Objetivo Estudar as diferentes formas dos infartos lacunares agudos, investigando os fatores de risco e o significado clinico daqueles com morfologia irregular. Métodos Os 204 pacientes com infartos lacunares agudos foram classificados em dois grupos: aqueles com morfologia regular e aqueles com morfologia irregular. Foram estudadas as características dos dois grupos e caracterizados os fatores de risco para infartos irregulares, deterioração neurológica e altos escores da escala de Rankin modificada. Resultados Variabilidade da pressão arterial é fator de risco independente para infartos lacunares irregulares. Tamanho do infarto, prevalência de leucoaraiose e formato irregular dos infartos lacunares são fatores de risco independentes para escores mais elevados na escala de Rankin modificada. Conclusões Variabilidade da pressão arterial está relacionada ao formato irregular dos infartos lacunares agudos. Este tipo de infarto e a leucoaraiose podem estar relacionado a desfechos clínicos desfavoráveis.

Objective Our study focused on acute lacunar infarct shapes to explore the risk factors and clinical significance of irregularly shaped lacunar infarctions. Methods Based on the shape of their acute lacunar infarct, patients (n=204) were classified into the “regular” group or “irregular” group. The characteristics of the lacunar infarction were compared between the regular and irregular groups, between patients with and without neurological deterioration, and between patients with different modified Rankin scale (mRS) scores. The risk factors for irregularly shaped lacunar infarctions, neurological deterioration, and high mRS scores were identified. Results Blood pressure variability (BPV) was an independent risk factor for irregularly shaped lacunar infarction. Infarction size, prevalence of advanced leukoaraiosis, and irregularly shaped lacunar infarcts were independent risk factors for higher mRS scores. Conclusions The irregularly shaped lacunar infarcts were correlated with BPV. Irregularly shaped lacunar infarctions and leukoaraiosis may be associated with unfavorable clinical outcomes.

OBJECTIVE: Silent brain infarctions are the silent cerebrovascular events that are distinguished from symptomatic lacunar infarctions by their 'silence'; the origin of these infarctions is still unclear. This study analyzed the characteristics of silent and symptomatic lacunar infarctions and sought to explore the mechanism of this 'silence'. METHODS: In total, 156 patients with only silent brain infarctions, 90 with only symptomatic lacunar infarctions, 160 with both silent and symptomatic lacunar infarctions, and 115 without any infarctions were recruited. Vascular risk factors, leukoaraiosis, and vascular assessment results were compared. The National Institutes of Health Stroke Scale scores were compared between patients with only symptomatic lacunar infarctions and patients with two types of infarctions. The locations of all of the infarctions were evaluated. The evolution of the two types of infarctions was retrospectively studied by comparing the infarcts on the magnetic resonance images of 63 patients obtained at different times. RESULTS: The main risk factors for silent brain infarctions were hypertension, age, and advanced leukoaraiosis; the main factors for symptomatic lacunar infarctions were hypertension, atrial fibrillation, and atherosclerosis of relevant arteries. The neurological deficits of patients with only symptomatic lacunar infarctions were more severe than those of patients with both types of infarctions. More silent brain infarctions were located in the corona radiata and basal ganglia; these locations were different from those of the symptomatic lacunar infarctions. The initial sizes of the symptomatic lacunar infarctions were larger than the silent brain infarctions, whereas the final sizes were almost equal between the two groups. CONCLUSIONS: Chronic ischemic preconditioning and nonstrategic locations may be the main reasons for the 'silence' of silent brain infarctions.