BACKGROUND: Perforating artery territorial infarction (PAI) is usually a small artery disease (SAD). However, it may also result from branch artery occlusion or arterial embolism from the proximal atherosclerotic lesions. We hypothesized that patients with PAI caused by a SAD may have a distinct pattern of systemic artery involvement from those with PAI caused by large artery diseases. METHODS: We investigated retrospectively 329 consecutive patients with PAI who had angiographic studies. Patients were grouped according to the presence or absence of atherosclerosis in the parent artery or relevant artery: no arterial lesion (NAL), relevant artery atherosclerosis (RAA) and parent artery atherosclerosis (PAA). The relevant artery was defined as any artery which can cause index stroke. The parent artery was defined as an original artery that branches out and forms small artery which was responsible for index PAI. Systemic evidence of atherosclerosis and risk factors were compared. RESULTS: Of the 329 patients with PAI, 109 had RAA, 45 had PAA and 175 had neither RAA nor PAA. There were no differences amongst the groups in the classic risk factors for atherosclerosis. Evidence of atherosclerosis in arterial beds other than the relevant artery to the infarction (other cerebral arteries, coronary arteries, descending aorta and peripheral arteries) was significantly lower in the NAL group (49.7%) than in either the PAA group (88.9%) or RAA group (93.6%). CONCLUSIONS: Perforating artery territorial infarction with RAA or PAA when compared to PAI without atherosclerosis showed different involvement patterns of systemic atherosclerosis, suggesting potentially different aetiological mechanisms.
BACKGROUND: Perforating artery territorial infarction (PAI) is usually a small artery disease (SAD). However, it may also result from branch artery occlusion or arterial embolism from the proximal atherosclerotic lesions. We hypothesized that patients with PAI caused by a SAD may have a distinct pattern of systemic artery involvement from those with PAI caused by large artery diseases. METHODS: We investigated retrospectively 329 consecutive patients with PAI who had angiographic studies. Patients were grouped according to the presence or absence of atherosclerosis in the parent artery or relevant artery: no arterial lesion (NAL), relevant artery atherosclerosis (RAA) and parent artery atherosclerosis (PAA). The relevant artery was defined as any artery which can cause index stroke. The parent artery was defined as an original artery that branches out and forms small artery which was responsible for index PAI. Systemic evidence of atherosclerosis and risk factors were compared. RESULTS: Of the 329 patients with PAI, 109 had RAA, 45 had PAA and 175 had neither RAA nor PAA. There were no differences amongst the groups in the classic risk factors for atherosclerosis. Evidence of atherosclerosis in arterial beds other than the relevant artery to the infarction (other cerebral arteries, coronary arteries, descending aorta and peripheral arteries) was significantly lower in the NAL group (49.7%) than in either the PAA group (88.9%) or RAA group (93.6%). CONCLUSIONS: Perforating artery territorial infarction with RAA or PAA when compared to PAI without atherosclerosis showed different involvement patterns of systemic atherosclerosis, suggesting potentially different aetiological mechanisms.