Hepatic T1-Time Predicts Cardiovascular Risk in All-Comers Referred for Cardiovascular Magnetic Resonance: A Post-Hoc Analysis.

BACKGROUND: Liver damage is frequently observed in patients with cardiovascular disease but infrequently quantified. We hypothesized that in patients with cardiovascular disease undergoing cardiac magnetic resonance, liver T1-times indicate liver damage and are associated with cardiovascular outcome. METHODS: We measured hepatic T1-times, displayed on standard cardiac T1-maps, in an all-comer cardiac magnetic resonance-cohort. At the time of cardiac magnetic resonance, we assessed validated general liver fibrosis scores. Kaplan-Meier estimates and Cox-regression models were used to investigate the association between hepatic T1-times and a composite endpoint of non-fatal myocardial infarction, heart failure hospitalization, and death. RESULTS: One thousand seventy-five participants (58±18 year old, 47% female) were included (972 patients, 50 controls, 53 participants with transient elastography). Hepatic T1-times were 590±89 ms in patients and 574±45 ms in controls (P=0.052). They were significantly correlated with cardiac size and function, presence of atrial fibrillation, NT-pro-BNP levels, and gamma-glutamyl-transferase levels (P<0.001 for all). During follow-up (58±31 months), a total of 280 (29%) events occurred. On Cox-regression, high hepatic T1-times yielded a significantly higher risk for events (adjusted hazard ratio, 1.66 [95% CI, 1.45-1.89] per 100 ms increase; P<0.001), even when adjusted for age, sex, left and right ventricular ejection fraction, NT-proBNP (N-terminal prohormone of brain natriuretic peptide), and myocardial T1-time. On receiver operating characteristic analysis and restricted cubic splines, we found that a hepatic T1-time exceeding 610 ms was associated with excessive risk. CONCLUSIONS: Hepatic T1-times on standard cardiac magnetic resonance scans were significantly associated with cardiac size and function, comorbidities, natriuretic peptides, and independently predicted cardiovascular mortality and morbidity. A hepatic T1-time >610 ms seems to indicate excessive risk. REGISTRATION: URL: https://www. CLINICALTRIALS: gov; Unique identifier: NCT04220450.

Comparison of Hepatic Tissue Characterization between T1-Mapping and Non-Contrast Computed Tomography.

Background: Non-contrast computed tomography (CT) is frequently used to assess non-alcoholic/metabolic fatty liver disease (NAFLD/MAFLD), which is associated with cardiovascular risk. Although liver biopsy is considered the gold standard for diagnosis, standardized scores and non-contrast computed tomography (CT) are used instead. On standard cardiac T1-maps on cardiovascular imaging (CMR) exams for myocardial tissue characterization hepatic tissue is also visible. We hypothesized that there is a significant correlation between hepatic tissue T1-times on CMR and Hounsfield units (HU) on non-contrast CT. Methods: We retrospectively identified patients undergoing a non-contrast CT including the abdomen, a CMR including T1-mapping, and laboratory assessment within 30 days. Patients with storage diseases were excluded. Results: We identified 271 patients (62 ± 15 y/o, 49% female) undergoing non-contrast CT and CMR T1-mapping within 30 days. Mean hepatic HU values were 54 ± 11 on CT and native T1-times were 598 ± 102 ms on CMR and there was a weak, but significant, correlation between these parameters (r = −0.136, p = 0.025). On age and sex adjusted regression analysis, lower liver HU values indicated a dismal cardiometabolic risk profile, including higher HbA1C (p = 0.005) and higher body mass index (p < 0.001). In contrast, native hepatic T1-times yielded a more pronounced cardiac risk profile, including impaired systolic function (p = 0.045) and higher NT-proBNP values (N-Terminal Brain Natriuretic Peptide) (p = 0.004). Conclusions: Hepatic T1-times are easy to assess on standard T1-maps on CMR but only weakly correlated with hepatic HU values on CT and clinical NAFLD/MAFLD scores. Liver T1-times, however, are linked to impaired systolic function and higher natriuretic peptide levels. The prognostic value and clinical usefulness of hepatic T1-times in CMR cohorts warrants further research.

Prognostic impact of sarcopenia in cirrhotic patients stratified by different severity of portal hypertension.

