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Vessel Wall (vessel + wall)
Kinds of Vessel Wall Selected Abstracts3D flow-independent peripheral vessel wall imaging using T2 -prepared phase-sensitive inversion-recovery steady-state free precessionJOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 2 2010Jingsi Xie BS Abstract Purpose: To develop a 3D flow-independent peripheral vessel wall imaging method using T2 -prepared phase-sensitive inversion-recovery (T2PSIR) steady-state free precession (SSFP). Materials and Methods: A 3D T2 -prepared and nonselective inversion-recovery SSFP sequence was designed to achieve flow-independent blood suppression for vessel wall imaging based on T1 and T2 properties of the vessel wall and blood. To maximize image contrast and reduce its dependence on the inversion time (TI), phase-sensitive reconstruction was used to restore the true signal difference between vessel wall and blood. The feasibility of this technique for peripheral artery wall imaging was tested in 13 healthy subjects. Image signal-to-noise ratio (SNR), wall/lumen contrast-to-noise ratio (CNR), and scan efficiency were compared between this technique and conventional 2D double inversion recovery , turbo spin echo (DIR-TSE) in eight subjects. Results: 3D T2PSIR SSFP provided more efficient data acquisition (32 slices and 64 mm in 4 minutes, 7.5 seconds per slice) than 2D DIR-TSE (2,3 minutes per slice). SNR of the vessel wall and CNR between vessel wall and lumen were significantly increased as compared to those of DIR-TSE (P < 0.001). Vessel wall and lumen areas of the two techniques are strongly correlated (intraclass correlation coefficients: 0.975 and 0.937, respectively; P < 0.001 for both). The lumen area of T2PSIR SSFP is slightly larger than that of DIR-TSE (P = 0.008). The difference in vessel wall area between the two techniques is not statistically significant. Conclusion: T2PSIR SSFP is a promising technique for peripheral vessel wall imaging. It provides excellent blood signal suppression and vessel wall/lumen contrast. It can cover a 3D volume efficiently and is flow- and TI-independent. J. Magn. Reson. Imaging 2010;32:399,408. © 2010 Wiley-Liss, Inc. [source] Local gene delivery to the vessel wallACTA PHYSIOLOGICA, Issue 1 2001R. C. Smith This review will provide an overview of delivery strategies that are being evaluated for vascular gene therapy. We will limit our discussion to those studies that have been demonstrated, utilizing in vivo model systems, to limit post-interventional restenosis. We also discuss the efficacy of the vectors and methods currently being used to transfer genetic material to the vessel wall. The efficiency of these techniques is a critical issue for the successful application of gene therapy. [source] Insulin resistance and endothelial dysfunction: the road map to cardiovascular diseasesDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 6 2006Eugenio Cersosimo Abstract Cardiovascular disease affects approximately 60% of the adult population over the age of 65 and represents the number one cause of death in the United States. Coronary atherosclerosis is responsible for the vast majority of the cardiovascular events, and a number of cardiovascular risk factors have been identified. In recent years, it has become clear that insulin resistance and endothelial dysfunction play a central role in the pathogenesis of atherosclerosis. Much evidence supports the presence of insulin resistance as the fundamental pathophysiologic disturbance responsible for the cluster of metabolic and cardiovascular disorders, known collectively as the metabolic syndrome. Endothelial dysfunction is an important component of the metabolic or insulin resistance syndrome and this is demonstrated by inadequate vasodilation and/or paradoxical vasoconstriction in coronary and peripheral arteries in response to stimuli that release nitric oxide (NO). Deficiency of endothelial-derived NO is believed to be the primary defect that links insulin resistance and endothelial dysfunction. NO deficiency results from decreased synthesis and/or release, in combination with exaggerated consumption in tissues by high levels of reactive oxygen (ROS) and nitrogen (RNS) species, which are produced by cellular disturbances in glucose and lipid metabolism. Endothelial dysfunction contributes to impaired insulin action, by altering the transcapillary passage of insulin to target tissues. Reduced expansion of the capillary network, with attenuation of microcirculatory blood flow to metabolically active tissues, contributes to the impairment of insulin-stimulated glucose and lipid metabolism. This establishes a reverberating negative feedback cycle in which progressive endothelial dysfunction and disturbances in glucose and lipid metabolism develop secondary to the insulin resistance. Vascular damage, which results from lipid deposition and oxidative stress to the vessel wall, triggers an inflammatory reaction, and the release of chemoattractants and cytokines worsens the insulin resistance and endothelial dysfunction. From the clinical standpoint, much experimental evidence supports the concept that therapies that improve insulin resistance and endothelial dysfunction reduce cardiovascular morbidity and mortality. Moreover, interventional strategies that reduce insulin resistance ameliorate endothelial dysfunction, while interventions that improve tissue sensitivity to insulin enhance vascular endothelial function. There is general agreement that aggressive therapy aimed simultaneously at improving insulin-mediated glucose/lipid metabolism and endothelial dysfunction represents an important strategy in preventing/delaying the appearance of atherosclerosis. Interventions that 1 correct carbohydrate and lipid metabolism, 2 improve insulin resistance, 3 reduce blood pressure and restore vascular reactivity, and 4 attenuate procoagulant and inflammatory responses in adults with a high risk of developing cardiovascular disease reduce cardiovascular morbidity and mortality. Whether these benefits hold when the same prevention strategies are applied to younger, high-risk individuals remains to be determined. Copyright © 2006 John Wiley & Sons, Ltd. [source] Increased infiltration of Chlamydophila pneumoniae in the vessel wall of human veins after perfusionEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 7 2008K. Kupreishvili ABSTRACT Background Several studies have suggested an association between Chlamydophila pneumoniae (Cp) infection and atherosclerosis. A recent study detected Cp DNA in the saphenous vein of 12% of all patients before bypass grafting and in 38% of failed grafts. We used a system in which human veins were perfused with autologous blood under arterial pressure. Materials and methods, Veins were surplus segments of saphenous veins