Luca Liberale1,2, Fabrizio Montecucco1,3,4, Aldo Bonaventura1, Ilaria Casetta5, Silva Seraceni6, Alessandro Trentini7, Marina Padroni5, Franco Dallegri1,3, Enrico Fainardi8, Federico Carbone1. 1. First Clinic of Internal Medicine, Department of Internal Medicine, University of Genoa, Genoa, Italy. 2. Center for Molecular Cardiology, University of Zürich, Schlieren, Switzerland. 3. Ospedale Policlinico San Martino, Genoa, Italy. 4. Centre of Excellence for Biomedical Research (CEBR), University of Genoa, Genoa, Italy. 5. Department of Biological, Psychiatric and Psychological Science, Azienda Ospedaliera-Universitaria, Ferrara, Italy. 6. Istitute for Maternal and Child Health 'IRCCS Burlo Garofolo', Trieste, Italy. 7. Section of Medical Biochemistry, Molecular Biology and Genetics, Department of Biomedical and Specialist Surgical Sciences, University of Ferrara, Ferrara, Italy. 8. Neuroradiology Unit, Azienda Ospedaliera-Universitaria Careggi, Florence, Italy.
Abstract
BACKGROUND: Acute ischaemic stroke (AIS) triggers both systemic and neurovascular inflammation, influencing poststroke recovery. In smokers with AIS, inflammation might be further upregulated, increasing ischaemia/reperfusion injury. Here, the predictive value of leucocyte and adhesion molecules levels on poststroke outcomes was investigated. MATERIALS AND METHODS: A total of 89 patients with AIS (n = 30 smokers and n = 59 nonsmokers) were recruited and evaluated 1, 7 and 90 days after the onset to assess stroke severity by the National Institute of Health Stroke Scale (NIHSS) score as well as clinical recovery at 90 days by the modified Rankin Scale (mRS). Lesion volume was assessed by noncontrast computed tomography. Haematological parameters, blood chemistry and soluble adhesion molecules were measured. RESULTS: Smokers experienced a more severe stroke and at a younger age with respect to nonsmokers, moreover, they had higher circulating levels of monocytes, neutrophils and soluble adhesion molecules. Baseline monocytes positively correlated with stroke severity and disability across all time points in the overall cohort. No correlation was shown between adhesion molecules and poststroke outcomes. A monocyte count >0·63 × 109 /L predicted worse stroke severity (defined as NIHSS ≥5) at day 90 independently of age, hypertension, thrombolysis and active smoking in the overall cohort. Similarly, a monocyte count >0·64 × 109 /L predicted poor neurological recovery at day 90 (defined as mRS > 2). CONCLUSIONS: Smoker had more severe AIS and higher leucocytes and adhesion molecule levels. In the overall cohort, monocyte count was an independent predictor of worse poststroke outcome. Although larger trials are needed, monocyte count might be a cheap prognostic parameter in AIS.
BACKGROUND: Acute ischaemic stroke (AIS) triggers both systemic and neurovascular inflammation, influencing poststroke recovery. In smokers with AIS, inflammation might be further upregulated, increasing ischaemia/reperfusion injury. Here, the predictive value of leucocyte and adhesion molecules levels on poststroke outcomes was investigated. MATERIALS AND METHODS: A total of 89 patients with AIS (n = 30 smokers and n = 59 nonsmokers) were recruited and evaluated 1, 7 and 90 days after the onset to assess stroke severity by the National Institute of Health Stroke Scale (NIHSS) score as well as clinical recovery at 90 days by the modified Rankin Scale (mRS). Lesion volume was assessed by noncontrast computed tomography. Haematological parameters, blood chemistry and soluble adhesion molecules were measured. RESULTS: Smokers experienced a more severe stroke and at a younger age with respect to nonsmokers, moreover, they had higher circulating levels of monocytes, neutrophils and soluble adhesion molecules. Baseline monocytes positively correlated with stroke severity and disability across all time points in the overall cohort. No correlation was shown between adhesion molecules and poststroke outcomes. A monocyte count >0·63 × 109 /L predicted worse stroke severity (defined as NIHSS ≥5) at day 90 independently of age, hypertension, thrombolysis and active smoking in the overall cohort. Similarly, a monocyte count >0·64 × 109 /L predicted poor neurological recovery at day 90 (defined as mRS > 2). CONCLUSIONS: Smoker had more severe AIS and higher leucocytes and adhesion molecule levels. In the overall cohort, monocyte count was an independent predictor of worse poststroke outcome. Although larger trials are needed, monocyte count might be a cheap prognostic parameter in AIS.