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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 31, No 3, May/June 2020

AFRICA

149

group. There was no significant difference in age, gender, systolic

arterial pressure, diastolic arterial pressure, body mass index,

hypertension, hyperlipidaemia, cigarette and alcohol use and

family history between the groups (

p

> 0.05). However, median

glycated haemoglobin (HbA

1c

) and Gal-3 levels were significantly

higher in patients with isolated CAE compared to the controls (

p

< 0.05). Demographic, clinical and laboratory characteristics of

the study population are shown in Table 1.

Table 2 shows frequency of distribution of ectatic coronary

arteries and the Markis classification in isolated CAE patients.

Ectasia occurred most frequently in the left anterior descending

artery (32%), followed by the circumflex artery (30%), right

coronary artery (26%) and left main coronary artery (15%).

Type 4 was the most common type of ectasia according to the

Markis classification in 36% of patients. Median Gal-3 levels

were significantly higher in isolated CAE patients than in the

controls [23.2 (23.9 ± 7.1) vs 16.8 ng/ml (17.8 ± 7.3);

p

< 0.001)

(Table 1, Fig. 1).

In patients with isolated CAE, there was no significant

association between Gal-3 levels and Markis classification or the

number of involved vessels (

p

= 0.41 and 0.093, respectively; Table

3). In univariate analysis, natural log (ln) Gal-3 was found to

have a significant impact for differentiating controls and patients

(

p

< 0.05). Multivariate logistic regression analysis demonstrated

that concentrations of ln Gal-3 were an independent predictor of

isolated CAE (Table 4). In ROC curve analysis, area under the

curve was 0.692 (0.581–0.803) for 16 ng/ml serum Gal-3 cut-off

value (91.8% sensitivity and 46.5% specificity) (

p

< 0.05) (Fig. 2).

Discussion

In this study, we investigated the relationship between serum

Gal-3 levels and isolated CAE. Our results showed significantly

increased Gal-3 levels as a novel cardiac biomarker among

isolated CAE patients, compared to controls. However, there was

no significant association between serum Gal-3 levels and the

extent of isolated CAE.

Despite uncertainties regarding the pathophysiological

mechanisms of CAE, the frequent occurrence of concurrent

CAD and the presence of atheromatous ulcerations in ectatic

segments suggest an important role for atherosclerosis in the

development of CAE.

19

Degeneration in the media layer of

the coronary artery, a common denominator of all conditions

resulting in coronary ectasia, has been reported to be associated

with advanced atherosclerosis.

7,20

Table 1. Baseline demographic, clinical and laboratory

characteristics of the study population

Control group

(

n

= 43)

Patient group

(

n

= 49)

p-

value

Mean ± SD,

n

(%) Mean ± SD,

n

(%)

Age, years

57.2 ± 8.3

60.6 ± 8.2

0.057

t

Gender

Female

24 (55.8)

18 (36.7)

0.067

*

Male

19 (44.2)

31 (63.3)

0.067

*

BMI (kg/m

2

)

31.9 ± 6.2

29.9 ± 0.0

0.084

t

Smoking

12 (27.9)

19 (38.8)

0.271

*

Alcohol

2 (4.7)

1 (2.0)

0.597

*

Hypertension

21 (48.8)

31 (63.3)

0.164

*

Diabetes

7 (16.3)

11 (22.4)

0.457

*

Hyperlipidaemia

13 (46.7)

22 (53.3)

0.148*

Family history

3 (7.0)

9 (18.4)

0.106*

SBP (mmHg)

117.9 ± 14.3

117.5 ± 13.5

0.933

m

DBP (mmHg)

68.9 ± 7.9

68.3 ± 7 .8

0.745

m

Fasting glucose (mg/dl)

110.1 ± 38.3

110.5 ± 34.5

(mmol/l)

(6.11 ± 2.13)

(6.13 ± 1.91)

0.488

m

Creatinine (mg/dl)

0.7 ± 0.2

1.1 ± 2.5

(μmol/l)

(61.88 ± 17.68)

(97.24 ± 221)

0.415

m

Total cholesterol (mg/dl)

200.4 ± 42.5

192.5 ± 60.7

0.790

m

(mmol/l)

(5.19 ± 1.10)

(4.99 ± 1.57)

LDL-C (mg/dl)

120.3 ± 38.0

129.1 ± 41.1

0.360

m

(mmol/l)

(3.12 ± 0.98)

(3.34 ± 1.06)

Triglycerides (mg/dl)

160.8 ± 80.4

143.9 ± 71.2

0.305

m

(mmol/l)

(1.82 ± 0.91)

(1.63 ± 0.80)

hs-CRP (mg/dl)

1.8 ± 1.5

3.2 ± 6.5

0.461

m

Fibrinogen (mg/dl)

305.8 ± 36.5

307.2 ± 76.8

0.554

m

WBC (× 10

3

)

8.1 ± 2.2

7.6 ± 1.8

0.158

m

HDL-C (mg/dl)

47.1 ± 11.8

43.5 ± 9

0.109

t

(mmol/l)

(1.22 ± 0.31)

(1.13 ± 0.23)

HbA

1c

(%)

6.0 ± 1.1

6.1 ± 0.9

0.044

m

Galectin-3 (ng/ml)

17.8 ±7.3

23.9 ±7.1

0.000

t

t

:

t-

test;

m

: Mann–Whitney

U

-test; *chi-squared test (Fisher’s exact test).

SD, standard deviation; BMI, body mass index; SBP, systolic blood pressure;

DBP, diastolic blood pressure; LDL-C, low-density lipoprotein cholesterol;

hs-CRP, high-sensitivity C-reactive protein; WBC, white blood cell count;

HDL-C, high-density lipoprotein cholesterol; HbA

1c

, glycated haemoglobin.

CAE group

Control group

Galectin-3 levels (ng/ml)

50

40

30

20

10

0

Fig. 1.

Comparison of galectin-3 levels of patients with CAE

and the control group (

p

< 0.001). CAE, coronary

artery ectasia.

Table 2. Distribution frequency of CAE and Markis classification

Number

Percent

CAE

LMCA

15

30.6

LAD

32

65.3

Cx

30

61.2

RCA

26

53.1

Markis classification

Type I

16

32.7

Type II

9

18.4

Type III

6

12.2

Type IV

18

36.7

CAE, coronary artery ectasia; Cx, circumflex coronary artery; LAD, left ante-

rior descending coronary artery; LMCA, left main coronary artery; RCA, right

coronary artery.