Arterial Neovascularization Research Articles

Chronic subdural hematoma recurrence due to contralateral neovascularization following middle meningeal artery embolization.

Chronic subdural hematoma (CSDH) is one of the most commonly encountered neurosurgical diseases. Middle meningeal artery embolization (MMAE) is a technique for the management of CSDH that has elicited promising results. Despite the encouraging results of MMAE, recurrence does occur. One uncommon mechanism for recurrence of CSDH is by means of neovascularization of the contralateral middle meningeal artery (MMA). We describe two cases of CSDH recurrence by means of contralateral middle meningeal artery neovascularization treated with contralateral MMAE. We identified two cases of recurrent subdural hematoma secondary to neovascularization following treatment with contralateral MMAE. Two patients initially treated with MMAE were identified with CSDH recurrence secondary to contralateral MMA neovascularization. There was no traumatic or coagulopathic contribution to CSDH recurrence. In both cases, patients underwent contralateral MMAE. Both patients were neurologically intact with radiographic improvement of CSDH at follow up. Re-accumulation of SDH following MMAE by means of contralateral MMA neovascularization is a rare subtype of subdural hematoma (SDH) recurrence following MMAE. Within the context of re-accumulation of SDH following MMAE, catheter angiography is an important diagnostic investigation to elucidate the etiology of the recurrence. Furthermore, when angiography reveals neovascularization of the contralateral MMA, embolization of the contralateral MMA achieves good clinical and radiographic result.

Hemoptysis after Lung Transplantation Caused by Bronchial Arterial Neovascularization: Angiographic Analysis and Successful Embolization

This report discusses 3 bilateral lung transplant recipients (2 female, 1 male) who presented with late hemoptysis (10 y, 18 y, and 19 y after transplantation). All patients had a history of pulmonary infections, bronchiectasis, and/or Aspergillus infection. Arteriography, through catherization of the common femoral artery, demonstrated spontaneous bronchial and systemic neovascularization arising from the thyrocervical trunk, internal thoracic artery, intercostal arteries, and dorsal scapular artery. Embolization was performed with microspheres, polyvinyl alcohol microparticles, and/or glue and effectively terminated hemoptysis. One patient died 10 d later as a result of fungal infection, and the 2 others remained in stable condition (18- and 26-mo postembolization follow-up available).

Physiopathologie de l’artérite à cellules géantes : de l’inflammation au remodelage vasculaire

Giant cell arteritis (GCA) is a large-vessel vasculitis involving the aorta and its main branches, especially supra aortic branches. Although much progress has been made, the pathophysiology remains incompletely understood. An initial trigger, suspected of infectious origin, lead to the maturation and recruitment of dendritic cells (DC). The lack of migration of these DC allows the local recruitment of T-lymphocytes (LT). These LT- CD4+ polarize in Type 1 helper (Th1), Th17 but also Th9. A qualitative and quantitative deficit in regulatory T cells (Treg) is observed under the influence of IL-21 overproduction. In addition, an imbalance in the Th17/Treg balance is favored by IL-6. The secretion of IFN-γ, IL-17, IL-6, IL-33 is responsible for a sustained local inflammatory reaction that is organized around tertiary lymphoid follicles. Locally recruited macrophages secrete reactive forms of oxygen together with VEGF and PDGF. These growth factors, together with neurotrophins and endothelin contribute to increase the proliferation of vascular smooth muscle cells (VSMCs). The imbalance between matrix metalloproteases (MMP)-2, MMP-9 and MMP-14 and tissue inhibitors of metalloproteases (TIMP)-1 and TIMP-2 also contribute to the remodeling process occurring in the vessel wall. Finally, arterial neovascularization contribute to the perpetuation of lymphocyte recruitment. This persistent remodeling is sometimes complicated by ischemic events responsible for the initial severity of the disease.

Limits of and Complications after Embolization of the Hepatic Artery and Portal Vein to Induce Segmental Hypertrophy of the Liver: A Large Mini-Pig Study

