Differences Between Ischemic Stroke Subtypes in Vascular Outcomes

Differences Between Ischemic Stroke Subtypes in Vascular Outcomes Support a Distinct Lacunar Ischemic Stroke Arteriopathy

Background and Purpose - Whether and how the arterial pathology underlying lacunar ischemic stroke differs from the atherothrombotic processes causing most other ischemic strokes is still debated. Different risks of recurrent stroke and MI after lacunar versus nonlacunar ischemic stroke may support a distinct lacunar arteriopathy.

Methods - We prospectively followed a hospital-based cohort of 809 first-ever ischemic stroke patients for 1 to 4 years. We compared risks of death, recurrent stroke, and MI in patients with lacunar versus nonlacunar stroke, and performed an updated meta-analysis of recurrent stroke subtype patterns.

Results - During 1725 person-years of follow-up, 109 patients had a recurrent stroke and 31 had MI. All patients at baseline, and 93% with recurrent stroke, had brain imaging and more than half with recurrent stroke had diffusion-weighted MRI. Overall, there was no difference in recurrence risk after lacunar vs nonlacunar stroke, although there was a trend toward a lower recurrence risk in the early weeks after lacunar stroke. Lacunar recurrence was more likely after lacunar than nonlacunar stroke (OR, 6.5; 95% CI, 2.4–17.5; updated meta-analysis OR, 6.8; 95% CI, 4.2–11.2). MI risk was nonsignificantly lower after lacunar than nonlacunar stroke (rate ratio, 0.5; 95% CI, 0.2–1.1; rate ratio after excluding patients with previous ischemic heart disease: 0.3; 95% CI, 0.1–0.9).

Conclusions - Our finding of a trend toward a lower MI risk after lacunar vs nonlacunar stroke and confirmation of both a lower early recurrence risk after lacunar stroke and a tendency of recurrent stroke subtypes to "breed true" support the notion of a distinct nonatherothrombotic lacunar arteriopathy.

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Approximately one-quarter of ischemic strokes are lacunar, presumed to result from occlusion, or perhaps leakiness, of one of the perforating arteries supplying the deep, subcortical areas of the brain. The underlying arterial pathology is poorly understood, but in most cases it is thought to be an intrinsic small vessel disease distinct from the atherothromboembolic processes causing most other ischemic strokes. In support of this is evidence that patients with lacunar ischemic stroke have a lower frequency than those with nonlacunar ischemic stroke of potential sources of thromboemboli (carotid stenosis and sources of cardiac emboli) and of previous ischemic heart disease (IHD), ie, coronary atherothrombosis.

If lacunar stroke is mainly caused by a distinct nonatherothrombotic arteriopathy, then we would also expect a lower early recurrent stroke rate compared with nonlacunar ischemic stroke (attributable to a lower frequency of active sources of thromboemboli); a tendency for recurrent stroke subtypes to "breed true" (ie, a further lacunar ischemic stroke would be more likely after a lacunar than a nonlacunar ischemic stroke); and a lower risk of MI among patients with lacunar vs nonlacunar ischemic stroke. We tested these hypotheses in a large, prospective, hospital-based cohort of well-characterized ischemic stroke patients.