Chung J-W, Bang OY, Lee MJ, Hwang J, Cha J, Choi J-H, et al. Echoing Plaque Activity of the Coronary and Intracranial Arteries in Patients With Stroke. Stroke. 2016
Atherosclerosis is a diffuse process that can affect both the coronary and carotid arteries, but while previous studies have suggested a strong correlation between coronary atherosclerosis and extracranial carotid atherosclerosis, the correlation with intracranial atherosclerosis is less clear. Whereas the mechanism of myocardial infarction from coronary atherosclerosis is likely more similar to ischemic stroke caused by extracranial atherosclerosis, ischemic stroke caused by intracranial atherosclerosis typically falls into two etiologies: branch occlusive disease-type (B-type), where atherosclerosis occludes a perforating artery, versus coronary-type plaque rupture of plaque (C-type), where the atherosclerotic plaque ruptures, causing a shower of multiple embolic infarcts distally. This study attempts to characterize intracranial plaque phenotypes and correlate asymptomatic coronary artery disease (CAD) with intracranial atherosclerotic disease (ICAD) burden.
A total of 81 patients were included the final analysis, drawn from a population of patients admitted within 7 days of symptom onset for treatment of acute ischemic stroke with intracranial atherosclerosis. Patients who had known histories of coronary artery disease were excluded. B-type ICAS was differentiated from C-type ICAS in both anterior and posterior territory strokes. An ICAD score was calculated on the basis of intracranial atherosclerotic burden, with 0 points given for stenosis less than 50%, 1 point for stenosis of 50-99% and 2 points for an occlusion, with all involved intracranial vessels summed for a total score
Asymptomatic CAD was quite common, with a prevalence of just over 80% in the study population. The prevalence of asymptomatic CAD was relatively similar in both B-type and C-type ICAS groups (48% vs 52%) and, as might be expected, the burden of ICAD was positively correlated with the burden of CAD, although non-calcified coronary artery plaque morphology was independently associated with C-type ICAS. As non-calcified coronary plaque increased, remodeling also increased in the symptomatic arteries of patients with ICAS.
This study provides evidence of a positive relationship between coronary and intracranial atherosclerotic burden, and that coronary artery plaque composition (calcified vs non-calcified) might predict intracranial atherosclerosis morphology. The investigators suggest that this should prompt us as clinician to take a more holistic approach to the entire vascular system, rather than solely focus on, for example, the cerebral vasculature, or the coronary arteries. Certainly this might prompt the clinician to, when faced with a stroke patient with C-type ICAS, be more cognizant of the type of likely associated CAD burden, but a study evaluating whether this might also be predictive of acute coronary syndrome, would be of additional benefit.