Imaging Sciences and Intervention Radiology

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    Imaging of indirect carotid cavernous fistula comparing advanced mri sequences with digital subtraction angiography
    (SCTIMST, 2019-12) Sathish K
    Carotid-cavernous fistulas (CCFs) are abnormal arteriovenous communications either directly between the internal carotid artery (ICA) and the cavernous sinus or between the dural branches of the internal and external carotid arteries. Several classification schemes have categorized CCFs according to aetiology (traumatic or spontaneous), hemodynamic features (high versus low flow), or the angiographic arterial architecture (direct or indirect). Direct CCFs usually arise after trauma or a ruptured aneurysm. These fistulae are less likely to resolve spontaneously and may require intervention if symptomatic. The remaining types are indirect and are best described as dural arteriovenous malformations. Their rate of flow and exact aetiology are variable. They have been associated with pregnancy, cavernous sinus thrombosis, sinusitis, and minor trauma. Most of the patients are managed conservatively and may require intervention if there is any deterioration during follow up. (1) Intra-arterial digital subtraction angiography (DSA) is the standard of reference for the diagnosis of CSDAVFs. Its high spatial and temporal resolution facilitates the accurate analysis of feeders, venous drainage, and fistula sites. However, DSA is invasive and not without possible complications; morbidity of 0.03% and mortality of 0.06% have been reported for patients undergoing diagnostic cerebral angiography(2,3). Therefore, a noninvasive, reliable method is needed for the appropriate selection of patients with CSDAVF with high risk (aggressive symptoms), exclusion of patients with CSDAVF considered benign and for follow-up. Carotid cavernous fistula descriptions are with type, location, laterality, size of fistula, feeding arteries, draining veins and cortical venous reflux. 7 Recently few studies are published on cranial dural arteriovenous fistulas (cDAVF) comparing the efficacy of advanced vascular MR imaging with DSA. Comparison of 3D-TOF (3T) with DSA in the evaluation of intracranial DAVF showed good intermodality agreement in the gross characterization of DAVF(4). Few studies showed SWI can reliably detect the fistulous point, presence of cortical venous reflux in cases of DAVF and also helps in differentiating nidus from haemorrhage and calcification in cases of brain AVM(5,6). Susceptibility-weighted angiography (SWAN) is a new 3D T2*- based gradient-echo sequence generating several echoes that are read out at different TE times, allowing high resolution visualization of both cerebral veins and arteries. SWAN sequence has a potential role for the diagnosis of intracranial DAVF in visualising intracranial arteriovenous shunt(7). Silence Magnetic resonance angiography is a relatively new technique available in 3.0 Tesla Magnetic Resonance scanners. The advantages of this arterial spin labelling (ASL) based ultra-short echo-time technique is that it is less affected by susceptibility effects and has excellent background suppression. Few preliminary studies have found that the vascular anatomy is better depicted on Silence magnetic resonance(8). To our knowledge, there are no systematic studies on the reliability of unenhanced 3T 3D TOF MRA, Silent MRA and SWAN for assessing feeders, fistula sites, and venous drainage of CSDAVFs. Thus, this intended to study the utility of these noninvasive magnetic resonance angiography techniques to determine the angiomorphology of CCF, in treatment planning and follow up. If found reliable it may supplant DSA in follow up imaging.
