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1.
F P Junqueira C M A O Lima A C Coutinho Jr D B Parente L K Bittencourt L G P Bessa R C Domingues E Marchiori 《The British journal of radiology》2012,85(1019):1446-1456
Pulmonary hypertension (PH) is a progressive disease that leads to substantial morbidity and eventual death. Pulmonary multidetector CT angiography (MDCTA), pulmonary MR angiography (MRA) and MR-derived pulmonary perfusion (MRPP) imaging are non-invasive imaging techniques for the differential diagnosis of PH. MDCTA is considered the gold standard for the diagnosis of pulmonary embolism, one of the most common causes of PH. MRA and MRPP are promising techniques that do not require the use of ionising radiation or iodinated contrast material, and can be useful for patients for whom such material cannot be used. This review compares the imaging aspects of pulmonary MRA and 64-row MDCTA in patients with chronic thromboembolic or idiopathic PH.Pulmonary hypertension (PH) is an insidious and progressive disease that leads to substantial morbidity and eventual death. PH results from a number of diseases with different physiopathologies, treatments and prognoses [1]. One of the most frequent causes of PH is chronic thromboembolic pulmonary hypertension (CTEPH).The current classification of PH (2], resulted from a review of the previous classification developed at the 2003 3rd World Symposium in Venice, Italy. During the 4th World Symposium on PH, an international group of experts agreed to maintain the general philosophy and organisation of the Evian–Venice classifications. However, in response to a questionnaire regarding the previous classification, a majority (63%) of experts felt that modification of the Venice classification was required to accurately reflect information published in the past 5 years and to provide clarification in some areas [2].
Open in a separate windowPH is a clinical and haemodynamic syndrome that results in increased vascular resistance in the pulmonary circulation, usually by a combination of mechanisms involving vasoconstriction and remodelling of the small vessels [3]. Haemodynamically, it is defined as a systolic pulmonary artery pressure of >35 mmHg, or a mean pulmonary artery pressure of >25 mmHg at rest or >30 mmHg with exertion [4,5]. An increase in pulmonary vascular resistance and subsequent compensatory right ventricular (RV) hypertrophy lead to elevated pulmonary pressure, which often results in increased RV afterload and failure. The disorder is progressive, leading to right heart failure and death within a median of 2.8 years after diagnosis [6,7].The development of RV failure in patients with pulmonary arterial hypertension (PAH) is an ominous sign with major adverse prognostic implications. Patients with severe PAH or right heart failure die usually within 1 year without treatment. In the National Institutes of Health registry, approximately 50% of deaths in patients with PAH are attributed to RV failure [6]. Numerous factors may indicate a poor prognosis in patients with PAH and secondary RV failure, including age >45 years at presentation, New York Heart Association (NYHA) Class III or IV functional classification, failure to improve to a lower NYHA class during treatment, pericardial effusion, large right atrial size, elevated right atrial pressure, septal shift during diastole, decreased pulmonary arterial capacitance (stroke volume/pulmonary arterial pulse pressure), increased N-terminal brain natriuretic peptide level and hypocapnia [8,9].Because patients with PH often present with non-specific symptoms, such as shortness of breath on minimal physical exertion, fatigue, chest pain and fainting, diagnosis often occurs late in the course of the disease, when the prognosis is poor and treatment options are limited [10]. A complete diagnostic evaluation includes a medical history, physical examination, pulmonary function tests, electrocardiogram, echocardiogram, cardiac catheterisation and advanced imaging. Invasive haemodynamic evaluation is mandatory, not only to confirm the diagnosis but also to address the prognosis and the patient''s eligibility for the use of calcium channel blockers through an acute vasodilator challenge. Non-invasive surrogate response markers to the acute vasodilator test have been sought. In other studies, mean pulmonary artery distensibility (mPAD) has been evaluated using MRI to assess pulmonary haemodynamics and diagnose pulmonary vascular disease [11,12]. The mPAD may reflect the degree of vascular remodelling, making it a very interesting marker for the evaluation of patients with idiopathic PAH (IPAH) [13]. Jardim et al [14] found that the cardiac index, calculated after the determination of cardiac output using MRI and pulmonary