Far Eastern University – Nicanor Reyes Medical Foundation
Internal Medicine 3A – Cardiology
Cardiomyopathies and Myocarditis
CARDIOMYOPATHY
 A disease of the heart muscle.
 Intended to exclude cardiac dysfunction that results from other
structural heart diseases.
 Ischemic Cardiomyopathy describes diffuse dysfunction
attributed to multivessel coronary artery disease.
 Non-ischemic Cardiomyopathy describes cardiomyopathy from
other causes.
 Defined as a heterogeneous group of diseases of the myocardium
associated with mechanical and/or electrical dysfunction that
usually exhibit inappropriate ventricular hypertrophy or dilation and
are due to variety of causes that are frequently genetic.
Clinical Classification of Cardiomyopathies
 Dilated and Restrictive cardiomyopathies can be distinguished on
the basis of left ventricular wall thickness and cavity dimension.
 Restrictive cardiomyopathy can have variable increased wall
thickness and chamber dimensions.
 It is now defined more on the basis of abnormal diastolic
function, which is also present on the other 2 types, but less
prominent.
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GENERAL PRESENTATION
 Early symptoms often relate to exertional intolerance with
breathlessness or fatigue, usually from inadequate cardiac reserve
during exercise.
 As fluid retention leads to elevation of resting filling pressure,
shortness of breath may occur during routine daily activities.
 May manifest as dyspnea or cough when lying down at night.
 Peripheral edema may be absent despite severe fluid retention.
 The non-specific term congestive heart failure is common to all 3
types of cardiomyopathies.
 All 3 types can be associated with:
 Atrioventricular valve regurgitation (tricuspid, mitral)
 Typical and atypical chest pain
 Atrial and ventricular tachyarrhythmias
 Embolic events
(See next page for table for presentation of symptomatic cardiomyopathies)
GENETIC ETIOLOGIES OF CARDIOMYOPATHY
 Careful family history should elicit not only known cardiomyopathy
and heart failure but also:
 Family members who have had sudden death often incorrectly
attributed to a massive heart attack
 Members who had atrial fibrillation
 Members who had pacemaker implantation by middle age
 Members with muscular dystrophy
 Most familial cardiomyopathies are inherited in an autosomal
dominant pattern, with occasional autosomal recessive and X-
linked inheritacnce.
 Missense mutation with amino acid substitutions are the most
common in cardiomyopathy.
 Mutant protein may interfere with function of the normal allele.
 Deletions or duplications are uncommon in cardiomyopathy.
 Desmin mutation impairs the transmission of force and signaling
for both cardiac and skeletal muscle associated with dilated
cardiomyopathy.
 SCN5A causes Brugada or Long QT Syndrome.
 Nuclear membrane proteins in the myocytes lead to skeletal
myopathy.
 Lamin – autosomal dominant
 Emerin – X-linked
DILATED CARDIOMYOPATHY
 An enlarged left ventricle with decreased systolic function as
measured by left ventricular ejection fraction.
 Systolic failure is more marked than diastolic dysfunction.
 Multiple etiologies but have common pathways of secondary
response and disease progression.
 Acquired cardiomyopathy attributed to infection / toxin exposure.
 When myocardial injury is acquired, some myocytes may die
initially, others may survive to undergo apoptosis, some
hypertrophy in response to increased wall stress.
 Local and circulating factors stimulate deleterious secondary
responses that contribute to progression of the disease.
 Dynamic remodeling of the interstitial scaffolding affects diastolic
function and the amount of ventricular dilation.
 Mitral regurgitation commonly develops as the valvular apparatus
is distorted and is usually substantial by the time heart failure is
severe.
 Even with long-standing disease, some patients have dramatic
improvement to near-normal ejection fractions during
pharmacologic therapy, particularly with beta blockers and RAAS
inhibitors.
 Microscopic specimen shows non-specific changes of interstitial
fibrosis and myocyte hypertrophy characterized by increased
myocyte size and enlarged, irregular nuclei.
