The impact of pre-existing blood pressure control in patients with acute aortic dissections

Amy B Reed1, Rumi Faizer1, R James Valentine1

  • 1Division of Vascular Surgery, Department of Surgery, 311816University of Minnesota Medical Center, Minneapolis, MN, USA.

Vascular
|September 17, 2021
PubMed

Insights

Pre-existing blood pressure control in patients with acute aortic dissection (AD) did not affect dissection extent or early outcomes. However, hypertension often worsens after AD, indicating a lasting impact on blood pressure regulation.

Area of Science:

  • Cardiovascular Medicine
  • Vascular Surgery
  • Hypertension Research

Background:

  • Arterial hypertension (HTN) is a primary risk factor for aortic dissection (AD).
  • Understanding the impact of pre-existing blood pressure (BP) control on AD outcomes is crucial for patient management.

Purpose of the Study:

  • To investigate whether pre-existing BP control influences the extent of acute AD.
  • To evaluate the effect of antecedent HTN control on the outcomes of patients with acute AD.

Main Methods:

  • Retrospective analysis of consecutive acute AD patients with BP records within 12 months prior to dissection.
  • BP categorized as normal, Stage I HTN, or Stage 2+ HTN based on published guidelines.
  • Number of antihypertensive medications (MEDs) used as a surrogate for HTN severity; genetic AD causes excluded.

Main Results:

  • Of 89 patients, 67% had elevated BP (Stage I or Stage 2+ HTN) prior to AD.
  • No significant differences observed in dissection extent, complications, hospital stay, or 30-day mortality between BP control groups.
  • Patients in all BP groups required more medications to control BP post-AD, persisting at follow-up.

Conclusions:

  • Pre-existing HTN control does not appear to influence the type, extent, or early outcomes of acute AD.
  • Acute AD significantly impacts BP regulation, leading to sustained increases in HTN severity post-dissection.
  • Further research is needed to understand the underlying pathological mechanisms of BP dysregulation following AD.
Abstract

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