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    Role of quantitative susceptibility weighted imaging in evaluating disease activity of lesions in multiple sclerosis
    (SCTIMST, 2019-12) Vinayagamani S
    Multiple sclerosis (MS) is an inflammatory demyelinating and neurodegenerative disease of the central nervous system. Majority of the patients start with a relapsing –remitting course, which has clearly defined episode of neurologic disability and recovery. Pathologic hallmark of MS was presence of focal plaques in white and gray matter associated with heavy infiltration of macrophages with myelin debris, lymphocytes, and large reactive multinucleated astrocytes called Creutzfeldt-Peters cells1 . The etiologic mechanism underlying this demyelinating disease is generally believed to be autoimmune inflammation however the intial triggerer and the further development of CNS plaques are not well established1 . Conventional magnetic resonance imaging (MRI) has been used routinely to diagnose and monitor the disease spatially and temporally. The use of conventional MRI to measure the disease activity and assess effects of therapy is now standard in clinical practice and drug trials. T2-weighted imaging (T2WI) is highly sensitive in the detection of hyperintensities in white matter but, hyperintensities on T2WI can correspond to a wide spectrum of pathology, ranging from edema and mild demyelination to lesions in which the neurons and supporting glial cells are replaced by glial scars or liquid necrosis. In MS , gadolinium enhancement on T1-weighted imaging (T1WI) can suggest an acute inflammation, which is a marker of disease activity2,3. It is becoming a consensus among many studies that iron is enriched within oligodendrocytes and myelin in both normal and diseased tissue. One explanation for such findings proposes that iron is associated with the biosynthetic enzymes of myelinogenesis4 . In MS , stages of relapse and remission alternate during disease progression, identification and characterization of active lesions are critical for correct diagnosis and therapy. In clinical practice, current active lesion assessment is based on gadolinium (Gd) enhancement on T1-weighted MR imaging2,3. However, because Gd enhancement reflects leakage of the blood-brain barrier, it is considered as an indirect measure of inflammation that is preceded and outlasted by infiltration of immune cells. The 8 activation of resident innate immune cells may not be captured on T1WI Gd5 . In addition, concerns over repeated Gd exposure have recently been raised, as new data showing long term Gd retention in the brain of patients with normal renal function who have undergone multiple Gd injections is emerging. In patients with MS in whom Gd retention seems also to be associated with secondary progression of the disease. 6,7 Therefore it has become a necessity to identify a ‗Gd-enhancing‘ or ‗active MS‘ lesions without the use of a contrast agent to reduce scan time, cost, Gd accumulation and adverse effects. A non-contrast based imaging modality to detect active lesions also helps in routine follow up / monitoring of MS patients on therapy. It is known that microglia and macrophages in an alternative activation, M2 type macrophages (ferritin poor macrophages) remove myelin debris from MS lesions which usually accumulate in the periphery of the active lesion, 8 whereas the classic pro inflammatory M1 type macrophages (ferritin rich macrophages)- which tend to accumulate iron- was more commonly present in the chronic lesions9 . Both M1 and M2 type macrophage accumulation varies in different types of lesions which may result in change in susceptibility values and iron content in them. Susceptibility weighted imaging (SWI) has been shown to be very sensitive to iron in the form of hemosiderin, ferritin, and deoxyhemoglobin, offering the ability to measure iron on the order of several µg/g of tissue in vivo10,11. SWI is a 3D, high-resolution, fully flow compensated gradient-echo sequence that uses magnitude and phase data both separately and together to enhance information about local tissue susceptibility. In the past, phase images were seldom used because artifacts from the background field destroyed the integrity of small changes seen in pristine tissue. As we know now, phase images contain a wealth of information that may not be observed from the magnitude images. Recently, SWI-filtered phase images were used to map out putative iron content in the brain11,12. Phase images are a direct measure of the sources of local susceptibility changes. MR imaging have demonstrated 9 that, the magnetic susceptibility of an MS lesion changes rapidly as the lesion evolves longitudinally which can be measured by various iron quantification methods. Our study was designed to assess whether Quantitative SWI (Routine SWI) is a viable technique to identify active enhancing MS lesions without Gd injection. In this study, we explore the routine SWI imaging with quantification of phase values and iron content. To best of our knowledge, this is the first study , in which the routinely available SWI sequence was used for quantification of iron content in MS lesions. The goal of this study is to investigate whether the measured phase values and iron content in the lesions will differentiate active lesions from inactive lesions.
