An eight-year prospective controlled study about the safety and diagnostic value of cardiac and non-cardiac 1.5-T MRI in patients with a conventional pacemaker or a conventional implantable cardioverter defibrillator.

OBJECTIVES: To investigate safety and diagnostic value of 1.5-T MRI in carriers of conventional pacemaker (cPM) or conventional implantable defibrillator (cICD). METHODS: We prospectively compared cPM/cICD-carriers undergoing MRI (study group, SG), excluding those device-dependent or implanted <6 weeks before enrolment or prior to 01/01/2000, with cPM/cICD-carriers undergoing chest x-ray, CT or follow-up (reference group, RG). RESULTS: 142 MRI (55 cardiac) were performed in 120 patients with cPM (n=71) or cICD (n=71). In the RG 98 measurements were performed in 95 patients with cPM (n=40) or cICD (n=58). No adverse events were observed. No MRI prolonged/interrupted. All cPM/cICD were correctly reprogrammed after MRI without malfunctions. One temporary communication failure was observed in one cPM-carrier. Immediately after MRI, 12/14 device interrogation parameters did not change significantly (clinically negligible changes of battery voltage and cICD charging time), without significant variations for SG versus RG. Three-12 months after MRI, 9/11 device interrogation parameters did not change significantly (clinically negligible changes of battery impedance/voltage). Non-significant changes of three markers of myocardial necrosis. Non-cardiac MRI: 82/87 diagnostic without artefacts; 4/87 diagnostic with artefacts; 1/87 partially diagnostic. Cardiac MRI: in cPM-carriers, 14/15 diagnostic with artefacts, 1/15 partially diagnostic; in cICD-carriers, 9/40 diagnostic with artefacts, 22 partially diagnostic, nine non-diagnostic. CONCLUSIONS: A favourable risk-benefit ratio of 1.5-T MRI in cPM/cICD carriers was reported. KEY POINTS: • Cooperation between radiologists and cardiac electrophysiologists allowed safe 1.5-T MRI in cPM/cICD-carriers. • No adverse events for 142 MRI in 71 cPM-carriers and 71 cICD-carriers. • Ninety-nine per cent (86/87) of non-cardiac MRI in cPM/cICD-carriers were diagnostic. • All cPM-carrier cardiac MRIs had artefacts, 14 examinations diagnostic, 1 partially diagnostic. • Twenty-three per cent (9/40) of cardiac MRI in cICD-carriers were non-diagnostic.

Time and diffusion lesion size in major anterior circulation ischemic strokes.

BACKGROUND AND PURPOSE: Major anterior circulation ischemic strokes caused by occlusion of the distal internal carotid artery or proximal middle cerebral artery or both account for about one third of ischemic strokes with mostly poor outcomes. These strokes are treatable by intravenous tissue-type plasminogen activator and endovascular methods. However, dynamics of infarct growth in these strokes are poorly documented. The purpose was to help understand infarct growth dynamics by measuring acute infarct size with diffusion-weighted imaging (DWI) at known times after stroke onset in patients with documented internal carotid artery/middle cerebral artery occlusions. METHODS: Retrospectively, we included 47 consecutive patients with documented internal carotid artery/middle cerebral artery occlusions who underwent DWI within 30 hours of stroke onset. Prospectively, 139 patients were identified using the same inclusion criteria. DWI lesion volumes were measured and correlated to time since stroke onset. Perfusion data were reviewed in those who underwent perfusion imaging. RESULTS: Acute infarct volumes ranged from 0.41 to 318.3 mL. Infarct size and time did not correlate (R2=0.001). The majority of patients had DWI lesions that were <25% the territory at risk (<70 mL) whether they were imaged <8 or >8 hours after stroke onset. DWI lesions corresponded to areas of greatly reduced perfusion. CONCLUSIONS: Poor correlation between infarct volume and time after stroke onset suggests that there are factors more powerful than time in determining infarct size within the first 30 hours. The observations suggest that highly variable cerebral perfusion via the collateral circulation may primarily determine infarct growth dynamics. If verified, clinical implications include the possibility of treating many patients outside traditional time windows.

Less is better? Intraindividual and interindividual comparison between 0.075 mmol/kg of gadobenate dimeglumine and 0.1 mmol/kg of gadoterate meglumine for cranial MRI.

