Impact of model-based iterative reconstruction on low-contrast lesion detection and image quality in abdominal CT: a 12-reader-based comparative phantom study with filtered back projection at different tube voltages.

OBJECTIVES: To evaluate the impact of model-based iterative reconstruction (MBIR) on image quality and low-contrast lesion detection compared with filtered back projection (FBP) in abdominal computed tomography (CT) of simulated medium and large patients at different tube voltages. METHODS: A phantom with 45 hypoattenuating lesions was placed in two water containers and scanned at 70, 80, 100, and 120 kVp. The 120-kVp protocol served as reference, and the volume CT dose index (CTDIvol) was kept constant for all protocols. The datasets were reconstructed with MBIR and FBP. Image noise and contrast-to-noise-ratio (CNR) were assessed. Low-contrast lesion detectability was evaluated by 12 radiologists. RESULTS: MBIR decreased the image noise by 24% and 27%, and increased the CNR by 30% and 29% for the medium and large phantoms, respectively. Lower tube voltages increased the CNR by 58%, 46%, and 16% at 70, 80, and 100 kVp, respectively, compared with 120 kVp in the medium phantom and by 9%, 18% and 12% in the large phantom. No significant difference in lesion detection rate was observed (medium: 79-82%; large: 57-65%; P > 0.37). CONCLUSIONS: Although MBIR improved quantitative image quality compared with FBP, it did not result in increased low-contrast lesion detection in abdominal CT at different tube voltages in simulated medium and large patients. KEY POINTS: • MBIR improved quantitative image quality but not lesion detection compared with FBP. • Increased CNR by low tube voltages did not improve lesion detection. • Changes in image noise and CNR do not directly influence diagnostic accuracy.

Variability of MRI Aortic Stiffness Measurements in a Multicenter Clinical Trial Setting: Intraobserver, Interobserver, and Intracenter Variability of Pulse Wave Velocity and Aortic Strain Measurement.

PURPOSE: To assess intraobserver, interobserver, and scan-rescan variability of MRI aortic stiffness measurements in a multicenter trial setting. MATERIALS AND METHODS: This study was a retrospective analysis of prospectively collected data in a multicenter prospective clinical trial (clinicaltrials.gov ID NCT01870739). Forty-five adult patients (31 men; mean age, 58 years ± 12 [standard deviation]; 15 patients per center; three centers) with arterial hypertension underwent standardized 3-T baseline MRI assessments between June and September 2014. Aortic strain was calculated from maximum and minimum aortic area measurements repeated three times by three readers at three aortic levels on three retrospectively gated axial gradient-echo (GRE) data sets. Pulse wave velocity (PWV) was assessed three times by five readers as Δx/Δt: Δx was measured on a parasagittal GRE image of the aortic arch, and Δt was extracted from ascending and descending aortic velocity curves created on three axial phase-contrast acquisitions. Intraobserver, interobserver, and scan-rescan variability was calculated using percentage coefficient of variation (COV). RESULTS: Aortic strain variability was lowest at the level of the distal descending aorta (DDA) with median COVs of 1.6% for intraobserver variability, 4.0% for interobserver variability, and 10.3% for scan-rescan variability. It was highest at the ascending aorta (AA) with COVs of 3.6% for intraobserver variability, 10.7% for interobserver variability, and 19.8% for scan-rescan variability. Variability of PWV was low: 0.7% for intraobserver variability, 1.5% for interobserver variability, and 8.1% for scan-rescan variability. CONCLUSION: Low variability can be achieved for aortic strain and PWV measurements in a multicenter trial setting using standardized MRI protocols. Although COV was lower when measuring aortic strain at DDA compared with AA, variability was acceptable at both anatomic locations.Supplemental material is available for this article.© RSNA, 2020.

Protection from hepatic ischemia/reperfusion injury and improvement of liver regeneration by alpha-lipoic acid.

