Echoing Plaque Activity of the Coronary and Intracranial Arteries in Patients With Stroke
Jong-Won Chung1, Oh Young Bang2, Mi Ji Lee1
1From the Departments of Neurology (J.-W.C., O.Y.B., M.J.L., J.H.) and Radiology (J.C., Y.H.C.), Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea; and Department of Medicine, Cardiovascular Imaging Center, Cardiac and Vascular Center, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea (J.-H.C.).
Insights
Vulnerable plaques in coronary arteries, specifically noncalcified ones, are linked to a specific type of intracranial atherosclerotic stroke. This suggests similar plaque behaviors across different arterial systems in the body.
Area of Science:
- Cardiovascular Medicine
- Neurology
- Radiology
Background:
- Atherosclerosis is a systemic condition affecting both coronary and intracranial arteries, particularly in the elderly.
- Intracranial atherosclerotic disease can lead to stroke via branch occlusive disease (B-type) or plaque rupture (C-type).
- Coronary artery disease (CAD) and intracranial atherosclerotic disease share common risk factors and pathological processes.
Purpose of the Study:
- To investigate the association between plaque characteristics in coronary arteries and intracranial arteries.
- To determine if specific coronary plaque features predict the type of intracranial atherosclerotic stroke.
Main Methods:
- Eighty-one patients with acute cerebral infarcts due to intracranial atherosclerotic disease were analyzed.
- Coronary artery disease burden and plaque characteristics were assessed using multidetector computed tomography.
- Intracranial atherosclerotic disease burden, vascular morphology, and plaque activation were evaluated using magnetic resonance angiography and high-resolution magnetic resonance imaging.
Main Results:
- A correlation was found between asymptomatic coronary artery disease burden and asymptomatic intracranial atherosclerotic disease burden.
- The prevalence of noncalcified coronary plaque was significantly higher in patients with C-type intracranial atherosclerotic stroke.
- The presence of noncalcified coronary plaque independently predicted C-type intracranial atherosclerotic stroke (OR, 3.38; P=0.041).
- Increased noncalcified coronary plaques were associated with positive remodeling and plaque enhancement in symptomatic intracranial arteries.
Conclusions:
- Plaque behavior in intracranial and coronary arteries is similar.
- The presence of vulnerable plaques in one arterial system warrants evaluation of other vascular beds.
- Identifying specific coronary plaque characteristics may aid in predicting the type of intracranial atherosclerotic stroke.
Background And Purpose:
Atherosclerosis is a systemic disease, and both coronary and intracranial atherosclerosis are common in the elderly. Unlike coronary artery disease (CAD), intracranial atherosclerotic disease can cause intracranial atherosclerotic stroke by branch occlusive disease (B-type) and coronary-type rupture of plaque (C-type). We hypothesized that plaque characteristics of intracranial arteries are associated with those of coronary arteries.
Methods:
Eighty-one patients with acute cerebral infarcts caused by intracranial atherosclerotic disease without history of CAD were analyzed. Asymptomatic CAD burden (number and degree of stenosis) and plaque characteristics (calcified, mixed, and noncalcified) were measured with multidetector computed tomography, whereas the asymptomatic intracranial atherosclerotic disease burden was measured using magnetic resonance angiography. The symptomatic intracranial artery was analyzed using high-resolution magnetic resonance imaging for vascular morphology (stenosis degree, remodeling index, and wall index) and plaque activation (enhancement pattern and volume).
Results:
The asymptomatic CAD burden was correlated with the asymptomatic intracranial atherosclerotic disease burden. The overall CAD burden did not differ between B- and C-type intracranial atherosclerotic stroke. However, the prevalence of noncalcified coronary plaque was much higher in C-type intracranial atherosclerotic stroke and the presence of coronary noncalcified plaque was independently associated with C-type intracranial atherosclerotic stroke (odds ratio, 3.38; 95% confidence interval, 1.05-10.85; P=0.041). As the number of coronary noncalcified plaques increased, positive remodeling and plaque enhancement increased in the symptomatic intracranial artery on high-resolution magnetic resonance imaging.
Conclusions:
Plaques within the intracranial and coronary arteries behave in similar ways. Our results suggest the need to evaluate and treat other vascular trees in patients with vulnerable plaques within a single arterial system.
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