3D angiography. Clinical interest. First applications in interventional neuroradiology. (1/1425)

3D angiography is a true technical revolution that allows improvement in the quality and safety of diagnostic and endovascular treatment procedures. 3D angiography images are obtained by reconstruction of a rotational angiography acquisition done on a C-arm (GE Medical Systems) spinning at 40 degrees per second. The carotid or vertebral selective injection of a total of 15 ml of non-ionic contrast media at 3 ml/sec over 5 seconds allows the selection of the "arterial phase". Four hundred sixty 3D angiographic studies were performed from December 1996 to September 1998 on 260 patients and have been analyzed in MIP (Maximum Intensity Projection) and SSD (Shaded Surface Display) views. The exploration of intracranial aneurysms is simplified and only requires, for each vascular axis, a biplane PA and Lateral run followed by a single rotational angiography run. The 3D angiography image is available on the workstation's screen (Advantage Workstation 3.1, GE Medical Systems) in less than 10 minutes after the acquisition of the rotational run. It therefore allows one to analyze, during the intervention, the aneurysm's angioarchitecture, in particular the neck, and select the best therapeutic technique. When endovascular treatment is the best indication, 3D angiography allows one to define the optimal angle of view and accurately select the microcoils dimensions. 3D angiography replaces the multiple oblique views that used to be required to analyze the complex aneurysms and therefore allows a reduction of the total contrast medium quantity, the patient X-ray dose and the length of the intervention time which is a safety factor. Also, in particular for complex cases, it brings additional elements complementing the results of standard 2D DSA and rotational angiograms. In the cervical vascular pathology, 3D angiography allows for a better assessment of the stenosis level and of dissection lesions. Our current research activities focus on the matching without stereotactic frame between 3D X-ray angiography and volumetric MR acquisition, which should allow us to improve the treatment of intracerebral arterio-venous malformations (AVMs).  (+info)

Rupture mechanism of a thrombosed slow-growing giant aneurysm of the vertebral artery--case report. (2/1425)

A 76-year-old male developed left hemiparesis in July 1991. The diagnosis was thrombosed giant vertebral artery aneurysm. He showed progressive symptoms and signs of brainstem compression, but refused surgery and was followed up without treatment. He died of rupture of the aneurysm and underwent autopsy in March 1995. Histological examination of the aneurysm revealed fresh clot in the aneurysmal lumen, old thrombus surrounding the aneurysmal lumen, and more recent hemorrhage between the old thrombus and the inner aneurysmal wall. The most important histological feature was the many clefts containing fresh blood clots in the old thrombus near the wall of the distal neck. These clefts were not lined with endothelial cells, and seemed to connect the lumen of the parent artery with the most peripheral fresh hemorrhage. However, the diameter of each of these clefts is apparently not large enough to transmit the blood pressure of the parent artery. Simple dissection of the aneurysmal wall by blood flow in the lumen through many clefts in the old thrombus of the distal neck may be involved in the growth and rupture of thrombosed giant aneurysms of the vertebral artery.  (+info)

Facial diplegia complicating a bilateral internal carotid artery dissection. (3/1425)

BACKGROUND AND PURPOSE: We report a case of facial diplegia complicating a bilateral internal carotid artery dissection. CASE DESCRIPTION: A 49-year-old patient presented with unilateral headache and oculosympathetic paresis. Cerebral angiography revealed a bilateral internal carotid artery dissection. A few days later, the patient developed a facial diplegia that regressed after arterial recanalization. An arterial anatomic variation may explain this ischemic complication of carotid dissection. CONCLUSIONS: Double carotid dissection should be included among the causes of bilateral seventh nerve palsy.  (+info)

Surgical transluminal iliac angioplasty with selective stenting: long-term results assessed by means of duplex scanning. (4/1425)

