Table 4.
Summary of the findings of the selected studies.
| Study design and subject's characteristics | Mean age (years) | Methods and MMPs measured | MMP-2 level in atherosclerotic CAD | NOS score | |
|---|---|---|---|---|---|
| Mogharrabi et al. [33] |
Case–control, double-blind, randomized clinical trial. 70 patients with CAD (40%–50% stenosis) were randomly assigned into two groups: (i) nanocurcumin group (given nanomicelle 80 mg/day) (ii) control group (given placebo) Treatment was given for 3 months |
>18 years old | The activity and expression of MMP-2 and MMP-9 in the serum were measured using RT–PCR and zymography analysis | MMP-2 mean relative gelatinase activity was significantly decreased in CAD patients treated with curcumin compared with the placebo group (p < 0.001) | 7 |
| Sai et al. [34] | Case–control clinical trial. 56 patients with AMI were randomly divided into: (i) study group (28 patients; 15 men and 13 women): given 20 mg rosuvastatin and 2.5 mg benazepril daily for 3 months. (ii) control group (28 patients; 14 men and 14 women): given 20 mg rosuvastatin daily for 3 months. 30 healthy volunteers were assigned as normal controls (18 men and 12 women) |
Study group: 53 ± 12 years old Control group: 54 ± 0.8 years old Normal control: 51 ± 1.2 years old |
Serum levels of MMP-2, MMP-9, and leukotriene B4 pre- and posttreatment were measured using ELISA | Serum levels of MMP-2 were significantly higher in AMI patients compared with the healthy subjects (p < 0.01). Serum levels of MMP-2 were significantly decreased in AMI patients treated with both benazepril and rosuvastatin compared with rosuvastatin alone (p < 0.05) |
8 |
| Li et al. [35] | Case–control study 80 patients with acute coronary syndrome: (i) acute group (40 patients; 19 male and 21 female, 26 AMI patients and 14 UAP patients, course of disease ranged from 1 to 6 years) (ii) stable group (40 patients; 18 male and 22 female, 25 AMI patients and 15 UAP patients. course of disease ranged from 2 to 8 years) 40 healthy subjects (control group) |
Acute group (37–73 years; mean age: 53.27 ± 1.45 years) Stable group (39–71 years; mean age: 53.04 ± 1.38 years) Control group (37–68 years; mean age: 52.85 ± 1.46 years) |
Serum MMP-2 levels were measured using ELISA | MMP-2 levels were significantly higher: (i) in the acute and stable groups compared with the control group (p < 0.05) (ii) in the acute group compared with the stable group (p < 0.05) (iii) in the AMI patients compared with the UAP patients (p < 0.01) |
9 |
| Murashov et al. [36] | Cross-sectional study 68 men with coronary atherosclerosis who underwent coronary bypass surgery with endarterectomy |
46–79 years old | MMP-2 expression in the stable (n = 21) and unstable (n = 31) atherosclerotic plaque in the coronary arteries was determined using immunohistochemistry (IHC) | Expression of MMP-2 in the unstable atherosclerotic plaque was 7.8 times higher in comparison with the stable atherosclerotic plaque (p < 0.05). MMP-2 was mostly expressed in the cytoplasm of foamy macrophages in the atheromatous core and in the caps of unstable plaque with lipid erosions |
4 |
| Murashov et al. [37] | Cross-sectional study 33 men with occlusive coronary atherosclerosis who underwent coronary bypass surgery with endarterectomy |
62.5 ± 10.9 years | MMP-2 expression was measured using IHC in different types of unstable coronary artery plaques, namely necrotic-degenerative type (64%), lipid type (23%), and inflammatory-erosive type (13%) | No significant difference in MMP-2 expression among the three different types of unstable atherosclerotic plaque, suggesting that accumulation of MMP-2 was present in all types of unstable plaque | 5 |
| Melin et al. [38] | Cross-sectional study 268 Type 1 diabetes (TID) patients with CVD, depression, thyroid disease, hypertension, and hyperlipidemia |
18–59 years old | Plasma levels of MMP-2, MMP-14, TIMP-2, and TIMP-3 were analyzed by ELISA | MMP-2 and CVD were independently associated with high levels of MMP-14 in T1D patients | 5 |
| Malkani et al. [39] | Case–control study 200 Pakistani subjects (i) 100 patients with coronary atherosclerosis (ii) 100 healthy controls |
NS | Genomic DNA was extracted from blood samples and subjected to RFLP-PCR analysis for two SNPs of the MMP-2 gene (rs 243865 and rs 243866) | Both allelic and genotype frequencies of rs243865 were higher in atherosclerosis patients than the healthy controls (p < 0.01) Only allelic frequency of rs243866 was higher in atherosclerosis patients than the healthy controls (p < 0.01) Haplotype analysis indicated that CA, CG, and TA haplotypes of the MMP-2 gene were significantly connected with atherosclerosis (p < 0.01) |
7 |
| Owolabi et al. [40] | Cohort study 64 subjects with AMI and stable CAD were divided into two main groups: (i) stable CAD (n = 15) (ii) acute MI (n = 49), which was further divided into atherothrombotic MI (n = 22) and non atherothrombotic MI (n = 12) |
>18 years old | Plasma MMP-2 levels were measured using multiplex immunoassay at two main time points: (i) acute phase (at the start of cardiac catheterization and 6 hr post catheterization) (ii) quiescent phase (at 3 months follow-up after acute phase) |
No significant difference in MMP-2 levels between acute MI vs. stable CAD, and atherothrombotic vs. nonatherothrombotic MI at any time point | 9 |
AMI, acute myocardial infarction; CAD, coronary artery disease; CVD, cardiovascular disease; ELISA, enzyme-linked immunosorbent assay; MI, myocardial infarction; MMP, matrix metalloproteinase; NS, not stated; RT–PCR, reverse transcription–polymerase chain reaction; RFLP–PCR, restriction fragment length polymorphismpolymerase chain reaction; TIMP, tissue inhibitor of matrix metalloproteinase,; UAP = unstable angina pectoris.