Cardiomyopathy, Myocarditis and pericarditis Flashcards

1
Q

dilated cardiomyopathy

A

heart condition where the ventricular function is impaired

- Can be a primary problem or the end result of almost any pathological insult to the myocardium

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2
Q

Causes of dilated cardiomyopathy?

A

ischaemia

valvular

genetic + familial - muscular dystrophy

inflammatory, infectious, autoimmune, postpartum

toxic:- drugs, exogenous chemicals, endocrine

injury, cell loss, scar replacement

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3
Q

which gene commonly causes cardio myopathy if altered

A

SCN5A gene

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4
Q

which chambers of the heart can dilated myocardiopathy affect/

A

Both L and R ventricles mainly but can also affect atria

Can be one chamber but most often all chambers become dilated and functionally impaired

So systolic and diastolic dysfunction can occur

thrombosis in chambers is not uncommon

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5
Q

when is flow slower through a ventricle?

A

when it is dysfunctional/ not contracting properly

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6
Q

Reversible causes of dilated cardiomyopathy (6)

A
Alcohol
endocrine
tropical disease
post partum - after having a baby - often fixes itself
haemaochromatosis sarcoid
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7
Q

is DCM common?

A

no

incidence = 5-8 per 100000

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8
Q

symptoms of DCM

A
Progressive
slow onset
dyspnoea
fatigue
orthopnoea
PND - paroxysmal nocturna dyspnoea
ankle swelling
weight gain of fluid overload
cough
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9
Q

what are you likely to find on examination of a patient with DCM? (10)

A

Poor superficial perfusion

thready pulse, irreg if in AF

SOB at rest

narrow pulse pressure
JVP elevated+/- TR waves

displaced apex

S3 and S4

MR murmur often

pulmonary, sacral and ankle oedema pleural effusions

acites - protein containing fluid in abdomen

hepatomegally

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10
Q

Basic investigations to carry out for DCM diagnosis? (7)

A

ECG - almost always abnormal

CXR - fluid overload, pleural effusion

ECHO - simplest, least invasive

basic bloods - FBC

CMRI - best imaging modality - show scar burden in myocardium and maybe see thrombus

coronary angiogram

sometimes a biopsy depending if caught at early stage or not

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11
Q

general treatment of DCM

A

Correct anaemia

Remove exacerbating drugs eg NSAIDs - these retain salt/water so not good if already have fluid overload

Correct any endocrine disturbance
Advise on fluid and salt intake, reduce it
Advise on managing weight to identify fluid overload
HF nurse referral

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12
Q

specific treatment of DCM

A
  • ACE Inhibitors, - Angiotensin II blockers - diuretics
  • Beta blockers
    Spironolactone
  • Anticoagulants as required
  • Sudden Cardiac Death risk assessment with ICD or CRT-D/P implant
  • Cardiac transplant – last resort, if everything else fails
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13
Q

prognosis of DCM? which cause of DCM shows worst outcome

A

generally poor and often influenced by the causes

Cardiomyopathy due to HIV

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14
Q

restrictive and infiltrative cardiomyopathy - what is it? prevalence?

A

not a high prevalence - cardiologist might see 1 a year?

heart is restricted - has to stretch to accommodate blood and increased venous return - ventricle can’t fill well due to reduced compliance

impairment of diastolic function

about 50% related to specific clinical conditions, the rest remain unknown

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15
Q

2 causes of infiltrative cardiomyopathy?

A

sarcoid - inflammation of organs

amyloid - protein collection in tissues/organs

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16
Q

storage diseases that can cause restrictive and infiltrative cardiomyopathy

A

haemachromatosis

Fabry’s disease - glycogen storage disease

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17
Q

endomyocardial causes of restrictive and infiltrative cardiomyopathy?

A

Fibrosis, carcinoid, radiation, drug effects

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18
Q

is there increased or reduced compliance in Restrictive and infiltrative cardiomyopathy?

A

reduced

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19
Q

is relaxation of the ventricular wall an active or passive process?

A

active

requires functioning intact myocytes

20
Q

investigations carried out for restrictive and infiltrative cardiomyopathy (10)

A

repeated ECG - note if there is Left bundle branch block (LBBB) -cardiac conduction abnormality seen on ECG. In this condition, activation of the left ventricle of the heart is delayed, which causes the left ventricle to contract later than the right ventricle.

CXR

BNP - increased in heart failure

Basic bloods FBC, U+E, be on the look out for sarcoid and haemachromatosis

Auto antibodies for sclerotic CT diseases

Amyloid needs non cardiac biopsy to help establish the diagnosis

Fabry; low plasma alpha galactosidase A activity

Echo

CMRI, probably best imaging modality

Biopsy more helpful but still has high false negative rate

21
Q

what are some specific measures put in place for restrictive and infiltrative cardiomyopathy

A

Limited diuretic use as low filling pressures will cause problems

Beta blockers limited ACE Inhibitor use

Anticoagulants as required

Sudden Cardiac Death risk assessment with Implantable cardiac defibrillator or Cardiac resynchronization therapy pacemaker implant

Cardiac transplant

If iron overload, specific forms of amyloid or Fabrys then specific treatments are available

Endomyocardial fibrosis has little specific treatment

22
Q

hypertrophic cardiomyopathy:- what is it? prevalence? genetic basis?

A

thickened heart muscle

impaired relaxation is a common feature. Ventricles can’t hold much blood, and the walls can’t relax properly and may stiffen. Behaves in restrictive manner

relatively high prevalence 1:500

over 1500 genes now identified - sarcomere gene defect

autosomal dominant but gene can be expressed differently and not known how until time passes

23
Q

what parts of the heart thicken in hypertophic cardiomyopathy?

