Association between intraplaque haemorrhage in the carotid atherosclerotic lesion, the degree of internal carotid artery stenosis and timing of ischaemic neurological events

Abstract

Abstract Background Expansion of carotid atherosclerotic plaques as a result of intraplaque haemorrhage has been implicated in the development of ischaemic neurological events. The relationship between the quantity of haemorrhage in the dominant atherosclerotic lesion, the degree of internal carotid artery (ICA) stenosis and the chronology of patients' symptoms was examined. Methods Consecutive patients undergoing carotid endarterectomy were included. The nature and timing of symptoms were recorded. Aortic arch injection digital subtraction angiography was performed before operation. Carotid endarterectomy specimens were serially sectioned and examined histologically. The amount of intraplaque haemorrhage was measured with digital image analysis. The influence of timing of symptoms on the quantity of intraplaque haemorrhage was compared with Kaplan–Meier analysis. Correlation between degree of ICA stenosis and quantity of intraplaque haemorrhage was assessed by means of regression analysis. Results Seventy-four patients (20 asymptomatic, 54 symptomatic) were included. The median latency of symptoms was 28 (1–600) days. Intraplaque haemorrhage was common: 54 (73 per cent) of 74 patients. Mean(s.e.m.) cumulative symptom-free survival before operation for patients with no intraplaque haemorrhage was 0·71(0·11), compared with 0·58(0·11) in those exhibiting haemorrhage in less than 50 per cent of the plaque area, and 0·20(0·07) in lesions with over 50 per cent (P = 0·002). A close correlation was observed between the degree of ICA stenosis and haemorrhagic content of the dominant atherosclerotic lesion (r2 = 0·433, P < 0·001). Conclusion These results confirm the association between intraplaque haemorrhage and the degree of ICA stenosis. They further demonstrate an association between the size of haemorrhage and timing of neurological events, suggesting a causative role for intraplaque haemorrhage in the development of ischaemic neurological events.