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. Author manuscript; available in PMC: 2014 Apr 3.
Published in final edited form as: Circ Cardiovasc Genet. 2013 May 20;6(3):230–237. doi: 10.1161/CIRCGENETICS.113.000037

Table 3. Characteristics of the 4 Subjects With Discordant Echo and CMR Determination of LVH.

Subject 1 Subject 2 Subject 3 Subject 4
Age at baseline study, y 17 36 34 23
Sex Male Male Female Male
Causal gene (mutation) MYH7 (Arg663Cys) MYBPC3 (Arg502Trp) MYBPC3 (Glu258Lys) MYH7 (Arg719Gln)
BSA, m2 2.3 1.8 1.8 1.9
IVS, mm
 Echo 10.0 10.4 9.4 9.7
 CMR 8.0 9.0 9.0 11.5
PWT, mm
 Echo 9.5 9.0 8.9 10.2
 CMR 9.5 6.6 7.6 12.6
LVEF, % 73 70 61 60
MWT, mm
 Echo 10.4 (M-IS) 11.8 (M-IS) 11.3 (B-AS) 11.9 (M-IS)
 CMR 13.9 (M-I) 13.5 (M-IS) 13.1 (M-AS) 12.6 (M-PW)
Echo quality Fair Poor Poor Good
CMR quality Fair Good Excellent Good
Time interval between echo and 0 days 0 days 0 days 0 days
CMR
LGE None None None None
Global Ea, cm/s 12.2 11.8 13.2 11.1
ECG Normal T wave Inversions Left atrial enlargement Normal
Follow-up findings Development of overt LVH over 24 mo Unchanged LV wall thickness (by echo) over 63 mo Unchanged LV wall thickness (by echo and CMR) over 48 mo Pending (baseline study performed during final year of study period)

B-AS indicates basal anteroseptum; BSA, body surface area; CMR, cardiac MRI; Ea, global early myocardial tissue Doppler relaxation velocity; Echo, echocardiography; IVS, interventricular septum; LGE, late gadolinium enhancement; LVEF, left ventricular ejection fraction; LVH, left ventricular hypertrophy; M-AS, anterior septum at midventricle; M-I, inferior wall at midventricle; M-IS, inferior septum at midventricle; M-PW, midventricle posterior wall; MWT, maximal wall thickness; and PWT, posterior wall thickness.