
wall
thickness

Atrial size ↑ ↑ ↑ Normal

Diagnosis •Echocardio •Echocardio •ECG •ECG

graphy graphy •Echocardio •Echocardio
•Cardiac •Cardiac graphy graphy
MRI MRI •Cardiac •Cardiac
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MRI MRI
Pathophysiology
Myocardium : thickest layer of the heart
Specialized form of striated muscle
Composed of cardiomyocytes connected
by intercalated discs
Structure, size, and arrangement of muscle fibers
and heart chambers optimized for pumping force
End effect of cardiomyopathies: structural
change in heart muscle
May cause hypertrophy or dilation of one or both
of the heart ventricles
Changes shape and capacity of ventricles

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Pathophysiology
Cause systolic or diastolic dysfunction, depending
on the disease process
Systolic dysfunction is characterized by a decrease
in heart muscle contractility.
Diastolic dysfunction is characterized by a decrease
in left ventricular relaxation and ability to fill with
blood and is often associated with increased filling
pressures.
Net end effect is inability to pump blood
efficiently:
Heart failure
Volume overload
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Diagnosis
 Diagnostic approach varies based on the type of
cardiomyopathy.
 Echocardiography with Doppler
 Used in evaluation of all cases
 Assesses cardiac size, anatomy, structure, and function
 Cardiac MRI:
 Advanced imaging technique
 Allows greater characterization of cardiac structure and function
 Used to determine extent of myocardial damage, infiltration,
and fibrosis
 ECG:
 Low sensitivity for diagnosis of cardiomyopathies
 Used to identify abnormal heart rhythms, such as associated
arrhythmias or conduction delays

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Management
Goals:
 Optimize cardiac output:
 Increase contractility.
 Allow for ventricular filling
 Optimize ejection fraction
 Treat or slow underlying disease progression.
 Manage symptoms of heart failure:
 Volume overload
 Blood pressure
 Manage symptoms caused by distortion of heart muscle:
 Arrhythmias: medication, pacemaker, or internal cardioverter–
defibrillator (ICD)
 Blood clots: anticoagulants
 In cases refractory to treatment, heart transplantation may
be indicated.
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Complications
Heart failure
Arrhythmias
Sudden cardiac death

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Dilated cardiomyopathy
 DCM is a disease of the cardiac
muscle associated with electrical and
mechanical dysfunction causing impaired
systolic function and featuring the dilatation
of 1 or both ventricles.

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Etiology
 Etiology
 Idiopathic in approximately 50% of cases
 Familial DCM:
 Caused by a multitude of gene mutations
 20%–35% of cases initially diagnosed as idiopathic are later found
to have a familial component after additional family screening
 Typical inheritance pattern is autosomal dominant; however, all
inheritance patterns have occurred.
 Ischemic heart disease/coronary artery disease (CAD)
 Untreated hypertension
 Long-standing valvular disease (e.g., mitral or aortic
regurgitation)
 Arrhythmias (particularly those that cause
sustained tachycardia, e.g., atrial fibrillation)
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Etiology
Infections
 Viral infections causing myocarditis (e.g., coxsackievirus, in
fluenza, or HIV)
 Chagas disease (protozoan infection due to Trypanosoma
cruzi)
Endocrine disorders (e.g., hyperthyroidism or diabetes)
Autoimmune or inflammatory conditions (e.g., lupus
or sarcoidosis)
Neuromuscular genetic conditions (e.g.,
Duchenne muscular dystrophy or Friedreich’s ataxia)
Deposition diseases
(e.g., hemochromatosis or amyloidosis)
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Etiology
 Medications that cause cardiotoxicity:
 Chemotherapeutic medications (classically an anthracycline, e.g.,
doxorubicin, or a monoclonal antibody, e.g., trastuzumab)
 Antiretrovirals (most classically azidothymidine; also known
as zidovudine)
 Hydroxychloroquine
 Radiation treatment (particularly to the chest)
 Peripartum cardiomyopathy
 :Secondary to hemodynamic changes associated with pregnancy
 Occurs in the last month of pregnancy or the 1st months after giving
birth
 Toxins:
 Alcohol abuse
 Cocaine and other illicit drug use
 Exposure to heavy metals (e.g., cobalt, arsenic, mercury, or lead)
 Nutritional deficiencies (e.g., thiamine, selenium, or carnitine)
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Pathophysiology
 Ventricular dilation caused by:
 Left ventricle (LV) failure
 Primary injury of heart muscle
 Ventricular dilatation leads to:
 Thinning of heart muscle wall
 Weakening and enlargement of heart
 Systolic failure:
 Cardiac muscle
 does not contract efficiently when deformed.
 Cardiac output
 decreases.
 Diastolic failure: valvular insufficiency due to distortion
 of cardiac architecture
 Heart failure
 (HF)
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Clinical Presentation
 Symptoms may develop and progress slowly over time, or
develop abruptly. Symptoms are similar to those seen with HF.
 Symptoms
 Dyspnea/shortness of breath (especially with exertion)
 Orthopnea (shortness of breath when lying down)
 Edema of lower extremities and abdomen
 Weight gain
 Dizziness
 Syncopal episodes
 Chest pain
 Palpitations
 Fatigue
 Weakness