of coronary artery bypass grafting (CABG) patients. Vein grafts were perfused with the blood of the same patient after CABG procedures. Veins were analysed for Cp -specific membrane protein using immunohistochemical and PCR analysis. Veins were analysed before and after perfusion (up to 4 h). The number of Cp positive cells was then quantified in the vein layers. Results Cp protein was detected within macrophages only. In non-perfused veins, Cp was present in the adventitia in 91% of all patients, in the circular (64%) and longitudinal (23%) layer of the media. No positivity was found in the intima. Perfusion subsequently resulted in a significant increase of Cp positive cells within the circular layer of the media that, however, differed strongly between different patients. Cp DNA was not detected by PCR in those specimens. Conclusion Cp protein was present in 91% of veins, but the number of positive cells differed remarkably between patients. Perfusion of veins resulted in increased infiltration of Cp into the circular layer. These results may point to a putative discriminating role of Cp with respect to graft failure between different patients. [source] Sphingosine-1-phosphate and FTY720 as anti-atherosclerotic lipid compoundsEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 3 2007M. Tölle Abstract All stages of atherosclerosis have been identified as a chronic vascular inflammatory disease. In the last few years there is increasing evidence that endogenous lysophospholipids such as sphingosine-1-phosphate (S1P) have potent anti-inflammatory properties. The S1P analogue FTY720 that has been developed as a potent, orally active, immunosuppressant in the field of transplantation and autoimmune disease has interesting effects on inflammatory processes in the arterial vessel wall. S1P targets five specific S1P receptors (S1P1,5), which are ubiquitously expressed. S1P1,3 receptor expression is identified in arterial vessels. S1P and FTY720 show potent silencing effects on some vascular proinflammatory mechanisms in endothelial and vascular smooth muscle cells. In addition, the interaction of monocytes with the vessel wall is inhibited. As shown recently, FTY720 can effectively reduce the progression of atherosclerosis in apolipoprotein E-deficient mice having a high-cholesterol diet. It is not entirely clear which S1P receptor subtype is mainly involved in this process. However, it is currently speculated that the S1P3 and probably the S1P1 is involved in the anti-atherosclerotic effects of FTY720. This review summarizes the current knowledge about S1P- and FTY720-effects on mechanisms of vascular inflammatory disease. In addition S1P receptor subtypes are identified which might be interesting for molecular drug targeting. [source] Measurement of the soluble angiopoietin receptor tie-2 in patients with coronary artery disease: development and application of an immunoassayEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 7 2003N. A. Y. Chung Abstract Background The angiopoietin family has emerged as a group of crucial growth factors to normal angiogenesis. They are essential to the development of the mature vessel wall and interact with the endothelium via endothelial cell-specific tyrosine kinase receptors, tie-1 and tie-2. The role of the tie-2 receptor has been extensively examined in neovascularization associated with malignancy, but little is known about the role it may play in atherosclerosis, a condition whose pathophysiology also involves angiogenesis. Soluble tie-2 has been detected in the plasma of healthy controls, but this has yet to be applied to patients in the clinical setting. Materials and methods We developed an ELISA to detect plasma tie-2 levels and applied these to a clinical setting. The intra- and interassay coefficients of variation for the assay were 4·7% and 9·6%, respectively. We then measured levels of tie-2, vascular endothelial growth factor (VEGF), another factor associated with angiogenesis, and the soluble VEGF receptor Flt-1 (sFlt-1) in 75 patients with coronary artery disease [25 with acute myocardial infarction (AMI), 25 with acute coronary syndromes (ACS) and 25 with stable angina] and 25 healthy controls. Results Median [IQR, interquartile range] levels of tie-2 were significantly higher in the coronary artery disease patients (AMI 12 [10,17] ng mL,1, ACS 10 [9,14] ng mL,1, stable angina 9 [3,11] ng mL,1) when compared with the controls (7·5 [7,9] ng mL,1P = 0·004). As expected, levels of VEGF and sFlt were significantly different from those in the healthy controls (P = 0·011 and P < 0·001, respectively). Significant correlations were found between levels of tie-2 and VEGF (Spearman r = 0·59, P < 0·001), tie-2 and sFlt-1 (r = 0·45, P < 0·001) and VEGF and sFlt-1 (r = 0·56, P < 0·001) in the whole study group. Conclusion We suggest that tie-2 may be potentially used as a marker of angiogenesis in atherosclerosis and may help elucidate the role of the angiopoietin/tie-2 system in atherogenesis. [source] Neuronal and vascular localization of histamine N-methyltransferase in the bovine central nervous systemEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 2 2000Masahiro Nishibori Abstract Histamine N-methyltransferase (HMT) (EC 2.1.1.8) plays a crucial role in the inactivation of the neurotransmitter histamine in the CNS. However, the localization of HMT remains to be determined. In the present study, we investigated immunohistochemical localization of HMT in the bovine CNS using a polyclonal antibody against bovine HMT. The HMT-like immunoreactivity was observed mainly in neurons. Strongly immunoreactive neurons were present in the oculomotor nucleus and ruber nucleus in the midbrain, the facial nucleus in the pons, the dorsal vagal nucleus and hypoglossal nucleus in the medulla oblongata and in the anterior horn as well as intermediolateral zone of the spinal cord. Intermediately immunoreactive neurons were present in the piriform cortex and the inferior olivary nucleus. The grey matter of the forebrain regions was diffusely and faintly stained. In the cerebellum and the striatum, the nerve fibres in the white matter were positive. The tuberomammillary nucleus, where histaminergic neurons are present, were weakly positive. The other immunoreactive structures in the CNS were blood vessels. Almost all of the blood vessel walls, irrespective of whether they were arterial or venous, were variably stained. The glial fibrillary acidic protein- (GFAP-) immunoreactive astrocytes were not stained. These findings indicated that histamine released from histaminergic nerve terminals or varicose fibres is methylated mainly in postsynaptic or extrasynaptic neurons rather than in astrocytes. The localization of HMT in the blood vessel wall may mean that blood-borne histamine and histamine released from mast cells