Key result
Long-term beta blockers in hypertension linked to ~70% greater risk of type A aortic dissection.
Why the study?
Recommendations for beta blockers in preventing aortic dissection and improving postdissection survival in nonsyndromic patients with hypertension are based on limited evidence.
Does long-term beta blocker use prevent aortic dissection or improve postdissection survival in nonsyndromic patients with hypertension?
Case-Control (n=17,796)
Does long-term beta blocker use prevent aortic dissection or improve postdissection survival in nonsyndromic patients with hypertension?
Effect estimate: OR 1.7 (95% CI 1.3-2.3)
In nonsyndromic patients with hypertension, long-term beta blocker use was associated with an increased risk of aortic dissection and higher post-dissection mortality, challenging current clinical practice.
May warrant caution with long-term beta blockers in nonsyndromic hypertension; leaves open causality and need for randomized confirmation.
BACKGROUND: Recommendations for beta blockers in preventing aortic dissection (AD) and improving postdissection survival in nonsyndromic patients with hypertension are based on limited evidence. METHODS: This nationwide, population-based study combined a nested case-control and historical cohort design. Using Danish health care registries, all hospitalized adult patients with AD from 1996 to 2016 were identified and validated. Patients with bicuspid aortic valves or connective tissue disorders were excluded. In the case-control analysis, 1657 validated AD cases were matched 1:10 (±1) with 16 139 controls with hypertension based on age, sex, index date, and cumulative antihypertensive drug use. Long-term beta blocker use was defined as ≥2000 defined daily doses (DDD). In the cohort analysis, 2120 validated survivors of AD were followed for 5 years to assess postdissection mortality stratified by beta blocker use. RESULTS: Long-term beta blocker use was associated with increased odds of AD type A (adjusted odds ratio [aOR], 1.7 [95% CI, 1.3-2.3]) and AD type B (aOR, 3.7 [95% CI, 2.7-5.2]) compared with never-users. A dose-dependent risk increase was observed for AD type B (aOR, 1.4 [95% CI, 0.8-2.2] for DDD 100-199; aOR, 3.9 [95% CI, 1.6-9.8] for DDD ≥10 000). Beta blocker use was associated with higher 5-year all-cause mortality in survivors of AD type A (adjusted hazard ratio [aHR], 1.5 [95% CI, 0.99-2.23]) and AD type B (aHR, 1.5 [95 %CI, 1.0-2.3]) compared with never-users. CONCLUSIONS: Beta blocker use did not reduce AD risk or improve outcomes in survivors of AD compared with other antihypertensive agents. Although clinically relevant data as aortic diameters and blood pressure were not available, these findings challenge current clinical practice and highlight the need for randomized trials.
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Liisberg et al. (2025) conducted a case-control in Hypertension and risk of aortic dissection (n=17,796). Beta blockers vs. Never-users of beta blockers (other antihypertensive agents) was evaluated on First-time aortic dissection type A (OR 1.7, 95% CI 1.3-2.3). Long-term beta blocker use in nonsyndromic patients with hypertension was associated with an increased risk of aortic dissection type A (OR 1.7) and type B (OR 3.7) compared with never-users.
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