 Below is a schematic diagram demonstrating the possible
progression from infection through direct, secondary, and
autoimmune responses to cardiomyopathy.
 Most of supporting evidences for this sequence is derived from
animal models. It is not known to what degree persistent infection
and/or ongoing immune responses contribute to ongoing
myocardial injury.
Causes
 Infection (Myocarditis)
 Toxic – environmental and pharmacologic agents
 Alcohol – most common
 Diastolic dysfunction, mild ventricular dilation.
 Atrial fibrillation is common.
 Marked improvement within 3-6 months of abstinence.
 Cocaine, amphetamines, related-catecholaminergic stimulants
 Excess consumption may contribute 10% of cases of heart failure.
 Toxicity attributed to alcohol and its primary metabolite aldehyde.
 Polymorphism of the genes encoding alcohol dehydrogenase and
the ACE.
 Estimated 6 drinks (4 ounces of pure ethanol) daily for 5 to 10
years but frequent binge drinking may also be sufficient.
 Pathology reveals tiny micro-infarct consistent with small vessel
ischemia.

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 Chemotherapy agents are the most common drugs implicated in
toxic cardiomyopathy.
 Anthracyclines cause histologic changes of vacuolar degeneration
and myofibrillar loss.
 Generation of ROS involving heme compounds.
 Disruption of the large titin protein may contribute to loss of
sarcomere organization.
 3 different presentation of anthracycline-induced CM:
 Heart failure can develop acutely during administration of
single dose but may resolve in few weeks.
 Early-onset doxorubicin cardiotoxicity develops in 3% of
patients during or shortly after a chronic course, relating to
the total dose.
 Chronic presentation differs according whether it was given
before or after puberty. When given early, doxorubicin
impairs development of the heart, leading to clinical heart
failure.
 Doxurubicin toxicity leads to relatively non-dilated ventricle due
to accompanying fibrosis (Stroke volume with 30-40% EF).
 Trastuzumab (Herceptin) – incidence of cardiotoxicity is lower, but
enhanced by co-administration with anthracyclines.
 Considered reversible, but cardiotoxicity do not always resolve
 Cyclophosphamide and Ifosfamide cardiotoxicity occurs acutely
with very high-doses.
 Alkylating agents (5-FU, Cisplatin) lead to depressed contractility
 IFN-α can cause hypotension and arrhythmias.
Metabolic Causes
 Hyperthyroidism and Hypothyroidism do not often cause clinical HF
in a normal heart, but exacerbates HF.
 Clinical signs may be masked so tests for thyroid function
should be part of routine evaluation.
 Hyperthyroidism should be considered with new-onset atrial
fibrillation or ventricular tachycardia.
 Most common current reason for thyroid abnormalities in the
cardiac population is the treatment of tachyarrhythmias with
amiodarone, a drug with substantial iodine content.
 Pheochromocytoma
 Should be considered when patient has HF and very labile BP
and HR, sometimes with episodic palpitations.
 Often have postural hypotension.
 Diabetes – most HF in DM result from epicardial coronary disease,
cardiomyopathy may result from insulin resistance and increased
advanced-glycosylation end product (impairs both systole/diastole)
 Obesity is associated with impaired excretion of excess volume
load, which, over time, can lead to increased wall stress and
secondary adaptive neurohormonal responses.
Nutritional Deficiencies
 Beri-beri heart disease due to thiamine deficiency can result from
poor nutrition.
 This is initially a vasodilated state with very high output heart
failure that can later progress to a low output state.
 Thiamine repletion can lead to prompt recovery.
 Carnitine metabolism abnormalities can cause dilated or restrictive
cardiomyopathies usually in children.
 Keshan’s disease – selenium deficiency, can lead to CM.
 Hypocalcemia can cause severe chronic heart failure, which can
be due to hypoparathyroidism or intestinal dysfunction.
 Hypophosphatemia can develop during starvation and early
refeeding following a prolonged fast, phosphate is needed for
efficient energy transfer and multiple signaling pathways.