Background: The aim of this study was to compare arterial embolization (AE) with portal vein embolization (PVE) for the induction of segmental hypertrophy regarding procedural efficacy, safety and outcome. Methods: A total of 29 mini pigs were subjected to PVE, AE or assigned to the sham (SO) group. Correspondingly, 75% of the hepatic artery or portal vein branches were embolized. Growth and atrophy of the liver lobes, calculating the liver-to-body weight index (LBWI), laboratory data, arteriography, portography, Doppler ultrasound (US) and histopathology were analyzed. Results: After PVE, 2 animals had to be excluded due to technical problems. After AE, 4 animals had to be excluded because of technical problems and early sacrifice. Postprocedural US demonstrated effective AE and PVE of the respective lobes. Four weeks after PVE, portography showed a slow refilling of the embolized lobe by collateral portal venous vessels. Four weeks after AE, arteriography revealed a slight revascularization of the embolized lobes by arterial neovascularization. Segmental AE led to extensive necrotic and inflammatory alterations in the liver and bile duct parenchyma. Significant hypertrophy of the non-embolized lobe was only noted in the PVE group (LBWI: 0.91 ± 0.28%; p = 0.001). There was no increase in the non-embolized lobe in the AE (LBWI: 0.45 ± 0.087%) and SO group (LBWI: 0.45 ± 0.13%). Conclusion: PVE is safe and effective to induce segmental hypertrophy. Portal reperfusion by collateral vessels may limit hypertrophy. AE did not increase the segmental hepatic volume but carries the risk of extensive necrotic inflammatory damage.

Transcapsular arterial neovascularization of liver transplants increases the risk of intraoperative bleeding during retransplantation

Arterial neovascularization of liver grafts can be a source of significant blood loss during retransplantation. This study evaluated the effect of transcapsular arterial neovascularization on intraoperative blood loss during retransplantation and long-term follow-up. Eleven consecutive patients with transcapsular arterial neovascularization (seven male, four female; nine children, two adults; mean age 12.3±16.3years) and the same number of matched control patients were analysed. Blood loss was calculated based on transfusion requirements. The volume of transfused units of red blood cells per kilogram bodyweight until hepatectomy and during the entire procedure was significantly higher in patients with neovascularization than in control patients (0.32±0.21 vs. 0.14±0.11, and 0.94±0.83 vs. 0.36±0.38 respectively; P-values 0.027). Neovascularization was associated with extensive intra-abdominal adhesions and a longer operating time until hepatectomy (175.6±52.1min vs. 124.3±34.9min, P-value 0.015). Postoperative revisions were performed more frequently in patients with neovessels. Graft survival did not differ between groups. Assessment for transcapsular arterial neovascularization should be included in preoperative Doppler ultrasound protocols to identify patients at risk of a complicated intra- and postoperative course in case of retransplantation.

Transcapsular Arterial Neovascularization after Liver Transplantation in Pediatric Patients Indicates Transplant Failure

To identify transcapsular arterial neovascularization with Doppler ultrasonography (US) in pediatric patients after liver transplantation and to assess the frequency of the finding, its underlying causes, and its relevance in terms of clinical outcome. The study was approved by the local ethics committee, with waived informed consent. All pediatric patients who underwent liver transplantation between January 2000 and December 2003 were retrospectively evaluated. Patients were followed up until June 2008, by using a predefined US protocol with prospective documentation. Of 182 consecutive liver transplantations performed in 162 patients (mean age, 4.5 years; range, 0.1-18.4 years) in this period, 25 patients with a total of 27 liver transplantations underwent US examinations conducted by multiple investigators and were primarily excluded. Student t tests and χ(2) tests were performed where appropriate. The Tarone-Ware test was used to compare transplant survival times. Transcapsular arterial neovascularization was noticed in 13 of 137 patients (9.5%) and in 13 of 155 liver transplants (8.4%). The mean time until arterial neovessels appeared was 157 days after liver transplantation (median, 97 days; range, 19-477 days). Arterial neovascularization was associated with pronounced transplant malperfusion and inflammatory changes (P < .001). Patients with transcapsular arterial neovascularization had a significantly shorter mean transplant survival time (1426.4 days ± 244.5 [standard error], with 95% confidence interval: 947.23, 1905.23, vs 2526.4 days ± 92.1, with 95% confidence interval: 2345.84, 2706.97; P = .008) and a higher retransplantation rate (53.8% vs 19.7%, P = .009). Transcapsular arterial neovascularization, detected with color Doppler US, occurred in 9.5% (13 of 137) of pediatric patients and 8.4% (13 of 155) of liver transplants and was associated with underlying malperfusion and inflammation. The diagnosis of transcapsular arterial neovascularization was associated with reduced graft survival times and a high retransplantation rate. The negative prognostic value of the sign may assist in a strategy of organ allocation.