artery catheterisation, showed excellent correlation, as did right atrial pressure and the RV ejection fraction. They also found that PAD was significantly higher in acute vasodilator test responders. A receiver operating characteristic curve analysis has shown that 10% distensibility can be used to differentiate responders from non-responders with 100% sensitivity and 56% specificity. This study suggested that MRI and PAD may be useful non-invasive tools for the evaluation of patients with PH. In some cases, definitive diagnosis requires a thoracoscopic lung biopsy [3]. Because CTEPH differs considerably from other forms of PH and may be treated surgically, an accurate diagnosis is essential [15].The depiction of occluding thrombotic material and concomitant perfusion defects is a prerequisite for the correct and reliable diagnosis of CTEPH. Until recently, pulmonary perfusion could be assessed only by using radionuclide perfusion scintigraphy and conventional pulmonary angiography. The former technique has substantial limitations with respect to spatial and temporal resolution, and the latter requires invasive catheterisation of the right side of the heart and produces only two-dimensional projection images [16].Pulmonary multidetector CT angiography (MDCTA), pulmonary MR angiography (MRA), and MR-derived pulmonary perfusion (MRPP) are non-invasive imaging techniques used to assess PH-related pulmonary vessel changes in the differential diagnosis [16]. MDCTA is considered the gold standard for the diagnosis of CTEPH because it depicts the occluding thrombotic material and concomitant lung changes [16]. However, the combined use of MRA and MRPP allows the evaluation of PH-related pulmonary vessel changes and concomitant perfusion defects without ionising radiation or iodinated contrast material, and can be useful for patients in whom such material cannot be used. Few studies to date have sought to determine the accuracy of MRA in distinguishing the various causes of PH [16-18].MRI also contributes to the cardiac evaluation of patients with PH. Cardiac MRI is the gold standard technique for the assessment of ventricular function and the quantification of volumes and mass without geometric assumptions [19]. Recently, myocardial delayed enhancement after the intravenous administration of a gadolinium-based contrast agent has been shown at the insertion points of the RV free wall in the interventricular septum in patients with PAH and impaired ventricular function [20]. McCann et al [21] also suggested that the extent of hyperenhancement was not correlated with any clinical or haemodynamic variable, but was inversely correlated with RV dysfunction measured on cardiac MRI.This review aims to compare the imaging aspects of pulmonary MRA and 64-row MDCTA in patients with CTEPH and IPAH, and to highlight the main differences between these techniques. Patients with other forms of PH are not considered here because CT is superior to MRI for the evaluation of lung parenchyma. 相似文献
Table 1
Classification of pulmonary hypertension according to the 4th World Symposium, Dana Point, CA, 2008 [2]1. Pulmonary arterial hypertension (PAH) |
1.1. Idiopathic PAH |
1.2. Heritable PAH |
1.2.1. Bone morphogenetic protein receptor type 2 |
1.2.2. Activin receptor-like kinase type 1 (ALK1) |
ALK1, endoglin (with or without hereditary haemorrhagic telangiectasia) |
1.2.3. Unknown |
1.3. Drug- and toxin-induced |
1.4. Associated with: |
1.4.1. Connective tissue diseases |
1.4.2. HIV infection |
1.4.3. Portal hypertension |
1.4.4. Congenital heart diseases |
1.4.5. Schistosomiasis |
1.4.6. Chronic haemolytic anaemia |
1.5. Persistent neonatal pulmonary hypertension |
1′. Pulmonary veno-occlusive disease and/or pulmonary capillary haemangiomatosis |
2. Pulmonary hypertension due to left heart disease |
2.1. Systolic dysfunction |
2.2. Diastolic dysfunction |
2.3. Valvular disease |
3. Pulmonary hypertension due to lung diseases and/or hypoxia |
3.1. Chronic obstructive pulmonary disease |
3.2. Interstitial lung disease |
3.3. Other pulmonary diseases with mixed restrictive and obstructive pattern |
3.4. Sleep-disordered breathing |
3.5. Alveolar hypoventilation disorders |
3.6. Chronic exposure to high altitude |
3.7. Developmental abnormalities |
4. Chronic thromboembolic pulmonary hypertension |
5. Pulmonary hypertension with unclear multifactorial mechanisms |
5.1. Haematological disorders: myeloproliferative disorders, splenectomy |
5.2. Systemic disorders: sarcoidosis, pulmonary Langerhans cell histiocytosis, lymphangioleiomyomatosis, neurofibromatosis, vasculitis |
5.3. Metabolic disorders: glycogen storage disease, Gaucher disease, thyroid disorders |
5.4. Other: tumoral obstruction, fibrosing mediastinitis, chronic renal failure on dialysis |
2.