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Physical exam findings
 Cardiac:
 Systolic heart murmur (from mitral or aortic regurgitation)
 S3 gallop
 Abdominal: ascites
 Pulmonary:
 Rales or crackles over lung fields (secondary to pulmonary
edema)
 Respiratory distress
 Low oxygen saturation
 Vascular: jugular venous distention
 Extremity:
 Pitting edema in lower extremities
 Signs of venous stasis with discoloration in lower extremities

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Management
 Treatment
 Medications:
 Angiotensin-converting enzyme inhibitors/angiotensin receptor blockers:
improve systolic function
 Beta-blockers: increase ejection fraction
 Diuretics: treat volume overload
 Vasodilators
 Oral anticoagulation (vitamin K antagonists, e.g., warfarin) if LVEF < 35%
 Device therapies (e.g., pacemaker or implanted cardioverter-defibrillator)
if:
 LVEF < 35%
 Arrhythmias or other conduction disorders
 LVEF > 35% with family history of sudden cardiac death or gene mutations
(e.g., LMNA) associated with a high risk for sudden cardiac death
 Syndromic diseases (e.g., muscular dystrophy)
 Heart transplant warranted in severe cases

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Restrictive cardiomyopathy
Restrictive cardiomyopathy (RCM) is a
disease of the heart muscle characterized by
decreased compliance of the ventricles,
nondilated heart muscle, and diastolic
dysfunction (impaired filling of the ventricles)

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Epidemiology
 Rarest cardiomyopathy
 5% of all cases
 Incidence and prevalence are etiology-dependent:
 Amyloidosis
 Most common RCM in the United States
 Men = women
 Common in elderly
 Sarcoidosis
 Women > men

 Highest incidence in Japan

 Highest prevalence among Black women

 Hemochromatosis
 1 in 200
 Men = women
 Loeffler endocarditis
 Increased incidence and frequent cause of death in the tropics of Africa, Asia, and

South and Central America

 Secondary to high incidence of endomyocardial fibrosis in those areas

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Pathophysiology
 Cardiac muscle becomes increasingly stiff owing to:
 Infiltration with abnormal cell/substances
 Excessive deposition of metabolic by-products
 Direct fibrosing injury
 Reduced compliance and impaired ability to expand →
impaired relaxation of the heart (diastole)
 Heart muscle cannot fill properly during diastole
 → increased filling pressures and diastolic dysfunction → atria
become dilated/enlarged secondary to the increased pressures
→ pulmonary and systemic congestion
 With increases in heart rate, heart is unable to adequately
↑ cardiac output
 Systolic function is usually normal.
 No ventricular dilation or thickening
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Clinical Presentation
Presentation is similar Swelling in lower
to that seen with extremities and
right heart failure possibly abdomen
Symptoms Weight gain
Dyspnea (shortness of Dizziness
breath), especially with Syncopal episodes
exertion
Chest pain
Orthopnea (shortness
Palpitations
of breath when lying
down, as while Cough
sleeping) Fatigue
Intolerance to exercise  Weakness
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Diagnosis
History and physical exam
Signs and symptoms suggestive of heart
failure:
Ascites
Dependent edema
Decreased exercise tolerance
Signs of causative pathologies:
Hemochromatosis: bronze skin
Amyloidosis: carpal tunnel syndrome
Sarcoidosis: respiratory symptoms