 Hypomagnesemia rarely becomes sufficiently profound to cause
clinical cardiomyopathy.
Hemochromatosis
 A metabolic/storage disease, included among the cause of
restrictive cardiomyopathy, but the clinical presentation is often that
of a dilated cardiomyopathy.
 The autosomal form is related to HFE gene.
 Can also be acquired from iron overload due to hemolytic anemia
and/or transfusions.
 Excess iron is deposited in the perinuclear compartments of the
myocytes with resulting disruption of intracellular architecture and
mitochondrial function.
 Inborn errors of metabolism occasionally present with dilated
cardiomyopathy, although they are most often associated with
restrictive cardiomyopathy.
FAMILIAL DILATED CARDIOMYOPATHY
 Recognized frequency has increased to over 30%.
 Mutations in TTN encoding the giant sarcomeric protein titin, are
the most common cause of dilated cardiomyopathy, accounting to
25% of familial disease.
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 Men with TTN develop CM a decade before women.
 Mutations in the thick and thin filament account for 8%.
 Most recognizable familial cardiomyopathy syndromes with extra-
cardiac manifestations are the muscular dystrophies.
 Both Duchenne’s and milder Becker’s dystrophy result from
abnormalities in the X-linked dystrophin gene of the
sarcolemmal membrane.
 Families with history of atrial arrhythmias, conduction system, and
cardiomyopathy have abnormalities in nuclear membrane lamin
protein.
 A prominent family history of sudden death or ventricular
tachycardia before clinical cardiomyopathy suggests genetic
defects in the desmosomal proteins.
 Affects the right ventricle (arrhythmogenic right ventricular
dysplasia), this disorder can affect both ventricles.
 Present first with ventricular tachycardia.
 Defects in demosomal proteins disrupt myocyte junctions and
adhesions, leading to replacement of myocardium by fats.
 Since demosomes are also important for skin and hair
elasticity, it is associated with wooly hair and thickened skin on
palms and soles.
 Left ventricular non-compaction is a condition of unknown
prevalence.
 Diagnostic criteria include presence of multiple trabeculations
in the left ventricle distal to the papillary muscle, creating a
spongy appearance of the apex.
 Associated with multiple genetic variants in the sarcomeric and
other genes such as TAZ (tafazzin).
 Three cardinal features:
 Ventricular arrhythmias
 Embolic events
 Heart Failure
TAKOTSUBO CARDIOMYOPATHY
 Apical ballooning syndrome or stress-induced cardiomyopathy
 Occurs typically in older women after sudden intense emotional or
physical stress.
 Ventricles show global ventricular dilation with basal contraction
forming the shape of the narrow-necked jar(takotsubo).
 Presentations include:
 Pulmonary edema
 Hypotension
 Chest Pain
 ECG changes mimicking acute infarction
IDIOPATHIC DILATED CARDIOMYOPATHY
 A diagnosis of exclusion.
 2/3 of dilated cardiomyopathies are still labeled as idiopathic.
MAJOR CAUSES OF DILATED CARDIOMYOPATHY

RESTRICTIVE CARDIOMYOPATHY
 Least common of the 3 types.
 Dominated by abnormal diastolic function, often with mildly
decreased contractility and ejection fraction (>30-50%).
 Both atria are enlarged, sometimes massively.
 Modest left ventricular dilation can be present, usually with an end-
diastolic dimension of <6cm.
 End-diastolic pressures are elevated in both ventricles, with
preservation of cardiac output until late disease.
 Subtle exercise intolerance is usually the first symptom but s often
not recognized until after clinical presentation with congestive
symptoms.
 Often present with more right-sided symptoms (edema, abdomen
discomfort, and ascites).
 Cardiac impulse is less displaced than in dilated CM and less
dynamic in hypertrophic CM.
 S4 is more common than S3 in sinus rhythm.
 Atrial fibrillation is common.
 JVP often show rapid y descents and may increase during
inspiration (positive Kussmaul’s sign).