associated with the blood vessels are catabolized in this structure. [source] Different pathways leading to cutaneous leukocytoclastic vasculitis in miceEXPERIMENTAL DERMATOLOGY, Issue 6 2001C. Sunderkötter Abstract: To investigate the pathomechanisms of leukocytoclastic vasculitis (LcV) we compared mouse models of LcV with non-vasculitic irritant contact dermatitis (ICD). Criteria for LcV as met by the immune complex-mediated Arthus reaction (Art-r) were also fulfilled by the localized Shwartzman reaction (Shw-r) and by cutaneous Loxoscelism (Lox) (injection of venom from Loxosceles reclusa containing sphingomyelinase D). After depletion of PMN (by ,-irradiation) vessel damage could not be elicited in these models, distinguishing them from models of direct endothelial insult (necrotizing ICD). Depletion of complement could only delay, but not inhibit the Art-r, and did not change ICD, Lox or the Shw-r. The Shw-r exclusively revealed a sustained local expression of vascular adhesion molecules for 24 h in the preparatory phase (LPS s.c.), not observed in the Art-r, in Lox or ICD. Subsequent challenge with LPS i.p. was associated with upregulation of Mac-1 and ICAM-1 on PMN, but not of VLA-4 or LFA-1 (FACS analysis). Cytokines which were able to replace LPS in priming for LcV in the Shw-r (TNF-, and IL-1,) also induced sustained expression of adhesion molecules, whereas IL-12 and IFN-, did neither. Neutralizing IL-12 or IFN-, also inhibited neither LcV nor sustained expression of adhesion molecules, whereas anti-TNF-, inhibited both. Anti-TNF-, had no marked inhibitory effects in the Art-r, in Lox or ICD. Combined (but not separate) neutralization of both E-selectin and VCAM-1 by antibodies suppressed LcV independent from reducing influx of PMN, proving that their sustained expression is decisive for the Shw-r and interferes with normal diapedesis. Since Loxosceles venom is known to dysregulate diapedesis and degranulation of PMN in vitro, since adherent immune complexes activate PMN at the vessel wall, and since adhesion molecules are dysregulated in the Shw-r, we suggest that LcV develops when activation of PMN coincides with vascular alterations which interfere with normal diapedesis. [source] Fibroblast growth factor (FGF)-23 and fetuin-A in calcified carotid atheromaHISTOPATHOLOGY, Issue 6 2010Mathias Voigt Voigt M, Fischer D-C, Rimpau M, Schareck W & Haffner D (2010) Histopathology56, 775,788 Fibroblast growth factor (FGF)-23 and fetuin-A in calcified carotid atheroma Aims:, Human atheroma calcification occurs secondary to repetitive injury/remodelling of the vessel wall and might be initiated by adherence of mineral-loaded fetuin-A whether or not professional matrix mineralizing cells are present. The aim was to investigate the contribution of fibroblast growth factor (FGF)-23 to ectopic mineralization. Methods and results:, Serial sections of formalin-fixed paraffin-embedded human carotid atheroma (n = 54) were investigated with respect to (i) size and distribution of calcific deposits, (ii) indicators of chondrogenic/osteogenic transformation, and (iii) expression of fetuin-A and FGF-23. All specimens were calcified and SOX-9, collagen type II, cathepsin-K, fetuin-A and FGF-23 expression was seen in 46, 53, 53, 54 and 48 specimens, respectively. The intracellular detection of FGF-23 (45/48) indicates local synthesis. Whereas fetuin-A expression was seen also within areas of vascular smooth muscle actin-positive cells adjacent to calcific deposits, FGF-23 expression was apparently restricted to the mineralization-prone areas. Both local expression and FGF-23 serum concentrations were significantly associated with the degree of atheroma calcification. Conclusions:, Besides the induction of bone islets and subsequent mineral deposition, severe remodelling of the vessel wall is sufficient to create a mineralizable fetuin-A-attracting microenvironment. FGF-23 might contribute to the formation of proper mineral, i.e. control local phosphate concentration. [source] Stuck long-term indwelling central venous catheters in adolescents: three cases and a short topical reviewACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 6 2010A. MORTENSEN We present three cases of fixated vascular injection ports. Two patients had cystic fibrosis and one had an immunological defect. All catheters were made from polyurethane and implanted in adolescent patients. Indwelling time were 6,8 years. One patient's catheter was entirely integrated in the vessel wall and impossible to remove. In the other two cases, catheters were removed with great difficulty by the interventional radiologists. These cases raise important questions concerning the maximum indwelling time and the choice of catheter material when implanting permanent central venous catheters (CVCs) in adolescents. Furthermore, it highlights the importance of not breaking a CVC in the attempt to remove it. [source] A novel simple technique for en face endothelial observations using water-soluble media ,,thinned-wall' preparationsJOURNAL OF ANATOMY, Issue 2 2008L. Jelev Abstract A new, easily applicable technique providing en face preparations for light microscopy observations of the rat aorta and human thin wall arteries is described here. The major steps of the technique include attachment of the fixed and flattened vessel with the endothelium face down on a glass slide, covered with a water-soluble adhesive medium; drying and softening the vessel wall with another water-soluble medium; removal of the adventitia and most of the media; detaching the layer by placing the glass slide in water; and final attachment of the layer with the endothelium upwards. On such ,thinned-wall' preparations, 40,50 µm in thickness, the stained endothelial cells are clearly visible. Because of the preparation thickness and the use of water-soluble media during the preparation, some subendothelial lipid accumulations, characteristic of the early stages of atherosclerosis process, are well preserved. [source] Salvianolic acid B attenuates VCAM-1 and ICAM-1 expression in TNF-,-treated human aortic endothelial cellsJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 3 2001Yung-Hsiang Chen Abstract Attachment to, and migration of leukocytes into the vessel wall is an early event in atherogenesis. Expression of cell adhesion molecules by the arterial endothelium may play a major role in atherosclerosis. It has been suggested that antioxidants inhibit the expression of adhesion molecules and may thus attenuate the processes leading to atherosclerosis. In the present study, the effects of a potent water-soluble antioxidant, salvianolic acid B (Sal B), and an aqueous ethanolic extract (SME), both derived from a Chinese herb, Salvia miltiorrhiza, on the expression of endothelial-leukocyte adhesion molecules by tumor necrosis factor-, (TNF-,)-treated