3.
M E Miquel A D Scott N D Macdougall R Boubertakh N Bharwani A G Rockall 《The British journal of radiology》2012,85(1019):1507-1512
Objective
To study the in vitro and in vivo (abdomen) variability of apparent diffusion coefficient (ADC) measurements at 1.5 T using a free-breathing multislice diffusion-weighted (DW) MRI sequence.Methods
DW MRI images were obtained using a multislice spin-echo echo-planar imaging sequence with b-values=0, 100, 200, 500, 750 and 1000 s mm−2. A flood-field phantom was imaged at regular intervals over 100 days, and 10 times on the same day on 2 occasions. 10 healthy volunteers were imaged on two separate occasions. Mono-exponential ADC maps were fitted excluding b=0. Paired analysis was carried out on the liver, spleen, kidney and gallbladder using multiple regions of interest (ROIs) and volumes of interest (VOIs).Results
The in vitro coefficient of variation was 1.3% over 100 days, and 0.5% and 1.0% for both the daily experiments. In vivo, there was no statistical difference in the group mean ADC value between visits for any organ. Using ROIs, the coefficient of reproducibility was 20.0% for the kidney, 21.0% for the gallbladder, 24.7% for the liver and 28.0% for the spleen. For VOIs, values fall to 7.7%, 6.4%, 8.6% and 9.6%, respectively.Conclusion
Good in vitro repeatability of ADC measurements provided a sound basis for in vivo measurement. In vivo variability is higher and when considering single measurements in the abdomen as a whole, only changes in ADC value greater than 23.1% would be statistically significant using a two-dimensional ROI. This value is substantially lower (7.9%) if large three-dimensional VOIs are considered.Diffusion-weighted (DW) MRI is based on the Brownian motion of water in biological tissues [1,2]. The technique has played a preponderant role in neuro-imaging over the last two decades and it is known to detect small changes before they are apparent on anatomical imaging [3,4].In recent years DW MRI has been increasingly used in other parts of the body, demonstrating great diagnostic potential in cancer imaging. To date, DW MRI has been successfully used for tissue characterisation and tumour staging. However, the apparent diffusion coefficient (ADC) is a potential biomarker that could be used to monitor treatment response or evaluate post-therapeutic changes. Details of the clinical use of DW MRI can be found in the 2009 consensus paper [5] or in general and organ-specific review articles [6-8].While DW MRI is a potentially powerful tool in diagnostic oncology, the lack of uniform protocols for imaging and data analysis hinder its clinical implementation. Large differences in ADC values are reported in the literature depending on the acquisition parameters, in particular the choice of b-values (e.g. see [9] for ADC values in the kidney or 5] highlighted the importance of quality analysis, validation and reproducibility studies. Although there are some emerging reproducibility and repeatability data in the abdomen [15,19-22], a recent review by Taouli and Koh [7] highlights the need for further work in this area. Recently, coefficients of variability of around 14% were published for both solid tumours [22] and bone marrow [23]. Other studies seem to indicate that only ADC changes of over 27% [20] or 30% [21] are significant. Substantial variations in ADC values have also been found between different scanners and vendors [24-26], further highlighting the difficulty of setting up multicentre trials.Table 1