 Most restrictive CM is due to infiltration of abnormal substances
between myocytes, storage of abnormal metabolic products, or
fibrotic injury (See Table 287-5, page 4).
 Differential diagnosis should include constrictive pericardial
disease, which may also be dominated by RSHF.
Infiltrative Disease
 Amyloidosis is the major cause of restrictive CM.
 Several proteins can self-assemble to form the beta-sheets of
amyloid proteins which can deposit with different consequences.
 Cardiac amyloid is classically suspected from thickened ventricular
walls with an ECG that shows low voltage.
 Characteristic refractile brightness in the septum on echo is
suggestive of diagnosis, but neither specific nor sensitive.
 Both atria are dilated and diastolic may be more obvious.
 Amyloid infiltration can be detected with gadolinium enhancement
MRI.
 An ECG showing thickened walls of both ventricles without major
chamber dilation.
 Atria are markedly dilated.
 Characteristic hyperrefractile glittering of the myocardium typical of
amyloid infiltration.
 Mitral and tricuspid valves are thickened.
 Pacing lead is visible in the RV and pericardial effusion is evident.
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 Therapy for all types of amyloid is predominantly for symptoms.
 Digoxin bound to amyloid fibrils can reach toxic levels, and should
therefore be used only in very low doses.
 No evidence regarding use of neurohormonal antagonists.
 Prognosis is worst for primary amyloid, median survival of 6-12
months after symptoms of heart failure.
(from Harrison)
Fibrotic Restrictive Cardiomyopathy
 Progressive fibrosis can cause restrictive myocardial disease
without ventricular dilation.
 Thoracic radiation can produce early/late restrictive CM.
 Patients with radiation cardiomyopathy can present with a possible
constrictive pericarditis, as the two often co-exist.
 Scleroderma causes small vessel spasm and ischemia that can
lead to a small, and stiff heart with reduced EF without dilation.
 Pulmonary hypertension associated with scleroderma may lead
to more clinical RSHF because of concomitant fibrotic disease.
 Doxurubicin causes direct myocyte injury, usually leading to dilated
cardiomyopathy, but limited degree of dilation may result from
increased fibrosis, which restricts remodeling.
Endomyocardial Disease
 Chronic hypereosinophilic syndrome (Loeffler’s Endocarditis)
 More common in men than in women.
 Persistent eosinophilia (>1,500 eosinophils/mm3) for 6 months
 In severe disease, the dense fibrotic layer can obliterate the
ventricular apices and extend to thicken and tether the AV
valve leaflets.
 Present with HF, embolic events, and atrial arrhythmias.
 Endomyocardial Fibrosis
 ¼ of HF in tropical countries,
 Partial obliteration of the ventricular apex with fibrosis leading
to valvular inflow tract and leaflets (like Loeffler’s), however, it
is not clear that the etiologies are the same.
 Pericardial effusions frequently accompany endomyocardial
fibrosis, but are not common in loefller’s.
 Medical treatment focuses on glucocorticoids and chemotherapy to
suppress hypereosinophilia when present.
 Diuretic therapy for fluid retention.
 Anticoagulation is recommended.
 Surgical resection of the apices and replacement of fibrotic valves
may improve symptoms.
 Carcinoid tumors secrete serotonin that can produce fibrous
plaques in the endocardium and right-sided cardiac valves.
HYPERTROPHIC CARDIOMYOPATHY
 Defined as left ventricular hypertrophy that develops in the
absence of causative hemodynamic factors.
 Previously termed as hypertrophic obstructive cardiomyopathy
(HOCM), asymmetric septal hypertrophy (ASH), and idiopathic
hypertrophic subaortic stenosis (IHSS).
 At the level of sarcomere, mutations lead to enhanced calcium
sensitivity, maximal force generation, and ATPase activity.
 Sarcomere mutations lead to abnormal energetics and impaired
relaxation. Characterized by misalignment and disarray of large
myofibrils and myocytes.
 Fibrosis and microvascular disease are also present.
 Microinfarction of hypertrophied myocardium is a hypothesized
mechanism for replacement scar formation.