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Diagnosis
Laboratory studies
↑ BNP:
BNP is a marker of heart failure.
Renal failure can also increase BNP, making it
less diagnostic in those cases.
Measure BUN and creatinine to monitor
renal function/perfusion.
To investigate underlying cause, perform
additional tests such as serum and urine
protein tests (amyloidosis).
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Management
Treatment
Treatment is aimed at managing heart failure
 and underlying secondary causes.
Goals of treatment:
↓ Pulmonary and systemic venous congestion
↓ Venous pressure
HR control to ↑ filling time (with caution to
avoid bradycardia)
Maintain atrial contractions.
Manage/correct conduction disturbances.
Manage/avoid anemia, electrolyte imbalances, nutrient
deficiencies, and calcium overload.
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Management
 Medication:
 Loop diuretics (i.e., furosemide (Lasix)) to ↓ edema/fluid overload
 Calcium channel blockers (i.e., verapamil) to control HR and ↑
filling time
 Beta-blockers may control HR, ↑ filling time, and ↑ ventricular
relaxation.
 ACE inhibitors or angiotensin II receptor blockers (ARBs) are
helpful in select cases.
 Oral anticoagulation, such as with warfarin, is necessary if atrial
fibrillation is present.
 Surgical intervention:
 Devices (pacemaker or implanted cardioverter–defibrillator) in
significant arrhythmias or conduction disorders
 Cardiac transplantation in patients with severe heart
failure refractory to treatment
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Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy (HCM) is the

most commonly inherited cardiomyopathy,
which is characterized by an asymmetric
increase in thickness (hypertrophy) of the left
ventricular wall, diastolic dysfunction, and
often left ventricular outflow tract
obstruction.

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Epidemiology
Prevalence: 1 in 200–500 adults
Higher prevalence in men than in women
Patients present most commonly in their 30s.
Well-known cause of sudden cardiac death in
athletes (approximately 50% of deaths
occurring during or immediately after
physical activity)
Left ventricular outflow tract obstructions
seen in 70%–75% cases

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Etiology
 Approximately 60–70% of cases are caused by mutations
affecting the thick or thin myofilament proteins of the
sarcomeres (contractile components of the heart).
 Mutations leading to hypertrophic cardiomyopathy (HCM)
found in 6 different genes over 4 different chromosomes
 50+ associated gene mutations identified
 The majority are missense mutations (single amino acid is
replaced).
 Inheritance pattern most commonly autosomal dominant
 De novo (sporadic) mutations without a familial pattern may
also occur.
 Penetrance and phenotypic expression vary due to a vast
number of mutations and sarcomeric genes that cause HCM.

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Pathophysiology
 Left ventricle (LV) becomes thickened and hypertrophied
(asymmetrically with septal predominance) → left ventricular
cavity becomes small/noncompliant → harder for the heart
to pump blood and relax to refill during diastole
 Depending on the location and severity of wall thickening within
the ventricle:
 Left ventricular outflow tract obstruction impairs blood flow
 from the heart to rest of the body, especially with exertional
activity:
 Dynamic and affected by ↑ LV contractility, ↓ preload, and ↓ afterload
 ↑ Left ventricular outflow tract obstruction → ↓ cardiac output
 Diastolic dysfunction
 Mitral regurgitation
 Myocardial ischemia
 Sudden cardiac death

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Pathophysiology

Mechanisms of left ventricular outflow tract obstruction:

 Anterior displacement of the mitral valve during systole, also
known as systolic anterior motion
 Venturi effect: High-velocity blood flow through the left
ventricular outflow tract during systole creates negative
pressure, pulling the mitral valve leaflets toward the
ventricular septum and pressing the leaflets against it.
 Abnormally elongated mitral valve leaflets in patients with
HCM
 Muscular obstruction due to a hypertrophic septum
narrowing cavity space
Hypertrophy or anomalous insertion of papillary muscle
may also occur, increasing left ventricular apical pressure
and the risk of apical ventricular aneurysms.
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Clinical Presentation
 Many individuals affected by HCM are asymptomatic throughout
their lives. For some, typically during adolescence,
 sudden cardiac death is the 1st symptom.
 History
 Symptoms:
 Shortness of breath, particularly with physical activity (most
common symptom)
 Chest pain, especially upon exertion
 Fatigue
 Palpitations
 Dizziness/light-headedness
 Syncope, particularly during exercise:
 15%–25% of patients report at least 1 episode of syncope.
 More common in individuals < 30 years of age
 Unexplained syncope = ↑ risk sudden cardiac death