PURPOSE: The safety of iliac angioplasty and selective stenting performed in the operating room by vascular surgeons was evaluated, and the short- and long-term results were assessed by means of serial duplex scanning. METHODS: Between 1989 and 1996, 281 iliac stenotic or occlusive lesions in 235 consecutive patients with chronic limb ischemia were treated by means of percutaneous transluminal angioplasty (PTA) alone (n = 214) or PTA with stent (n = 67, 23.8%). There were 260 primary lesions and 21 restenosis after a first PTA, which were analyzed separately. Stents were implanted in selected cases, either primarily in totally occluded arteries or after suboptimum results of PTA (ie, residual stenosis or a dissection). Data were collected prospectively and analyzed retrospectively. Results were reported in an intention-to-treat basis. Clinical results and patency were evaluated by means of symptom assessment, ankle brachial pressure index, and duplex scanning at discharge and 1, 3, 6, and every 12 months after angioplasty. To identify factors that may affect outcome, 12 clinical and radiological variables, including the four categories of lesions defined by the Standards of Practice Committee of the Society of Cardiovascular and Interventional Radiology, were analyzed separately. The statistical significances of life-table analysis of patency were determined by means of the log-rank test. RESULTS: There were no postoperative deaths or amputations. Local, general, and vascular complications occurred in 2.1%, 1.3% and 4.7% of cases, respectively (total, 8.1%). The mean follow-up period was 29.6 months. The cumulative patency rates +/- SE of the 260 PTAs (including 55 PTAs plus stents) were 92.9% +/- 1.5% at 1 month, 86. 5% +/- 1.7% at 1 year, 81.2% +/- 2.3% at 2 years, 78.8% +/- 2.9% at 3 years, and 75.4% +/- 3.5% at 5 and 6 years. The two-year patency rate of 21 redo PTAs (including 11 PTAs plus stents) was 79.1% +/- 18.2%. Of 12 predictable variables studied in the first PTA group, only the category of the lesion was predictive of long-term patency. The two-year patency rate was 84% +/- 3% for 199 category 1 lesions and 69.7% +/- 6.5% for 61 category 2, 3, and 4 lesions together (P =. 02). There was no difference of patency in the stented and nonstented group. CONCLUSION: Iliac PTA alone or with the use of a stent (in cases of occlusion and/or suboptimal results of PTA) offers an excellent long-term patency rate. Categorization of lesions remains useful in predicting long-term outcome. PTA can be performed safely by vascular surgeons in the operating room and should be considered to be the primary treatment for localized iliac occlusive disease.  (+info)

Plaque area increase and vascular remodeling contribute to lumen area change after percutaneous transluminal angioplasty of the femoropopliteal artery: an intravascular ultrasound study. (5/1425)

OBJECTIVE: The aim of the study was to assess the change in lumen area (LA), plaque area (PLA), and vessel area (VA) after percutaneous transluminal angioplasty (PTA) of the femoropopliteal artery. METHODS: This was a prospective study. Twenty patients were studied with intravascular ultrasound (IVUS) immediately after PTA and at follow-up examination. Multiple corresponding IVUS cross-sections were analyzed at the segments that were dilated by PTA (ie, treated sites; n = 168), including the most stenotic site (n = 20) and the nondilated segments (ie, reference sites; n = 77). RESULTS: At follow-up examination, both the PLA increase (13%) and the VA decrease (9%) resulted in a significant LA decrease (43%) at the most stenotic sites (P =.001). At the treated sites, the LA decrease (15%) was smaller and was caused by the PLA increase (15%). At the reference sites, the PLA increase (15%) and the VA increase (6%) resulted in a slight LA decrease (3%). An analysis of the IVUS cross-sections that were grouped according to LA change (difference >/=10%) revealed a similar PLA increase in all the groups: the type of vascular remodeling (VA decrease, no change, or increase) determined the LA change. At the treated sites, the LA change and the VA change correlated closely (r = 0.77, P <.001). At the treated sites, significantly more PLA increase was seen in the IVUS cross-sections that showed hard lesion or media rupture (P <.05). No relationship was found between the presence of dissection and the quantitative changes. CONCLUSION: At the most stenotic sites, lumen narrowing was caused by plaque increase and vessel shrinkage. Both the treated sites and the reference sites showed a significant PLA increase: the type of vascular remodeling determined the LA change at follow-up examination. The extent of the PLA increase was significantly larger in the IVUS cross-sections that showed hard lesion or media rupture.  (+info)

Intimal tear without hematoma: an important variant of aortic dissection that can elude current imaging techniques. (6/1425)