human aortic endothelial cells (HAECs) were investigated. When pretreated with SME (50 and 100 ,g/ml), the TNF-,-induced expression of vascular adhesion molecule-1 (VCAM-1) was notably attenuated (77.2,±,3.2% and 80.0,±,2.2%, respectively); and with Sal B (1, 2.5, 5, 10, and 20 ,g/ml), 84.5,±,1.9%, 78.8,±,1.2%, 58.9,±,0.4%, 58.7,±,0.9%, and 57.4,±,0.3%, respectively. Dose-dependent lowering of expression of intercellular cell adhesion molecule-1 (ICAM-1) was also seen with SME or Sal B. In contrast, the expression of endothelial cell selectin (E-selectin) was not affected. SME (50 ,g/ml) or Sal B (5 ,g/ml) significantly reduced the binding of the human monocytic cell line, U937, to TNF-,-stimulated HAECs (45.7,±,2.5% and 55.8,±,1.2%, respectively). SME or Sal B significantly inhibited TNF-,-induced activation of nuclear factor kappa B (NF-,B) in HAECs (0.36- and 0.48-fold, respectively). These results demonstrate that SME and Sal B have anti-inflammatory properties and may explain their anti-atherosclerotic properties. This new mechanism of action of Sal B and SME, in addition to their previously reported inhibition of LDL, may help explain their efficacy in the treatment of atherosclerosis. J. Cell. Biochem. 82:512,521, 2001. © 2001 Wiley-Liss, Inc. [source] 3D flow-independent peripheral vessel wall imaging using T2 -prepared phase-sensitive inversion-recovery steady-state free precessionJOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 2 2010Jingsi Xie BS Abstract Purpose: To develop a 3D flow-independent peripheral vessel wall imaging method using T2 -prepared phase-sensitive inversion-recovery (T2PSIR) steady-state free precession (SSFP). Materials and Methods: A 3D T2 -prepared and nonselective inversion-recovery SSFP sequence was designed to achieve flow-independent blood suppression for vessel wall imaging based on T1 and T2 properties of the vessel wall and blood. To maximize image contrast and reduce its dependence on the inversion time (TI), phase-sensitive reconstruction was used to restore the true signal difference between vessel wall and blood. The feasibility of this technique for peripheral artery wall imaging was tested in 13 healthy subjects. Image signal-to-noise ratio (SNR), wall/lumen contrast-to-noise ratio (CNR), and scan efficiency were compared between this technique and conventional 2D double inversion recovery , turbo spin echo (DIR-TSE) in eight subjects. Results: 3D T2PSIR SSFP provided more efficient data acquisition (32 slices and 64 mm in 4 minutes, 7.5 seconds per slice) than 2D DIR-TSE (2,3 minutes per slice). SNR of the vessel wall and CNR between vessel wall and lumen were significantly increased as compared to those of DIR-TSE (P < 0.001). Vessel wall and lumen areas of the two techniques are strongly correlated (intraclass correlation coefficients: 0.975 and 0.937, respectively; P < 0.001 for both). The lumen area of T2PSIR SSFP is slightly larger than that of DIR-TSE (P = 0.008). The difference in vessel wall area between the two techniques is not statistically significant. Conclusion: T2PSIR SSFP is a promising technique for peripheral vessel wall imaging. It provides excellent blood signal suppression and vessel wall/lumen contrast. It can cover a 3D volume efficiently and is flow- and TI-independent. J. Magn. Reson. Imaging 2010;32:399,408. © 2010 Wiley-Liss, Inc. [source] MRI of early- and late-stage arterial remodeling in a low-level cholesterol-fed rabbit model of atherosclerosisJOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 4 2007John A. Ronald MS Abstract Purpose To monitor early- and late-stage arterial remodeling following low-level cholesterol (CH) feeding in rabbits using a standardized MRI protocol. Materials and Methods New Zealand White rabbits were fed a CH diet (0.25% w/w) (n = 15) or normal chow (n = 6) and imaged either at 0, 2, 6, 8, and 11 months ("early-stage") or 12, 14, 16, 18, and 20 months ("late-stage"). T2-weighted fast-spin-echo images (,200 ,m in-plane resolution) of aortic lesions were collected using either a 1.5 or 3.0T MR scanner interfaced with a customized surface RF coil. Luminal (LA), outer vessel wall boundary (OVBA), and vessel wall areas (VWA) were assessed. Results Among CH-fed animals in the early-stage group, increased VWA associated with decreased OVBA and a more pronounced decrease in LA was first detectable at 8 months. These changes became more evident between 8 and 11 months. In the late-stage group, lesions continued to grow in response to CH-feeding, as VWA significantly increased at regular 2-month intervals. Beyond 16 months, signal intensity differences (reflecting increased lesion complexity) within the vessel wall were noted. Conclusion This often-overlooked rabbit model combined with customized MR technology holds tremendous promise for studying the natural progression, regression, and remodeling of atherosclerotic lesions. J. Magn. Reson. Imaging 2007;26:1010,1019. © 2007 Wiley-Liss, Inc. [source] MR coronary vessel wall imaging: Comparison between radial and spiral k-space samplingJOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 5 2006Marcus Katoh MD Abstract Purpose To compare radial and spiral k-space sampling in navigator-gated ECG-triggered three-dimensional (3D) coronary vessel wall imaging. Materials and Methods The right coronary artery (RCA) vessel walls of eight healthy subjects were imaged using a modified double-inversion prepulse in concert with radial and spiral data acquisition. For data analysis, two investigators blinded to the sequence parameters subjectively assessed image quality in terms of artifacts and vessel wall visualization. Objective measures of the signal-to-noise ratio (SNR), contrast-to-noise ratio (CNR), and vessel wall definition were also determined. Results Radial k-space sampling demonstrated fewer artifacts and led to improved visualization of the coronary vessel wall compared to spiral imaging (P < 0.05). This finding was also reflected in a better vessel wall definition using radial data acquisition (P < 0.05). SNR and CNR were found to be higher when spiral k-space sampling was used (n.s.). Conclusion Radial k-space sampling in concert with free-breathing navigator-gated cardiac-triggered MRI of the coronary vessel wall resulted in fewer motion artifacts and improved vessel wall definition compared to spiral k-space sampling. The proposed approach therefore appears to be preferable. J. Magn. Reson. Imaging 2006. © 2006 Wiley-Liss, Inc. [source] Comparison between three-dimensional volume-selective turbo spin-echo imaging and two-dimensional ultrasound for assessing carotid artery structure and functionJOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 3 2005Lindsey A. Crowe PhD Abstract Purpose To compare a volume-selective three-dimensional turbo spin echo (TSE) technique with