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MYOCARDIAL DISEASE (MYOCARDITIS, CARDIOMYOPATHY) (HYPERTROPHIC…

- - - - idiopathic (50%)
        
        when primary and secondary causes have been eliminated
      - genetic (25%)
        
        inherited as autosomal dominant: a variety of single gene mutations have been identified. there are also autosomal recessive, x-linked (esp duchenne's and becker's muscular dystrophies), and mitochondrial inheritance patterns
      - alcohol
        
        chronic consumption is implicated in the development - potentially reversible
      - infective
        
        frequently occurs as a sequela of viral myocarditis.
        
        VIRAL causes: PARVOVIRUS, COXSACKIE A & B, INFLUENZA, ADENOVIRUS, ECHOVIRUS, CMV, HIV
        
        NON VIRAL causes: CHAGAS DISEASE; endemic in south america develops 10-20yrs after infections
      - other causes
        
        hypothyroidism
        
        peripartum cardiomyopathy
        
        chemotherapy
        
        sarcoidosis
  - - - presents with heart failure symptoms: breathlessness, peripheral oedema, fatigue, syncope, sporadic chest pain
      - arrhythmia - eg AF or sudden cardiac death due to ventricular arrhythmia
      - asymptomatic - may be an incidental finding
      - thromborembolism
    - - Remember to ask about a history of viral illness or myocarditis in the past and a pos fam hx may be helpful
      - presents with a displaced heart beat secondary to LV dilatation
      - signs of HF
      - s3 and s4 gallop
  - - - ECG
        
        Changes are non specific
      - CXR
        
        features of HF, cardiomegaly
      - Bloods
        
        including LFTs, electrolytes, TFTs, and ferritin (note that haemochromatosis is an important reversible cause)
      - ECHO
        
        GOLD STANDARD
    - - cardiac biopsy can establish definitive diagnosis but its use is controversial
      - cardiac MRI may be useful
  - - - treat identifiable underlying cause
      - manage HF symptoms
        
        ACEi/ARBSs also reduce risk of sudden arrhythmic death
        
        loop and thiazide diuretics
        
        B-blockers and ACEi/ARBs improve survival
        
        spirinolactone also improves survival
      - prevent complications
        
        anticoagulation is not routinely offered
        
        generally prescribed if pts have AF or evidence of LV thrombus
        
        implantable cardioverter defibrillator (ICD) and cardiac resynchronisation therapy (CRT)
        
        anti-arrhythmics
        
        heart transplantation may eventually be an option for the select few where maximal medical therapy has failed
- - - - obstructive (hypertrophic obstructive cardiomyopathy)
        
        involves narrowing of the ventricular outflow tract due to a thickened interventicular septum
        
        the anterior mitral valve leaflet is sucked towards the hypertrophied septum, which may lead to obstruction. this is known as systolic anterior motion (SAM) of the mitral valve. these pts are prone to mitral regurg but is not a major feature
      - Non obstructive
  - - - most people with hypertrophic cardiomyopathy are asymptomatic
      - may present similar to aortic stenosis if there is LV outflow tract obstruction
      - symptoms - ANGINA, DYSPNOEA, PRE-SYNCOPE/SYNCOPE ON EFFORT, SUDDEN DEATH
      - syncope in hypertrophic cardiomyopathy may occur due to arrhythmias that develop because of abnormal cardiac myocytes
      - AF is the most common arrhythmia seen in hypertrophic cardiomyopathy
      - sudden death is usually caused by arrhythmias or severe ventricular outflow tract obstruction
    - - signs of LV outflow obstruction are exaggerated by standing up (reduced venous return), inotropes and vasodilators (eg GTN spray)
      - The double impulse is caused by the combination of the contraction of the hypertrophied atrium and ventricle
      - SIGNS - jerky pulse, palpable LV hypertrophy, double impulse at apex, pansystolic murmur (due to mitral regurg)
      - EXAM ESSENTIAL
        
        valsalva manoevure (forced expiration against a closed glottis) reduces venous return to the heart and will increase the murmur intensity by bringing the hypertrophied septum closer to the mitral valve and increasing obstruction to blood flow. in contrast the murmur of aortic stenosis will decrease in intensity as flow is reduced
  - - - CXR
      - BLOODS: LFTs, electrolytes, BNP, TFT
      - ecg: CHANGES MOSTLY INVOLVE LV HYPERTROPHY AND t WAVE INVERSION
      - ECHO - GOLD STANDARD. DILATATION IS NOT SEEN AND MOST PTS HAVE A THICKENED IV SEPTUM
      - GENETIC TESTING
        
        50% of pts with HCM have an identifiable mutation on genotype analysis - used to screen first degree family members if mutation found in the proband (first person identified)
    - - Cardiac MRI is useful for evaluating ventricular wall thickness and the presence of replacement myocardial fibrosis
  - - - alcohol septal ablation is another option (alcohol injected directly into the coronary artery causing small iatrogenic MI to reduce septal thickness)
      - institute HF treatment as disease progresses to HF in later stages
      - surgical myectomy is the treatment of choice for those who do not resond to best medical therapy
      - heart transplantation may be required in severe cases
      - initially, use B blockers rate limiting CCBs (verapamil)
    - - anti-arrhythmics for any arrhythmia
      - pts at risk for sudden death may benefit from ICD
      - pts with AF should receive treatment with warfarin (if not contraindicated)
- - - - ECG
        
        changes are non specific
      - CXR
        
        reveals features of HF
      - BLOODS
        
        including LFTs, electrolytes, cardiac enzymes
      - ECHO
    - - endomyocardial biopsy
        
        GOLD STANDARD
      - COMPLEX IMAGING MODALITIES (eg CT, MRI) and diagnostic angiography
        
        used to distinguish restrictive cardiomyopathy from constrictive pericarditis because the latter is correctable with surgery
- - - - in its typical form the LV apex in systole has a similar shape to that of the bulging trap
        it is characterised by apical ballooning akinesia or dyskinesia of the apical one-half to two-thirds of the LV), non obstructive coronary artery disease and impaired LV systolic function, which typically recovers within 1-4 wks