PURPOSE: To retrospectively compare a reduced dose (RD) (0.075 mmol/kg) of gadobenate dimeglumine (RD-gadobenate) with standard single dose (SSD) (0.1 mmol/kg) of gadoterate meglumine (SSD-gadoterate) for cranial MRI. MATERIALS AND METHODS: Thirty-one patients (12 males; aged 52 ± 16 years) underwent cranial MRI with SSD-gadoterate and repeated the examination with RD-gadobenate after a median interval of 10 months. Signal-to-noise ratio (SNR) was obtained on contrast-enhanced images for enhancing lesions (n=10) as well as for right and left transverse venous sinuses, internal carotid arteries, and parotid glands. Moreover, a consecutive series of 100 cranial MRI with SSD-gadoterate (49 males; aged 51 ± 19 years) was compared with a consecutive series of 100 cranial MRI with RD-gadobenate (45 males; aged 54 ± 18 years). Two blinded neuroradiologists (R1, R2) judged contrast enhancement as sufficient, good, or optimal. Wilcoxon, Mann-Whitney, χ(2), and Cohen κ statistics were used. RESULTS: At intraindividual analysis, median SNR ranged 57-88 for SSD-gadoterate and 79-99 for RD-gadobenate, the latter being systematically higher, the difference being significant for both transverse venous sinuses (p ≤ 0.011), not significant for both internal carotid arteries and both parotid glands, and enhancing lesions (p ≤ 0.101). The two series of interindividual analysis were not significantly different for gender/age (p>0.415). Contrast enhancement was optimal in 59% (R1) and 76% (R2) of patients using RD-gadobenate, in 39% (R1) and 49% (R2) of patients using SSD-gadoterate (p ≤ 0.016), with substantial reproducibility (κ ≥ 0.606). CONCLUSION: Both analyses showed an equal or better contrast enhancement when using RD-gadobenate compared to SSD-gadoterate for routine cranial MRI. The high relaxivity of gadobenate allowed for a 25% dose reduction.

Evaluation of inflammatory status of atherosclerotic carotid plaque before thromboendarterectomy using delayed contrast-enhanced subtracted images after magnetic resonance angiography.

OBJECTIVE: To investigate the correlation among carotid plaque contrast enhancement (CPCE) at MRI, inflammatory cell infiltration (ICI) at histopathology, and carotid stenosis degree. MATERIALS AND METHODS: Twenty-eight patients (19 males; mean age 67±9 years) scheduled for thromboendarterectomy prospectively underwent 1.5-T MR imaging using: (a) axial T1-weighted gradient-echo (T1wGRE) sequence centered on carotid bifurcations; (b) contrast-enhanced MR angiography (CE-MRA) with 0.1 mmol/kg of gadobenate dimeglumine; (c) enhanced axial T1wGRE sequence as in (a), 3 min after contrast injection. A three-point score system (absent, focal, wide) was used to assess CPCE on native and subtracted MRI images (c minus a) and ICI at histopathology. Carotid stenosis degree was determined on CE-MRA. RESULTS: Six CPCE studies were discarded due to patient movement. In the remaining 22 studies, CPCE was absent, focal and wide in 13, 6 and 3 cases, respectively; ICI was absent, focal and wide in 13, 7 and 2 cases, respectively (k=0.57). On CE-MRA 21/28 stenoses were severe and 7/28 moderate. There was no correlation either with ICI (p=1.000, n=28) or CPCE (p=0.747, n=22). CONCLUSION: The correlation between CPCE and ICI suggests a role for CPCE as an independent marker of plaque inflammation.

Optimizing dose and administration regimen of a high-relaxivity contrast agent for myocardial MRI late gadolinium enhancement.