The aim of this study was to characterize the in vivo action of lipoic acid (LA) in hepatic ischemia/reperfusion injury (IRI) and its effects on liver regeneration involving the investigation of mechanisms of action and effects on animal survival. Two groups of rats were compared: one group received 500 micromol alpha-LA injected via the inferior vena cava 15 min before the induction of 90 min of selective ischemia. The untreated group received vehicle. Influence of LA on IRI of the liver was determined in short- and long-term experiments. Cellular damage was decreased under preconditioning conditions with LA. Caspase 3, 8, and 9 activities were significantly lower in the LA group accompanied by a decrease in terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive hepatocytes. Electron micrographs in the untreated group showed massive mitochondrial damage. The survival rate as end point of liver function was markedly increased after pretreatment with LA. Increased levels of tumor necrosis factor alpha was shown by enzyme-linked immunosorbent assay as well as real-time reverse transcription-polymerase chain reaction in the LA group accompanied by increased mitotic index and Ki-67 staining in liver tissue. Attenuation of IRI of the rat liver in vivo by LA is accompanied by reduction of necrosis and apoptosis-related cell death, whereas liver regeneration is increased.

Protective effects of ischemic preconditioning and application of lipoic acid prior to 90 min of hepatic ischemia in a rat model.

AIM: To compare different preconditioning strategies to protect the liver from ischemia/reperfusion injury focusing on the expression of pro- and anti-apoptotic proteins. Interventions comprised different modes of ischemic preconditioning (IP) as well as pharmacologic pretreatment by alpha-lipoic acid (LA). METHODS: Several groups of rats were compared: sham operated animals, non-pretreated animals (nt), animals receiving IP (10 min of ischemia by clamping of the portal triad and 10 min of reperfusion) prior to sustained ischemia, animals receiving selective ischemic preconditioning (IPsel, 10 min of ischemia by selective clamping of the ischemic lobe and 10 min of reperfusion) prior to sustained ischemia, and animals receiving 500 micromol alpha-LA injected i.v. 15 min prior to the induction of 90 min of selective ischemia. RESULTS: Cellular damage was decreased only in the LA group. TUNEL-positive hepatocytes as well as necrotic hepatocyte injury were also decreased only by LA (19 +/- 2 vs 10 +/- 1, P < 0.05 and 29 +/- 5 vs 12 +/- 1, P < 0.05). Whereas caspase 3- activities in liver tissue were unchanged, caspase 9- activity in liver tissue was decreased only by LA pretreatment (3.1 +/- 0.3 vs 1.8 +/- 0.2, P < 0.05). Survival rate as the endpoint of liver function was increased after IP and LA pretreatment but not after IPsel. Levels of lipid peroxidation (LPO) in liver tissue were decreased in the IP as well as in the LA group compared to the nt group. Determination of pro- and anti-apoptotic proteins showed a shift towards anti-apoptotic proteins by LA. In contrast, both our IP strategies failed to influence apoptotic cell death. CONCLUSION: IP, consisting of 10 min of ischemia and 10 min of reperfusion, protects only partly against ischemia/reperfusion injury of the liver prior to 90 min of selective ischemia. IPsel did not influence ischemic tolerance of the liver. LA improved tolerance to ischemia, possibly by downregulation of pro-apoptotic Bax.

Reduction of ischemia reperfusion injury after liver resection and hepatic inflow occlusion by alpha-lipoic acid in humans.

AIM: To evaluate the protective effects of preconditioning by alpha-lipoic acid (LA) in patients undergoing hepatic resection under inflow occlusion of the liver. METHODS: Twenty-four patients undergoing liver resection for various reasons either received 600 mg LA or NaCl 15 min before transection performed under inflow occlusion of the liver. Blood samples and liver wedge biopsy samples were obtained after opening of the abdomen immediately after inflow occlusion of the liver, and 30 min after the end of inflow occlusion of the liver. RESULTS: Serum levels of aspartate transferase and alanine transferase were reduced at all time points in patients who received LA in comparison to those who received NaCL. This was accompanied by reduced histomorphological features of oncosis. We observed TUNEL-positive hepatocytes in the livers of the untreated patients, especially after 30 min of ischemia. LA attenuated this increase of TUNEL-positive hepatocytes. Under preconditioning with LA, ATP content was significantly enhanced after 30 min of ischemia and after 30 min of reperfusion. CONCLUSION: This is the first report on the potential for LA reducing ischemia/reperfusion injury (IRI) of the liver in humans who were undergoing liver surgery. Beside its simple and rapid application, side effects did not occur. LA might therefore represent a new strategy against hepatic IRI in humans.

A very rare cause of low-back pain and sciatica: deep vein thrombosis due to absence of the inferior vena cava mimicking the clinical and radiological signs of lumbar disc herniation.

