Objective: Smoking causes cardiovascular risk, which may alter the stability between the production and degradation of the extracellular matrix. Matrix metalloproteinase-9 (MMP-9) is a zinc-containing endopeptidase that degrades the extracellular matrix and is involved in tissue remodelling and several physiological processes. As a result, smoking-induced elevated serum MMP-9 levels, particularly at a younger age, raise the risk of coronary heart disease (CHD). Thus, this study aimed to determine the possible relationship between smoking-induced circulating MMP-9 and the risk of cardiovascular disease in young smokers. Methods: In this cross-sectional study, the patients were divided into three groups. Each group contains 120 study participants. Group one consisted of 120 healthy individuals with no physical and mental illness, group two consisted of 120 active smokers with a heart disease, and group three consisted of 120 active smokers with a heart disease and diabetes, who attended Sri Ramaswamy Memorial Hospital for cardiology checkup at the age of 20-55 years. The serum MMP-9, high-sensitivity C-reactive protein (hs-CRP), and apolipoprotein-E (APO-E) levels were analyzed using the ELISA method, and the lipid levels were measured enzymatically using AU480 automatic analyzer (Beckman Coulter). Results: Compared with non-smokers, the study shows that the mean serum MMP-9, hs-CRP, and APO-E levels were significantly higher in smokers (p<0.001). A strong relationship was also found between MMP-9 and hs-CRP, APO-E, smoking load, and smoking intensity. Conclusions: A significant association was found between cigarette smoking with MMP-9, and relative exposure to circulating inflammation markers plays a potential role in the pathogenesis of CHD.

IntroductionCigarette smoking promotes angiotensin-converting enzyme (ACE) production and causes a substantial change in inflammation and oxidative stress, resulting in an increase in antioxidant activity and lipid peroxidation. ObjectiveThe study's goal is to determine the role of cigarette smoking on serum ACE and its relation with inflammatory markers and lipid peroxidation. MethodsThe cross-sectional study consists of three groups. The study participants are all men between the age group of 20 to 55 years. Group 1 includes 120 healthy controls as nonsmokers, Group 2 consists of 120 active smokers with coronary heart disease (CHD) and Group 3 includes 120 active smokers with diabetic CHD patients attending the SRM Medical College Hospital in Tamil Nadu for cardiology and medical Outpatient. Measurements of serum ACE, oxidized low-density lipoprotein (oxLDL), high-sensitivity Creactive protein (hsCRP), and matrix metalloprotease-9 (MMP-9) were performed using the ELISA method (enzyme-linked immunosorbent assay). Using a spectrophotometric approach, the total antioxidant capacity and lipid peroxidation, particularly Malondialdehyde (MDA), were assessed. ResultsThe mean serum ACE (92.35±10.28), oxLDL (48.59±8.56), hs-CRP (5.87±1.62), and MDA (1.146±0.198) levels were significantly (p-value <0.0001) higher in smokers with CHD and diabetes (group 3) when compared to group 1 and group 2. On the other hand, the total antioxidant capacity (0.413±0.097) of smokers of group 3 was found to be (p<0.0001) significantly lower than those of group 1 and group 2. The study also demonstrated a significant correlation between ACE with MDA, ox-LDL, total antioxidant capacity, hs-CRP, MMP-9, smoking load, and smoking intensity in smokers. ConclusionThe study concludes a substantial correlation exists in smokers owing to ACE modification, which results in inflammation and lipid peroxidation activation. This is strongly associated with an increased risk of major cardiovascular events.