Mean number and range of perforating branches per parent artery identified in the 7T postcontrast TOF-MRA images.

<p>^aIn one patient the posterior communicating artery was absent bilaterally.</p><p>^bOnly scans containing this segment within the FOV were taken into account.</p><p>Mean number and range of perforating branches per parent artery identified in the 7T postcontrast TOF-MRA images.</p

Typical images of intracranial perforators from different patients, obtained by postcontrast TOF-MRA at 7T.

<p>(A) A medial lenticulostriate artery (arrowhead), arising from the A1 segment of the ACA (transverse slab MIP, thickness 10mm), (B) lateral lenticulostriate arteries arising from the right MCA (arrows) and medial lenticulostriate arteries arising from the left ACA (arrowheads; coronal slab MIP, thickness 10 mm), (C) artery of Percheron (arrowheads), arising from the P1 segment of the PCA (coronal slab MIP, thickness 10mm), (D) perforating branch (arrowheads) arising from the right AChA (sagittal slab MIP, thickness 10mm), (E) thalamoperforating artery (arrowhead), arising from the left PCoA (transverse slab MIP, thickness 6mm), (F) pontine arteries (arrowheads) arising from the BA (transverse slab MIP, thickness 4mm), and (G) the intracranial feeders of the anterior spinal artery (arrows) with an adjacent vein (dashed arrow, transverse slab MIP angulated anterior-posterior in line with the BA, thickness 10mm). ACA = anterior cerebral artery; AChA = anterior choroidal artery; BA = basilar artery; ICA = intracranial carotid artery; MCA = middle cerebral artery; MIP = maximum intensity projection; PCA = posterior cerebral artery; PCoA = posterior communicating artery; P1 = first segment of the PCA; VA = vertebral artery.</p

7T TOF-MRA MIP images of different intracranial perforating arteries.

<p><b>On the left (A,C,E) the precontrast images with the corresponding postcontrast images of the same patient on the right (B,D,F)</b>. In B, D and F, longer arterial trajectories can be seen after contrast administration as compared to the corresponding unenhanced image in A, C and E (white boxes). (A and B) Sagittal slab MIP, thickness 10mm; (B and C) sagittal slab MIP, thickness 10mm; (E and F) coronal slab MIP, thickness 10mm. MIP = maximum intensity projection.</p

Three-component model fit parameters of UTE signal intensity as function of TE.

<p>Listed parameters are: n = number of mice, fractions of the fast (I_fast), slow (I_slow) and lipid (I_lipid) pool, and the T2*_fast (μs) and T2*_slow (ms) for control hearts, infarct and remote tissue in post-MI hearts, and the TAC hearts. Indicated are:</p><p>* (<i>P</i><0.05)</p><p>† (<i>P</i><0.01)</p><p>‡(<i>P</i><0.001) of the TAC hearts or the remote tissue in post-MI hearts as compared to the control hearts, or between the infarct core and remote tissue in post-MI hearts. The change of T2*_slow in remote tissue of post-MI hearts, as compared to control hearts, did not reach statistical significance (<i>P</i> = 0.09, respectively), so as the change of T2*_slow in TAC hearts as compared to control hearts (<i>P</i> = 0.18).</p><p>Three-component model fit parameters of UTE signal intensity as function of TE.</p

Relative infarct size determined from histology compared to MRI.

<p>(A) Long axis cross sections through <i>ex vivo</i> ΔUTE images in post-MI mouse hearts obtained from subtraction of a long-TE (4 ms) from a short-TE (21 μs) T2*-weighted image. The left panels show a post-MI heart 2 days after surgery. The right panels show a post-MI heart with a chronic MI 7 days after surgery. A positive contrast is observed in the ΔUTE image, which corresponds to the location of the chronic MI. Corresponding Picrosirius red stained slices showed hardly any collagen in the MI heart 2 days after surgery, whereas excessive replacement fibrosis was present (arrows) in the chronic MI. (B) Correlation between the infarct size as percentage of the total heart volume determined from histology and the <i>ex vivo</i> ΔUTE images of control (n = 3) and MI hearts (n = 8). The solid line is a linear fit.</p

<i>Ex vivo</i> and <i>in vivo</i> signal intensity time curves.

<p>Representative ROI-based T2*-weighted signal intensity curves as a function of echo time (TE) for <i>ex vivo</i> (top row) and <i>in vivo</i> (bottom row) measurements in control hearts, remote tissue and infarct area of the post-MI hearts and the TAC hearts, together with the corresponding model fit (gray line, top row) and lines to guide the eye (bottom row). Signal intensities were normalized to the signal intensity at TE = 21 μs.</p

<i>In vivo</i> signal difference between long and short-TE.

<p><i>In vivo</i> signal difference between long and short-TE, in control, post-MI and TAC mouse hearts. The signal difference between the short-TE (21 μs) and long-TE images (1.429 ms) is larger for remote and infarct tissue in post-MI hearts, and in TAC hearts, compared to control hearts. * (<i>P</i><0.05) and † (<i>P</i><0.01). Error bars indicate SD.</p

T2*-weighted MR images of a post-MI mouse heart.

<p>Two short-axis and long-axis cross-sections through an <i>in vivo</i> T2*-weighted dataset (TE = 21 μs) of a post-MI mouse heart. Indicated are the right ventricle (RV), left ventricle (LV), the papillary muscles (PM) and some small artefacts (↖). A dark saturation band with low signal intensity is visible in the two long-axis images.</p

<i>In vivo</i> T2*-weighted images in control heart, a MI heart and a TAC heart.

<p>Examples of a short-axis cross-section of a control heart (top row), a MI heart (middle row) and a TAC heart (bottom row) obtained with the T2*-weighted 3D sequence (short-TE, long-TE and ΔUTE image). LGE scans were obtained in control and post-MI mice (right column). The arrows indicate the infarcted areas.</p

A 73-year-old female patient presented with subacute infarcts of the left parietal cortex and left internal borderzone area.

<p>(A) On the transverse 3D time-of-flight magnetic resonance angiography two stenoses can be appreciated, one in the left M1 segment of the middle cerebral artery (arrowhead) and one in M2 segment of the middle cerebral artery (arrow). The transverse T₁w VIRTA, after contrast administration, shows a corresponding vessel wall lesion in the M2 segment (B), this lesion is however missed by the transverse reconstruction of the sagittal T₁w VIRTA sequence, also after contrast administration (C) because of its limited field-of-view (indicated by the dashed lines in A).</p