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Cardiomyopathies

Cardiomyopathies refer to diseases of the heart muscle that cause it to be structurally and functionally abnormal without other causes like coronary artery disease. The main types are hypertrophic, dilated, restrictive, and arrhythmic right ventricular dysplasia. Causes can be genetic, mixed genetic and acquired, or acquired. Dilated cardiomyopathy is characterized by enlarged ventricles and reduced contraction. Causes include viral infections like influenza, inflammatory conditions, toxins, metabolic issues, and inherited defects. Symptoms may include heart palpitations, shortness of breath, and edema. Diagnosis involves echocardiogram, EKG, blood tests and endomyocardial biopsy. Treatment focuses on managing heart failure

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139 views4 pages

Cardiomyopathies

Cardiomyopathies refer to diseases of the heart muscle that cause it to be structurally and functionally abnormal without other causes like coronary artery disease. The main types are hypertrophic, dilated, restrictive, and arrhythmic right ventricular dysplasia. Causes can be genetic, mixed genetic and acquired, or acquired. Dilated cardiomyopathy is characterized by enlarged ventricles and reduced contraction. Causes include viral infections like influenza, inflammatory conditions, toxins, metabolic issues, and inherited defects. Symptoms may include heart palpitations, shortness of breath, and edema. Diagnosis involves echocardiogram, EKG, blood tests and endomyocardial biopsy. Treatment focuses on managing heart failure

Uploaded by

yvasparks
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd
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Cardiomyopathies

Disease

Cardiomyop
athy

Definition

Types/Phenot
ypes

Classification

Disease of heart
muscle

1. Hypertrophi
c
2. Dilated
3. Restrictive
4. Arrhythmic
RV
dysplasia
5. LV noncompaction

Primaryly:
affecting the
heart
MAG
Mixed genetic
& acquired
Acquired
Genetic

Myocardial disorder in
which the heart muscle is
structurally and
functionally abnormal
in the absence of
coronary artery disease,
hypertension, valvular
disease and congenital
heart disease sufficient to
explain the observed
myocardial abnormality

5-10% of 5-6 million HF


pts in US
**excludes disease of
heart caused by CAD,
valvular disease, HTN

Secondary:
Systemic
Disease

General
Presentatio
n
**Exertion,
dsynpea, or
fatigue
*Progresses
to dyspnea
with minimal
activity and
then at rest
(Class 4)
*FH
Cardiomyopa
thy and HF
Muscular
Dstrophy
A-fib
Pacemaker
Implant
Sudden
death

Cause/Etiology

Treatment

Genetic: heredity
hypertrophic and
dilated (30%)
cardiomyopathy

Usually based on
phenotype rather
than genetic

Autosomal
dominant
Different defects
affect different
aspects of cellular
metabolism

Cardiomyopathies

Disease/Di
sorder

Signs/Sympt
oms

Dilated
Cardiomyo
pathy

Signs

2 types:
Familial
(1/3) &
Sporadic/A
cquired 2/3

Raised JVP
Displaced apex
beat
Functional
mitral and
tricuspid
regurgitations
3rd heart sound
Symptoms
Systolic
dysfunction
predominates
with reduced EF
Diastolic
dysfunction
frequently
present but not
prominent
unless volume
overload is
present

Causes

***Many causes idiopathicpresumed post-viral***


Inflammation
Infectious Causes
Viral (Coxsackie, Adeno, Influenza most
common- HIV, Hep C)
Parasitic (T cruze, causes Chaga disease,,
toxoplasmosis)
Bacterial (diphtheria)
Spirochetal (Lymes disease)
Richettsial (Q fever)
Fungal (with system infection)
Non Infectious Causes
Granulomatous inflammatory disease
(sarcoidosis, giant cell myocarditis)
Hypersensitivity myocarditis
Polymyositis
Collagen vascular disease
Peripartum
Transplant rejection
Toxins
**Alcohol
Catecholamines, amphetamines, cocaine,
drugs
Chemotherapeutic agents
Interferon
Other therapeutic agents (chloroquine,
hydrochloroquine)
Heavy Metals, lead/mercury
Occupational exposure (hydrocarbons,
arsenicals)
Metabolic Causes
Nutritional Deficiencies (thiamine,
selenium, carnitine)
Electrolyte Deficiencies ( calcium,
phosphate, magnesium)
Endocrinopathy (thyroid disease,

Investigations/Fin
dings
Diagnosis
Chest x-ray:
generalized cardiac
enlargement
ECG: diffuse, nonspecific ST segment
and T wave changes
*sinus tachycardia
*conduction defects
*a-fib, ventricular
premature
contractions or v-tach
Echocardiogram:
CONFIRMS dilation
of left and/or right
ventricle with poor
global contraction
function
BMP: Troponin and
CK may be elevated
Acute and
convalescent viral
titres
Cardiac MRI:
edema, increase in
gadolinium
enhancement (DYE)
in mid wall (distinct
from cad) abnormal

Treatment

With
appropriate HF
and specific
therapy
progress (slow
or fast),
stabilize, or
completely
recover
*1/2 recover to
normal
function