ultrasound (US) for assessing carotid artery wall structure and function. Materials and Methods A three-dimensional volume-selective TSE technique was used to image the carotid artery in 10 healthy subjects and five hypertensive subjects (each of whom were scanned three times while they received different hypertension treatments). Lumen and wall area were measured on MR images. Two-dimensional US measurements of the intima-media thickness (IMT) and lumen diameter were taken in three orientations through a single cross section. The lumen area change over the cardiac cycle was used to determine distension. For validation, a Bland-Altman analysis was used to compare the vessel wall and lumen areas measured by three-dimensional MRI volumes with those obtained by US scans. Results Agreement between the two methods was found. The mean difference in distension between US and MRI was 1.2% (±5.1%). For the wall area measurements, good agreement was shown, but there was a systematic difference due to the visualization of the adventitia by MRI. Both techniques offer an easy way to objectively measure lumen indices. MRI can provide the complete circumference over the length of a vessel, while US is flexible and relatively inexpensive. The application of US is limited, however, when subjects are poorly echogenic. A difference between hypertensive and healthy subjects was found. Conclusion There was a good agreement between MRI and the clinically established two-dimensional US method. The MRI method has the advantage of providing increased vessel coverage, which permits one to assess localized abnormalities without assuming vessel uniformity. J. Magn. Reson. Imaging 2005;21:282,289. © 2005 Wiley-Liss, Inc. [source] Intramyocardial arterial narrowing in dogs with subaortic stenosisJOURNAL OF SMALL ANIMAL PRACTICE, Issue 9 2004T. Falk Earlier studies have described intramyocardial arterial narrowing based on hyperplasia and hypertrophy of the vessel wall in dogs with subaortic stenosis (SAS). In theory, such changes might increase the risk of sudden death, as they seem to do in heart disease in other species. This retrospective pathological study describes and quantifies intramyocardial arterial narrowing in 44 dogs with naturally occurring SAS and in eight control dogs. The majority of the dogs with SAS died suddenly (n=27); nine had died or been euthanased with signs of heart failure and eight were euthanased without clinical signs. Dogs with SAS had significantly narrower intramyocardial arteries (P<0.001) and more myocardial fibrosis (P<0.001) than control dogs. Male dogs and those with more severe hypertrophy had more vessel narrowing (P=0.02 and P=0.02, respectively), whereas dogs with dilated hearts had slightly less pronounced arterial thickening (P=0.01). Arterial narrowing was not related to age, but fibrosis increased with age (P=0.047). Dogs that died suddenly did not have a greater number of arterial changes than other dogs with SAS. This study suggests that most dogs with SAS have intramyocardial arterial narrowing and that the risk of dying suddenly is not significantly related to the overall degree of vessel obliteration. [source] ORIGINAL ARTICLE: Venous thromboembolism and subsequent diagnosis of subarachnoid hemorrhage: a 20-year cohort studyJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 8 2010H. T. SŘRENSEN Summary.,Background:,Venous thromboembolism is a predictor of subsequent risk of ischemic stroke and intracerebral hemorrhage, but no data are available regarding its association with risk of subarachnoid hemorrhage. Objectives:,To examine this issue, we conducted a nationwide cohort study in Denmark. Patients and methods: Between 1977 and 2007, we identified 97 558 patients with a hospital diagnosis of venous thromboembolism and obtained information on risk of subsequent subarachnoid hemorrhage during follow-up in the Danish Registry of Patients. The incidence of subarachnoid hemorrhage in the venous thromboembolism cohort was compared with that of 453 406 population control cohort members. Results:,For patients with pulmonary embolism (PE), there was clearly an increased risk of subarachnoid hemorrhage, both during the first year of follow-up [relative risk 2.69; 95% confidence interval (CI), 1.32,5.48] and during later follow-up of 2,20 years (relative risk 1.40; 95% CI, 1.05,1.87). For patients with deep venous thrombosis (DVT) the risk was likewise clearly increased during the first year of follow-up (relative risk 1.91; 95% CI, 1.13,3.22), but not during later follow-up (relative risk 1.04; 95% CI, 0.81,1.32). Conclusions:,We found evidence that PE is associated with an increased long-term risk of subarachnoid hemorrhage. The two diseases might share etiologic pathways affecting the vessel wall or share unknown risk factors. [source] A snake venom metalloproteinase, kistomin, cleaves platelet glycoprotein VI and impairs platelet functionsJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 9 2008C. C. HSU Summary.,Background and objectives:,Injuries to the vessel wall and subsequent exposure of the matrix of the subendothelial layer resulted in thrombus formation. Platelet glycoprotein (GP) Ib and VI play a crucial role in matrix-induced activation and aggregation of platelets. Methods and results:,In the present study, we reported that the GPIb-cleaving snake venom metalloproteinase (SVMP), kistomin, inhibited collagen-induced platelet aggregation. Moreover, kistomin inhibited platelet aggregation induced by convulxin (CVX, a GPVI agonist) and a GPVI-specific antibody in a concentration and time-dependent manner. Kistomin treatment decreased platelet GPVI but not integrin ,2,1 and ,IIb,3, accompanied with the formation of GPVI cleavage fragments, as determined by flow cytometric and Western blot analyses. In addition, intact platelet GPVI and recombinant GPVI were digested by kistomin to release 25- and 35-kDa fragments, suggesting that kistomin cleaved GPVI near the mucin-like region. We designed four synthetic peptides ranging from Leu180 to Asn249 as the substrates for kistomin and found that kistomin cleaved these synthetic peptides at FSE205/A206TA and NKV218/F219TT, as analyzed by MALDI-TOF-MS. In addition, GPVI-specific antibody-induced tyrosine kinase phosphorylation in platelets was reduced after kistomin pretreatment, and platelet adhesion to collagen but not to fibrinogen was attenuated by kistomin. Conclusions:,We provided here the first evidence that a P-I snake venom metalloproteinase, kistomin, inhibits the interaction between collagen and platelet GPVI through its proteolytic activity on GPVI, thus providing an alternative strategy for developing new anti-thrombotic agents. [source] Increased metastatic potential of tumor cells in von Willebrand factor-deficient miceJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 