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    Comparison of 3d rotational angiography with digital subtraction angiography and correlation of angioarchitecture with clinical presentations in cerebral arteriovenous malformations
    (SCTIMST, 2019-12) Somnath Pan
    Brain arteriovenous malformations (AVM) are an intriguing disease entity involving the intracranial vasculature where arteries and veins are interconnected through a low resistance dysplastic nidus bypassing the normal intervening capillary network.[1] There are several morphological aspects of AVM that need to be assessed prior to planning therapeutic approach and intervention. These include location, feeding arteries, draining veins, nidus and size of the lesion.[2] The presence of feeding artery, intranidal and perinidal aneurysms, venous pouches, venous dilatations, fistulas, venous stenosis and venous thrombosis are the other factors which necessitate therapy in brain arteriovenous malformations.[3,4] An ideal imaging modality should reliably reveal these parameters. Digital subtraction angiography (DSA) very reliably predicts the presence of these varied parameters. DSA is the standard imaging procedure for AVM. However, although it gives a good impression of the spatial relationships between the vessels, it is limited by overprojection of early draining veins on arterial feeders and nidus and cannot give a true three-dimensional (3D) view from every angle. The 3D rotational angiographic (RA) images have excellent resolution, and can be rotated in any direction to show the structures from any required angle, including views that would be impossible to obtain by radiographic projections alone. An improved understanding of the 3D vascular morphology helps to ensure optimum positioning of the image intensifier during the intervention for guideline positioning of catheters, coils, balloons and stents.[5] There are few studies comparing the utility of 3D RA in cerebral aneurysm.[6,7] Hochmuth A et al., in their study have concluded that compared with DSA, 3D RA allows more exact 2 depiction of anatomic details that are important in planning surgery and interventional therapy for intracranial aneurysms and also RA depicted more aneurysms.[8] The current gold standard in imaging of brain AVM is superselective microcatheter angiography. We intended to study the effect of addition of 3D RA in better delineation of angioarchitecture of the lesions. Cerebral AVM has varied clinical presentations. Broadly it can present because of haemorrhage and unbled lesions can manifest with seizure, headache, neurodeficit or vague neurologic symptoms. Also asymptomatic lesions are detected incidentally due to neuroimaging for inexplicit symptoms. Various angiographic features like deep venous drainage, deep location, infratentorial location, distal flow related & intranidal aneurysm, previous haemorrhage has been implicated as risk factors or predictors of haemorrhagic complications.[9] Few studies have attributed manifestation of seizure in AVM to angiographic features like cortical location of feeder, feeder by MCA, absence of aneurysm, varix/varices in venous drainage.[10] Other clinical manifestations like headache and neurodeficit in unbled AVM has not been studied in relation to specific angiomorphologic attribute. Combining the 2D DSA & 3D RA is expected to generate the best possible angiomorphology of AVM. We intend to analyse the angiographic predictors for clinical manifestations of haemorrhage, seizure, headache & neurodeficit; thereby prompting necessary therapeutic intervention.
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    Myocardial t1 mapping: relation of t1 values to myocardial perfusion, early gadolinium enhancement and late gadolinium enhancement in hypertrophic cardiomyopathy
    (SCTIMST, 2019-12) Harshit
    Hypertrophic cardiomyopathy (HCM) is a disorder of myocardium with a genetic basis, characterized by an increase in myocardial thickness, non-dilated left ventricle and increased in ejection fraction(1). Incidence is believed to be 1 in 500 people(2) with heterogeneous phenotypic expression. Natural history is variable presenting as sudden cardiac death, heart failure or arrhythmias. HCM is usually a diagnosis of exclusion, while other ethology of LV hypertrophy needs to be ruled out. Most common differential diagnosis are hypertension, valvular heart diseases and infiltrative cardiomyopathies(2). HCM is defined as a wall thickness of > 15 mm either any echocardiography, Computed tomography or cardiac magnetic resonance imaging (CMR), without any identifiable cause(3). Cardiac involvement is usually asymmetric, most commonly involving the basal septum, followed by apical and mid cavity involvement. Echocardiogram is usually the first modality for diagnosis and assessment of HCM. CMR is the established modality for diagnosis, risk stratification, and management of the patients diagnosed with HCM. Myocardial fibrosis has proven to be associated with severe hypertrophy, and an increase in fibrosis reflects onto failing LV function and risk of sudden cardiac death secondary to arrythmias in patients of HCM(4). Myocardial fibrosis determined by Late gadolinium enhancement (LGE) has been established as the maker for future risk of sudden cardiac death(5). Increase in myocardial crypts in phenotype positive HCM is associated with particular gene mutations(6). These crypts can be assessed using Early gadolinium enhancement (EGE) sequence which can predict areas of subtle changes even before fibrosis sets in. Assessment of LGE requires CMR contrast for fibrosis quantification. T1 mapping is a novel technique which can assess the local/diffuse fibrosis without the requirement of an MR contrast agent. Native T1 maps have proven to be a cost-effective method or fibrosis assessment without 10 exposure to gadolinium-based contrast agent(7). Microvascular perfusion defects in HCM patients is an important marker of prognosis and future arrhythmic episodes causing sudden cardiac death(8). This study was aimed at determining the relationship between Early gadolinium enhancement (EGE)/Late gadolinium enhancement (LGE) and native T1 values in patients of hypertrophic cardiomyopathy.
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