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Flashcards in cardiomyopathy Deck (20)
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1
Q

what sort of cardiomyopathy does the anthracyclines cause?

A

restrictive

2
Q

what is the diagnostic criteria for DCM?

A

LVEF < 45% and dilated LVEDD (>117% when corrected for age and BSA)

3
Q

how is fractional shortening calculated?

A

this is (LVEDD - LVESD) / LVEDD

4
Q

what CMP phenotype do hypertensive and ischaemic heart disease have?

A

typically long standing HTN, as well as ischaemia, cause a dilated heart.

however, these have been excluded from the DCM classification in more recent definitions

5
Q

what are some causes of the DCM?

A
  1. tachyarrhythmias
  2. infectious causes
  3. nutritional abnormalities
  4. electrolyte
  5. endocrine
  6. infiltrative (incl amyloid, HCM, sarcoid)
  7. neuromusculars
  8. toxins, such as HART, amphetamines, clozapine, cocaine
6
Q

what are the best treatments for dilated cardiomyopathy?

A
  1. ACEi - shown to have mortality improvement.
  2. diuretics for symptomatic pulm vessel congestion
  3. beta blockers - standard of care
  4. CRT - if LVEF < 30 - 45%; LBBB (QRS > 120 - 150 depending on study) on ECG
7
Q

what are the indications for ICD therapy in DCM?

A
  • VT/VF arrest
  • spontaneous sustained VT
  • syncope of uncertain origin
  • VT/VF at EPS
  • LVEF 1 year
8
Q

what role do VAD play?

A

ventricular assist devices are really only as a bridge to transplant.

they are not, currently, suitable as destination therapy

9
Q

what is the genetics of HCM?

A

this is a disease of the sarcomere

it is AD

many different abnormalities, with variable penetrance

10
Q

What are the most common causes of sudden death in young athletes in the US

A

most common:

  • HCM (~35%!)
  • congenital coronary artery anomaly

less common

  • myocarditis
  • aortic rupture (Marfan)
  • MVP

uncommon:

  • ARVC
  • CAD
  • conduction system abnormalities
  • aortic valve stenosis
11
Q

what happens with HCM on echo?

A
  1. there is systolic anterior movement of the anterior leaflet of the mitral valve
  2. there is dynamic LVOT obstruction (depends on afterload, preload, contractility) (this is only about 25% of patients, however)
  3. MR occurs secondary to the aortic leaflet movement
  4. diastolic dysfunction is an important finding. this is because the LV is stiff. This leads to elevated LVEDP, elevated LA pressure and elevated pulm pressures
12
Q

What are the clinical findings in HCM?

examination?

ECG?

A

examination has a systolic murmur, that is quieter on squatting and louder with standing

ecg is abnormal in about 95%. usually LVH with repol abnormalities

13
Q

how do we diagnose HCM?

A

DNA analysis is actually Gold Standard, however there is a bit of a miss rate with genetic screen (not all abnormalities have been identified)

2D echo can demonstrate the anatomy - 90-95% see asymmetric hypertrophy, the rest see concentric

Doppler echo shows the pathophysiology such as LVOT, MR, diastolic dysfunction

14
Q

what are some of the RF for sudden cardiac death in the HCM population?

A

high risk features:

  1. prior cardiac arrest or spont sustained VT
  2. FH of prematured HCM-related SCM
  3. syncope
  4. repetitive bursts of nsVT on Holter
  5. hypotension on response to exercise
  6. extreme LVH > 30mm
15
Q

what is the role of septal ablation in HCM?

A

it is used to cause a localised infarct and reduce a LVOT obstruction

(they introduce alcohol down a small coronary artery)

16
Q

what does the echo normally look like with restrictive cardiomyopathy?

A

usually we have normal or reduced ventricular volumes, normal or near normal systolic function, significant atrial dilatation

the pathophysiology is dominated by diastolic filling abnormalities

17
Q

what is ARVC?

A

likely AD, progressive fibrofatty replacement of right myocardium, initially RV, then LV with relative sparing of the septum

it is diagnosed based on major and minor criteria

it is associated with many presentations, including arrhythmias and also heart failure

18
Q

what are some of the findings on ECG for ARVC?

A

Epsilon waves are important, and they are associated with low amplitude signals between QRS and T wave

there can also be LBBB on nsVT etc

19
Q

what is the best clinical predictor of sudden cardiac death?

A

previous arrest, probably

syncope is stronger than LVEF <25% and ECG changes

20
Q

what is the most specific finding for HCM on echo?

A

asymmetrical wall thickening is probably number 1