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Cardiomyopathy

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Cardiomyopathy Dr.mirdamadi Cardiologist, fellowship of echocardiograpy Apical HCM Apical hypertrophy Giant negative T wave on the ECG Spade shaped LV cavity ... – PowerPoint PPT presentation

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Title: Cardiomyopathy


1
Cardiomyopathy
  • Dr.mirdamadi
  • Cardiologist, fellowship of echocardiograpy

2
Definition
  • Group of diseases that primarily affect the heart
    muscle and are not the result of congenital,
    acquired, valvular, hypertensive , coronary
    arterial or pericardial abnormalities

3
Classification
Dilated
primary myocardial involvement
Restrictive
secondary myocardial involvement
Hypertrophic
( infective,

Metabolic,

Connective tissue
disorders

Infiltration,

toxin,

peripartum)
4
Dilated cardiomyopathy (DCM)
5
  • 1/3 of CHF is due to DCM
  • LV and/or RV systolic function is impaired
    leading to progressive cardiac dilation
  • No cause detected in many cases, but familial
    (1/4-1/3 of cases) or secondary cause like
    infectious, metabolic or toxic agents present.

6
  • Reversible form may be found with alcohol abuse,
    pregnancy, thyroid disease, cocaine use and
    chronic uncontrolled tachycardia.

7
Clinical features
  • symptoms of left and right sided CHF.
  • some patients have LV dilation for months or
    even years before becoming symptomatic
  • vague chest pain (typical angina is unusual and
    suggestive of IHD)
  • syncope due to arrhythmias
  • systemic embolism

8
Physical examination
  • Narrow pulse pressure and elevated JVP in
    advanced disease
  • S3
  • S4
  • MR
  • TR

9
Laboratory examination
  • CXR cardiomegaly , pulmonary congestion
  • ECG Sinus tachycardia or AF , Ventricular
    arrhythmias, Non specific changes
  • Echocardiography LV dilation , systolic
    dysfunction
  • Angiography to exclude IHD

10
  • Endomyocardial biopsy
  • is not necessary in idiopathic or familial
    DCM but may be helpful in the recognition of
    secondary CMP like amyloidosis and myocarditis

11
  • most patient has progressive course
  • patients gt 55 years die within 4 years of the
    onset of symptoms
  • Spontaneous improvement in about one- quarter of
    patient
  • death is due to progressive HF or ventricular
    arrhythmia or brady arrhythmia

12
Alcoholic cardiomyopathy
13
  • large quantities (gt90g/d) of alcohol over many
    years cause DCM
  • Risk of developing CMP is partially genetically
  • patient with severe CHF have a poor prognosis (lt
    1/4 of such patients survive 3 years)

14
  • Second presentation of alcoholic cardiotoxicity
    is recurrent supraventricular or ventricular
    tachyarrhythmias
  • Holiday heart syndrome AF, Atrial flutter or
    frequeut PVC after a drinking binge.

15
Peripartum cardiomyopathy
16
  • Cardiac dilation and CHF may develop during the
    last trimester of pregnancy or within 6 months of
    delivery.
  • Mortality rate is 10.
  • Patient who recover from peripartum CMP should be
    encouraged to avoid further pregnancy .

17
Drugs
18
  • A variety of drugs may damage the myocard?ium
    acutely (myocarditis) or they may lead to chronic
    damage (like DCM)
  • Anthracycline derivatives
  • Doxorubicin cardiotoxicity may occur acutely but
    more commonly develops 3 months after the last
    dose.
  • TCA antidepressants, phenothiazines , lithium
  • Cocaine abuse (SCD , myocarditis , DCM, acute MI
    )

19
Arrhythmogenic right ventricular cardiomyopathy
/ Dysphasia (ARVC/D)
20
  • ARVD is a familial CMP with progressive
    fibrofatty replacement of the RV and to a much
    lesser degree LV.
  • Patients may present by RV failure or ventricular
    tachycardia

21
Others
  • Neuromuscular disease
  • Tako tsubo (stress) CMP
  • Non compaction CMP

22
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23
Hypertrophic cardiomyopathy
24
  • characterized by LV hypertrophy without obvious
    cause
  • It is 1 in 500 of general population
  • two features af HCM asymmetric LV hypertrophy ,
    Dynamic LVOT obstruction

25
  • There is a bizarre and disorganized arrangement
    of myocytes with variable degree of fibrosis.
  • About a half of patients have a positive family
    history compatible with autosomal dominant
    transmission

26
Normal and HCM cellular
arrengement
27
  • Screening by echocardiography of first- degree
    relatives between the age 12 and 20 should be
    done every 12-24 months unless diagnosis
    evaluated by genetic testing

28
Clinical features
  • Clinical course is variable , from asymptomatic
    to SCD
  • SCD frequently occur in children and young adult
    during or after physical exertion.
  • HCM is the most common cause of SCD in young
    competitive athletes
  • Other symptom dyspnea , syncope , angina and
    fatigue.