High-Resolution Duplex Ultrasound Imaging Proves a High Incidence of an Arterial Neovascularization Phenomenon Associated with venous Thrombosis

Introduction We have recently observed an interesting phenomenon of prominent arterial neovascularization (ANV) within the thrombus and vein wall of patients with major venous thrombosis, sometimes intense enough to mimic small arteriovenous fistula. A prospective study was therefore conducted in 50 patients to further characterize this process. Aims We sought to determine the incidence of ANV; to characterize the process in more detail; and to determine whether there was an eventual recanalization of the thrombosed vein and favorable clinical outcome Methods All patients presenting with lower-extremity venous thrombus were prospectively imaged with Philips HDI 5000 and IU22 ultrasound systems using a standard protocol, including spectral and color Doppler analysis. Blood flow patterns in and around the thrombus were closely observed and recorded. In each patient, the phenomenon was assigned a grading from 0 to III according to prominence and penetration of the neovascularization process into the thrombosed vein. Results A total of 50 consecutive patients (age range; 35–80 years) were included in the study. 32 patients had DVT and 18 patients had superficial venous thrombus (SVT). ANV was observed as small vessels demonstrating a low-resistive arterial signature appearing predominantly on the vein wall and/or within the thrombus. The typical vessel diameter was 0.3–3.0 mm. ANV was present in 80% of patients examined and in 97% of cases with thrombus aged less than a year old. It was more common with SVT (100%). The process was most prominent at the 2–4 month interval after venous thrombosis. Conclusion There is a process of neovascularization that commonly occurs in association with venous thrombus. This was detected in 97% of patients with thrombus less than a year old. ANV appears to be a normal component of the recanalization process and may result from an inflammatory reaction. Further studies will be required to determine if the grade of this process can be correlated with favorable long-term outcome.

Arterial Neovascularization and Inflammation in Vulnerable Patients: Early and Late Signs of Symptomatic Atherosclerosis

Arterial Neovascularization and Inflammation in Vulnerable Patients: Early and Late Signs of Symptomatic Atherosclerosis

Arterial Neovascularization and Inflammation in Vulnerable Patients

Atherosclerosis is complicated by cardiovascular events such as myocardial infarction, stroke, or peripheral arterial occlusive disease. Inflammation and pathological neovascularization are thought to precipitate plaque rupture or erosion, both causes of arterial thrombosis and cardiovascular events. We tested the hypothesis that arterial inflammation and angiogenic events are increased throughout the arterial tree in vulnerable patients, ie, in patients who suffered from cardiovascular events, compared with patients who never suffered from complications of atherosclerosis. In a postmortem study, we quantified the inflammatory infiltrate and microvascular network in the arterial wall of iliac, carotid, and renal arteries. Tissue microarray technology was adapted to investigate full-thickness arterial sectors. We compared 22 patients with symptomatic atherosclerosis with 27 patients who never had suffered from any cardiovascular event. The absolute intimal macrophage content was 2- to 4-fold higher in vulnerable patients at all 3 arterial sites analyzed (P<0.05). Patients with symptomatic atherosclerosis had a denser network of vasa vasorum than patients with asymptomatic disease (33+/-2 versus 25+/-2 adventitial microvessels per 1 mm2; P=0.008). Hyperplasia of vasa vasorum was an early and macrophage infiltration was a late sign of symptomatic atherosclerosis. High intimal macrophage content and a hyperplastic network of vasa vasorum characterize vulnerable patients suffering from symptomatic atherosclerosis. These changes are uniformly present in different arterial beds and support the concept of symptomatic atherosclerosis as a panarterial disease.

Coronary Artery Neovascularization in Chronic Constrictive Pericarditis

Neovascularity in the region of the left atrial appendage was demonstrated by coronary arteriography in a patient with tuberculous constrictive pericarditis. The presence of neovascularity may have been caused by the chronic nature of the constrictive pericarditis, which allowed time for tissue reaction and organization.

Cardiopulmonary Bypass in a Patient with Moyamoya Disease

Cardiopulmonary Bypass in a Patient with Moyamoya Disease

A review of the pathophysiology of exercise-induced pulmonary haemorrhage in the equine athlete

