Key result
Smoking increased the activity of MMP9 in patients with acute myocardial infarction compared to non-smokers with the condition.
Why the study?
Does smoking increase the activity of MMP2 and MMP9 in patients with acute myocardial infarction?
Case-Control (n=400)
No
Does smoking increase the activity of MMP2 and MMP9 in patients with acute myocardial infarction?
Smoking is associated with increased activity of the matrix-degrading enzyme MMP9 in AMI patients, potentially contributing to plaque vulnerability.
Answers are grounded in this paper and cite their sources.
Smoking may heighten plaque vulnerability via MMP9 in AMI; hypothesis-generating and requires prospective confirmation.
INTRODUCTION: Many risk factors are involved in the course and pathogenesis of Acute Myocardial Infarction (AMI). Smoking can significantly increase the AMI mortality and morbidity. Matrix metalloproteinases (MMPs), a class of Zn containing enzymes, are involved in the erosion of the fibrous cap and rupture of the plaque which leads to AMI. AIM: To evaluate the activity of MMP2 and MMP9 in AMI patients, with or without the habit of smoking. MATERIALS AND METHODS: The study group consists of 300 AMI patients and 100 sex and age matched control subjects with and without the habit of smoking. MMP2 and MMP9 activities were measured in the blood samples of these patients and controls by sandwich enzyme immunoassay and the values were noted and compared. RESULTS: Both MMP2 and MMP9 were found to be significantly elevated in all the AMI patients when compared to the normal controls subjects irrespective of the habit of smoking. However MMP9 showed a significant elevation when compared to MMP2 in patients with the habit of smoking. CONCLUSION: The results of the present study shows increased concentration of both MMPs in AMI patients. However, concentration of MMP9 was found to be more in patients with the habit of smoking when compared to MMP2, indicating that smoking can increase the activity of MMP9 in these patients. Hence apart from producing the free radicals, the smoke can increase the activities of matrix degrading enzymes which in turn contribute to the vulnerability of plaque.
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Sreekanth K Sivaraman (2014) conducted a case-control in Acute Myocardial Infarction (n=400). Smoking vs. Non-smoking was evaluated on MMP2 and MMP9 activity (p=<0.01). Smoking increased the activity of MMP9 in patients with acute myocardial infarction compared to non-smokers with the condition.
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