Apparent diffusion coefficient values measured in normal liver at 1.5 TReference | Mean ADC (10−3 mm2 s−1) | Standard deviation | Range | Number of subjects | b-values (s mm−2) | Comments |
Taouli et al [10] | 1.60 | 0.13 | 1.44–1.88 | 10 v | 0, 500 | Conventional |
1.52 | 0.15 | 1.28–180 | With parallel imaging | |||
1.51 | 0.21 | 1.27–1.99 | Diffusion tensor/parallel imaging | |||
Mürtz et al [11] | 0.92–0.96a | 0.09–0.14 | 0.62–1.20 | 12 v | 50, 300, 700, 1000, 1300 | Pulse triggered |
1.03–1.14 | 0.22–0.40 | 0.67–2.57 | Non-triggered | |||
Kim et al [12] | 1.05/1.02b | 0.30/0.25 | 6 v/126 p | 3, 57, 192, 408, 517, 850 | ||
1.55/1.16 | 0.37/0.42 | 3, 57, 192, 408, 192, 408 | ||||
4.8/3.55 | 2.37/1.75 | 3, 57 | ||||
Ichikawa et al [13] | 2.28 | 1.23 | 46 p | 1.6, 55 | ||
Taouli et al [14] | 1.83 | 0.36 | 1.4–2.55 | 66 p | 0, 500 | |
1.51 | 0.49 | 1.12–2.71 | 0, 134, 267, 400 | |||
Kwee et al [15] | 1.60/1.62/1.57c | 0.14/0.18/0.15 | 11 v | 0, 500 | Breath-hold | |
2.13/2.27/2.07 | 0.33/0.47/0.43 | Respiratory triggered | ||||
1.65/1.62/1.65 | 0.09/0.16/0.17 | Free breathing (7 mm slice) | ||||
1.64/1.66/1.57 | 0.13/0.11/0.19 | Free breathing (5 mm slice) | ||||
Yamada et al [16] | 0.87 | 0.26 | 78 p | 30, 300, 900,1100 | ADC | |
0.76 | 0.27 | Diffusion coefficient (DC) | ||||
Müller et al [17] | 1.39 | 0.16 | 10 v+9 p | 8 b-values; bmax 328–454 | ||
Namimato et al [18] | 0.69 | 0.31 | 51 p | 30, 1200 | ||
This study | 1.04 | 0.05 | 0.95–1.11 | 10 v | 100, 200, 500, 750, 1000 | Free breathing |
4.
Non-cutaneous melanomas (NCM) are diverse and relatively uncommon. They often differ from cutaneous melanomas in their epidemiology, genetic profile and biological behaviour. Despite the growing body of evidence regarding the utility of positron emission tomography (PET)/CT in cutaneous melanoma, the data on its use in NCM are scarce. In this review, we will summarize the existing literature and present cases from our experience with NCM to illustrate current knowledge on the potential role and limitations of fluorine-18 fludeoxyglucose PET/CT in NCM.Non-cutaneous melanomas (NCM) are classified according to origin: ocular, mucosal or unknown primary. Ocular melanomas may arise from the uvea or conjunctiva. Mucosal melanomas may originate from mucosal surfaces in the head and neck (oral cavity, nasal and paranasal sinuses) and gastrointestinal and genitourinary tracts. NCM are relatively rare, with ocular and mucosal melanomas accounting for only 5.5% and 1.3% of all melanomas in North America, respectively. The incidence of mucosal melanoma may vary according to the population studied (range, 0.2–10.0%) and is higher in Asian populations. By contrast, uveal melanomas are more common in Caucasians. 1,2 Staging and management of NCM varies by location and differs from cutaneous melanoma. In NCM, primary therapy consists of local resection, often with adjuvant radiotherapy. There may be a role for chemotherapy and immunotherapy; however, this approach has largely been extrapolated from experience with cutaneous tumours.