BACKGROUND: The modern imaging techniques of transesophageal echocardiography, CT, and MRI are reported to have up to 100% sensitivity in detecting the classic class of aortic dissection; however, anecdotal reports of patient deaths from a missed diagnosis of subtle classes of variants are increasingly being noted. METHODS AND RESULTS: In a series of 181 consecutive patients who had ascending or aortic arch repairs, 9 patients (5%) had subtle aortic dissection not diagnosed preoperatively. All preoperative studies in patients with missed aortic dissection were reviewed in detail. All 9 patients (2 with Marfan syndrome, 1 with Takayasu's disease) with undiagnosed aortic dissection had undergone >/=3 imaging techniques, with the finding of ascending aortic dilatation (4.7 to 9 cm) in all 9 and significant aortic valve regurgitation in 7. In 6 patients, an eccentric ascending aortic bulge was present but not diagnostic of aortic dissection on aortography. At operation, aortic dissection tears were limited in extent and involved the intima without extensive undermining of the intima or an intimal "flap." Eight had composite valve grafts inserted, and all survived. Of the larger series of 181 patients, 98% (179 of 181) were 30-day survivors. CONCLUSIONS: In patients with suspected aortic dissection not proven by modern noninvasive imaging techniques, further study should be performed, including multiple views of the ascending aorta by aortography. If patients have an ascending aneurysm, particularly if eccentric on aortography and associated with aortic valve regurgitation, an urgent surgical repair should be considered, with excellent results expected.  (+info)

Pathogenetic sequence for aneurysm revealed in mice underexpressing fibrillin-1. (7/1425)

Dissecting aortic aneurysm is the hallmark of Marfan syndrome (MFS) and the result of mutations in fibrillin-1, the major constituent of elastin-associated extracellular microfibrils. It is yet to be established whether dysfunction of fibrillin-1 perturbs the ability of the elastic vessel wall to sustain hemodynamic stress by disrupting microfibrillar assembly, by impairing the homeostasis of established elastic fibers, or by a combination of both mechanisms. The pathogenic sequence responsible for the mechanical collapse of the elastic lamellae in the aortic wall is also unknown. Targeted mutation of the mouse fibrillin-1 gene has recently suggested that deficiency of fibrillin-1 reduces tissue homeostasis rather than elastic fiber formation. Here we describe another gene-targeting mutation, mgR, which shows that underexpression of fibrillin-1 similarly leads to MFS-like manifestations. Histopathological analysis of mgR/mgR specimens implicates medial calcification, the inflammatory-fibroproliferative response, and inflammation-mediated elastolysis in the natural history of dissecting aneurysm. More generally, the phenotypic severity associated with various combinations of normal and mutant fibrillin-1 alleles suggests a threshold phenomenon for the functional collapse of the vessel wall that is based on the level and the integrity of microfibrils.  (+info)

Observations on the treatment of dissection of the aorta. (8/1425)

The results are presented of treatment in twenty-three patients with dissection of the thoracic aorta, in four of whom it was acute (less than 14 days' duration), and in nineteen chronic (more than 14 days' duration). Sixteen patients had Type I and II dissection (involving the ascending aorta) and five Type III (descending aorta at or distal to the origin of the left subclavian artery); in two, dissection complicated coarctation of the aorta in the usual site. Thirteen patients had aortic regurgitation. Three of the patients with acute dissection were treated medically; two, both with Type I dissection, died, and the third, with Type III, survived. The remaining acute patient was treated surgically and also died. Of the patients with chronic dissection, eight were treated medically and eleven surgically. None of the medical group died in hospital; three died between 3 months and 1 year, and five have survived from periods of 12-72 months. Eleven patients with chronic dissection were treated surgically; four died in hospital at or shortly after operation; and the remaining seven lived for periods of 12-84 months. The presentation, indications for surgical treatment and results are discussed. It is concluded that surgical treatment of chronic dissection may carry a higher initial mortality than medical, but that there may be slightly better overall long term results in the former. As this series was not selected randomly, because patients with complications were selected for surgery, and there are only a few patients in each group, the results do not permit firm conclusion regarding the relative merits of medical and surgical treatment. It is suggested that all patients should initially be treated medically but that surgical treatment should be considered if the dissection continues, if aortic regurgitation is severe, if an aneurysm develops or enlarges, if cardiac tamponade develops or there is evidence of progressive involvement of the branches of the aorta. Attention is drawn to the important syndrome of chronic dissecting aneurysm of the ascending aorta with severe aortic regurgitation which requires definitive surgical treatment and aortic valve replacement. The importance of adequate visualization of the origin and extent of the dissection as a preliminary to surgical treatment is stressed.  (+info)

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