 Macroscopically, it manifests as non-uniform ventricular thickening.
 Interventricular septum is the typical location of maximal
hypertrophy, other patterns include concentric or midventricular.
 Left ventricular outflow tract obstruction represents the most
common focus of diagnosis and intervention.
 Diastolic dysfunction, myocardial fibrosis and microvascular
ischemia also contribute to contractile dysfunction.


 Apical Hypertrophic Cardiomyopathy

 Systolic obstruction is initiated by drag forces, which push an

anteriorly displaced and enlarged mitral leaflet into contact with  ¼ of patients with hypertrophic cardiomyopathy in Japan.
hypertrophied interventricular septum.  ECG: Deep T-wave inversions in precordial leads.
 In order to maintain stroke volume, the ventricle generates higher  Echo: Spade-like appearance with apical obliteration
pressures, leading to high wall stress / myocardial oxygen demand.
 Smaller chamber size and increased contractility exacerbate the
severity of the obstruction.
 Conditions with low preload (dehydration) and low afterload
(arterial vasodilation) may lead to transient hypotension and near-
syncope.
 Systolic ejection murmur of the left ventricular outflow tract
obstruction is harsh and late peaking can be enhanced by
bedside maneuvers that diminish ventricular volume and worsends
obstruction (standing from squatting, or Valsalva maneuver).
 They may be decreased by increasing ventricular volume or
vascular resistance (squatting or handgrip).
 S4 is commonly heard due to decreased ventricular compliance.
 Palpation of carotid pulse may reveal a bifid systolic impulse from
early and delayed ejection.

Diagnosis
 Patients may be diagnosed after undergoing evaluations triggered
by abnormal PE (murmurs) or symptoms of exertional dyspnea,
angina, or syncope.
 Dyspnea on exertion is the most common presenting symptom,
reflecting elevated intracardiac filling pressures.
 Chest pain with either an atypical or typical exertional pattern
occurs in more than half of symptomatic patients and is attributed
to myocardial ischemia from high demand and abnormal intramural
coronary arteries in the hypertrophied myocardium.
 Palpitations may result from atrial fibrillation or ventricular
arrhythmias.
 First manifestation may be sudden cardiac death.
 Cardiac imaging is central to diagnosis due to insensitivity of
examination and ECG.
 Rigorous athletic training may cause intermediate degrees of
physiologic hypertrophy difficult to differentiate from mild
hypertrophic cardiomyopathy.
Medical Treatment
 Management focuses on the treatment of symptoms and
prevention of sudden death and stroke.
 Obstruction can be controlled by beta blocker and L-type calcium
channel blockers (verapamil), these are first-line agents that
reduce the severity of obstruction by slowing heart rate, increase
diastolic filling and decrease contractility.
 Exertional dyspnea or chest pain can be controlled by addition of
disopyramide, an antiarrhythmic agent with potent negative
inotropic properties.
 Refractory patients may undergo surgical myectomy or alcohol
septal ablation may be effective.
 Vigorous physical activity and competitive sports are prohibited.
 Atrial fibrillation is common and may lead to hemodynamic
deterioration and embolic stroke.
 Rapid ventricular response is poorly tolerated.
 Beta blockers and L-type calcium channel blockers slow AV nodal
conduction and improve sypmtoms.
 Cardiac glycosides should be avoided, as they may increase
contractility and worsen obstruction.
 Anticoagulation therapy is recommended.

 This ECG shows asymmetric hypertrophy of the septum.

 Mitral valve is moving anteriorly toward the hypertrophied septum
in systole
 Left atrium is enlarged.
 In ECG, there are often prominent septal Q waves.

Page 5 of 8
MYOCARDITIS
 Inflammation of the heart can result from multiple causes but is
most commonly attributed to infective agents that can injure the
myocardium via direct invasion, production of toxin, or chronic
inflammation.
 May be a precursor to idiopathic dilated cardiomyopathy.