In the United States, more than 75% of equine athletes are reported to suffer from exercise-related haemorrhage of the respiratory tract (Voynick and Sweeney, 1986; Sweeney et al., 1990). Fiberoptic endoscopy has traced the source of blood to beyond the bifurcation of the trachea. In 1981, the term exercise-induced pulmonary haemorrhage (EIPH) was introduced (Pascoe et al., 1981). Racehorses of all breeds, polo ponies and three-day event horses of mixed heritage, even foxhunters, may 'bleed' (Voynick and Sweeney, 1986; Pascoe et al., 1981; Sweeney and Soma, 1983; Hillidge, 1986). Any horse working at speeds greater than 240 m/min is at risk (Voynick and Sweeney, 1986). The impact of exercise-induced pulmonary haemorrhage is difficult to assess. Most attempts to demonstrate statistically a negative correlation between EIPH and performance have been unrewarding, largely due to the number of uncontrollable variables (Pascoe et al., 1981; Raphel and Soma, 1982). In racing thoroughbreds (Mason et al., 1983) and standard breeds (MacNamara et al., 1990) approximately half as many EIPH-positive as EIPH-negative horses were placed in their races. Based on extensive intrapulmonary haemorrhage, a 3-year prospective study of sudden deaths in exercising thoroughbreds concluded that 9 out of 11 deaths were attributable to EIPH (Gunson et al., 1988). By correlation of clinical signs, thoracic radiographs, ventilation/perfusion scintigraphy, gross and subgross pathology and histopathology in 26 affected thoroughbreds, EIPH has been associated with chronic small airway inflammation, proliferation of subpleural, peribronchial and septal bronchial arterioles, interstitial connective tissue fibrosis and alveolar septal disruption in the dorsocaudal lung lobes (O'Callaghan et al., 1987). From this work it was proposed that the initial insult of EIPH started as focal, dorsocaudal pulmonary peribronchial inflammation which resulted in bronchial arterial neovascularization. Haemorrhage then occurred when, during exercise, bronchial blood pressure increased in fragile capillary buds. The incidence of bronchitis/bronchiolitis, regardless of aetiology, has been estimated to be 30% in non-racing equine athletes and close to 100% in one group of racing thoroughbreds (Sweeney et al., 1989). Histological study of lungs from horses with mild, moderate and severe chronic small airway disease consistently revealed a greater density of lesions in the diaphragmatic lobes (Winder and von Fellenberg, 1988). To understand further the aetiology and/or pathophysiology of EIPH, we will first explore some aspects of general mammalian and specific equine pulmonary and bronchial vascular anatomy and physiology. Exercise-related changes in these systems in normal and EIPH-positive horses will be briefly reviewed.(ABSTRACT TRUNCATED AT 400 WORDS)

Neovascularization and coronary atherosclerotic plaque: Cinematographic localization and quantitative histologic analysis

A new technique was developed for analyzing the neovascularization associated with coronary artery atherosclerosis: cinematography during silicone polymer injection of the coronary arteries of fixed and cleared human hearts, followed by histologic analysis in routine and 1-micron-thick, Epon-embedded sections. Twenty-two hearts obtained at autopsy were studied. On the basis of cinematographic findings, individual regions of the coronary arteries were classified as negative, positive, or abundantly positive for neovascularization. Positive and abundantly positive areas, which invariably occurred in segments exhibiting changes of atherosclerosis, contained numerous small vessels in the adventitia and outer media (4.7 +/- 1.5 and 9.8 +/- 1.3 [SE] vessel profiles/artery cross-section in positive and abundantly positive areas, versus 1.0 +/- 0.6 in negative regions). Abundantly positive areas, which occurred in coronary artery segments demonstrating the most extensive atherosclerotic change, contained numerous small vessels in the inner media or in the plaque itself. Some of these microvessels were in close proximity to mast cells, which represent potentially rich sources of mediators affecting vascular tone and permeability. Vessels were not observed in the inner media or in atherosclerotic plaque in areas designated either positive or negative by cinematography. These findings show how our approach can be used both to define the three-dimensional, in situ configuration of coronary artery neovascularization and to characterize the histology of this process in detail. They also confirm previous work indicating that areas of coronary arteries involved by atherosclerosis frequently exhibit extensive neovascularization.

ROENTGENOLOGIC DEMONSTRATION OF SPONTANEOUS REVERSAL OF PORTAL BLOOD FLOW IN CIRRHOSIS AND PRIMARY CARCINOMA OF THE LIVER

ROENTGENOLOGIC DEMONSTRATION OF SPONTANEOUS REVERSAL OF PORTAL BLOOD FLOW IN CIRRHOSIS AND PRIMARY CARCINOMA OF THE LIVERKUNIO OKUDA, M.D., MIKIO MORIYAMA, M.D., MASATAKE YASUMOTO, M.D., SHIGENOBU JINNOUCHI, M.D., YUTAKA SHIMOKAWA, M.D., TOSHIMICHI NAKAYAMA, M.D., YOSHIRO KANDA, M.D., YOSHIO FUKYUAMA, M.D., HIROTAKA MUSHA, M.D, SHINTARO KURATOMI, M.D. and TOSHIRO NAKASHIMA, M.D.Audio Available | Share