1. Dr. Syed Waleem Pasha Assistant Professor Yenepoya Medical College
COMPARISON OF SERUM PARAOXONASE LEVELS IN PATIENTS WITH ACUTE CORONARY SYNDROME AND NORMAL SUBJECTS: CASE CONTROL STUDY
Dr. Syed Waleem Pasha
Assistant Professor
Yenepoya Medical College

2. Background
Materials and methods
Results
Conclusion

3. Background
Atherosclerosis
Role of HDL
Risk factors

6. Risk factors conventional newer hs-CRP Markers of inflammation
Smoking
Hypertension
Elevated LDL
Low HDL
Insulin resistance and diabetes
Obesity
Mental stress and depression
hs-CRP
Markers of inflammation
Homocysteine
Fibrinogen and D-dimer
Lipoprotein (a)
Paraoxonase 1

7. Paraoxonase 1 (PON 1) Synthesized in liver Transported along HDL
Antioxidant function – prevents LDL oxidation
Activity exclusively associated with HDL

8. Materials and Methods 60 patients with Acute Coronary Syndrome (ACS)
30 matched controls
Serum paraoxonase (PON) levels, blood sugar, lipid profile
History of smoking and alcohol intake
History of diabetes and hypertension

9. Paraoxonase assay: Lipid profile: UV spectrophotometer
Enzymatic activity
Reference range: 53 – 186 kU/L
Lipid profile:
Fasting
Total cholesterol, High density lipoprotein and trigycerides – enzymatic method
Low density lipoprotein – friedwald’s formula

10. Inclusion criteria: Exclusion criteria: Age > 18 yrs
Cases: patients diagnosed as acute coronary syndrome
Controls: patients with ACS (history and investigations)
Exclusion criteria:
Renal failure
Hepatic parenchymal disease
Prior IHD, stroke, peripheral vascular disease in last three months
Anti-lipid treatment for more than three months

11. Analysis:
SPSS (statistical package for the social sciences) version 18
Department of statistics, Manipal university

12. Results

13. Age distribution

14. Age distribution AGE (YRS) CASES CONTROLS N PON 1 31-40 6 54.67 7
93.86
41-50 9
49.67 5
71.6
51-60 23
59.26 10
78.3
61-70 12
54.75 8
71.25
>70 50
TOTAL 60 30
P Value
0.307
0.098

15. Gender distribution GENDER CASES CONTROLS N PON 1 MALE 50 54.1 24
74.88
FEMALE 10 59 6
95.17
TOTAL 60 30
P Value
0.203
0.129

16. Smoking SMOKER CASES CONTROLS N PON 1 YES 36 53.06 14 82.21 NO 24
57.71 16
76.06
TOTAL 60 30
P value
0.266
0.865

17. Alcohol ALCOHOLIC CASES CONTROLS 23 N PON 1 YES 16 50.06 7 83.71 NO 44
56.68
77.48
TOTAL 60 30
P value
0.99
0.252

18. Diabetes DIABETIC CASES CONTROLS N PON 1 YES 36 52.89 9 78.78 NO 24
57.96 21 79
TOTAL 60 30
P value
0.81
0.435

19. Hypertension HYPERTENSIVE CASES CONTROLS N PON 1 YES 31 54.58 14 77.21NO 29
55.28 16
80.44
TOTAL 60 30
P value
0.244
0.578

20. Total cholesterol TC (mg/dl) CASES CONTROLS N PON 1 <100 2 65 87.5 11
55.27 4
66.5 19
57.16 10
84.8 21
58.1
85.8
>250 7
35.86
55.25
TOTAL 60 30
P value
0.642
0.055

21. Triglycerides TG (mg/dl) CASES CONTROLS N PON 1 <80 11 60.73 7 90
81-160 30
57.1 12
83.8 16
48.12 10
66.55
>240 3 48 1 59
TOTAL 60
P value
0.247
0.702

22. HDL HDL (mg/dl) CASES CONTROLS N PON 1 <30 23 41.87 9 60.89 31-4525
61.56 18
84.11
46-60
64.56 3
102
>60
71.33
TOTAL 60 30
P value
0.166
0.086

23. LDL LDL (mg/dl) CASES CONTROLS N PON 1 <100 11 56.82 5 78.4 101-12520
58.15 8
74.38 12
61.5 7
92.14 9
50.44
83.4
>175
39.38
63.8
TOTAL 60 30
P value
0.238
0.074

24. Master CASES (N=60) CONTROLS (N=30) P value TC 193.4 197.23 0.663 TG
140.13
135.13
0.865
LDL
124.06
129.69
0.791
HDL
35.77
34.43
0.213
RBS
150.02
142.27
0.541
PON 1
54.92
78.93
0.034

25. Comparative study SINGH et al PRESENT STUDY CONTROLS (191) CASES (120)
PON 1
64.92
57.19
<0.05
54.92
78.93
0.034 TC
155.38
160.81
197.23
193.4
0.663 TG
150.4
131.45
135.13
140.13
0.791
LDL
84.77
97.59
<0.01
129.69
124.06
HDL
41.82
36.92
<0.001
34.43
35.77
0.213

26. Conclusion
Cases had significantly lower serom PON 1 levels when compared to controls
Low PON 1 levels can be an independent risk factor for IHD

27. Future Target for prophylaxis Marker of morbidity/ mortality
Risk stratification
Other organ dysfunction (atherosclerosis)

28. Limitations: Small sample size Obesity not considered
Stable angina not considered
Wide reference range

29. References
Mackness MI, Bouiller A, Hennuyer M, Mackness B, Hall M, Tailleux A, et-al. Paraoxonase activity is reduced by a pro-atherosclerotic diet in rabbits. Biochem Biophys Res Commun. 2000; 269:
Mackness MI, Arrol S, Durrington PN. Paraoxonase prevents accumulation of lipoproteins in LDL. FEBS Lett. 1991; 286:
Watson AD, Berliner JA, Hama SY, La Du BN, Fault KF, Fogelman AM. Protective effect of HCL associated paraoxonase: inhibition of the biological activity of minimally oxidised LDL. J Clin Invest. 1995; 96:

30. Thank you