 Infectious myocarditis has been associated to all types of infective
agents, but most commonly associated with viruses and
Trypanosoma cruzi.
VIRAL MYOCARDITIS
 Viral invasion and replication lead directly to myocardial injury and
lysis, proteases degrade the protein, dystrophin, in the myocyte
membrane complex.
 After they enter circulation via the respiratory or gastrointestinal
tract, they can infect other organs possessing specific receptors,
such as the coxsackie-adenovirus receptor on the heart.
 Viral antigens activate immune responses that help to contain the
initial infection but may persist into later phases.
Clinical Presentation
 Acute Viral Myocarditis often presents with signs and symptoms of
heart failure.
 Chest pain – may suggest MI or pericarditis
 Atrial or ventricular tachyarrhythmia
 Pulmonary or systemic emboli from intracardiac thrombi
 ECG abnormalities are also detected.
 Typically young to middle-aged adult who develops progressive
dyspnea and weakness within few days to weeks after a viral
syndrome accompanied with fever and myalgia.
Page 6 of 8
 Some present with fulminant myocarditis with rapid progression
from severe febrile respiratory syndrome to cardiogenic shock.
 Aggressive support, with high level of of inotrophic therapy,
more than half with acute presentation survive with marked
improvement within the first few weeks.
 Often returns to near-normal systolic function.

 Chronic Viral Myocarditis is often invoked but rarely proven.
 A diagnosis when no other cause of dilated cardiomyopathy
can be identified.
 Some will be later recognized to be due to illicit drug use or
excess alcoholic consumption.
Laboratory Evaluation
 Initial evaluation include:
 ECG
 Echocardiogram
 Serum levels of troponin and creatine phosphokinase fractions.
 MRI is increasingly used, supported by evidence of increased
tissue edema and gadolinium enhancement.
 Endomyocardial biopsy is not often indicated, unless ventricular
tachyarrhythmia may suggest possible etiologies (sarcoidosis or
giant cell myocarditis).
 Dallas Criteria for myocarditis - Lymphocytic infiltration with
evidence of myocyte necrosis
 Troponin is often mildly elevated.
 Creatine kinase may be released from the cardiac injury or skeletal
muscle involvement.
Patients with recent or on-going viral syndromes can be classified into:
1.) Possible sub-clinical acute myocarditis is not diagnosed when a
patient has a typical viral syndrome but no cardiac symptoms, with one
or more of the following:
 Elevated biomarkers (troponin, CK-MB)
 ECG findings of suggestive acute injury
 Reduced left ventricular EF or regional wall motion
 Abnormality on cardiac imaging, usually echo.
2.) Possible acute myocarditis is diagnosed when the above criteria
are met and also accompanied also by cardiac symptoms.
3.) Definite myocarditis, diagnosed when there is histologic or
immunohistologic evidence does not require any other lab/clinical
criteria.
(from Harrison’s)
Viruses implicated in Myocarditis
 Picornavirus family of RNA viruses – Enteroviruses, Coxsackie,
Echovirus, and Poliovirus.
 Influenza is also implicated.
 Of the DNA viruses – adenovirus, vaccinia (smallpox vaccine), and
herpesviruses – varicella zoster, CMV, EBV, HHV6 are well
recognized.
 HIV was associated with an incidence of dilated CM (1-2%).
 Hepatitis C has been repeatedly implicated.
 Mumps, RSV, Arboviruses (Dengue, yellow fever), and Arenavirus
Treatment
 Currently no specific therapy recommended.
 During acute infection, anti-inflammatory or immunosuppressive
medications are avoided.
 Patients with persistent inflammatory myocarditis and a
progressive downhill course over weeks may be treated empirically
with glucocorticoids in an attempt to avoid the need for cardiac
transplantation.
PARASITIC MYOCARDITIS
Chagas’ Disease
 The third most common parasitic infection and most common
infective cause of cardiomyopathy.
 The protozoan T. cruzi is transmitted by the bite of the reduviid bug
 Transmission can also occur through blood transfusion, organ
donation, mother to fetus, and occasionally orally.