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Clinical Presentation
Family history:
Important to determine the history of HCM to
help in the diagnosis
History of sudden cardiac death in a family
member worsens prognosis:
Sometimes, sudden cardiac death is not known
as the cause of a family member’s death.
Important to ask about unexplained deaths
(drowning, car accidents, etc)

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Diagnosis
Initial diagnosis based on history and physical
examination:
 Given the prevalence of a lack of symptoms, physical
examination and screening of all athletes annually
during pre-participation is essential.
 May require further investigation:
 Unexplained chest pain, shortness of breath on
exertion, syncope, palpitations
 Family history of HCM or sudden cardiac death at an early
age
 Systolic heart murmur

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  ECG: Abnormal in > 90% of cases
 Echocardiography with Doppler:
 Assessment for:
 Cardiac size and structure

 Systolic and diastolic function

 Presence and severity of left ventricular outflow tract obstruction

or mitral regurgitation
 Findings suggestive of HCM
 Asymmetric thickening of the left ventricular wall
 Variable wall thickening, most commonly seen in interventricular
septum
 The majority of patients have normal left ventricular ejection
fraction (LVEF).

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Management
 Treatment
 No pharmacological treatment is known to improve prognosis.
 Goals of treatment:
 Reduce symptoms.
 Reduce left ventricular outflow tract obstruction.
 Control HR to ↑ filling time (with caution to avoid bradycardia)
 Maintain atrial contractions.
 Manage/correct any conduction disturbances.
 Avoid volume depletion.
 Asymptomatic cases:
 Observed with routine follow up and surveillance (including
repeat ECG and echocardiography)
 Avoid strenuous exercise.

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  In setting of heart failure symptoms without left ventricular
outflow tract obstruction:
 Beta-blockers (treatment of choice) or nondihydropyridine calcium-
channel blockers (CCBs)
 Diuretics if signs or symptoms of fluid overload
 If severe symptoms persist and in case of reconfirmation of the
absence of left ventricular outflow tract obstruction, a heart
transplant may be needed.
 In setting of heart failure symptoms and left ventricular
outflow tract obstruction:
 Monotherapy with beta-blockers: 1st-line treatment
 Monotherapy with nondihydropyridine CCBs (i.e., verapamil) may be
used if:
 Beta-blockers are contraindicated or not tolerated
 No signs or symptoms of hypotension, volume overload, or
severe dyspnea
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  If monotherapy is not sufficient:
 Addition of disopyramide (should not be used as monotherapy or
in a setting of prolonged QT interval on ECG)
 Combination therapy beta-blocker + nondihydropyridine CCBs
 Avoid
 Diuretics and vasodilators such as dihydropyridine
 CCBs (i.e., amlodipine)
 ACE inhibitors
 Angiotensin II receptor blockers (ARBs)
 If limiting symptoms persist:
 Surgical septal myectomy (partial resection of the thickened
septal wall)
 Septal ablation with alcohol (ethanol) via cardiac
catheterization (creates localized myocardial infarct resulting in
cardiac remodeling)
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Complications
Concurrent atrial fibrillation:
Beta-blockers, CCBs, or antiarrhythmic drug
therapy
Cardioversion as a last resort
Atrial
fibrillation: thromboembolism prophylaxis with a
blood thinner such as warfarin
Ventricular arrhythmias: Implantable cardioverter-
defibrillator (ICD) should be considered.
LV
apical aneurysm: thromboembolism prophylaxis w
ith a blood thinner such as warfarin
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Takotsubo Cardiomyopathy
Takotsubo cardiomyopathy (also known as
stress cardiomyopathy, or “broken heart
syndrome”) is a type of non-ischemic
cardiomyopathy in which there is transient
regional systolic dysfunction of the left
ventricle.
Patients present with symptoms of acute
coronary syndrome, including chest pressure
and shortness of breath.