29
Physical examination
  • Double or triple apical precordial impulse
  • Fourth heart sound
  • Harsh , diamond shaped systolic murmur in LSB
    due to LVOT obstruction
  • Holosystolic and blowing systolic murmur at
    apex due to MR

30
Hemodynamic
  • Obstruction in LVOT is dynamic (not fixed) and is
    due to narrowing of the LVOT by systolic
    anterior motion (SAM) of mitral valve against the
    hypertrophied septum.

31
Hemodynamic
  • Three mechanisms are involved dynamic obstruction
  • 1) increased LV contractility (exercise)
  • 2) decreased ventricular preload (strain phase of
    valsalva maneuver , standing )
  • 3) decreased ventricular after load

32
  • Squatting , sustained handgrip position with
    leg raising , expansion of volume in pregnancy
    decreased obstruction

33
Laboratory evaluation
  • ECG LVH and deep broad Q waves (mistake as a
    MI)
  • CXR Cardiomegaly
  • Echocardiography septal hypertrophy (
    septumgt1.3 times of posterior wall )
  • SAM of mitral valve with MR.

34
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35
Apical HCM
  • Apical hypertrophy
  • Giant negative T wave on the ECG
  • Spade shaped LV cavity

36
Management
  • Competitive sports and very strenuous activities
    should be proscribed
  • dehydration should be avoided.

37
  • B- blockers ameliorate angina and syncope
    in1/3-1/4 of patients
  • Varapamil and diltiazem may reduce the
    stiffness of LV
  • Amiodaron reduced risk of SCD and arrhythmia
  • Digitalis,diuretics,nitrates, dihydropyridine
    calcium blockers, vasodilators and B- agonists
    are best avoided.

38
  • Surgical myotomy / myectomy of septum and ethanol
    injections into the septal artey are the invasive
    treatment.
  • ICD should be considered in high- risk patients

39
Restrictive cardiomyopthy
40
  • Hallmark of the RCM is abnormal diastole
    function.
  • Myocardial fibrosis,hypertrophy or infiltration
    caused rigid LV walls

41
  • Amyloidosis,
  • hemochromatosis,
  • glycogen storage disease,
  • endomyocardial fibrosis,
  • sarcoidosis,
  • hypereosinophilic disease,
  • sceleroderma,
  • following mediastinal irradiation

42
  • Inability of the ventricles to fill, caused
    decrease cardiac out put
  • exercise intolerance and dyspnea
  • elevated systemic venous pressure cause edema
  • ascitis and elevated JVP

43
Laboratory examinations
  • in infiltrative disease
  • ECG often shows low voltage, nonspecific
    ST/T change and various arrhythmias.
  • Echocardiography , CT and MRI showed thickened LV
    walls with normal LV systolic function and
    dilated atria.

44
Differentiation of RCM from Constrictive
pericarditis important.
45
  • Management is usually disappointing except for
    hemochromatosis and fabrys disease.

46
Myocarditis
47
  • myocarditis is most commonly the result of
    infectious process, frequently complicated by
    autoimmunity.
  • myocarditis may also result from
    hypersensitivity to drugs (TCA ,
    antibiotics,antipsychotics) or may be caused by
    irradiation, chemicals or physical agents.

48
  • Most common cause is viruses especially
    coxsakievirus B
  • adenovirus
  • hepatitis C
  • and HIV
  •  

49
  • Patients with viral myocarditis may give a
    history of upper respiratory febrile illness or a
    flu like syndrome ,
  • and viral nasopharyngitis or tonsillitis may
    be evident.

50
Clinical manifestation
  • clinical spectrum ranges from an asymptomatic
    state to fulminant condition with arrhythmias,
    acute CHF and death.

51
  • sometime myocarditis simulates an acute coronary
    syndrome ( chest pain, ECG change and elevated
    troponin level ) but typically in patients
    younger than those with coronary atherosclerosis.

52
  • Viral myocarditis is most often self-limited and
    without sequelae but sometime may progress to a
    chronic from and to DCM.

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