 The parasite itself can cause myocyte lysis and primary neuronal
damage and specific immune responses may recognize the
parasites or related antigens and lead to chronic immune activation
in the absence of detectable parasites.
 Additional factor in progression of Chagas’ disease is the
autonomic dysfunction and microvascular damage that may
contribute to cardiac and GIT disease.
 Acute phase of Chagas’ disease with parasitemia is usually
unrecognized, may present clinically with non-specific symptoms.
 In the absence of anti-parasitic therapy, the silent stage progresses
slowly over 10-30 years to manifest in cardiac and GIT in the
chronic stages.
 Features typical of Chagas’ disease:
 Sinus Node and AV node dysfunction
 Right Bundle Branch Block
 Atrial fibrillation and ventricular tachyarrhythmia
 Small ventricular aneurysms are common, particularly at the
ventricular apex.
 Dilated ventricles giving rise to pulmonary and systemic emboli
 Serologic tests for specific IgG antibodies lack sufficient specificity
and sensitivity, thereby requiring 2 separate positive tests.
 Treatment include:
 Heart failure medications
 Pacemaker-defibrillators
 Anticoagulation
Page 7 of 8
 Increased attention is directed to anti-parasitic therapy.
 Most common effective are benznidazole and nifurtimox
 Associated with severe reactions including dermatitis, GIT
distress and neuropathy.
African Trypanosomiasis
 Results from the tsetse fly bite and can occur in travelers exposed
during trips to Africa.
 West African form is caused by Trypanosoma brucei gambiense
and progresses silently over the years.
 East African form is caused by Trypanosoma brucei rhodesiense
can progress rapidly through perivascular infiltration to myocarditis
and heart failure with frequent arrhythmias.
 Diagnosis is made by identification of trypanosomes in blood,
lymph nodes, or other affected sites.
 Anti-parasitic therapy has limited efficacy and is determined by the
specific type and stage of infection (hemolymphatic or neurologic)
Toxoplasmosis
 Contracted thought undercooked infected beef or pork,
transmission from feline feces, organ transplantation, transfusion,
or maternal-fetal transmission.
 May present with encephalitis or chorioretinitis and, in the heart,
can cause myocarditis, pericardial effusion, constrictive pericarditis
and heart failure.
 Diagnosis is made when the IgM is positive, and IgG becomes
positive later on.
 Sampling occasionally reveals the cysts in the myocardium.
 Treatment: Pyrimethamine and Sulfadiazine or Clindamycin.
Trichinellosis
 Caused by Trichinella spiralis larva infested w/ undercooked meat.
 Larvae migrating into skeletal muscles cause myalgia, weakness,
and fever.
 Periorbital and facial edema and conjunctival and retinal
hemorrhage may also be seen.
 Larva may invade the myocardium, clinical HF is rare.
 When HF is observed, it is attributed to the eosinophilic
inflammatory response.
 Diagnosis is made from the specific serum antibody and is further
supported by the presence of eosinophilia.
 Treatment: Albendazole, Mebendazole, Glucocorticoids
Echinococcosis
 Cardiac involvement is rare.
 Cysts can form and rupture in the myocardium and pericardium
BACTERIAL INFECTIONS
 Most can involve the heart through direct invasion and abscess
formation, but do so rarely.
 Systemic inflammatory responses depress contractility in severe
infection and sepsis.
Diphteria
 Affects the heart in almost ½ of cases.
 Cardiac involvement is the most common cause of death in
patients with this infection.
 Bacilli release toxin that impairs protein synthesis and may
particularly affect the conduction system.
 Anti-toxin should be administered as soon as possible, with higher
priority than antibiotic therapy.
 Other systemic bacterial infections:
 Brucellosis
 Chlamydophila
 Legionella
 Meningococcus
 Mycoplasma
 Psittacosis
 Salmonellosis
Clostridial Infection  Immunosuppresive treatments are more effective for
 Causes myocardial damage from the released toxin. arrhythmias than for heart failure.
