Abstract 138: Perfusion Imaging of Intracranial Atherosclerotic Disease in SAMMPRIS

• Published in: Stroke (1970) 2015-02, Vol.46 (suppl_1)
• Main Authors: Liebeskind, David S, Derdeyn, Colin P, Sanossian, Nerses, Cotsonis, George A, Scalzo, Fabien, Prabhakaran, Shyam, Romano, Jose G, Turan, Tanya N, Johnson, Mark S, Lynn, Michael J, Fiorella, David J, Hess, David C, Chimowitz, Marc I, Feldmann, Edward
• Format: Article
• Language: English
• ISSN: 0039-2499; 1524-4628
• DOI: 10.1161/str.46.suppl_1.138

Abstract only Background: Noninvasive perfusion imaging with CT (CTP) or MRI (PWI) provides key physiologic data regarding hemodynamics of intracranial atherosclerotic disease (ICAD). Parameters of delayed perfusion such as Tmax, time to peak (TTP), mean transit time (MTT) and cerebral blood volume (CBV) or flow (CBF) may disclose important mechanisms of stroke in ICAD. We analyzed CTP and PWI acquired in SAMMPRIS to identify the principal perfusion patterns, correlation with conventional angiography and potential links with clinical outcome. Methods: CTP and PWI were identified in the SAMMPRIS imaging archive. Perfusion datasets were processed with Olea Sphere® to yield Tmax, TTP, MTT, CBV and CBF maps graded by 2 expert readers to identify markers of decreased, normal, or increased perfusion in the symptomatic territory. The resultant multiparametric perfusion patterns were correlated with clinical and angiographic variables, using Fisher’s exact test and Kaplan-Meier methods followed by log-rank tests. Results: Perfusion imaging was available in 59 subjects at baseline and 42 at follow-up. Baseline perfusion included Tmax (decreased in 2, normal in 18, increased in 39); TTP (decreased in 2, normal in 18, increased in 39); MTT (decreased in 2, normal in 27, increased in 30); CBV (decreased in 5, normal in 42, increased in 12); CBF (decreased in 7, normal in 48, increased in 4). The baseline Tmax increases in 66% of subjects were associated with the combined (TICI and collaterals) diminished angiographic flow patterns (p=0.016) and with increased 30-day SIT (p=0.015). Baseline CBV changes were associated with stroke as a qualifying event (p=0.007), NIHSS (p=0.039), presenting symptoms of hypoperfusion (p=0.071), severity of stenosis (p=0.015), and angiographic flow patterns (p=0.009). Follow-up CTP or PWI revealed similar patterns to baseline, although delay maps normalized in patients after stenting. Conclusions: Noninvasive perfusion imaging with CT or MRI discloses delayed flow caused by ICAD, often compensated by autoregulatory vasodilation (increased CBV) to maintain CBF in the downstream territory. Perfusion imaging parameters may reflect angiographic collateral flow patterns in ICAD, warranting further investigation as predictors of stroke risk.