BACKGROUND AND AIMS: Portal hypertension (PH) and sarcopenia are common in patients with advanced chronic liver disease (ACLD). However, the interaction between PH and sarcopenia and their specific and independent impact on prognosis and mortality has yet to be systematically investigated in patients with ACLD. METHODS: Consecutive patients with ACLD and hepatic venous pressure gradient (HVPG) ≥10 mm Hg with available CT/MRI imaging were included. Sarcopenia was defined by transversal psoas muscle thickness (TPMT) at <12 mm/m in men and <8 mm/m in women at the level of the third lumbar vertebrae. Hepatic decompensation and mortality was recorded during follow-up. RESULTS: Among 203 patients (68% male, age: 55 ± 11, model for end-stage liver disease [MELD]: 12 [9-15]), sarcopenia was observed in 77 (37.9%) and HVPG was ≥20 mm Hg in 98 (48.3%). There was no correlation between TPMT and HVPG (r = .031, P = .66), median HVPG was not different between patients with vs without sarcopenia (P = .211). Sarcopenia was significantly associated with first/further decompensation both in compensated (SHR: 3.05, P = .041) and in decompensated patients (SHR: 1.86, P = .021). Furthermore, sarcopenia (SARC) was a significant predictor of mortality irrespective of HVPG (HVPG < 20-SARC: SHR: 2.25, P = .021; HVPG ≥ 20-SARC: SHR: 3.33, P = .001). On multivariate analysis adjusted for age, HVPG and MELD, sarcopenia was an independent risk factor for mortality (aHR: 1.99, 95% confidence interval: 1.2-3.3, P = .007). CONCLUSION: Sarcopenia has a major impact on clinical outcomes both in compensated and in decompensated ACLD patients. The presence of sarcopenia doubled the risk for mortality independently from the severity of PH.

Deep learning detection and quantification of pneumothorax in heterogeneous routine chest computed tomography.

BACKGROUND: Automatically detecting and quantifying pneumothorax on chest computed tomography (CT) may impact clinical decision-making. Machine learning methods published so far struggle with the heterogeneity of technical parameters and the presence of additional pathologies, highlighting the importance of stable algorithms. METHODS: A deep residual UNet was developed and evaluated for automated, volume-level pneumothorax grading (i.e., labelling a volume whether a pneumothorax was present or not), and pixel-level classification (i.e., segmentation and quantification of pneumothorax), on a retrospective series of routine chest CT data. Ground truth annotations were provided by radiologists. The fully automated pixel-level pneumothorax segmentation method was trained using 43 chest CT scans and evaluated on 9 chest CT scans with pixel-level annotation basis and 567 chest CT scans on a volume-level basis. RESULTS: This method achieved a receiver operating characteristic area under the curve (AUC) of 0.98, an average precision of 0.97, and a Dice similarity coefficient (DSC) of 0.94. This segmentation performance resulted to be similar to the inter-rater segmentation accuracy of two radiologists, who achieved a DSC of 0.92. The comparison of manual and automated pneumothorax quantification yielded a Pearson correlation coefficient of 0.996. The volume-level pneumothorax grading accuracy was evaluated on 567 chest CT scans and yielded an AUC of 0.98 and an average precision of 0.95. CONCLUSIONS: We proposed a deep learning method for the detection and quantification of pneumothorax in heterogeneous routine clinical data that may facilitate the automated triage of urgent examinations and enable treatment decision support.

The value of different CT-based methods for diagnosing low muscle mass and predicting mortality in patients with cirrhosis.

BACKGROUND & AIMS: Low muscle mass impacts on morbidity and mortality in cirrhosis. The skeletal-muscle index (SMI) is a well-validated tool to diagnose muscle wasting, but requires specialized radiologic software and expertise. Thus, we compared different Computed tomography (CT)-based evaluation methods for muscle wasting and their prognostic value in cirrhosis. METHODS: Consecutive cirrhotic patients included in a prospective registry undergoing abdominal CT scans were analysed. SMI, transversal psoas muscle thickness (TPMT), total psoas volume (TPV) and paraspinal muscle index (PSMI) were measured. Sarcopenia was defined using SMI as a reference method by applying sex-specific cut-offs (males: <52.4 cm2 /m2 ; females: <38.5 cm2 /m2 ). RESULTS: One hundred and nine patients (71.6% male) of age 57 ± 11 years, MELD 16 (8-26) and alcoholic liver disease (63.3%) as the main aetiology were included. According to established SMI cut-offs, low muscle mass was present in 69 patients (63.3%) who also presented with higher MELD (17 vs 14 points; P = .025). The following optimal sex-specific cut-offs (men/women) for diagnosing low muscle mass were determined: TPMT: <10.7/ <7.8 mm/m, TPV: <194.9/ <99.2 cm3 and PSMI <26.3/ <20.8 cm2 /m2 . Thirty (27.5%) patients died during a follow-up of 15 (0.3-45.7) months. Univariate competing risks analyses showed a significant risk for mortality according to SMI (aSHR:2.52, 95% CI: 1.03-6.21, P = .043), TPMT (aSHR: 3.87, 95% CI: 1.4-8.09, P = .007) and PSMI (aSHR: 2.7, 95% CI: 1.17-6.23, P = .02), but not TPV (P = .18) derived low muscle mass cut-offs. In multivariate analysis only TPMT (aSHR: 2.82, 95% CI: 1.20-6.67, P = .018) was associated with mortality, SMI (aSHR: 1.93, 95% CI: 0.72-5.16, P = .19) and PSMI (aSHR: 1.93, 95% CI: 0.79-4.75, P = .15) were not. CONCLUSION: Low muscle mass was highly prevalent in our cohort of patients with cirrhosis. Gender-specific TPMT, SMI and PSMI cut-offs for low muscle mass can help identify patients with an increased risk for mortality. Importantly, only TPMT emerged as an independent risk factor for mortality in patients with cirrhosis.

Dysbalanced sex hormone status is an independent predictor of decompensation and mortality in patients with liver cirrhosis.

