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cardiomyopathies Flashcards

1
Q

what is the myocardium?

A

thickest layer of the heart. Composed of cardiac muscle§

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2
Q

what is the functional unit of the myocardium?

A

sarcomere

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3
Q

what is a cardiomyopathy?

A

any disease of the myocardium that can’t be explained by coronary artery narrowing or abnormal loading of ventricles

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4
Q

what are primary cardiomyopathies?

A

genetic, mixed (genetic and nonmixed) or non-genetic (acquired) causes and are confined solely to the heart

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5
Q

what are secondary cardiomyopathies?

A

affect the heart as part of a systemic disease

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6
Q

what are the main categories of cardiomyopathies?

A 
o Hypertrophic (HCM)
o Dilated (DCM)
o Restricted (RCM)
o (Also: Arrhythmogenic right ventricular (ARVC) and unclassified CM)
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7
Q

what is DCM characterised by?

A

Characterised by dilation of chambers and decreased systolic function (usually L side)

Right ventricular dilation and dysfunction might be present – not necessary for diagnosis

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8
Q

when does DCM occur?

A

Occurs in the absence of abnormal loading conditions (hypertension, valve disease) or coronary artery disease)

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9
Q

what are the causes of DCM?

A

genetic mutations, infections, inflammation, autoimmune diseases, exposure to toxins and endocrine or neuromuscular causes

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10
Q

what are the most common causes of DCM?

A

Idiopathic and familial disease

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11
Q

describe the histopathology in DCM

A

remodelling of myocardium occurs. Cardiomyocytes are interspersed with necrotic and fibrotic patches and intermittent calcifications

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12
Q

what is the pathophysiology of DCM in the early stages?

A

Myocyte injury –> decreased contractility –> decreased stroke volume –> decreased cardiac output

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13
Q

how does the CVS compensate for a reduction in CO in DCM?

A

o Frank Starling mechanism
o Neurohormonal mechanism; SNS activates increased HR and contractility
o Activation of the renin-angiotensin-aldosterone system

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14
Q

what are the detrimental effects of the compensation mechanisms for DCM?

A
  • Increased preload and afterload –> more difficult for the LV to eject blood
  • Angiotensin II and aldosterone contribute to pathogenic cardiac remodelling
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15
Q

what are the signs and symptoms of DCM and why do they occur?

A
  • Decreased CO – tiredness/fatigue
  • Pulmonary oedema – dyspnoea/crackles
  • Ascites and peripheral oedema in legs and ankle
  • Enlarged heart – leftward displacement of apical beat and possibly 3rd heart sound
  • Mitral regurgitation – blood goes back into LA
  • Palpitations – caused by arrhythmias
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16
Q

what are methods of diagnosing DCM?

A

signs/symptoms/family history, physical exam, blood tests, ECG, CXR – enlarged heart silhouette, echocardiogram, exercise stress test, cardiac catheterization, CT scan, MRI

17
Q

what are the main treatment methods for DCM?

A
  • medication to control heart failure symptoms
  • prevention and treatment of arrhythmias
  • cardiac surgery/transplantation
18
Q

what medications can be used to control heart failure symptoms and how do they work?

A
  • Beta blockers – control heart rate
  • Anti-coagulants – reduce chance of blood clots forming
  • Diuretics – reduce build-up of fluid
  • ACE inhibitor/ARBs – lower blood pressure
19
Q

what are the methods to prevent and treat arrhythmias for DCM?

A
  • Medication to control arrhythmias
  • Blood thinners to prevent blood clots
  • Pacemaker – implanted to control the rhythm of the heart
  • Implantable cardioverter defibrillators or ICDs to control the rhythm and chock the heart if it goes out of normal rhythm
20
Q

how are the different types of HCM classified?

A

depending on location and thickening on different areas of muscle - usually LV, but can be in the septum or RV

21
Q

how is the volume of the ventricle affected in HCM?

A

volume of ventricle may be normal or reduced

22
Q

what can happen if septal thickening occurs in HCM?

A

LV outflow tract obstruction or mitral valve dysfunction may be caused

23
Q

how many mutations can cause HCM and what proteins do these affect?

A

Caused by more than 1400 mutations in at least 13 genes coding for proteins of the sarcomere and Z disc (most commonly affected are myosin-binding protein C and B-myosin heavy chain)

24
Q

what is the inheritance pattern of HCM?

A

autosomal dominant

25
Q

what are the symptoms of HCM and what causes them?

A
  • Palpitations – caused by arrhythmias.
  • Chest pain – reduced oxygen levels getting to the heart.
  • Dizziness or fainting – reduced oxygen levels or blood flow to the brain.
  • Breathlessness (or dyspnoea) – pulmonary oedema, making it harder to breathe.
  • Tiredness – reduced cardiac output.
26
Q

how can you diagnose HCM?

A
  • Medical history, physical exam, ECG, exercise ECG, holter monitoring
  • Echocardiogram – type of ultrasound scan which uses sound waves to make echoes when they hit different body parts. Shows heart structure
  • MRI scan
  • Treatment - Medication, devices and surgery
27
Q

what is restrictive cardiomyopathies characterised by? what does this lead to?

A

Characterised by increased stiffness of the myocardium that causes increased pressure in one or both ventricles

• Ventricular relaxation impaired  atria enlarge in response to increased pressure in some patients

28
Q

give examples of restrictive cardiomyopathies

A

non-infiltrative (idiopathic), infiltrative, storage diseases, endomyocardial diseases

29
Q

what are the causes of RCM?

A

• Fibrosis or scarring of the endomyocardium
• Infiltration of myocardium by an abnormal substance
• Genetic and run in the family
o Mutations in troponin I recognised as primary mutation in famial RCM

30
Q

what is Loeffler’s disease?

A

infiltration of the heart and lungs by eosinophils in response to a parasitic infection

31
Q

what are signs and symptoms of RCM?

A
  • Decreases CO – fatigue (tiredness)
  • Systemic congestion
  • Jugular venous distension
  • Peripheral oedema
  • Arrhythmias – palpitations
  • Possible conduction block
  • Signs of congestive heart failure may also be present e.g. pulmonary crackles
32
Q

how do you diagnose RCM?

A

medical history, physical exam, ECG, CXR, CT and MRI

33
Q

what is the prognosis of RCM?

A

Poor prognosis except when the underlying cause can be treated

34
Q

how is arrhythmogenic RVCM inherited?

A

autosomal dominant or recessive pattern

35
Q

what do the most common mutations in RCMs affect?

A

mutation affects cardiac desmosomes  structural and functional alterations – associated with cardiomyocyte apoptosis

36
Q

name a hallmark of ARVC?

A

Adipose and fibrotic tissue that replace cardiomyocytes are a hallmark of ARVC – primarily in the RV (LV affected later)

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