PMC6230418_01
Magnetic resonance images of the affected arteries. High-grade stenosis of the right vertebral and the left distal internal carotid artery ((a), arrow) on a contrast enhanced magnetic resonance angiography. Long stenosis of the left ICA with tapering aspect ((b), arrows) on a follow-up time of flight MRI. Vessel wall enhancement of both internal carotid arteries ((c), arrows), and the right vertebral artery ((d), arrow), visible on a "dark blood" sequence. Contrast enhancement of both superficial temporal arteries ((e), arrows).
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MRI scan with a 3T whole-body system (Verio, Siemens Medical 22 AG, Erlangen, Germany) and a 12-channel reception head coil. MRI angiography revealed short high-grade stenosis of the right vertebral artery (VA) in the V3 segment (Figure 2(a)), a hypoplastic left VA, and a patent posterior communicating artery on the right side. The C6 and C7 segments of the left internal carotid artery (ICA) also showed high-grade stenosis (Figure 2(a)). On a follow-up MRA three weeks later especially the stenosis in the left ICA was longer, but also the stenosis of the right VA (Figure 2(b)). ICA (Figure 2(c)), the left temporal artery (TA), and the right VA (Figure 2(d)) were thickened with contrast enhancement, so were the walls of the superficial temporal arteries (Figure 2(e)). In addition, a left-sided pontine infarct was present.
Perfusion weighted imaging prior to and after therapy. Prior to therapy (a): prolonged mean transit time in large parts of the left middle cerebral artery territory as well as both posterior cerebral artery territories and an area with only moderately elevated transit time was found in the left insular cortex (white circle). After endovascular therapy (b): improvement of cerebral perfusion in both posterior cerebral artery territories and partly the left middle cerebral artery territory, with a now moderately elevated transit time in the border zone between middle and posterior cerebral artery territories, in addition to the area in the insular cortex (circles).
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PWI showed that the MTT, but none of the other perfusion parameters, was inhomogeneously prolonged in the left middle cerebral artery (MCA) territory and in both posterior cerebral artery (PCA) territories (see Figure 3(a)). The fitting model was composed of 15 Lorentzian-shaped exponentially decaying sinusoids; however, for this patient only the calculation of the metabolite ratio of Pi/PCr was taken into account, as this ratio can be seen as a marker for the energy reserve. 31P MRS revealed a decreased Pi/PCr ratio (Table 1) in both PCA and central left MCA territories in areas which showed a moderately prolonged (3.432 sec) but shorter MTT (Figure 3(a), Table 1) than surrounding areas (3.776 sec, reference value contralateral MCA territory = 3.279 sec). The Pi/PCr ratio in the MCA territory was higher than in the first scan and higher than in the contralateral hemisphere (Table 1). 31P MRS showed a newly decreased Pi/PCr ratio in the border area between MCA and PCA territories and the insular cortex of the left side (Figure 3(b); Table 1), again in an area with a moderately increased MTT (3.462 sec), which was shorter than in the ventral adjacent MCA territory (3.962 sec; Figure 3(b)).
Conventional angiography prior to and after angioplasty. Contrast injections in the right vertebral artery, displaying a high-grade stenosis of the right vertebral artery ((a), arrow), which improved after stent angioplasty ((b), arrow). After angioplasty a new cross-flow via the left posterior communicating artery to the left distal internal carotid artery is seen ((c), arrow).
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With the intention to improve the perfusion of the ACM territory via the posterior communicating artery, the high-grade stenosis in the V3 segment of the right vertebral artery was corrected via balloon angioplasty and stenting (Figure 4).