Key result
The presence of at least either the AGT CC genotype or ACE D allele was associated with increased 5-year all-cause mortality after acute myocardial infarction compared to having neither variant (HR 2.07).
Why the study?
Do RAAS genetic variants (specifically the combination of AGT CC genotype and ACE D allele) increase 5-year mortality in survivors of acute myocardial infarction?
Observational (n=3,149)
Yes
Do RAAS genetic variants (specifically the combination of AGT CC genotype and ACE D allele) increase 5-year mortality in survivors of acute myocardial infarction?
Hazard Ratio: 2.07 (95% CI 1.18–3.65)
p-value: p=0.012
The combination of the AGT CC genotype and ACE D allele is associated with increased 5-year mortality in survivors of acute myocardial infarction, highlighting the importance of gene-gene interactions in risk stratification.
May inform post-MI genetic risk models; leaves open whether RAAS genotyping improves outcomes in prospective trials.
This study sought to evaluate whether genetic variants in the renin-angiotensin-aldosterone system (RAAS) have an impact on long-term mortality after acute myocardial infarction (AMI) in the percutaneous coronary intervention (PCI) era. We investigated the impacts of individual and combinations of 4 major RAAS genetic variants, angiotensinogen (AGT) T1311C, angiotensin-converting enzyme (ACE) insertion/deletion (I/D), angiotensin 2 type 1 receptor A1166C, and aldosterone synthase T4660C on 5-year mortality in 3149 post-AMI patients using multivariate Cox regression analysis. The predictive accuracy of all possible RAAS genetic combinations was evaluated using Cox regression analysis, and the best combination that affected prognosis was determined based on the minimal Akaike Information Criterion. There were 220 deaths during a median follow-up of 4.9 years. Independent analyses of any single RAAS variant did not show significant impacts on 5-year mortality. However, analyses in combination revealed that absence of both AGT CC genotype and ACE D allele was associated with lower 5-year mortality (log-rank P = 0.005). Patients with at least either of the AGT CC or ACE D allele had increased mortality with adjusted hazard ratios of 2.07 (95% confidence interval 1.18-3.65, P = 0.012), compared with those with neither the AGT CC nor ACE D allele. Among the 4 RAAS genetic variants examined, a combination of AGT and ACE polymorphisms was associated with 5-year mortality after AMI.
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Hara et al. (2014) conducted an observational in Acute Myocardial Infarction (n=3,149). Presence of at least either the AGT CC genotype or ACE D allele vs. Absence of both AGT CC genotype and ACE D allele was evaluated on 5-year all-cause mortality (HR 2.07, 95% CI 1.18-3.65, p=0.012). The presence of at least either the AGT CC genotype or ACE D allele was associated with increased 5-year all-cause mortality after acute myocardial infarction compared to having neither variant (HR 2.07).
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