Abstract 3431: A High Vascular Risk Factors Profile Predicts Lacunar Stroke Progression
Background. Lacunar stroke (LS) accounts for a quarter of all ischemic strokes and is considered to have a benign prognosis. However, 20-30% of patients experience worsening of neurological deficit in hours or days after stroke onset. Mechanisms of progression are not known and no reliable clinical predictor has been identified. Aim of this study was to explore vascular risk factors and baseline clinical or laboratory features potentially associated with progression in LS.
Methods. We performed a retrospective analysis of consecutive patients with LS admitted to the Stroke Unit of Careggi University Hospital (Florence, Italy) between January 2002 and December 2010. Patients were included in the study if they presented with a lacunar syndrome according to OCSP classification and/or small vessel disease according to TOAST classification and/or a lacunar infarct on neuroimaging consistent with the clinical deficit. Patients were divided into “progressive” and “non progressive”. Progression was defined as an increase of at least one point on one of the motor items of the NIHSS during the first 72 hours after stroke onset. Factors associated with progression after univariate analysis were entered into a multiple logistic regression model in order to select independent determinants of progression.
Results. Out of 1502 patients with ischemic stroke admitted during the study period, 156 met the inclusion criteria. Thirty-nine (25%) patients showed neurological worsening. Latency of progression was 25.7 hours. Patients who progressed were younger than those who did not (mean age: 67.9±10.7 vs 70.6±13.0). There were no significant differences for single vascular risk factors distribution, laboratory parameters and baseline stroke severity comparing the two groups. When considering the presence of one versus more than one factor among hypertension, diabetes, smoking and hypercholesterolemia, the risk of progression increased with increasing number of risk factors: neurological worsening was observed in 0% (0/17) of patients with no risk factor, 24% (15/62) of those with one risk factor and 31% (24/77) of those with more than one risk factor (p=0.025). After adjustment for univariate predictors (age, sex, diastolic hypertension and lesion location in pons or internal capsule), the presence of multiple vascular risk factors maintained an independent effect on progression: risk of progression increased with an OR=1.7 (95%IC=1.1-2.8) for any additional risk factor.
Conclusion. Our results suggest that a high risk factors profile is associated with an increased risk of progression. Translating this observation into a hypothetical pathological setting, it could support the hypothesis of mural atheroma involving the parent artery and proximal portion of the perforating arteries, eventually leading to the progressive enlargement of the ischemic area as a putative mechanism of progressive LS.
- © 2012 by American Heart Association, Inc.