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Carotid plaques and retinal emboli: a clinical, angiographic and morphological study
Insights
Carotid plaque complications, like ulceration and hemorrhage, were common in patients with symptomatic lesions. Retinal emboli suggest embolization is a key cause of stroke.
Area of Science:
- Vascular Surgery
- Neurology
- Pathology
Background:
- The exact criteria for carotid lesion significance and the role of embolic vs. hemodynamic factors in stroke are unclear.
- Understanding these factors is crucial for effective stroke prevention strategies.
Purpose of the Study:
- To correlate clinical features, retinal emboli, and angiographic findings with carotid plaque morphology in patients with symptomatic carotid lesions.
- To investigate the pathogenetic mechanisms of stroke in these patients.
Main Methods:
- A study of 32 consecutive patients with symptomatic carotid lesions.
- Evaluation of clinical presentation, retinal emboli, intraoperative carotid bifurcation appearance, and excised plaque morphology.
- Correlation of angiographic estimates with intraoperative findings and plaque characteristics.
Main Results:
- Retinal emboli were present in 22% of patients, even those without amaurosis fugax.
- Carotid plaques frequently showed complications (ulceration, hemorrhage, debris) in 91% of cases.
- Intraoperative stenosis correlated with angiographic estimates, but plaque complications were not reliably predicted by angiography.
Conclusions:
- Embolization appears to be the primary mechanism for stroke in most patients with symptomatic carotid lesions.
- Angiography has limitations in predicting complex plaque morphology and associated embolic risk.
Abstract:
The angiographic criteria for the significance of a carotid lesion and the contribution of embolic versus haemodynamic factors in stroke pathogenesis are currently unresolved. This study evaluated correlations between the clinical features, presence of retinal emboli, angiographic appearance of the carotid bifurcation and morphology of the surgically excised plaque in 32 consecutive patients with symptomatic carotid lesions. Retinal emboli were found in 22% of patients, including some without a history of amaurosis fugax. The carotid plaques were complicated by ulceration, intraplaque haemorrhage and/or intraluminal debris in 91% of cases. The degree of carotid stenosis seen at operation correlated well with the angiographic estimate. Plaque complications could not be accurately predicted angiographically, however. The high frequency of plaque complications, and the presence of retinal emboli, suggested that embolisation was the likely pathogenetic mechanism of stroke in most of these patients.