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Table 3 Mean (± Standard deviation) interventricular septum, posterior wall thickness, left ventricular wall thickness, age at the diagnostis and body mass index values, and frequency of cases with affected relatives, according to the AT1R genotype in the 205 HCM-patients without sarcomeric mutations, the 40 patients with a sarcomeric mutation, and the 145 patients with hypertensive LVH

From: Functional polymorphisms in genes of the Angiotensin and Serotonin systems and risk of hypertrophic cardiomyopathy: AT1R as a potential modifier

 

IVS

(mm)

PWT

(mm)

LVWT

(mm)

Age (years)

BMI

Familial

HCM#

HCM-No mutation 1

      

CC (n = 27)

21 ± 4

13 ± 3

34 ± 5

49 ± 18

26 ± 5

10 (37%)

AC (n = 94)

21 ± 5

13 ± 4

33 ± 4

46 ± 18

27 ± 4

40 (43%)

AA (n = 84)

19 ± 5

13 ± 4

32 ± 4

48 ± 16

27 ± 5

25 (30%)

HCM-Mutation 2

      

CC (n = 5)

23 ± 4

16 ± 3

39 ± 4

38 ± 4

21 ± 4

4 (80%)

AC (n = 14)

22 ± 5

14 ± 5

35 ± 5

36 ± 5

21 ± 5

12 (86%)

AA (n = 21)

18 ± 5

14 ± 4

31 ± 5

45 ± 5

20 ± 5

14 (67%)

Hypertensive-LVH

      

CC (n = 13)

16 ± 4

10 ± 5

25 ± 5

60 ± 8

28 ± 2

ND

AC (n = 60)

16 ± 3

9 ± 4

25 ± 4

58 ± 7

27 ± 2

ND

AA (n = 72)

15 ± 2

10 ± 5

24 ± 4

59 ± 9

28 ± 3

ND

  1. # We did not determine (ND) the existence of a family history of LVH in the hypertensive-LVH group.
  2. 1P = 0.016, IVS CC + AC vs. AA.
  3. 2P = 0.017, IVS CC + AC vs. AA.