1.Treat HF
2.Treat
arrhythmias
3.ICD for
recurrent vtachs
3.Cardiac
transplantation
for end stage
HF

Complicati
ons
Sudden
death
Embolism
HF
arrhythmias

Cardiomyopathies
pheocrhomocytoma, DM)
Obesity
Hemocromatosis
Inherited Metabolic Cause
Defects occur at multiple sites w/in cell
(45 defects)
Skeletal & cardiac myopathy (9 defects)
Arrythmogenic RV Dysplasia
Causes of DCM following RCM
Hemochromatosis
Amylidosis
Hypertropic CM burned out
Miscellaneous Cause
Arrythmogenic RV dysplasia (may effect
LV also)

Disease/Di
sorder
Dilated
Cardiomyop
athy:
Infective
Myocarditis

Pathology
Failure of systolic
function with
inadequate
contractibility
Affected myocardium
unable to generate
pressures required to
maintain cardiac
output (normal
Ejection rate 50%,
30-35% in
DC)ventricles
become stretched
and volume
overloaded
Valves become
stretcheddont
close
properlyregurgitati
on of blood in atria
diastolic (present if
volume overload)
and systolic

myocardial fibrosis
*identifying
myocardial thrombus
Endomyocardial
biopsy: 10-20% show
lymphatic infiltrationmost just show
edema
Coronary
Angiography:
exclude CAD (usually
in pts >40)

Signs/Sympt
oms

Causes

Clinical Presentations

Symptoms
*May occur
without
symptoms for
years
Heart
flutters/arrhyth
mia
Shortness of
breath
Cold extremities
Thromboemboli
sm
FH of sudden
death
Signs
*reduced cardiac
output & poor
ventricular
contractility weak
pulse/compensatory
tachycardia /poor
peripheral perfusion
(pale mucous
membranes and cold
extremities

Viral
Trypanazoma cruzi (Chagas
disease)
Endomyocardial fibrosis- Africa

Viral
*young adults with
progressive dyspnea,
weakness/fatique for
weeks/days with recent viral
infection causing
fever/myalgias
*may have pericarditis pain
(pleuritic, pericardial, angina
type)
*may have ventricle
arrhythmias (consider
sarcoid or giant cell)

Virus infects through GI or


respiratory tractattach to
myocytes with injury and cell
lysis (vulnerable cells, mostly)
Chagas
-3rd most common parasitic
infection in world & parasitic
cause of CM
- 100,000 people in US have it
- Most common cause of HF in
S. America
- transmitted by bite/ingestion
(bug or its feces) of the
reduvidd bug (endemic to rural
S./C. America
- transmitted via blood
infusion, organ donation,
mother to fetus

Fulminant Myocarditis
(inflammatory process that
occurs in myocardium;
causes acute onset CHF
virally mediated myocyte
dysfunction and immunemediated tissue
injuryreplication and
necrosis/ventricular dysfunction
occur): pts progress to severe
HF/Cardiogenic shock
(inadequate circulation of blood
due to ventricle dysfunction)

Diagnosis/
Treatment
Echocardiograph confirms
Consider presence of
myocarditis:
Troponin, CK elevated, viral
titres (acute and convaslcent)
MRI-> edema, increased
gadolinium in mid wall
Biopsy of heart mucscle (1020% show lymphatic
infiltration/most just show
edema)
Acute Treatment of Myocarditis
Acute treatment *stabilize
hemodynamic status
*ACE/ARB + BB (long term
treatment recommended)
*Steroids no benefit, use
glucocorticoids if condition
quickly getting worse

Chagas

Cardiomyopathies
dysfunction (more
common) dysfunction
Atrial pressure
increases, atria
become dilated,
pressure in the veins
behind
heart(backward
failure)=
pulmonary edema,
causing dyspnea
tachyopnea/fast
breatingHF
-LITTLE TO NO wall
hypertrophy

* S3 gallop sound
heard on
auscultation over
the left and/or right
heart apex
* Murmurs of mitral
and/or tricuspid
regurgitation are
usually heard, but
they can be very
quiet and difficult to
appreciate,
particularly if there
is a dysrhythmia,
such as atrial
fibrillation
* distended jugular
veins,
hepatomegaly,
ascites and a
percussable pleural
fluid line

Other parasitic causes


Toxoplasmosis
Trinchinellosis
African trypanosomiesis
Bacterial
Diptheria
Clostridia
Steptococcus/ B-hemolytic ARF
Tuberculosis (mainly
pericardium)
Spirochetal myocarditis
(Lymes disease)
Usually associated with
arthritis & conduction system
disease resolves w/in 1-2
weeks

*need AGGRESSIVE inotropic


(force altering)/mechanical
ventricle support (1/2
recover in a few weeks with
normal function/minimal
damage)
Chagas Clinical Features
*Conduction System Disease
*A-fib
*Ventricular arrhythmia
*Ventricular dilation &
aneurysm
*Thromboemoboli from LV

Treatment
HF treatment regimes
Pacemaker/Defib
Anticoagulation
Antiparastic
therapy(Benznidazole,
Nifurtimox)
Occasional transplant need
life long antiparasitic therapy

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