Related Experiment Video
Updated: Jul 29, 2026

Intracoronary Acetylcholine Provocation Testing for Assessment of Coronary Vasomotor Disorders
Published on: August 18, 2016
Stromelysin promoter 5A/6A polymorphism is associated with acute myocardial infarction
M Terashima1, H Akita, K Kanazawa
1First Department of Internal Medicine, Kobe University School of Medicine, Kobe, and Himeji Cardiovascular Center, Hyogo, Japan.
Background:
Rupture of the fibrous cap of an atherosclerotic plaque is a key event that predisposes to acute myocardial infarction (AMI). Matrix metalloproteinases (MMPs) may contribute to weakening of the cap, which favors rupture. Stromelysin, a member of MMP family, is identified extensively in human coronary atherosclerotic lesions. It can degrade most of the constituents of extracellular matrix as well as activating other MMPs, which suggests that it may play an important role in plaque rupture. Recently, a common variant (5A/6A) in the promoter of the stromelysin gene has been identified. The 5A/6A polymorphism could regulate the transcription of the stromelysin gene in an allele-specific manner.
Methods And Results:
To investigate the relation between the 5A/6A polymorphism in the promoter of the stromelysin gene and AMI, we conducted a case-control study of 330 AMI patients and 330 control subjects. The prevalence of the 5A/6A+5A/5A genotype was significantly more frequent in the patients with AMI than in control subjects (48.8% vs 32.7%, P<0.0001). In logistic regression models, the odds ratio of the 5A/6A+5A/5A was 2.25 (95% CI, 1.51 to 3.35). The association of 5A/6A polymorphism with AMI was statistically significant and independent of other risk factors.
Conclusions:
The 5A/6A polymorphism in the promoter of the stromelysin gene is a novel pathogenetic risk factor for AMI.
Insights
A common genetic variant, the 5A/6A polymorphism in the stromelysin gene promoter, is a significant risk factor for acute myocardial infarction (AMI). This finding highlights a novel pathway contributing to heart attacks.
Area of Science:
- Cardiovascular Genetics
- Molecular Biology
- Pathogenesis of Atherosclerosis
Background:
- Plaque rupture is a critical event leading to acute myocardial infarction (AMI).
- Matrix metalloproteinases (MMPs), including stromelysin, are implicated in weakening atherosclerotic plaque caps.
- A common 5A/6A polymorphism in the stromelysin gene promoter may influence gene transcription.
Purpose of the Study:
- To investigate the association between the stromelysin gene 5A/6A polymorphism and the risk of AMI.
- To determine if this genetic variant is an independent risk factor for AMI.
Main Methods:
- A case-control study was conducted with 330 AMI patients and 330 control subjects.
- Genotyping for the 5A/6A polymorphism in the stromelysin gene promoter was performed.
- Statistical analysis, including logistic regression, was used to assess the association.
Main Results:
- The 5A/6A+5A/5A genotype was significantly more prevalent in AMI patients (48.8%) compared to controls (32.7%).
- The odds ratio for AMI associated with the 5A/6A+5A/5A genotype was 2.25.
- The association remained statistically significant and independent of other cardiovascular risk factors.
Conclusions:
- The 5A/6A polymorphism in the stromelysin gene promoter represents a novel pathogenetic risk factor for AMI.
- This genetic variant may play a role in the development and progression of acute myocardial infarction.
Related Concept Videos
Drugs Affecting Neurotransmitter Release or Uptake
Heart Failure Drugs: Inotropic Agents
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
Heart Failure Drugs: β-Blockers
Acute Coronary Syndrome I: Introduction
Cardiopulmonary Resuscitation IV: Pharmacological Management

