What is the clinical evidence from this study?

Study design: Case-Control. Population: Hypertension and risk of aortic dissection (n=17796). Intervention: Beta blockers vs. Never-users of beta blockers (other antihypertensive agents). Primary outcome: First-time aortic dissection type A (OR 1.7, 95% CI 1.3-2.3).

What does this research mean for the field?

Long-term beta blocker use in nonsyndromic patients with hypertension is associated with an increased risk of aortic dissection type A and type B, and higher all-cause mortality in survivors, compared with never-users. Novelty: ClaimNovelty.CONTRADICTORY. Consensus alignment: ConsensusAlignment.CHALLENGES_CONSENSUS.

June 11, 2025Open Access

Beta Blockers as Primary and Secondary Prevention for Aortic Dissections in Nonsyndromic Patients With Hypertension

MLMads LiisbergOdense University Hospital JLJes S. LindholtVascular Medicine KKKatrine Lawaetz KristensenUniversity of Southern Denmark

Key Result

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.

Study Design

Type

Case-Control (n=17,796)

Structured PICO

Does long-term beta blocker use prevent aortic dissection or improve postdissection survival in nonsyndromic patients with hypertension?

Population

1,657 validated adult cases of aortic dissection matched with 16,139 controls with hypertension (case-control analysis), and a cohort of 2,120 validated survivors of aortic dissection (cohort analysis). Excluded: patients with bicuspid aortic valves or connective tissue disorders.

Intervention

Long-term beta blocker use (defined as ≥2000 defined daily doses [DDD])

Comparator

Never-users of beta blockers (using other antihypertensive agents)

Outcome

Occurrence of aortic dissection (type A and B) for primary prevention, and 5-year all-cause mortality for secondary preventionhard clinical

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.

Main Result

Effect estimate: OR 1.7 (95% CI 1.3-2.3)

Limitations

Observational study design can only identify risk associations, not causation.
Potential residual confounding and confounding by indication.
Inability to meaningfully analyze nonselective beta blockers due to low consumption.
Lack of clinical variables such as aortic diameters, accurate blood pressure readings, and smoking status in the registries.
Limited ethnic and geographic diversity, primarily comprising individuals of European descent.

Abstract

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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