3 2006V. TERRAUBE Summary.,Background:,The key role played by von Willebrand factor (VWF) in platelet adhesion suggests a potential implication in various pathologies, where this process is involved. In cancer metastasis development, tumor cells interact with platelets and the vessel wall to extravasate from the circulation. As a potential mediator of platelet,tumor cell interactions, VWF could influence this early step of tumor spread and therefore play a role in cancer metastasis.Objectives:,To investigate whether VWF is involved in metastasis development.Methods:,In a first step, we characterized the interaction between murine melanoma cells B16-BL6 and VWF in vitro. In a second step, an experimental metastasis model was used to compare the formation of pulmonary metastatic foci in C57BL/6 wild-type and VWF-null mice following the injection of B16-BL6 cells or Lewis lung carcinoma cells.Results:,In vitro adhesion assays revealed that VWF is able to promote a dose-dependent adhesion of B16-BL6 cells via its Arg-Gly-Asp (RGD) sequence. In the experimental metastasis model, we found a significant increase in the number of pulmonary metastatic foci in VWF-null mice compared with the wild-type mice, a phenotype that could be corrected by restoring VWF plasma levels. We also showed that increased survival of the tumor cells in the lungs during the first 24 h in the absence of VWF was the cause of this increased metastasis.Conclusion:,These findings suggest that VWF plays a protective role against tumor cell dissemination in vivo. Underlying mechanisms remain to be investigated. [source] Mathematical modeling of 980-nm and 1320-nm endovenous laser treatmentLASERS IN SURGERY AND MEDICINE, Issue 3 2007Serge R. Mordon PhD Abstract Background and Objectives Endovenous laser treatment (ELT) has been proposed as an alternative in the treatment of reflux of the great saphenous vein (GSV) and small saphenous vein (SSV). Numerous studies have since demonstrated that this technique is both safe and efficacious. ELT was presented initially using diode lasers of 810 nm, 940 nm, and 980 nm. Recently, a 1,320-nm Nd:YAG laser was introduced for ELT. This study aims to provide mathematical modeling of ELT in order to compare 980 nm and 1,320 nm laser-induced damage of saphenous veins. Study Design/Materials and Methods The model is based on calculations describing light distribution using the diffusion approximation of the transport theory, the temperature rise using the bioheat equation, and the laser-induced injury using the Arrhenius damage model. The geometry to simulate ELT was based on a 2D model consisting of a cylindrically symmetric blood vessel including a vessel wall and surrounded by an infinite homogenous tissue. The mathematical model was implemented using the Macsyma-Pdease2D software (Macsyma, Inc., Arlington, MA). Calculations were performed so as to determine the damage induced in the intima tunica, the externa tunica and inside the peri-venous tissue for 3 mm and 5 mm vessels (considered after tumescent anesthesia) and different linear endovenous energy densities (LEED) usually reported in the literature. Results Calculations were performed for two different vein diameters: 3 mm and 5 mm and with LEED typically reported in the literature. For 980 nm, LEED: 50 to 160 J/cm (CW mode, 2 mm/second pullback speed, power: 10 W to 32 W) and for 1,320 nm, LEED: 50 to 80 J/cm (pulsed mode, pulse duration 1.2 milliseconds, peak power: 135 W, repetition rate 30 Hz to 50 Hz). Discussion and Conclusion Numerical simulations are in agreement with LEED reported in clinical studies. Mathematical modeling shows clearly that 1,320 nm, with a better absorption by the vessel wall, requires less energy to achieve wall damage. In the 810,1,320-nm range, blood plays only a minor role. Consequently, the classification of these lasers into hemoglobin-specific laser wavelengths (810, 940, 980 nm) and water-specific laser wavelengths (1,320 nm) is inappropriate. In terms of closure rate, 980 nm and 1,320 nm can lead to similar results and, as reported by the literature, to similar side effects. This model should serve as a useful tool to simulate and better understand the mechanism of action of the ELT. Lasers Surg. Med. 39:256,265, 2007. © 2007 Wiley-Liss, Inc. [source] Vascular response to laser photothermolysis as a function of pulse duration, vessel type, and diameter: Implications for port wine stain laser therapyLASERS IN SURGERY AND MEDICINE, Issue 2 2002Sol Kimel PhD Abstract Background and Objective Treatment of port wine stains (PWS) by photothermolysis can be improved by optimizing laser parameters on an individual patient basis. We have studied the critical role of pulse duration (tp) on the treatment efficacy. Study Design/Materials and Methods The V-beam laser (Candela) allowed changing tp over user-specified discrete values between 1.5 and 40 milliseconds by delivering a series of 100 microsecond spikes. For the 1.5 and 3 millisecond pulses, three spikes were observed at intervals tp/2 and for tp,,,6 milliseconds, four spikes separated by tp/3. The ScleroPlus laser (Candela) has a smooth output over its fixed 1.5 milliseconds duration. Blood vessels in the chick chorioallantoic membrane (CAM) were irradiated at fixed wavelength (595 nm), spot size (7 mm), radiant exposure (15 Jcm,2), and at variable tp. The CAM contains an extensive microvascular network ranging from capillaries with diameter D,<,30 ,m to blood vessels of D,,,120 ,m. The CAM assay allows real-time video documentation, and observation of blood flow in pre-capillary arterioles (A) and post-capillary venules (V). Vessel injury was graded from recorded videotapes. Mathematical modeling was developed to interpret results of vessel injury when varying tp and D. A modified thermal relaxation time was introduced to calculate vessel wall temperature following laser exposure. Results Arterioles. For increasing tp, overall damage was found to decrease. For fixed tp, damage decreased with vessel size. Venules. For all D, damage was smaller than for corresponding arterioles. There was no dependence of damage on tp. For given tp, no variation of damage with D was observed. Photothermolysis due to spiked (V-beam) vs. smooth (Scleroplus) delivery of laser energy at fixed tp (1.5 milliseconds), showed similar vessel injuries for al values of D (P>0.05). Conclusions The difference between initial arteriole and venule damage could be explained by the threefold higher absorption coefficient at 595 nm in (oxygen-poor!) arterioles. In human patients, PWS consist of ectatic venules (characterized by higher absorption), so that these considerations favor the use of 595-nm irradiation for laser photothermolysis. For optimal treatment of PWS it is proposed that tp be between 0.1 and 1.5 milliseconds. This is based