Prevalence of nonstenosing, complicated atherosclerotic plaques in cryptogenic stroke
Tobias M Freilinger1, Andreas Schindler, Caroline Schmidt
1Department of Neurology, Ludwig-Maximilians-University Munich, Klinikum Großhadern, Munich, Germany. tobias.freilinger@med.unimuenchen.de
Insights
Complicated carotid plaques (American Heart Association type VI) were found in 37.5% of patients with cryptogenic stroke. These nonstenosing plaques, featuring intraplaque hemorrhage or rupture, may cause arterio-arterial embolism, explaining some cryptogenic strokes.
Area of Science:
- Vascular Neurology
- Cardiovascular Imaging
- Cerebrovascular Disease
Background:
- Cryptogenic stroke, accounting for up to 40% of ischemic strokes, lacks a definitive cause despite thorough investigation.
- Nonstenosing carotid plaques with complex features may be an underrecognized cause of stroke.
- American Heart Association (AHA) type VI lesions represent complicated plaques characterized by hemorrhage, thrombus, or fibrous cap rupture.
Purpose of the Study:
- To determine the prevalence of AHA type VI plaques in the carotid arteries of patients diagnosed with cryptogenic stroke.
- To investigate the potential role of nonstenosing complicated carotid plaques as an etiology for cryptogenic stroke.
Main Methods:
- A cohort of 32 patients with cryptogenic stroke and nonstenosing (<50%) eccentric carotid plaques underwent comprehensive clinical workup to exclude other stroke causes.
- High-resolution 3-Tesla black-blood carotid MRI was performed to assess plaque composition and morphology.
- Prevalence of AHA type VI plaques was determined based on established MRI criteria.
Main Results:
- AHA type VI plaques were identified in 12 out of 32 carotid arteries (37.5%) ipsilateral to the stroke.
- No AHA type VI plaques were detected in the contralateral carotid arteries (p = 0.001).
- The most frequent features of AHA type VI plaques were intraplaque hemorrhage (75%), fibrous plaque rupture (50%), and luminal thrombus (33%).
Conclusions:
- This pilot study suggests that complicated, nonstenosing carotid atherosclerotic plaques (AHA type VI) may contribute to arterio-arterial embolism in a subset of patients with cryptogenic stroke.
- Future research should include clinical and imaging follow-up to evaluate event rates and confirm the significance of AHA type VI plaques in cryptogenic stroke.
Objectives:
Our goal was to assess the prevalence of complicated American Heart Association (AHA) lesion type VI plaques in the carotid arteries of patients with cryptogenic stroke.
Background:
In up to 40% of ischemic stroke patients, no definite cause can be established despite extensive workup (i.e., cryptogenic stroke). To test the hypothesis if nonstenosing complicated carotid plaques may be the underlying etiology in some of these patients, we used high-resolution black-blood carotid magnetic resonance imaging (MRI), which can quantitatively assess plaque composition and morphology with good correlation to histopathology. Specifically, we focused on AHA type VI plaques, which are characterized by hemorrhage, thrombus, or fibrous cap rupture.
Methods:
Thirty-two consecutive patients (22 male; mean age 71.7 ± 11.9 years) with cryptogenic stroke and nonstenosing (<50%) eccentric carotid plaques were recruited from a single stroke unit. All patients underwent extensive clinical workup (brain MRI, duplex sonography, electrocardiography and Holter monitoring, transthoracic and transesophageal echocardiography, and laboratory investigations) to exclude other causes of stroke. All patients received a black-blood carotid MRI at 3-T with fat-saturated pre- and post-contrast T-1-, proton density-, and T-2-weighted and time-of-flight images using surface coils and parallel imaging techniques. Prevalence of AHA type VI plaque was determined in both carotid arteries on the basis of previously published MRI criteria.
Results:
AHA type VI plaques were found in 12 of 32 arteries (37.5%) ipsilateral to the stroke, whereas there were no AHA type VI plaques contralateral to the stroke (p = 0.001). The most common diagnostic feature of AHA type VI plaques was intraplaque hemorrhage (75%), followed by fibrous plaque rupture (50%) and luminal thrombus (33%).
Conclusions:
This pilot study suggests that arterio-arterial embolism from complicated, nonstenosing carotid atherosclerotic plaques may play a role in a subgroup of patients previously diagnosed with cryptogenic stroke. To further evaluate the significance of AHA type VI plaques in cryptogenic stroke, future studies will have to analyze both clinical and imaging follow-up data, including event rates for secondary strokes.
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