Cardiology Board Review in cardiomyopathy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Classification

CMPs can be divided into genetic, mixed and acquired ones.

Dilated CMP

  • Look for reversible causes alcohol, hemochromatosis, and soa

Restrictive Cardiomyopathy

  • 5 yr survival only 64%, CCB, diuresis are mainstays. SOmewhat preload dependent. Slow heart rate and may drop CO., transplant may be best option.
  • Atrial bigger than ventricles, hige atria to fill ventricles
  • Little atrial contribution to filling since pressure so high
  • Non-hypertrophied ventricles
  • Restrictive physiology not the same as restr cmp
  • Classic square root sign

Muscle or Myocardial

===Endomay

Hypereosinophilia

  • Bright endomyocardium on echocardiogram
  • May affect valve function with progressive scarring
  • Mobile scars may require chemotherapy

Amyloid Cardiomyopathy

  • Small volts on EKG
  • Shimmering on Echo
  • Very thick myocardium
  • Often a small pericardial effusion

Arrhythmogenic Right Ventricular Dysplasia

  • Fibrofatty replacement of RV free wall, almost no muscle left
  • Repol abn on EKG
  • 30% have + FH
  • AICD and avoid athletics

Non-Compaction Cardiomyopathy

  • More commonly diagnoses now
  • Heart muscle does not compact down in utero
  • Beta myosin heavy chain most common
  • See crypts and ressesin wall
  • MRI a good imaging modality
  • Dyspnea is the most common symptom, may not have may sx
  • Increased risk of SCD
  • If systolic function normal: Risk strat for SCD using HCM criteria, treat with stage B CHF
  • Low EF: treat like HCM

Class 2B recommendation fo AICD If +FH, SVT put in AICD

HOCM

  • Thick walls
  • Myocardial disarray
  • Prevalence is 1:500
  • Average age of death not that different than gen pop
  • 1% / ye ris of SCD
  • Autosomal dom inheritacne
  • Contrainidcations to competitive athletics, but can hav e ehalthy lifestyle
  • Meds only to reat symptoms
  • Pt with +FH, 2/6 murmur, brisk carotid upstroke in HCM, apical impulse bifid or trifid, bearin down increases murmur, loud whenyou stand up after qauting, most dynamic of the murmurs, EKG narrow symmetric inverted t waves. 5% have normal ECG.
  • thick walss on echo Ithink amyloid, renal failure, glycogen storage dz, anderson Fabrys, or Fredierichs
  • Athletes heart: does not exist in as many people as you think. 1% have increased will thickness. 18-22 mm is too big. Not common in weekend warriors.

Distinguish HCM vs athletic ehart. More wall than cavity then HOCM,

  • Spetum, base can be involved. THere is an apical variant
  • Apical treated no differently, not benign
  • Genetics:
  • abnromal sarcomere genetics, 14 mutations, dont know final common pathway. 50% of HOCM have a genetic abn. Limits role of testing

genotype doesnt teel you if patient will respon to a therpay Only identifies family memebrs

  • Family screening: screening start at puberty or onset of adolescence if child of an HCM patient, then every yeart ill no longer a athlelet. One time echo not good enough stop in adults at age 60 q 5 years as an adilt. iF a mutation is present in a pt, then screen first degree family memb. If no mutation in a ptiatient, screen family with imaging

Tx

  • Avoid heavy weight lifting, comp sports,
  • 40% of young athlete deaths are due to HCM
  • Avoid dehdration
  • Avoid caffiene
  • no diuretics
  • no inotropes
  • hydrate
  • take meds away
  • Debate over myectom and ablation.
  • Indications for myecotmy

LVOT > 40, sx refractory drugs are indications for ablation or myectomr Opmort 0.5% gradient 67 to 3 95% become class 1 or 2. Survivla = age matched chohort Less need for AICD, myectomy patients have less discharge of their AICD Dont tell patients it may save lives, but it might.

Ablation

  • If it works it works as well as myectomy

20-30% dont respond complicaitons like chb in 20% mortalityr ate is 1.9%, not going down, similar to infarcts of same size since we are creating an infarct. if pre-existing LBBB, the ablation wacks out RBB a dn they will need PPM. Younger pts due better with myectomy

Guidelines

  • Indicated if drug refractory symptoms

if surg candidate then myecoty 2a, ablation 2b not surg candate then ablation a 2a indication

Prognosis

  • 1% per year risk of SCD
  • IndependentRisk factors:
  • LVOT obstrution, syncope, worse with exercise
  • serverity of LVH
  • Fibrosis on MRI
  • Fh

Who needs a defib

  • Class 1: Prior CPR
  • Class 2a:

FH SCD, wall > 30 mm, unexplained syncope Non sustained VT and abnormal exercise response and + hyperencehament 2b

Bottom Line

No risk factors: Reassure Prior SCD: AICD Sustained VT: AICD

Pathophysiology

  • Diastolic dysfun in 100%
  • 70% have dynamic obstruction
  • Suendo ischemia
  • MR proportion to gradient
  • Gradient reduces forward CO
  • Sx vary from day to day due to graient, Na intake, temperature. AS sx are constant with constant graient
  • Mitarl vale like your hand hanging out a car and gets pulled back
  • MR anteriorly directed means there may be a primary problemw ith the mitral voalve
  • Sx with reduced pre load and increased contractily



References