ObjectivesCardiac magnetic resonance (CMR) was used to investigate the extracellular compartment and myocardial fibrosis in patients with aortic stenosis, as well as their association with other measures of left ventricular decompensation and mortality.BackgroundProgressive myocardial fibrosis drives the transition from hypertrophy to heart failure in aortic stenosis. Diffuse fibrosis is associated with extracellular volume expansion that is detectable by T1 mapping, whereas late gadolinium enhancement (LGE) detects replacement fibrosis.MethodsIn a prospective observational cohort study, 203 subjects (166 with aortic stenosis [69 years; 69% male]; 37 healthy volunteers [68 years; 65% male]) underwent comprehensive phenotypic characterization with clinical imaging and biomarker evaluation. On CMR, we quantified the total extracellular volume of the myocardium indexed to body surface area (iECV). The iECV upper limit of normal from the control group (22.5 ml/m2) was used to define extracellular compartment expansion. Areas of replacement mid-wall LGE were also identified. All-cause mortality was determined during 2.9 ± 0.8 years of follow up.ResultsiECV demonstrated a good correlation with diffuse histological fibrosis on myocardial biopsies (r = 0.87; p < 0.001; n = 11) and was increased in patients with aortic stenosis (23.6 ± 7.2 ml/m2 vs. 16.1 ± 3.2 ml/m2 in control subjects; p < 0.001). iECV was used together with LGE to categorize patients with normal myocardium (iECV <22.5 ml/m2; 51% of patients), extracellular expansion (iECV ≥22.5 ml/m2; 22%), and replacement fibrosis (presence of mid-wall LGE, 27%). There was evidence of increasing hypertrophy, myocardial injury, diastolic dysfunction, and longitudinal systolic dysfunction consistent with progressive left ventricular decompensation (all p < 0.05) across these groups. Moreover, this categorization was of prognostic value with stepwise increases in unadjusted all-cause mortality (8 deaths/1,000 patient-years vs. 36 deaths/1,000 patient-years vs. 71 deaths/1,000 patient-years, respectively; p = 0.009).ConclusionsCMR detects ventricular decompensation in aortic stenosis through the identification of myocardial extracellular expansion and replacement fibrosis. This holds major promise in tracking myocardial health in valve disease and for optimizing the timing of valve replacement. (The Role of Myocardial Fibrosis in Patients With Aortic Stenosis; NCT01755936)
Lung cancer is the most common cause of death from cancer in males, accounting for more than 1.4 million deaths in 2008. It is a growing concern in China, Asia and Africa as well. Accurate staging of the disease is an important part of the management as it provides estimation of patient's prognosis and identifies treatment sterategies. It also helps to build a database for future staging projects. A major revision of lung cancer staging has been announced with effect from January 2010. The new classification is based on a larger surgical and non-surgical cohort of patients, and thus more accurate in terms of outcome prediction compared to the previous classification. There are several original papers regarding this new classification which give comprehensive description of the methodology, the changes in the staging and the statistical analysis. This overview is a simplified description of the changes in the new classification and their potential impact on patients' treatment and prognosis.
Lung cancer is the leading cause of cancer death in both men and women. Clinical staging plays a crucial role in predicting survivor as well as influencing management option in lung cancer patients. Guidelines are constantly being reviewed as more data becomes available to provide the most accurate prognostic markers, hence aiding in the clinical detection and staging of lung cancer. Since its introduction in the 1970s, the TNM staging has undergone significant revisions with the latest, 8 edition, being effective internationally from 2018. This edition re-categorizes the tumour size and other non-quantitative tumour descriptors (T), and further subclassifies extra-thoracic metastases (M). The clinical nodal (N) classifier is unchanged as the earlier version correlates well with prognosis. The downstream effects on staging to accommodate for the new T and M classifications are highlighted. The survival is inversely proportional to every centimeter increase in tumour size up till 7 cm, where the same prognosis as a T4 disease is reached. Hence, some of the T-classifiers based on size of the tumour is upstaged to reflect that. Invasion of the diaphragm is considered T4 instead of T3. On the other hand, involvement of the main bronchus regardless of tumour distance to carina as well as atelectasis is down-staged from a T3 to a T2 disease. Since the 7 edition, new entities of lung tumour known as adenocarcinoma in situ (AIS) and minimally invasive adenocarcinoma (MIA) have been introduced. The T-defining features are also described in this manuscript. Extrathoracic metastases that were classified as M1b in the 7 edition is further subcategorized into M1b and M1c in the 8 edition, to better define oligometastasis which has a better prognosis, and may benefit from more aggressive local therapy. This overview aims to provide radiologists with a description of the changes in the latest edition including staging of subsolid and multiple nodules, outline potential limitations of this 8 edition, as well as discussion on the implications on treatment.
BackgroundMRI of the lung is recommended in a number of clinical indications. Having a non-radiation alternative is particularly attractive in children and young subjects, or pregnant women.MethodsProvided there is sufficient expertise, magnetic resonance imaging (MRI) may be considered as the preferential modality in specific clinical conditions such as cystic fibrosis and acute pulmonary embolism, since additional functional information on respiratory mechanics and regional lung perfusion is provided. In other cases, such as tumours and pneumonia in children, lung MRI may be considered an alternative or adjunct to other modalities with at least similar diagnostic value.ResultsIn interstitial lung disease, the clinical utility of MRI remains to be proven, but it could provide additional information that will be beneficial in research, or at some stage in clinical practice. Customised protocols for chest imaging combine fast breath-hold acquisitions from a “buffet” of sequences. Having introduced details of imaging protocols in previous articles, the aim of this manuscript is to discuss the advantages and limitations of lung MRI in current clinical practice.ConclusionNew developments and future perspectives such as motion-compensated imaging with self-navigated sequences or fast Fourier decomposition MRI for non-contrast enhanced ventilation- and perfusion-weighted imaging of the lung are discussed.Main Messages• MRI evolves as a third lung imaging modality, combining morphological and functional information.• It may be considered first choice in cystic fibrosis and pulmonary embolism of young and pregnant patients.• In other cases (tumours, pneumonia in children), it is an alternative or adjunct to X-ray and CT.• In interstitial lung disease, it serves for research, but the clinical value remains to be proven.• New users are advised to make themselves familiar with the particular advantages and limitations.
This study aimed to produce an acellular human tissue scaffold with a view to recellularization with autologous cells to produce a tissue-engineered pericardium that can be used as a patch for cardiovascular repair. Human pericardia from cadaveric donors were treated sequentially with hypotonic buffer, SDS in hypotonic buffer, and a nuclease solution. Histological analysis of decellularized matrices showed that the human pericardial tissue retained its histioarchitecture and major structural proteins. There were no whole cells or cell fragments. There were no significant differences in the hydroxyproline (normal and denatured collagen) and glycosaminoglycan content of the tissue before and after decellularization (p > 0.05). There were no significant changes in the ultimate tensile strength after decellularization (p > 0.05). However, there was an increased extensibility when the tissue strips were cut parallel to the visualized collagen bundles (p = 0.005). No indication of contact or extract cytotoxicity was found when using human dermal fibroblasts and A549 cells. In summary, successful decellularization of the human pericardium was achieved producing a biocompatible matrix that retained the major structural components and strength of the native tissue.
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