Open in a separate windowBRAF, v-raf murine sarcoma viral oncogene homologue B; C-Kit, receptor tyrosine kinase for stem cell factor; UIACC, Union for International Cancer Control. 相似文献
Table 1.
Comparison of cutaneous and non-cutaneous melanoma1,2Patient/tumour characteristics | Cutaneous | Non-cutaneous |
---|---|---|
Age (years) | 55 | 67 |
Ultraviolet light association | Yes | No clear association |
Incidence over time | Increasing | Stable |
Distant metastases at presentation | 12% | Ocular, 3%; mucosal, 23% |
Staging scheme | UIACC/American Joint Committee on Cancer and TNM | No single validated system |
Genetic profile | ||
C-Kit mutations | 1.7% | 15.6% (mucosal) |
BRAF mutations | Common | Rare |
5-year survival | 80% | Ocular, 74.6%; mucosal, 23%; unknown primary, 29.1% |
5.
R Girometti G Brondani L Cereser G Como M Del Pin M Bazzocchi C Zuiani 《The British journal of radiology》2010,83(988):351-361
Post-cholecystectomy syndrome (PCS) is defined as a complex of heterogeneous symptoms, consisting of upper abdominal pain and dyspepsia, which recur and/or persist after cholecystectomy. Nevertheless, this term is inaccurate, as it encompasses biliary and non-biliary disorders, possibly unrelated to cholecystectomy. Biliary manifestations of PCS may occur early in the post-operative period, usually because of incomplete surgery (retained calculi in the cystic duct remnant or in the common bile duct) or operative complications, such as bile duct injury and/or bile leakage. A later onset is commonly caused by inflammatory scarring strictures involving the sphincter of Oddi or the common bile duct, recurrent calculi or biliary dyskinesia. The traditional imaging approach for PCS has involved ultrasound and/or CT followed by direct cholangiography, whereas manometry of the sphincter of Oddi and biliary scintigraphy have been reserved for cases of biliary dyskinesia. Because of its capability to provide non-invasive high-quality visualisation of the biliary tract, magnetic resonance cholangiopancreatography (MRCP) has been advocated as a reliable imaging tool for assessing patients with suspected PCS and for guiding management decisions. This paper illustrates the rationale for using MRCP, together with the main MRCP biliary findings and diagnostic pitfalls.Post-cholecystectomy syndrome (PCS) consists of a group of abdominal symptoms that recur and/or persist after cholecystectomy [1, 2]. It is defined as early if occurring in the post-operative period and late if it manifests after months or years.Although this term is used widely, it is not completely accurate, as it includes a large number of disorders, both biliary (1, 2]. It has been reported that ∼50% of these patients suffer from organic pancreaticobiliary and/or gastrointestinal disorders, whereas the remaining patients are affected by psychosomatic or extra-intestinal diseases. Moreover, in 5% of patients who undergo laparoscopic cholecystectomy, the reason for chronic abdominal pain remains unknown [1]. Probably because of the uncertainty in nosographic definition, the reported prevalence of PCS ranges from very low [2] to 47% [1]. Symptoms include biliary or non-biliary-like abdominal pain, dyspepsia, vomiting, gastrointestinal disorders and jaundice, with or without fever and cholangitis [1, 2]. Severe symptoms are more likely to represent a complication of cholecystectomy if they occur early or to express a definite treatable cause when compared with non-specific, dyspeptic or mild symptoms. A non-biliary aetiology of PCS should be suspected if no calculi or gallbladder abnormalities are found at cholecystectomy and symptoms are similar to those suffered pre-operatively [1]. Treatment for PCS is tailored to the specific cause and includes medication, sphincterotomy, biliary stenting, percutaneous drainage of bilomas and surgical revision for severe strictures [1–4].