A

doesn’t have to be whole heart, can be part of it

Can be apical, septal or generalised

24
Q

if septal hypertrophy what can an additional defect in the mitral valve lead to?

A

Left ventricular outflow tract obstruction

25
Q

common further heart/vessel problems associated with hypertrophic cardiomyopathy

A

Coronary arteries also affected with small vessel narrowing and consequent ischaemia and fibrosis

arrhythmias are common

26
Q

symptoms of hypertrophic cardiomyopathy

A

Breathless, palpitations, syncope, exertional symptoms, Sudden Cardiac Death

Asymptomatic for many
fatigue
dyspnoea
anginal like chest pain 
exertional pre syncope
syncope related to arrhythmias or LVOT obstruction
27
Q

examination findings:- hypertrophic cardiomyopathy

A

Can be none!

Notched pulse pattern

Irreg pulse if in AF or ectopy

Double impulse over apex, thrills and murmurs, often dynamic, LVOT murmur will increase with valsalve and decrease with squatting

JVP can be raised in very restrictive filling

28
Q

investigations/tests for hypertrophic cardiomyopathy?

A

ECG - often abnormal but a few are normal where phenotype is poorly expressed in genotype +ve individuals

Echo - see thickness in muscle and dynamic effects of blood flow

CMRI

Risk stratification for Sudden Cardiac Death, may need ICD
Holters repeatedly (monitors heart rate)
29
Q

general measures suggested for hypertrophic cardiomyopathy

A

Avoid heavy exercise

Avoid dehydration

Explore FH and first degree relatives, ECGs and echoes may be required

Consider genetic testing

Regular follow up to re appraise the risks and progress

30
Q

specific measures suggested for hypertrophic cardiomyopathy

A

Drugs to try and enhance relaxation, variable results but often if symptomatic, beta blockers, verapamil, disopyrimide

If in AF anticoagulate

Obstructive form; surgical or alcohol septal ablation

ICD if required based on risk stratification

31
Q

myocarditis:- what is it? acute/chronic? prevalence?

A

can be acute or chronic
inflammation of the myocardium

canimpair myocardial function, conduction and generate arrhythmia

8-10 100000
most common is viral

32
Q

common viruses causing myocarditis?

A
adenovirus
parvovirus B19
influenza 
hep C 
epstein barr virus
33
Q

pathology of myocarditis?

A

Infiltration of inflammatory cells into the myocardial layers, reduced function and heart failure, heart block as conduction system is involved and arrhythmias

34
Q

symptoms of myocarditis

A

Heart failure with fatigue, SOB, Chest Pain in only 26%

Shorter course of a few weeks
May not have fever
Signs of Heart Failure

35
Q

Expected investigation/test outcomes for myocarditis?

A

ECG usually abnormal

Biomarkers often elevated but not falling in a pattern consistent with MI

Echo, can get RWMA (regional wall motion abnormalities - LV wall motion abnormalities usually)

CMRI can see oedema in certain images

Low threshold for biopsy

Viral DNA PCR
Auto antibodies
Step antibodies
Lyme B burgdorferi
HIV
36
Q

general measures/management for myocarditis

A

Supportive with treatment of heart failure and support for brady and tachy arrhythmias

Immunotherpay if biopsy or other Ix point to a specific diagnosis

Stop possible drugs or toxic agent exposure

20% mortality at 1 year and 56% by 4 years.

37
Q

pericarditis

A

Inflammation of the pericardial layers with or without myocardial involvement

38
Q

causes of pericarditis (10)

A
idiopathic
viral - infectious
bacterial 
post MI
perforation
dissection of proximal aorta 
neoplasia - presence or formation of new, abnormal growth of tissue
immune-inflammatory 
trauma
congenital
39
Q

symptoms of pericardial disease

A

Usually 1-2/52 week duration

chest pain with pleuritic features and postural features, sitting forward usually improves it lying back makes it worse

Fever

40
Q

signs of pericardial disease

A

Raised temp

pericardial rub Left Sternal Edge

look for JVP as if an effusion is present and substantial or haemodynamically relevant then it will be raised

low BP

muffled HS and raised JVP should make you consider not just pericarditis but effusion

High fever and very unwell despite no effusion may suggest bacterial

41
Q

investigations for pericardial disease

A

ECG and echo,

troponin (protein in muscle fibres) may be raised if myocardial involvement too (myocardial injury)

42
Q

general measures/management for pericardial disease:- viral, idiopathic and bacterial

A

Viral is conservative - non invasive treatment

idiopathic gets colchicine and limited use of NSAIDs

Bacterial must be drained even if small effusion and antimicrobials, high death rate

If large effusion present and some haemodynamic effects then drain

43
Q

what signs and symptoms would a patient present with if tamponade was present

A

signs:- raised JVP, low BP, +/- rub or muffled HS. Large drop in stroke vol, systolic BP and pulse wave
amplitude during inspiration (pulsus paradoxus)

symptoms:- fatige, SOB, dizzy with low BP, occasionally chest pain.

44
Q

tests/investigations:- tamponade

A

urgent echo
CXR - show large cardiac shadow

drainage - treatment
mechanical circulatory support

45
Q

what does persistant effusion need

A

a surgical pericardial window made to allow flow to abdomen

46
Q

constrictive pericarditis

A

rare, impaired filling although myocardium is normal most of the time

causes: - idiopathic, radiation, post-op, autoimmune, renal failure, sarcoid
symptoms: - fatigue, SOB, cough
signs: - more of RHF with oedema, ascites, high JVP, jaundice, hapetomegally, AF, TR, pleural effusion
investigations: - echo, RH catheter to differentiate from restrictive cardiomyopathy - v difficult
treatment: - careful and limited diuretics and pericardectomy