Key result
Stromelysin-1 5A allele linked to ~115% greater young MI risk, with synergistic risk among smokers.
Why the study?
The association between stromelysin-1 (MMP-3) promoter 5A/6A polymorphism and smoking in the pathogenesis of young acute myocardial infarction was unclear.
Does the stromelysin-1 promoter 5A/6A polymorphism and smoking synergistically increase the risk of premature acute myocardial infarction in young adults?
Population
150 young acute MI patients under 45 years and 150 age- and sex-matched controls in Taiwan
Comparison
5A allele carriers with smoking vs 6A/6A genotype and non-smoking
Design
Case-control study
Authors
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May support intensified smoking cessation in 5A carriers to reduce premature MI risk; leaves open validation in prospective cohorts before any clinical use.
Case-Control (n=300)
Does the stromelysin-1 promoter 5A/6A polymorphism and smoking synergistically increase the risk of premature acute myocardial infarction in young adults?
Odds Ratio: 2.15 (95% CI 1.3–6.8)
Absolute Event Rate: 35% vs 20%
p-value: p=<0.001
The 5A allele of the stromelysin-1 promoter polymorphism and smoking have a synergistic effect, significantly increasing the risk of premature acute myocardial infarction.
Liu et al. (2003) conducted a case-control in Young acute myocardial infarction (n=300). 5A allele of the stromelysin-1 (MMP-3) promoter polymorphism vs. Control subjects / 6A allele was evaluated on Acute myocardial infarction under age 45 (OR 2.15, 95% CI 1.30 to 6.80, p=<0.001). The 5A allele of the stromelysin-1 promoter was associated with an increased risk of young acute MI (OR 2.15; 95% CI 1.30-6.80), with a synergistic 10-fold higher risk among smokers.
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