The authors report a very rare cause of low-back pain and sciatica in a patient with iliac vein thrombosis attributed to absence of the infrarenal segment of the inferior vena cava (IVC) with massively dilated venous collaterals draining via a paraspinal plexus into the azygous system. This 21-year-old man presented with acute low-back pain radiating to the left ventral thigh. The initial CT scan revealed an intraspinal lesion that mimicked lumbar disc herniation. Further clarification revealed an iliac vein thrombosis, which was triggered by the absence of the infrarenal segment of the IVC, a very rare vascular anomaly. Collateral venous return was developed and led to lumbar varicosities and epidural vein engorgements. Laboratory examinations revealed factor V mutation as a predisposing factor for thrombosis. The patient's symptoms were relieved with anticoagulation and antiinflammatory therapy. Absence of the infrarenal IVC associated with iliac vein thrombosis should be regarded as a very rare cause of radicular and low-back pain, and this condition can mimic the clinical and radiological signs of lumbar disc herniation. Sciatica might be the first clinical manifestation of this rare venous anomaly.

Bcl-2 upregulation after 3-nitropropionic acid preconditioning in warm rat liver ischemia.

We aimed to determine whether 3-nitropropionic acid (3-NPA) preconditioning protects rat livers against warm ischemia/reperfusion injury. We hypothesized that 3-NPA mediates its protective effects by Bcl-2 upregulation. Brown-Norway rats (200 g) were injected with 3-NPA (10 mg/kg intraperitoneally) 24 h before 90 min of selective warm in situ ischemia. In additional experiments, 30-day survival was studied after 90 min of warm liver ischemia and resection of nonischemic liver tissue. We demonstrate increased mRNA and protein levels of Bcl-2 by real-time polymerase chain reaction, immunohistochemistry, and Western blot analysis in 3-NPA-pretreated rats. All treated animals survived, whereas all untreated rats died within 3 days after selective ischemia and resection of the nonischemic tissue. This corresponded well with a significant decrease of caspases 3 and 9 activity at 1 h of reperfusion after preconditioning with 3-NPA as compared with untreated rats. The histological sections showed protection of liver tissue after 3-NPA by reduction of apoptotic and oncotic tissue damage. Lipid peroxidation in liver tissue was reduced after 3-NPA preconditioning. We show that subtoxic doses of the mitochondrial toxin 3-NPA induces tolerance to warm liver ischemia in rats associated by synthesis of Bcl-2. Bcl-2 upregulation might protect against the postischemic burst of reactive oxygen species and therefore reduces apoptotic- and oncotic-related cell death.

Different protection mechanisms after pretreatment with glycine or alpha-lipoic acid in a rat model of warm hepatic ischemia.

BACKGROUND/AIM: Alpha-lipoic (LA) acid pretreatment has previously been described to reduce ischemia/reperfusion injury (IRI) after warm liver ischemia, whereas glycine pretreatment has been shown to be protective mostly in models of cold hepatic ischemia. The aim of this study was to determine whether glycine decreases IRI after warm hepatic ischemia. Furthermore we investigated whether doses of LA other than those used previously are also protective against IRI after warm hepatic ischemia. METHODS: Selective liver ischemia was maintained over a period of 90 min. In long-term as well as short-term experiments we studied IRI in several groups comparing animal survival as the pivotal endpoint. RESULTS: Animal survival was improved by glycine and 5,000 micromol LA, whereas all animals died within 3 days after pretreatment with 50 micromol LA. In the glycine group we observed a tendency towards decreased apoptosis-related cell death measured by the activity of caspase-3 in liver tissue and the percentage of TUNEL-positive hepatocytes in comparison to the untreated group. Serum alpha-glutathione S-transferase, lipid peroxidation, and caspase-3 activity as well as the percentage of TUNEL-positive hepatocytes and the percentage of liver necrosis were only significantly decreased by 5,000 micromol LA pretreatment. Liver tissue levels of tumor necrosis factor (TNF)alpha were reduced only in the glycine group whereas TNFalpha was increased in the untreated as well as the LA group. Levels of TNFalpha mRNA were upregulated in both the glycine- and LA-pretreated groups. CONCLUSION: Our data show that increased animal survival by glycine was accompanied by a reduced TNFalpha content in liver tissue. Protection by glycine is likely to result from a reduction in adverse TNFalpha effects. Administration of high-dose LA on the other hand led to a significant reduction in necrosis- and apoptosis-related cell death in IRI of the liver without a reduction in liver TNFalpha.