Thrombus Characteristics Are Related to Collaterals and Angioarchitecture in Acute Stroke

Abstract

Background: We have theorized that clots with stasis are longer. We therefore explored the relationship between thrombus imaging characteristics on noncontrast computed tomography (NCCT) and magnetic resonance imaging (MRI) with clot length and pial collaterals on baseline computed tomography angiography (CTA). Methods: Prospective study of acute ischemic stroke patients (2005)(2006)(2007)(2008)(2009)) from Keimyung University. Patients with known stroke symptom onset time, baseline CTA, MRI, and with M1-Middle Cerebral Artery (MCA) ± intracranial internal carotid artery (ICA) occlusions were included. Clot length and pial collaterals were measured on baseline CTA. Results: A total of 104 patients (mean age 65.1 ± 12.28 years, 56.7% male, median baseline National Institutes of Health Stroke Scale 13) with intracranial ICA + MCA (n = 50) or isolated M1-MCA (n = 54) occlusions were included. Hyperdense sign on NCCT had a median clot length of 42.3 mm versus 29.5 mm when hyperdense negative (p = 0.02). Clots showing blooming artifact on gradient recall echo MRI had a median length of 39.1 mm versus 24.5 mm without blooming (p = 0.005). Patients with poor baseline collaterals on CTA had longer clots than those with intermediate/good collaterals (median clot length 49.4 mm vs 34.9 mm vs 20.5 mm respectively, p < 0.001). In censored logistic regression modeling, clot length was an independent predictor of hyperdense sign (p = 0.05) and of the presence of blooming artifact (p = 0.006). Conclusions: Clot length and baseline collateral status are independent predictors of clot hyperdensity on NCCT and blooming artifact on gradient recall echo. Longer clots are more likely to be hyperdense and to bloom more, probably because portions of these clots are freshly formed locally due to of stasis of blood around the original clot. This stasis could be because of poor collaterals and inefficient angio-architecture within the cerebral arterial tree.RÉSUMÉ: Les caractéristiques du thrombus sont associées aux collatérales et à l'architecture vasculaire dans l'accident vasculaire cérébral aigu. Contexte: Nous avons émis l'hypothèse que les caillots avec stase sont plus longs. Nous avons donc exploré la relation entre les caractéristiques du caillot, à l'imagerie par tomodensitométrie (CT) sans agent de contraste (CTSAC) et à l'imagerie par résonance magnétique (IRM), et la longueur du caillot et les vaisseaux collatéraux pie-mériens à l'angiographie CT initiale (CTA). Méthode: Cette étude prospective porte sur des patients ayant subi un accident vasculaire cérébral ischémique entre 2005 et 2009 qui ont consulté à l'Université Keinyung. Les patients dont le moment du début des symptômes d'AVC était connu, dont le CTA initial et l'IRM étaient au dossier et qui présentaient une occlusion de l'artère cérébrale moyenne M1 (ACM) ± de la carotide interne intracrânienne (CIIC), ont été inclus dans l'étude. La longueur du caillot et les collatérales pie-mériennes ont été mesurées sur le CTA initial. Résultats: Cent quatre patients...

Is Unexplained Early Neurological Deterioration After Intravenous Thrombolysis Associated With Thrombus Extension?

“…Mean age was 69±15 years, median National Institutes of Health Stroke Scale was 16 (interquartile range, [12][13][14][15][16][17][18][19][20], and proximal occlusion (internal carotid artery or M1) was present in 83% of patients. Unexplained END occurred in 22 patients.…”

“…First, in situ extension of the original thrombus may be caused by (1) pathological thrombosis pathways, such as increased coagulation activity and resistance to fibrinolysis, or (2) activation of the physiological coagulation cascade because of blood stasis adjacent to the original thrombus (eg, because of poor collateral flow or inefficient vascular architecture). 13 Second, proximal thrombus extension could be explained by re-embolization in the same territory from a proximal embolic source. END indicates early neurological deterioration; ICA, internal carotid artery; M1, proximal part of the middle cerebral artery (MCA); M2, insular MCA segment; >M2, more distal MCA segment; MRA, magnetic resonance angiography; MRI, magnetic resonance imaging; NIHSS, National Institute of Health Stroke Scale; and SVS, susceptibility vessel sign.…”

Multimodality CT based imaging to determine clot characteristics and recanalization with intravenous tPA in patients with acute ischemic stroke

“…To better explain clot formation and organization over time within the intracranial tree in patients with acute ischemic stroke, we recently suggested a theoretical framework wherein intracranial clots have two components [10]. The first is the "original clot" that comes from a proximal source or is formed in-situ due to endo-luminal factors, and the second is new clot that forms over time from stasis of blood flow around the original clot (Figs.…”

“…2 and 3). The extent of new clot formation due to stasis around the original clot is dependent on the patient's collateral status and [10] branching pattern of vessels around the clot (angioarchitecture) ( Figs. 1 and 2).…”

“…The average width of the middle cerebral artery (MCA; the most common site of occlusion in AIS) is 3-4 mm [16]. Scans that [10] exceed this width and are of average signal may potentially miss detecting the hyperdense sign because of the phenomenon of partial volume averaging. Thin slice NCCT (≤2.5 mm) minimizes volume averaging, significantly improving the signal to noise ratio and producing higher object contrast.…”