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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 30, No 5, September/October 2019

AFRICA

287

Comparison between the groups in terms of the culprit vessel

affected andmultivessel frequency showed no significant differences.

The incidence of MACE and major and minor bleeding

during the hospital stay and at follow up are shown in Table

3. Only one patient developed major bleeding due to upper

gastrointestinal bleeding. Five patients developed minor bleeding

in group A (three patients developed access-site bleeding and two

developed haematuria). In group B, one patient developed major

bleeding in the lower gastrointestinal system and four developed

haematuria.

Discussion

Diabetic patients usually have microangiopathy and

microvascular dysfunction. After restoration of normal blood

flow in the coronary arteries, there is still insufficient myocardial

tissue reperfusion (i.e. no reflow and slow flow) in up to 30%

of patients.

19,20

Higher incidence of re-infarction, heart failure,

stroke and death was previously documented in diabetic than in

non-diabetic patients.

21

The main cause of slow flow and no reflow is thrombosis and

microvascular embolisation. These microvascular complications

are higher in AMI and primary PCI. Visible thrombus in

coronary angiography can be removed by a suction catheter, but

it was found that 61% of the thrombus was invisible in AMI.

22

Imperfect inhibition of platelet aggregation during PCI may

increase the MACE. The use of adjuvant medical drugs such as

GPIs considerably decrease the incidence of distal embolisation

and thrombotic outcomes in STEMI patients.

23,24

This study demonstrated that IC tirofiban administered for

thrombotic complications or bail-out situations, in addition to

loading oral antiplatelets in diabetic patients, was associated

with greater reduction of peak hs-TnT, CK-MB levels and

ST-segment resolution compared with IV tirofiban. Both

regimens showed similar results for MACE and major and minor

bleeding events during hospitalisation and after one month of

follow up. The risk of bleeding did not appear to increase with

Table 1. Baseline characteristics of both groups

Parameters

Group A (IV)

(

n

=

50)

Group B (IC)

(

n

=

45)

t/

χ

2

p-

value

Age (mean

±

SD)

58.56

±

10.18 55.90

±

11.66 0.72 0.41

Gender,

n

(%)

Male

27 (54)

23 (51.1) 0.69 0.49

Female

23 (46)

22 (48.9)

Body mass index

(kg/m

2

)

(mean + SD)

26.1

±

6.5

25.4

±

8.2 0.1

0.78

Smoking,

n

(%)

34 (68)

31 (68.8) 0.69 0.48

Hypertension,

n

(%)

20 (40)

19 (42)

0.08 0.78

Family history of coronary

artery disease,

n

(%)

9 (18)

7 (15.5) 0.61 0.54

Killip class > 1,

n

(%)

9 (18)

11 (24)

1.025 0.33

Aspirin,

n

(%)

49 (98)

43 (95.5) 0.05 0.87

Clopidogrel,

n

(%)

50 (100)

44 (97.7) 0.84 0.64

Beta-blockers,

n

(%)

41 (82)

39 (86.6) 0.06 0.85

ACEI or ARBs,

n

(%)

39 (78)

36 (80)

0.12 0.79

Statin,

n

(%)

44 (88)

39 (86.6) 0.15 0.73

Warfarin,

n

(%)

3 (6)

1 (2.2)

0.8

0.068

Onset-to-balloon time (min)

(mean

±

SD)

167

±

12.4

151

±

18.3 5.8

0.089

Door-to-balloon time (min)

(mean

±

SD)

46.8

±

8.9

44

±

7.6 1.72 0.38

Fasting glucose (mg/dl)

(mean

±

SD)

168

±

29.8

192

±

46.6 3.64 0.074

Glycated haemoglobin

(HbA

1c

) (mean

±

SD)

7.8

±

2.2

9

±

1.3 3.1

0.087

Creatinine (mg/dl)

(mean

±

SD)

1.17

±

0.41 1.08

±

0.56 2.56 0.251

Low-density lipoprotein choles-

terol (mg/dl) (mean

±

SD)

132.6

±

46 147.09

±

51 2.79 0.091

ACEI: angiotensin converting enzyme inhibitor; ARB: angiotensin II receptor

blocker.

Group A

Group B

80

60

40

20

0

Fig. 1.

Frequency of 50% ST-segment resolution in the

groups.

Table 2. Comparison between the groups regarding cardiac

biomarkers and left ventricular ejection fraction

Parameters

Group A (IV)

(

n

=

50)

Group B (IC)

(

n

=

45)

t

p-

value

Peak CK-MB (U/l)

192.4

±

86 155.68

±

121 6.43 0.021*

Time to peak CK-MB (s)

12.9

±

5.8

8.96

±

3.2 11.4 0.001*

Peak hs-TnT (ng/dl)

#

5342

±

286 4291

±

334 5.9 0.035*

Time to peak hs-TnT (s)

13.5

±

3.1

9.24

±

2.8 10.7 0.001*

50% ST-segment resolution (%)

56

77

7.6 0.016*

LVEF at 48 hours (%)

38.6

±

5.3

41.5

±

3.2 0.84 0.632

LVEF at 30 days (%)

42.6

±

4.2

48.2

±

6.1 6.23 0.023*

Maximum C-reactive protein

level (ng/dl)

9.2

±

2.3

5.7

±

1.4 6.1 0.026*

#

Normal high-sensitivity troponin level up to 14 ng/dl.

CK-MB: creatine kinase-muscle/brain; hs-TnT: high-sensitivity troponin T;

LVEF: left ventricular ejection fraction.

0

I

II

III

100

75

50

25

0

Group A

Group B

Fig. 2.

Comparison of TIMI flow post intervention in the

groups.