Key result
RASi at one year post-AMI shows no benefit over no RASi for two-year all-cause mortality.
Why the study?
RASi have shown survival benefits after acute MI, but the role of routine long-term use of RASi remains unclear.
Does long-term use of renin-angiotensin-system inhibitors (RASi) at 1-year follow-up reduce 2-year all-cause mortality in patients after acute myocardial infarction?
Cohort (n=10,822)
Yes
Does long-term use of renin-angiotensin-system inhibitors (RASi) at 1-year follow-up reduce 2-year all-cause mortality in patients after acute myocardial infarction?
Effect estimate: HR 1.04 (95% CI 0.82-1.31)
p-value: p=0.758
Routine long-term continuation of RASi at 1-year post-MI is not associated with improved 2-year survival, suggesting a potential role for tailored medication strategies rather than universal long-term use.
Continued RASi at 1 year post-MI was not associated with lower mortality; leaves open tailored discontinuation pending randomized trials.
Introduction Renin-angiotensin-system inhibitors (RASi) have shown survival benefits after acute myocardial infarction (MI), but the role of routine long-term use of RASi remains unclear. Thereby, we explored the therapeutic effects of RASi medication at 1-year follow-up from acute MI. Methods Using the nationwide Korea Acute Myocardial Infarction Registry-National Institutes of Health (KAMIR-NIH) registry, we included and analyzed 10,822 subjects. Patients were stratified into those taking RASi at 1-year follow-up ( n = 7,696) and those not taking RASi at 1-year follow-up ( n = 3,126). Patients were followed up for 2-years from the 1-year follow-up; 2-year all-cause mortality and cardiac mortality were analyzed as primary and secondary outcomes, respectively. Results The use of RASi at 1-year follow-up was not associated with decreased all-cause mortality (log-rank P = 0.195) or cardiac mortality (log-rank P = 0.337). In multivariate analyses, RASi medication at 1-year follow-up did not reduce all-cause mortality ( P = 0.758) or cardiac mortality ( P = 0.923), while RASi medication at discharge substantially reduced 1-year all-cause and cardiac mortality. Treatment with either an angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker at 1-year follow-up did not show survival benefits from 1-year follow-up, respectively. The use of RASi at 1-year follow-up did not show a prognostic interaction between previous history of chronic kidney disease, post-MI acute heart failure, concomitant use of beta-blockers at 1-year follow-up, or 1-year LVEF. Conclusion Acute MI patients taking RASi at 1-year follow-up were not associated with improved 2-year all-cause mortality or cardiac mortality from the 1-year follow-up. This study provides valuable information regarding tailored medication strategy after acute MI. Clinical trial registration [ www.ClinicalTrials.gov ], identifier [KCT0000863].
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Park et al. (2022) conducted a cohort in Acute myocardial infarction (n=10,822). Renin-angiotensin-system inhibitors (RASi) vs. No RASi at 1-year follow-up was evaluated on 2-year all-cause mortality (HR 1.04, 95% CI 0.82-1.31, p=0.758). Renin-angiotensin-system inhibitors at 1-year follow-up after acute myocardial infarction did not reduce 2-year all-cause mortality (HR 1.04) compared to no RASi.