AIMS: Endocrinological abnormalities, including low testosterone levels, are prevalent in cirrhosis. We assessed sexual hormone status in regard to hemodynamic abnormalities and its impact on hepatic decompensation and survival. METHODS: Males with cirrhosis were prospectively included in this study since 2010. Sexual hormones including bioavailable testosterone, total testosterone, luteinizing hormone, follicle-stimulating hormone, prolactin, and sex hormone-binding globulin as well as Child-Pugh score, Model for End-stage Liver Disease (MELD) score, and hepatic venous pressure gradient were recorded. Sarcopenia was also assessed in patients with available computed tomography scans. Clinical follow-up for hepatic decompensation, liver transplantation, and death was recorded until May 2017. RESULTS: One hundred fourteen male cirrhotic patients were included: age 55 ± 9.4 years, MELD 13.5 (range, 7-20.7). Etiologies were alcoholic liver disease in 61(53.5%) patients, viral in 30 (26.3%) patients, and other in 23 (20.2%). Child-Pugh scores were A in 32 (28.1%) patients, B in 48 (42.1%), and C in 34 (29.8%). Levels of bioavailable testosterone and total testosterone decreased with advanced Child-Pugh score (P < 0.001 and P < 0.001) whereas prolactin increased (P = 0.002). Median bioavailable testosterone (0.8 ng/mL [0.1-2] vs. 1.68 ng/mL [0.07-2.65]; P = 0.004) and total testosterone (2.7 ng/mL [0.23-12.34] vs. 7 ng/mL [0.25-10]; P = 0.041) levels were lower in patients with severe portal hypertension (hepatic venous pressure gradient >12 mmHg). Median bioavailable testosterone (0.25 ng/mL [0.07-1.7] vs. 0.97 ng/mL [0.15-2.74)]; P = 0.017) and total testosterone levels (1.28 ng/mL [0.25-7.32] vs. 4.32 ng/mL [0.43-13.47]; P = 0.031) were significantly lower in sarcopenic patients. Median follow-up was 13 months (0.2-75 months) and liver-related events were recorded in 46 patients (40.4%; death, 31 [27.2%]). Low total testosterone was associated with an increased risk for hepatic decompensation and/or death, even after adjusting for Child-Pugh score, MELD, and other relevant factors (Child-Pugh score model: hazard ratio 2.503, 95% confidence interval, 1.214-5.157, P = 0.013; MELD model: hazard ratio 3.065, 95% confidence interval, 1.523-6.169, P = 0.002). CONCLUSION: In parallel to increasing severity of cirrhosis, levels of testosterone decline whereas prolactin levels increase. However, low testosterone levels are independently associated with a higher risk for hepatic decompensation and mortality.

Influence of Contrast Media on Bone Mineral Density (BMD) Measurements from Routine Contrast-Enhanced MDCT Datasets using a Phantom-less BMD Measurement Tool.

Aim To evaluate the differences in phantom-less bone mineral density (BMD) measurements in contrast-enhanced routine MDCT scans at different contrast phases, and to develop an algorithm for calculating a reliable BMD value. Materials and Methods 112 postmenopausal women from the age of 40 to 77 years (mean age: 57.31 years; SD 9.61) who underwent a clinically indicated MDCT scan, consisting of an unenhanced, an arterial, and a venous phase, were included. A retrospective analysis of the BMD values of the Th12 to L4 vertebrae in each phase was performed using a commercially available phantom-less measurement tool. Results The mean BMD value in the unenhanced MDCT scans was 79.76 mg/cm³ (SD 31.20), in the arterial phase it was 85.09 mg/cm³ (SD 31.61), and in the venous phase it was 86.18 mg/cm³ (SD 31.30). A significant difference (p < 0.001) was found between BMD values on unenhanced and contrast-enhanced MDCT scans. There was no significant difference between BMD values in the arterial and venous phases (p = 0.228). The following conversion formulas were calculated using linear regression: unenhanced BMD = -2.287 + 0.964 * [arterial BMD value] and -4.517 + 0.978 * [venous BMD value]. The intrarater agreement of BMD measurements was calculated with an intraclass correlation (ICC) of 0.984 and the interobserver reliability was calculated with an ICC of 0.991. Conclusion Phantom-less BMD measurements in contrast-enhanced MDCT scans result in increased mean BMD values, but, with the formulas applied in our study, a reliable BMD value can be calculated. However, the mean BMD values did not differ significantly between the arterial and venous phases. Key points · BMD can be assessed on routine CT scans using a phantom-less tool.. · i. v. contrast agent significantly elevates BMD values measured on routine CT scans.. · BMD values measured in the arterial and venous phase did not differ significantly.. · Conversion formulas were defined for the calculation of a reliable BMD.. · The phantom-less tool showed good reliability and is a promising method.. Citation Format · Toelly A, Bardach C, Weber M et al. Influence of Contrast Media on Bone Mineral Density (BMD) Measurements from Routine Contrast-Enhanced MDCT Datasets using a Phantom-less BMD Measurement Tool. Fortschr Röntgenstr 2017; 189: 537 - 543.