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Etiology
The exact cause for this condition is unknown, but it
is associated with the following:
Emotional stressors
 Loss of a loved one
 Financial distress
Physical stressors
 Domestic abuse and physical assault
 Severe medical illness
 Surgery
 Drug or alcohol abuse
Underlying psychiatric or neurologic disorders
appear to increase a patient’s risk.
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Pathophysiology

 Mechanism is not well understood.

 Postulated pathogenesis:
 Stress-induced catecholamine release
 → direct myocardial toxicity
 and vascular dysfunction → transient ↓ In left ventricular
function (“stunning”) → ↓ contractility → systolic
dysfunction and ↓ cardiac output
 It is not clear why the mid-cavity and apex of the left ventricle
are affected.
 Left ventricular outflow tract (LVOT) obstruction can
develop due to a compensated hyperkinesis of the left
ventricular basal segments.
 Patients may also develop mitral regurgitation due to
involvement of the anterior mitral valve leaflet.
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10/17/2024 48
Clinical Presentation
Patients will present similar to those with ACS
or heart failure:
Symptoms
Acute substernal chest pain (most common)
Dyspnea
Syncope
Palpitations
Fatigue
Dizziness
Nausea

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Clinical Presentation
Physical exam
May be nonspecific
Hypotension from cardiogenic shock
Hypoxia from pulmonary edema
Tachyarrhythmias or bradyarrhythmias
Diaphoresis
Crackles from pulmonary edema
Late-peaking systolic murmur from mitral
regurgitation and left ventricular outflow
tract obstruction
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10/17/2024 51
Diagnostic tests
Initial testing:
Electrocardiogram (ECG)
ST segment elevations, usually in the precordial
leads
ST segment depressions
QT prolongation
T wave inversions
Troponin
↑ In most cases
Brain natriuretic peptide (BNP)
↑ In most cases, but not required for diagnosis
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Diagnostic tests
Next steps:
Cardiac catheterization
Often done emergently to rule out ACS
No critical coronary artery disease
 will usually be found.
Left ventriculogram will show
apical ballooning.
 Contrast dye is injected into the left ventricle to
visualize systolic function.

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Diagnostic tests
Next steps:
Echocardiography
 Should be done in all patients with suspected
takotsubo cardiomyopathy
 Demonstrates regional wall-motion abnormalities
and systolic dysfunction:
 Mid and apical hypokinesis of the left ventricle
 Left ventricular apical ballooning
 ↓ Left ventricular ejection fraction (LVEF)
 Abnormalities will not follow a vascular distribution.
 May reveal LVOT obstruction
 Evaluates for a thrombus in the ventricle
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Diagnosis
Diagnostic criteria
The following 4 criteria are required for diagnosis:
Transient left ventricular systolic
dysfunction (hypokinesis, akinesis, or dyskinesis)
observed on echocardiogram
Absence of obstructive coronary disease or
acute plaque rupture observed on coronary
angiography
New electrocardiogram abnormalities observed
on ECG or modest elevation in cardiac troponin
Absence of pheochromocytoma or myocarditis
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Treatment
The acute management prior to diagnosis follows the
typical protocol for ACS.
Management after diagnosis is confirmed:
 Resolve and prevent stressors.
 Treat heart failure.
 Beta blockers (metoprolol)
 Angiotensin-converting enzyme (ACE) inhibitors (lisinopril)
 Diuretics, if evidence of volume overload
 Consider anticoagulation in patients with an LVEF < 30% to
prevent thromboembolism.
 Follow-up echocardiogram to confirm resolution
 May discontinue ACE inhibitors
 once systolic function improves
 Consider continuing long-term beta-blocker therapy.
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Complications
Cardiogenic shock
 With LVOT obstruction:
 Beta blockers
 Cautious intravenous fluid resuscitation to increase preload
 Vasopressors (phenylephrine, vasopressin)
 Avoid inotropic support, as it can worsen LVOT obstruction
and shock.
 Without LVOT obstruction:
 Inotropic support (milrinone, dobutamine, dopamine)

 Vasopressors as a 2nd-line therapy

Arrhythmias: monitor on telemetry

Intraventricular thrombus: anticoagulation until LVEF
normalizes and thrombus is no longer seen
on echocardiogram
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