on a modified relaxation time ,d,, defined as the time required for heat conduction into the full thickness of the vessel wall, which is assumed to have a thickness ,D ,,0.1D. The corresponding ,d, will be a factor of about six smaller than given in the literature. For vessels with D between 30 and 300 ,m, ,d, ranges from 0.1 to 1.5 milliseconds. Lasers Surg. Med. 30:160,169, 2002. © 2002 Wiley-Liss, Inc. [source] Liposome-enhanced MRI of neointimal lesions in the ApoE-KO mouseMAGNETIC RESONANCE IN MEDICINE, Issue 5 2006Willem J.M. Mulder Abstract Conventional high-resolution MRI is capable of detecting lipid-rich atherosclerotic plaques in both human atherosclerosis and animal models of atherosclerosis. In this study we induced neointimal lesions in ApoE-KO mice by placing a constrictive collar around the right carotid artery. The model was imaged with conventional multispectral MRI, and the thickened wall could not be distinguished from surrounding tissue. We then tested paramagnetic liposomes (mean size = 90 nm) for their ability to improve MRI visualization of induced thickening, using Gd-DTPA as a control. T1 -weighted (T1 -w), black-blood MRI of the neck area of the mice was performed before and 15 min, 45 min, and 24 hr after intravenous injection of either paramagnetic liposomes or Gd-DTPA. The collared vessel wall of mice that were injected with liposomes showed a pronounced signal enhancement of ,100% immediately after injection, which was sustained largely until 24 hr postinjection. In contrast, the vessel wall of all controls (left carotid artery and animals injected with Gd-DTPA) did not show significant contrast enhancement at those time points. This study demonstrates that intimal thickening in ApoE-KO mice can be effectively detected by contrast-enhanced (CE)-MRI upon injection of paramagnetic liposomes. Magn Reson Med, 2006. © 2006 Wiley-Liss, Inc. [source] A Computer-Based Method for Determination of the Cell-Free Layer Width in MicrocirculationMICROCIRCULATION, Issue 3 2006SANGHO KIM ABSTRACT Objectives: The cell-free layer between the erythrocyte column and the vessel wall is an important determinant of hydrodynamic resistance in microcirculatory vessels. The authors report a method for continuous measurement of the width of this layer. Methods: The light intensity of a linear array of pixels perpendicular to the vessel axis is continuously determined from a video image of a microcirculatory vessel. A threshold level based on Otsu's method is used to establish the interface between the cell-free layer and the erythrocyte column. To test the method, video images at 750,4500 frames/s were obtained from venules and arterioles in rat spinotrapezius muscle at normal and reduced arterial pressures before and after induction of erythrocyte aggregation with Dextran 500. The current measurements were compared to manual measurements of the same images. Results: Values obtained by the manual and the new methods were in agreement within the 95% confidence limit by the Bland-Altman analysis and within 90,95% range by the correlation coefficient (R2). The more frequent measurements reveal substantial, rapid variations in cell-free layer width and changes in mean values with alteration of arterial pressure and red cell aggregability. Conclusions: A new, computer-based technique has been developed that provides measurements of rapid, time-dependent variations in the width of the cell-free layer in the microcirculation. [source] Transient Osmotic Absorption of Fluid in Microvessels Exposed to Low Concentrations of Dimethyl SulfoxideMICROCIRCULATION, Issue 1 2006CATHERINE A. GLASS ABSTRACT Dimethyl Sulfoxide (DMSO) is a common solvent for pharmacological agents. It is a small, lipophilic molecule thought to be relatively highly permeable through the cell membrane. While measuring the effect of low concentrations of DMSO (0.05,0.5% v/v) on capillary hydraulic conductivity as a vehicle control for pharmacological agents, the authors noticed what appeared to be an unusual transient absorption of fluid across the vessel wall. This absorption occurred during occlusion of the vessel, but dissipated quickly (1.7,8.6 s). The transient reabsorption reappeared upon each successive occlusion. To determine the nature of this transient absorption, the authors have measured the effect of increasing the pressure of the perfusing solution, of the concentration and time of perfusion of DMSO, and of superfusing the DMSO. They found that the absorption rate, but not the filtration rate, was concentration dependent, and was significantly correlated with the osmotic pressure of the DMSO. Moreover, the time taken for completion of the transient, i.e., time to reversal of flow, was inversely proportional to the hydraulic conductivity of the vessel. Furthermore, the transient absorption could be reduced and eventually abolished by increasing the hydrostatic pressure. These results strongly suggested that perfusion with low concentrations of DMSO could set up a significant osmotic pressure gradient across the vessel wall. This proposed mechanism for the absorption was confirmed by the measurement of a significant osmotic reflection coefficient of the vessel wall to DMSO (0.11 ± 0.01). Relatively low concentrations (0.05,0.5%) of DMSO were therefore able to stimulate a significant osmotic transient across the blood vessel walls. [source] Ischemia,Reperfusion Impairs Ascending Vasodilation in Feed Arteries of Hamster Skeletal MuscleMICROCIRCULATION, Issue 7 2005MIRIAM C. J. DE WITH ABSTRACT Objective: Vasodilation originating within the microcirculation ascends into proximal feed arteries during muscle contraction to attain peak levels of muscle blood flow. Ascending vasodilation (AVD) requires an intact endothelium, as does conducted vasodilation in response to acetylcholine (ACh). Whereas ischemia,reperfusion (I-R) can affect endothelial cell function, the effect of I-R on AVD is unknown. The authors tested the hypothesis that I-R (1h,1h) would impair AVD. Methods: Using the retractor muscle of anesthetized hamsters, contractions were evoked using field stimulation (200 ms at 40 Hz every 2 s for 1 min) and ACh was delivered using microiontophoresis (1 ,m tip, 500,4000 ms pulse at 800 nA). Feed artery responses were monitored 500,1500 ,m upstream. Results: Neither resting (51 ± 4 ,m) nor maximal diameter (81 ± 5 ,m; 10 ,m sodium nitroprusside) following I-R (n = 8) were different from time-matched controls (n = 10). With peak active tension of 23 ± 4 mN · mm,2, control AVD was 26 ± 2 ,m. Following I-R, active tension fell by 48% (p < .05) and AVD by 57% (p < .05). Stimulation at 70 Hz restored active tension but AVD remained depressed by nearly half (p < .05), as did local and conducted responses to ACh. Nevertheless, control responses to 500 ms ACh were restored by