OBJECTIVES: To investigate the time-course of late gadolinium enhancement of infarcted myocardium using gadobenate dimeglumine at different dosages and administration regimens. MATERIALS AND METHODS: After institutional review board approval and informed consent, we studied 13 patients (aged 63±11 years) with chronic myocardial infarction. They underwent two gadobenate dimeglumine-enhanced MR examinations (interval 24-48 h) using short-axis inversion-recovery gradient-echo sequences, with the following two different protocols, in randomized order: 0.05 mmol/kg and imaging at the 2.5th, 5th, 7.5th and 10th minute plus 0.05 mmol/kg and imaging at the 12.5th, 15th, 17.5th and 20th minute; the same as before but using 0.1 mmol/kg for both contrast injections. Contrast-to-noise ratios (CNRs) between infarcted myocardium, non-infarcted myocardium and left ventricle cavity were calculated for each time-point (2.5-min steps). Friedman ANOVA was used for comparing the CNR time-course; Wilcoxon test for comparing CNR at the 10th and the 20th minute. RESULTS: The CNR between infarcted and non-infarcted myocardium obtained at the 20th minute with 0.05 plus 0.05 mmol/kg resulted significantly higher than that obtained at the 10th minute with 0.05 mmol/kg (P=0.033) while not significantly different from that obtained at the 10th (0.1mm/kg) or at the 20th minute with 0.1 plus 0.1 mmol/kg. The CNR between infarcted myocardium and the left ventricle cavity obtained at the 20th minute with 0.05 plus 0.05 mmol/kg resulted significantly higher than all other measured values (P≤0.017). CONCLUSION: Using gadobenate dimeglumine, 0.05 plus 0.05 mmol/kg allows for a higher CNR between infarcted myocardium and the left ventricle cavity allowing for reliable assessment of the sub-endocardial infarctions.

In vivo assessment of coronary stents with 64-row multidetector computed tomography: analysis of metal artifacts.

OBJECTIVE: To evaluate stent-induced artifacts by 64-row multidetector computed tomography (MDCT). METHODS: We studied 26 stented patients with MDCT before conventional coronary angiography (CCA). The CT values were measured. Stents were classified as occluded, with significant stenosis, with nonsignificant stenosis, or patent. For the patent stents, mean in-stent and out-stent CT values were compared; stents 3 mm or smaller were compared with stents larger than 3 mm. Multidetector CT was compared with CCA. RESULTS: We analyzed 42 stents. At CCA, 34 stents were patent, 5 were nonsignificantly stenosed, 1 was significantly stenosed, and 2 were occluded. At MDCT, 33 of 34 patent stents, 2 occluded stents, and 1 stent with significant stenosis were correctly diagnosed; nonsignificant stenoses were undetected, 1 patent stent was misdiagnosed as occluded (κ = 0.727). The out-stent CT value was lower than in-stent CT value both in stents 3 mm or smaller (P = 0.001) and stents larger than 3 mm (P < 0.001). The in-stent CT value of stents 3 mm or smaller was higher (P = 0.011) than that of stents larger than 3 mm. CONCLUSIONS: Metal artifacts cause overlooking of nonsignificant stenosis.

Evaluation of carotid vessel wall enhancement with image subtraction after gadobenate dimeglumine-enhanced MR angiography.

OBJECTIVES: This study was aimed at testing the value of image subtraction for evaluating carotid vessel wall enhancement in contrast-enhanced MR angiography (MRA). MATERIALS AND METHODS: IRB approval was obtained. The scans of 81 consecutive patients who underwent carotid MRA with 0.1 mmol/kg of gadobenate dimeglumine were reviewed. Axial carotid 3D T1-weighted fast low-angle shot sequence before and 3 min after contrast injection were acquired and subtracted (enhanced minus unenhanced). Vessel wall enhancement was assigned a four-point score using native or subtracted images from 0 (no enhancement) to 3 (strong enhancement). Stenosis degree was graded according to NASCET. RESULTS: With native images, vessel wall enhancement was detected in 20/81 patients (25%) and in 20/161 carotids (12%), and scored 2.0+/-0.6 (mean+/-standard deviation); with subtracted images, in 21/81 (26%) and 22/161 (14%), and scored 2.5+/-0.6, respectively (P<0.001, Sign test). The overall stenosis degree distribution was: mild, 41/161 (25%); moderate, 77/161 (48%); severe, 43/161 (27%). Carotids with moderate stenosis showed vessel wall enhancement with a frequency (17/77, 22%) significantly higher than that observed in carotids with mild stenosis (1/41, 2%) (P=0.005, Fisher exact test) and higher, even though with borderline significance (P=0.078, Fisher exact test), than that observed in carotids with severe stenosis (4/43, 9%). CONCLUSION: Roughly a quarter of patients undergoing carotid MRA showed vessel wall enhancement. Image subtraction improved vessel wall enhancement conspicuity. Vessel wall enhancement seems to be an event relatively independent from the degree of stenosis. Further studies are warranted to define the relation between vessel wall enhancement and histopathology, inflammatory status, and instability.