Angioedema associated with thrombolysis for ischemic stroke: analysis of a case‐control study

Abstract

Background Bradykinin‐mediated angioedema (AE) is a complication associated with thrombolysis for acute ischemic stroke. Risk factors are unknown and management is discussed. Objectives To clarify risk factors associated with bradykinin‐mediated AE after thrombolysis for acute ischemic stroke. Methods In a case‐control study conducted at a French reference centre for bradykinin angiœdema, patients with thrombolysis for acute ischemic stroke and a diagnosis of bradykinin‐mediated angiœdema, were compared to controls treated with thrombolysis treatment without angiœdema. Results Fifty‐three thrombolysis‐related AE were matched to 106 control subjects. The sites of attacks following thrombolysis for ischemic stroke mainly included tongue (34/53, 64%) and lips (26/53, 49%). The upper airways were involved in 37 (70%) cases. Three patients required mechanical ventilation. Patients with bradykinin‐mediated angiœdema were more frequently women [33 (62%) vs. 44 (42%); P = 0.01], had higher frequency of prior ischemic stroke [12 (23%) vs. 9 (8%); P = 0.01], hypertension [46 (87%) vs. 70 (66%); P = 0.005], were more frequently treated with angiotensin‐converting enzyme inhibitor [37 (70%) vs. 28 (26%); P < 0.001] and were more frequently hospitalized in intensive care medicine [ICU; 11 (21%) vs. 5 (5%); P = 0.004]. In multivariate analysis, factors associated with thrombolysis‐related AE were female sex [odds ratio (OR), 3.04; 95% confident interval (CI), 1.32–7.01; P = 0.009] and treatment with angiotensin‐converting enzyme inhibitors [(OR), 6.08; 95% (CI), 2.17–17.07; P < 0.001]. Conclusions This case‐control study points out angiotensin‐converting enzyme inhibitors and female sex as risk factors of bradykinin AE associated with thrombolysis for ischemic stroke.

Clinical Significance and Value of Serum Homocysteine and Urine 11 Dehydrothromboxane B2 Combined with Transferrin-Specific Peptide in the Diagnosis of Cerebral Apoplexy

“…Oxidative stress is the basic pathological mechanism of ischemic brain injury and reperfusion injury. The accumulation of reactive oxygen species in the infarcted area and ischemic penumbra (that is, the surrounding area of the infarcted area) can lead to the damage of cell membrane, DNA, and polypeptides, as well as the destruction of redox balance of various biochemical systems [ 22 ]. Meanwhile, in the acute phase of stroke, the peripheral blood vessels of the body can release a large number of reactive oxygen species and proinflammatory factors, further aggravating the injury of vascular endothelium [ 23 ].…”

Bradykinin Metabolism and Drug-Induced Angioedema

“…The recombinant serine proteases cleave plasminogen to plasmin, and in addition to their thrombolytic effects, activate the kinin pathway by converting Factor XII to Factor XIIa, with increased production of BK and AE usually appearing a few hours after thrombolytic treatment. AE is asymmetric in many cases, and mainly contralateral to the ischemic hemisphere, suggesting that infarction of the insular cortex could lead to contralateral autonomic dysfunction [101][102][103]. In addition, cerebral damage secondary to brain ischemia can lead to BK release [104].…”

Intravenous thrombolysis in ischemic stroke: 10 rules for the practical neurologist

“…Другим возможным осложнением ВТ является ангиоэдема, которая развивается у 0,4-5,1% и обычно прояв-ляется оролингвальным отеком, но может привести к обструкции верхних дыхательных путей и анафилактическому шоку. К основным факторам риска ангиоэдемы относятся женский пол и прием ингибиторов АПФ до инсульта [57,58]. При возникновении ангионевротического отека необходимо прекратить введение тромболитика; обеспечить проходимость дыхательных путей; решить вопрос о необходимости эндотрахеальной интубации; ввести метилпреднизолон в дозе 125 мг, дифенгидрамин 50 мг, ранитидин 50 мг или фамотидин 20 мг; при дальнейшем прогрессировании отека ввести адреналин (0,1%) 0,3 мл подкожно [39].…”