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Table 1 Baseline characteristics of studied groups

From: Temporal changes in regulatory T cell subsets defined by the transcription factor Helios in stroke and their potential role in stroke-associated infection: a prospective case–control study

 

Stroke patients D1 N = 52

Disease controls N = 34

p value

Age, years

69 (± 12)

68 (± 13)

0.66

BMI (kg/m2)

25.4 (23.6–28.4)

27.0 (25.1–31.1)

0.37

Females, n (%)

25 (48)

13 (38)

0.39

Hypertension, n (%)

42 (81)

30 (88)

0.56

Diabetes, n (%)

10 (19)

6 (18)

 > 0.99

Ischemic heart disease, n (%)

19 (37)

14 (41)

0.82

Atrial fibrillation, n (%)

20 (39)

3 (9)

< 0.01

Hyperlipidemia (%)

16 (31)

12 (35)

0.81

Smoking, n (%)

18 (35)

7 (21)

0.23

Treatment, n (%)

 Thrombolysis

16 (31)

 

 Antiplatelet drugs

45 (87)

34 (100)

0.72

 Anticoagulant

7 (14)

0

0.04

 ACEI

20 (39)

17 (50)

0.37

 Diuretics

23 (44)

12 (35)

0.51

 CCB

22 (42)

17 (50)

0.51

 β-blockers

9 (17)

8 (24)

0.58

 ARB

7 (14)

1 (3)

0.14

 Statins

14 (27)

15 (44)

0.11

 Hypoglycemics

8 (15)

4 (13)

0.78

 Insulin

3 (6)

3 (9)

0.68

Stroke etiology (TOAST classification), n (%)

 LVD

13 (25)

 SVD

12 (23)

 CE

22 (42)

 OE

5 (10)

 UE

0

Stroke location, n (%)

 TACI

6 (12)

 PAC

22 (42)

 POCI

13 (27)

 LACI

10 (8)

Stroke lesion volume, mL

 Day 1

2.1 (0.3–11.2)

 Day 90

1.0 (0.4–4.7)

  1. ACEI angiotensin convertase enzyme inhibitors, CCB calcium channel blockers, ARB angiotensin receptor blockers, LVD large vessel disease, SVD small vessel disease, CE cardioembolic stroke, OE stroke of other etiology, UE stroke of unknown etiology, TACI total anterior circulation infarcts, PACI partial anterior circulation infarcts, POCI posterior circulation infarcts, LACI lacunar infarcts