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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.
Objective:
To evaluate current UK practice of periprocedural haematological management for image-guided procedures in relation to Cardiovascular and Interventional Radiological Society guidelines, which provide recommendations according to bleeding risk of procedures from Category 1 (lowest) to 3 (highest).Methods:
Survey of practice in UK radiology departments conducted over a 1-year periodResults:
48 radiology departments responded. The percentage of departments that stop antithrombotics pre-procedurally are as follows (for Category 1, 2 and 3, respectively): aspirin (31.3%, 43.8%, 54.2%); clopidogrel (54.2%, 68.8%, 72.9%); therapeutic low-molecular-weight heparin (56.3%, 77.1%, 75.0%). The percentage of departments that perform pre-procedural laboratory testing are as follows (for Category 1, 2 and 3, respectively): international normalized ratio (INR; 81.3%, 95.8%, 93.8%); activated partial thrombin time ratio (APTTR; 60.4%, 75.0%, 93.8%); platelet (77.1%, 91.7%, 95.7%); haemoglobin (70.8%, 85.4%, 87.5%). Mean threshold (standard deviation) of laboratory results for conducting procedures (Level 1, 2 and 3, respectively) are as follows: INR [1.53 (0.197), 1.47 (0.186), 1.47 (0.188)]; APTTR [1.50 (0.392), 1.50 (0.339), 1.48 (0.344)]; platelet count (x103 cells per microlitre) [74.4 (28.7), 79.9 (29.1), 80.5 (29.3)]; haemoglobin (grams per decilitre) [9.05 (1.40), 9.00 (1.33), 8.92 (1.21)]. No department practices conformed to current recommendations for (1) pre-procedural cessation of antithrombotics and (2) pre-procedural laboratory testing. Two (4.2%) department practices conformed to recommendations for thresholds of haematological parameters.Conclusion:
Current peri-procedural haematological management is variable and often does not conform to existing recommendations. Further research into the impact of this variation in practice on patient outcome is requiredAdvances in Knowledge:
This study demonstrates wide variation in practice in haematological management for image-guided procedures.Periprocedural haematological management, such as correction of coagulopathy, cessation of antithrombotics and pre-procedural laboratory testing (e.g. for haemoglobin levels and platelet count), is an important consideration for patients undergoing image-guided procedures.1 The challenges of periprocedural haematological management are multifactorial in aetiology. In addition to the increasing range of complex image-guided procedures being performed, the patient population undergoing such procedures may also be complicated.2 Many of these patients have comorbidities requiring antithrombotic therapy, or may have liver and marrow dysfunction, which can affect bleeding risk. Decisions on the optimal periprocedural haematological management are also confounded by the lack of high-level evidence, and existing guidelines within the literature can be variable even for equivalent procedures. For example, in two separate internationally accepted guidelines, the recommended international normalized ratio (INR) for chest drain insertion is <1.5 and <2.0.3,4 There is also limited scope to transfer existing evidence on haematological management from other domains such as open surgery to image-guided interventions. Unlike conventional open surgical procedures where bleeding may be visualized immediately and controlled by direct pressure or vessel ligation, bleeding from image-guided procedures may be difficult to control owing to issues with access and identification.5The lack of high-level evidence is unsurprising, given the potential ethical issues in conducting the necessary studies; it would be difficult to justify the randomization of patients to receiving or not receiving coagulopathy correction prior to undergoing various image-guided procedures for the purpose of research.6 As a result, current evidence is often based on retrospective studies. To address this complex issue, the Society of Interventional Radiology in conjunction with the Cardiovascular and Interventional Radiological Society of Europe (CIRSE) has previously produced guidelines based on existing evidence and expert consensus on periprocedural haematological management for image-guided procedures which are stratified into three categories according to the bleeding risk (4 However, despite the existence of such guidelines, from our experience, significant variation in practice exists between clinicians, even within our own institution.Table 1.
Society of Interventional Radiology/Cardiovascular and Interventional Radiological Society of Europe consensus guidelines on periprocedural haematological management for image-guided procedures according to category of bleeding risk| Guideline item | Guidance according to category of bleeding risk | |||
|---|---|---|---|---|
| Category 1 (low risk) | Category 2 (intermediate risk) | Category 3 (high risk) | ||
| Examples of procedures | ||||
| Vascular | Venography, IVC filter, PICC line | Arterial intervention (access size up to 7 French), chemoembolization, uterine fibroid embolization | TIPS | |
| Non-vascular | Thoracentesis, paracentesis, superficial aspiration and biopsy | Intra-abdominal abscess drainage, lung biopsy, percutaneous cholecystostomy | Renal biopsy, biliary interventions (new tract), nephrostomy | |
| Antiplatelet/anticoagulation cessation | ||||
| Aspirin | Do not withhold | Do not withhold | Withhold 5-day pre-procedure | |
| Clopidogrel | Do not withhold | Withhold 5-day pre-procedure | Withhold 5-day pre-procedure | |
| Therapeutic LMWH | Withhold one-dose pre-procedure | Withhold one-dose pre-procedure | Withhold for 24 h/up to two doses | |
| Pre-procedural testing | ||||
| INR | On warfarin/with liver disease | All patients | All patients | |
| APTTR | On unfractionated heparin | On unfractionated heparin | On unfractionated heparin | |
| Platelet count | Not routinely recommended | Not routinely recommended | All patients | |
| Haemoglobin | Not routinely recommended | Not routinely recommended | All patients | |
| Threshold for correcting parameter/withholding procedure | ||||
| INR | INR >2.0 | >1.5 (89% consensus) | >1.5 (95% consensus) | |
| APTTR | No consensus | No consensus | >1.5 times control | |
| Platelet count | Transfusion if <50 × 103 μl−1 | Transfusion if <50 × 103 μl−1 | Transfusion if <50 × 103 μl−1 | |
| Haemoglobin | No recommended threshold | No recommended threshold | No recommended threshold | |
3.
4.
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 T| Reference | 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 |
5.
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 melanoma1,2| Patient/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% |
6.
S Kritsaneepaiboon P Siriwanarangsun P Tanaanantarak A Krisanachinda 《The British journal of radiology》2014,87(1041)