increasing stimulus duration to 4000 ms. Conclusions: Ischemia,reperfusion impairs the initiation of feed artery dilation with muscle contraction and with ACh while conduction along the vessel wall is preserved. Respective components of endothelial cell signaling events may differ in their susceptibility to I-R. [source] Interactions of Platelets with Subendothelium and EndotheliumMICROCIRCULATION, Issue 3 2005JUNMEI CHEN PhD ABSTRACT In this review, the authors summarize how platelets interact with subendothelium when the vessel wall is damaged or with intact endothelium in the inflammatory state. When subendothelium is exposed to rapidly flowing blood upon vessel damage, platelets adhere rapidly to the exposed surface, decelerate, and aggregate to arrest bleeding. Under high shear stress, such as is found in the microcirculation, the interaction between subendothelial von Willebrand factor (VWF) and its platelet receptor, glycoprotein (GP) Ib-IX-V, is required to slow down platelets and allow the platelet collagen receptors ,2,1 and GP VI to bind to collagen. GP VI and ,2,1 play important roles to activate platelets in the early stage and work with GP Ib-IX-V to fully activate platelets to form thrombi. GP Ib-IX-V and GP VI employ similar signaling pathways for platelet activation and the signals from both receptors are down-modulated by PECAM-1 (platelet,endothelial,cell adhesion molecule 1) to prevent unnecessary platelet activation under high shear. During inflammatory states, intact endothelial cells release VWF and P-selectin from their Weibel-Palade bodies. Both molecules are ligands for GP Ib-IX-V. The newly released VWF is larger and stickier than the form normally found in plasma and binds platelets spontaneously. Normally, VWF is processed by proteolysis by the plasma metalloprotease ADAMTS-13. Failure of this processing results in the microvascular thrombotic disorder thrombotic thrombocytopenic purpura. In this review, the authors also use available crystal structures of platelet receptors and ligands to explain the details of their interactions. [source] Detection of peripherally inserted central catheter occlusion by in-line pressure monitoringPEDIATRIC ANESTHESIA, Issue 7 2002Junichi Arai MD SummaryBackground: Peripherally inserted central catheters (PICC) are being increasingly used in neonatal practice. Their use is not without technical difficulty. This report describes the use of continuous pressure monitoring to detect catheter occlusion in critically ill neonates. Methods: In-line venous pressure of the PICC line was monitored by pressure transducer in neonates; 28-gauge 20 cm PICC or 29-gauge 25 cm PICC were used. Results: In-line pressure of the PICC was monitored 64 times in 50 neonates. Increases in the in-line pressure were observed when the catheter tip was against the vessel wall and the catheter was obstructed partially or completely. Decreases were observed when the infusion syringe was changed and when an inappropriate infusion rate was set. Two infants experienced marked variations of blood pressure due to intermittent catheter occlusion of the tip against the vessel wall. These infants were receiving dopamine via a PICC line. Conclusions: In critically ill infants, in-line pressure monitoring of the PICC is helpful in detecting the occlusion of the catheter. [source] Erythema Toxicum Neonatorum: An Immunohistochemical AnalysisPEDIATRIC DERMATOLOGY, Issue 3 2001Giovanna Marchini M.D., Ph.D. The recruitment of leukocytes to tissues implicates the involvement of adhesion molecules, cytokines, and chemokines. We therefore performed immunohistochemistry on punch biopsy specimens from cutaneous lesions of ten 1-day-old infants with erythema toxicum using specific monoclonal antibodies directed against a variety of adhesion molecules, cytokines, chemokines, and cell type-specific membrane markers. Biopsy specimens of noninflamed skin from four matched newborns and four adults served as controls. The immunohistologic features of erythema toxicum in all 10 infants included a strong staining of the adhesion molecule E-selectin in the vessel wall and the presence of numerous inflammatory cells that were identified as dendritic cells (CD1a, CD83, HLA-DR, CD40, and ICAM-1 positive), eosinophils (EG2 positive), neutrophils (CD15 positive), macrophages (CD14, CD68, and Mac387 positive), and E-selectin-expressing cells. Furthermore, the lesions showed a high incidence of the proinflammatory cytokines interleukin (IL)-1, and IL-1, and of the chemokines IL-8 and eotaxin. This immunologic activity was reduced or absent in noninflamed skin from newborn controls and adults. We conclude that there is an accumulation and activation of immune cells in the lesions of erythema toxicum, also present in noninflamed skin of 1-day-old infants, but to a lower level. The physiologic significance of the rash remains to be elucidated. [source] Fluorescence Kinetics of Protoporphyrin-IX Induced from 5-ALA Compounds in Rabbit Postballoon Injury Model for ALA-PhotoangioplastyPHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 5 2008Oh-Choon Kwon Protoporphyrin IX (PpIX) is one of the photodynamically active substances that are endogenously synthesized in the metabolic pathway for heme as a precursor. Aminolevulinic acid-esters are more lipophilic than conventional 5-aminolevulinic acid (ALA) and some of them are currently being approved as new drugs for photodynamic diagnosis (PDD) and photodynamic therapy (PDT). In order to investigate the pharmacokinetics of ALA and ALA-ethyl ester (ALA-ethyl) in the atheromatous plaque and normal aortic wall of rabbit postballoon injured artery, each 60 mg kg,1 of ALA or ALA-ethyl was injected intravenously followed by serial detection of PpIX fluorescence of harvested arteries at 0,48 h post-injection. Maximum PpIX build-up in the atheromatous plaque was seen at 2 h after injecting ALA. In contrast, it occurred at 9 h after injecting ALA-ethyl. In addition, the selective build-up of ALA in the atheromatous plaque compared to normal vessel wall was much higher (10 times) than that of ALA-ethyl. The time of maximum fluorescence intensity of PpIX was employed as drug-light-interval for subsequent PDT treatment of the atheromatous plaque with 50,150 J cm,1 of light dose. Significant reduction in plaque was observed without damage of the medial wall at both groups, but smooth muscle cell (SMC) was still present in the media region below the PDT-treated atheromatous plaque. In conclusion, ALA may be a more effective compound for endovascular PDT treatment of the atheromatous plaque compared with ALA-ethyl based on their pharmacokinetics, but further optimization of PDT methodology remains to remove completely residual SMC in the media for preventing potential restenosis. [source] | ||||||||||||||||||||||||||||||||||||||||