Premorbid Use of Beta-Blockers or Angiotensin-Converting Enzyme Inhibitors/Angiotensin Receptor Blockers in Patients with Acute Ischemic Stroke

Abstract

This study was designed to investigate the impact of the preexisting use of beta-blockers, angiotensin-converting enzyme inhibitors (ACEIs), or angiotensin receptor blockers (ARBs) on the cellular immune response in peripheral blood and the clinical outcomes of patients with acute ischemic stroke. We retrospectively collected clinical data from a cohort of 69 patients with premorbid beta-blockers and 56 patients with premorbid ACEIs/ARBs. Additionally, we selected a cohort of 107 patients with acute ischemic stroke to be the control of the same age and sex. We analyzed cellular immune parameters in peripheral blood 1 day after the appearance of symptoms, including the frequencies of circulating white blood cell subpopulations, the neutrophil-to-lymphocyte ratio (NLR), and the lymphocyte-to-monocyte ratio (LMR). We found that the count of lymphocytes and the lymphocyte-to-monocyte ratio were significantly higher in the peripheral blood of patients treated with beta-blockers before stroke than in matched controls. However, the premorbid use of ACEIs/ARBs did not considerably impact the circulating immune parameters listed above in patients with acute ischemic stroke. Furthermore, we found that premorbid use of beta-blockers or ACEIs/ARBs did not significantly change functional outcomes in patients 3 months after the onset of stroke. These results suggest that premorbid use of beta-blockers, but not ACEIs/ARBs, reversed lymphopenia associated with acute ischemic stroke. As cellular immune changes in peripheral blood could be an independent predictor of stroke prognosis, more large-scale studies are warranted to further verify the impact of premorbid use of beta-blockers or ACEIs/ARBs on the prognosis of patients with ischemic stroke. Our research is beneficial to understanding the mechanism of the systemic immune response induced by stroke and has the potential for a therapeutic strategy in stroke interventions and treatment.