 Gas bubbles can be detected in the myocardium, and occasionally  Pacemakers and implantable defibrillators are generally
abscesses can form within the myocardium and pericardium. indicated.
 Giant Cell Myocarditis – less common, accounts to 10-20% of
Streptococcal Infection biopsy-positive cases of myocarditis.
 Infection with β-hemolytic streptococci is most commonly  Presents with rapidly progressive HF and tachyarrhythmia
associated with acute rheumatic fever.  Diffuse granulomatous lesions surrounded by extensive
 Characterized by inflammation and fibrosis of cardiac valves and inflammatory infiltrate.
systemic connective tissue.  Associated conditions are thymomas, thyroiditis, pernicious
 Can also lead to myocarditis with focal or diffuse infiltrates of anemia and other autoimmune disease, occasionally recent
mononuclear cells. infections.
 Glucocorticoid therapy is less effective
Tuberculosis  Eosinophilic Myocarditis – important manifestation of
 Can involve the myocardium directly as well as through hypereosinophilic syndrome, often idiopathic, may be seen in
tuberculouse pericarditis. Churg-Strauss syndrome or malignancies.
 Rarely does so when it is treated with antibiotic.  Hypersensitive Myocarditis – an unexpected diagnosis, biopsy
reveals infiltration with lymphocytes and mononuclear cells with
Whipple’s Disease high proportion of eosinophils.
 Caused by Tropheryma whipplei.  Most commonly attributed to antibiotics.
 Usual manifestations are in GIT, but pericarditis, coronary arteritis,  Can also be to thiazides, anticonvulsants, indomethacin, and
valvular lesions, and occasionally HF may also occur. methyldopa.
 Smallpox vaccines have also been implicated.
OTHER INFECTIONS  Polymyositis and Dermatomyositis affect skeletal and cardiac
Spirochetal Myocarditis muscles.
 Has been diagnosed from myocardial biopsies containing Borrelia
burgdorferi that causes Lyme disease. Postpartum Cardiomyopathy (PPCM)
 Lyme carditis most often presents with arthritis and conduction  Develops during last trimester or within first 6 months after
system disease that resolves within 1-2 weeks of antibiotic pregnancy, 1:2000 and 1:15,000 deliveries.
treatment.  Risk factors:
 Only rarely implicated in chronic HF.  Increased maternal age
 Increased parity
Fungal Myocarditis  Twin pregnancy
 Can occur due to hematogenous or direct spread.  Malnutrition
 Described for:  Tocolytic therapy for premature labor
 Aspergillosis  Preeclampsia
 Actinomycosis  Toxemia of pregnancy
 Blastomycosis
 Candidiasis
 Coccidioidomycosis
 Cryptococcosis
 Histoplasmosis
 Mucormycosis
 Cardiac involvement is rarely the dominant clinical feature.

Rickettsial Infections
 Q fever, Rocky Mountain spotted fever, and scrub typhus are
frequently accompanied by ECG changes.
 Most manifestations relate to systemic vascular involvement

NON-INFECTIVE MYOCARDITIS
 Myocardial inflammation can occur without apparent preceding
infection.
 The paradigm of non-infective inflammatory myocarditis is cardiac
transplant rejection.
 Most commonly diagnosed non-infective inflammation is
granulomatous myocarditis, including both sarcoidosis and giant
cell myocarditis.
 Sarcoidosis – a multisystem disease most commonly affecting the
lungs, high risk for cardiac involvement.
 Patients may present with rapid-onset heart failure and
ventricular tachyarrhythmia, conduction block, chest pain
syndromes, or;
 Minor cardiac findings in the setting of ocular involvement, an
infiltrative skin rash or a non-specific febrile illness.
“Hen sȳndrorro, ōños. Hen ñuqīr, perzys. Hen morghot, glaeson”
 Ventricles may appear restrictive or dilated.
(From darkness, light. From ashes, fire. From death, life.)
 Often right ventricular predominance in both dilation and
ventricular arrhythmias, attributed to ARVD.

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