Open in a separate window
Open in a separate windowThe traditional imaging approach to PCS includes ultrasonography and/or CT, followed by direct cholangiography, as the gold standard [2]. Biliary scintigraphy has been advocated as a reliable non-invasive tool to evaluate sphincter of Oddi activity. Nevertheless, it has limited diagnostic accuracy compared with sphincter of Oddi manometry (SOM), which represents the gold standard for assessing functional forms of PCS [5]. Magnetic resonance cholangiopancreatography (MRCP) is a non-invasive and reliable alternative to direct cholangiography for the evaluation of the biliary tract. This has led to an increasing demand for MRCP to be used in patients with suspected PCS, despite the fact that its role in patient management has been assessed only briefly [1, 2]. The main advantages of using MRCP are its non-invasiveness and its capability to provide a road-map for interventional treatments [1–4]. Heavily T2 weighted images with a high bile duct-to-background contrast may be obtained either with a set of single breath-hold, single-shot turbo spin-echo projective thick slabs or by using a respiratory-triggered three-dimensional (3D) turbo spin-echo sequence for a detailed representation of the biliary tree, together with multiplanar reformations and volumetric reconstructions [2–4]. Alternatives to the standard MRCP techniques include the use of fat-saturated 3D spoiled gradient-echo sequences in conjunction with intravenous contrast agents excreted (to a varying degree) via the biliary system, such as mangafodipir trisodium, gadobenate dimeglumine or gadoxetic acid. Advantages over fluid-based techniques include biliary function assessment, background suppression of ascites and bowel fluid, and identification of biliary leaks following cholecystectomy, with a reported sensitivity and specificity of 86% and 83%, respectively (Figure 1) [6].Open in a separate windowFigure 1A 31-year-old female patient presenting with right upper abdominal pain 1 week after laparoscopic cholecystectomy. (a) T2 weighted projective magnetic resonance cholangiopancreatography image shows an elongated hyperintense fluid collection proximal to the cystic duct stump, along with a small amount of subhepatic free fluid, which is well delineated in the axial T2 weighted single-shot fast spin-echo image. (b) An aberrant right intrahepatic bile duct is visible (arrow in (a)). (c) Coronal and (d) axially reformatted T1 weighted fat saturated three-dimensional gradient echo images obtained 20 min after intravenous injection of gadoxetic acid document the passage of contrast agent from the cystic duct stump into the fluid collection and the subhepatic space, demonstrating the presence of a bile leak. (Courtesy of Celso Matos, MD, Brussels, Belgium.) 相似文献
Table 1
Main biliary causes of post-cholecystectomy syndrome (PCS) related to cholecystectomy. (Biliary malignancies are the most frequent causes of PCS unrelated to cholecystectomy [1])Early PCS |
Retained stones in the cystic duct stump and/or common bile duct |
Bile duct injury/ligature during surgery |
Bile leakage |
Late PCS |
Recurrent stones in the common bile duct |
Bile duct strictures |
Cystic duct remnant harbouring stones and/or inflammation |
Gallbladder remnant harbouring stones and/or inflammation |
Papillary stenosis |
Biliary dyskinesia |
Table 2
Main extrabiliary causes of post-cholecystectomy syndrome (modified from [1])Gastrointestinal causes | Extra-intestinal causes |
Acute/chronic pancreatitis (and complications) | Psychiatric and/or neurological disorders |
Pancreatic tumours | Coronary artery disease |
Pancreas divisum | Intercostal neuritis |
Hepatitis | Wound neuroma |
Oesophageal diseases | Unexplained pain syndromes |
Peptic ulcer disease | |
Mesenteric ischaemia | |
Diverticulitis | |
Organic or motor intestinal disorders |
6.
S Kritsaneepaiboon P Siriwanarangsun P Tanaanantarak A Krisanachinda 《The British journal of radiology》2014,87(1041)