Table 1.
Controls (n = 63) | Subclinical HCM (n = 79) | Overt HCM (n = 50) | P-value for global test | P-valuea, control vs. subclinical | P-valuea, control vs. overt | P-valuea, subclinical vs. overt | |
---|---|---|---|---|---|---|---|
Age (years)b | 32.9 ± 13.1 | 24.9 ± 13.1 | 44.1 ± 13.4 | 0.0004 | <0.0001 | <0.0001 | |
Female, n (%)c | 31 (49.2%) | 47 (59.5%) | 18 (36.0%) | 0.239 | 0.184 | 0.012 | |
BSA (m2)b | 1.89 ± 0.29 | 1.70 ± 0.33 | 1.96 ± 0.24 | 0.0004 | 0.163 | <0.0001 | |
Septal thickness (mm) | 9.3 ± 0.2 | 9.4 ± 0.3 | 16.2 ± 0.7 | <0.0001 | 0.707 | <0.0001 | <0.0001 |
Posterior wall thickness (mm) | 8.9±0.2 | 8.7 ± 0.2 | 10.6 ± 0.3 | <0.0001 | 0.437 | <0.0001 | <0.0001 |
LV end-diastolic diameter (mm) | 45.8 ± 0.7 | 45.5 ± 0.5 | 40.2 ± 0.8 | <0.0001 | 0.709 | <0.0001 | <0.0001 |
LVEDVid(mL/m2) | 59.2 ± 1.6 | 54.7 ± 1.6 | 43.8 ± 2.1 | <0.0001 | 0.023 | <0.0001 | <0.0001 |
LVESVid (mL/m2) | 38.6 ± 1.6 | 33.4 ± 1.5 | 25.0 ± 2.3 | <0.0001 | 0.007 | <0.0001 | 0.005 |
LVEF (%) | 65.1 ± 0.7 | 67.7 ± 0.8 | 69.3 ± 1.3 | 0.003 | 0.011 | 0.003 | 0.311 |
LA diameter (cm) | 3.4 ± 0.1 | 3.4 ± 0.1 | 3.8 ± 0.1 | 0.013 | 0.969 | 0.002 | 0.001 |
LVOT diameter (mm) | 21.8 ± 0.3 | 21.3 ± 0.3 | 21.8 ± 0.3 | 0.20 | |||
Causal gene, n (%)e | |||||||
MYH7 | Not applicable | 35 (44.3%) | 18 (36.0%) | ||||
MYBPC3 | 35 (44.3%) | 29 (58.0%) | |||||
TNNT2 | 5 (6.3%) | 3 (6.0%) | |||||
TNNI3 | 4 (5.1%) | 3 (6.0%) |
BSA, body surface area; LA, left atrium; LV, left ventricle; LVEDVi, LV end-diastolic volume indexed for BSA; LVEF, left ventricular ejection fraction; LVESVi, LV end-systolic volume indexed for BSA; LVOT, left ventricular outflow tract.
P-values reflect adjustment for age, sex, BSA, and family relations unless otherwise stated. A P-value <0.017 was considered statistically significant for pairwise comparisons between status groups.
Values expressed as unadjusted mean ± simple standard deviation, and groups compared using two-tailed Student’s t-test.
Group comparisons using Fishers Exact test.
BSA was not included in multivariable models given that BSA was already incorporated in the dependent variable.
Cumulative percentage exceeds 100% in overt HCM cohort because 1 patient had a mutation in MYH7 and MYBPC3 genes, 1 patient had a mutation in MYBPC3 and TNNT2 genes, and 1 patient had a mutation in MYBPC3 and TNNI3 genes.