SILENT BRAIN INFARCTS IN 755 CONSECUTIVE PATIENTS WITH A FIRST-EVER SUPRATENTORIAL ISCHEMIC STROKE - RELATIONSHIP WITH INDEX-STROKE SUBTYPE, VASCULAR RISK-FACTORS, AND MORTALITY

Background and Purpose We wanted to establish independent dent associa tions of various clinical variables, computed tomographic (CT) scan fe atures, presenting stroke subtypes, and outcome with the presence of s ilent infarcts on CT. Methods We studied 755 consecutive patients in a prospective registration of patients with first-ever supratentorial a therothrombotic, cardioembolic, or lacunar stroke or stroke of undeter mined cause by multiple logistic regression analysis. Results Two hund red six patients (27%) with a first symptomatic territorial or small d eep ischemic stroke had one or more silent infarcts on CT. Of all sile nt lesions, 169 (82%) were small and deep. Silent infarcts were signif icantly more strongly associated with a lacunar than atherothrombotic (odds ratio [OR], 1.59; 95% confidence interval [CI], 1.02 to 2.47; P= .039) or cardioembolic (OR, 1.89; 95% CI, 1.2 to 2.99; P=.005) index s troke. Silent territorial lesions were more strongly associated with c ardioembolic than with lacunar stroke but not with atherothrombotic st roke. In this respect, no differences were found between the atherothr ombotic and undetermined-cause group. Advanced age and hypertension we re the only risk factors that were significantly associated with silen t infarcts (OR, 1.76; 95% CI, 1.14 to 2.71; P=.011; and OR, 1.58; 95% CI, 1.13 to 2.21; P=.007; respectively), mainly because of a strong in dependent association of these risk factors with silent small deep inf arcts (OR, 1.75; 95% CI, 1.10 to 2.79; P=.018; and OR, 1.57; 95% CI, 1 .09 to 2.24; P=.014; respectively). A cardioembolic source or atrial f ibrillation in specific was not independently associated with any type or number of silent infarcts. Significant carotid stenosis (diameter reduction >50%) was not significantly associated with any type of sile nt lesion. Initial severe handicap (Rankin Scale score >3), 30-day cas e fatality rate, and 1-year mortality were not affected by the presenc e of silent infarcts. Conclusions The strong association of silent sma ll deep lesions with first symptomatic small deep infarcts suggests a common underlying mechanism (presumably small-vessel vasculopathy), wh ereas cardiogenic embolism and large-vessel thromboembolism are the mo st likely causes in both silent and first symptomatic territorial infa rcts. Single or multiple silent infarcts do not predict a cardioemboli c stroke mechanism in first symptomatic supratentorial brain infarcts. As silent infarcts do not predict the cause of carotid embolic stroke in first symptomatic brain infarcts, their presence should not influe nce the decision on carotid surgery. Silent infarcts do not affect the degree of initial handicap, 30-day case fatality, or 1-year mortality . The significance of silent infarcts for predicting possible future c ognitive decline and risk of recurrent stroke deserves further study.