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G Sangiorgi

Publications and source records attributed to G Sangiorgi.

36 records · Page 2Linked to original sources
PubMed1998

Adventitial vasa vasorum in balloon-injured coronary arteries: visualization and quantitation by a microscopic three-dimensional computed tomography technique.

OBJECTIVES: The objective of this study was to examine the quantitative response of the adventitial vasa vasorum to balloon-induced coronary injury. BACKGROUND: Recent attention has focused on the role of vasa vasorum in atherosclerotic and restenotic coronary artery disease. However, the three-dimensional anatomy of these complex vessels is largely unknown, especially after angioplasty injury. The purpose of this study was to visualize and quantitate three-dimensional spatial patterns of vasa vasorum in normal and balloon injured porcine coronary arteries. We also studied the spatial growth of vasa vasorum in regions of neointimal formation. A novel imaging technique, microscopic computed tomography, was used for these studies. METHODS: Four pigs were killed 28 d after coronary balloon injury, and four pigs with uninjured coronary arteries served as normal controls. The coronary arteries were injected with a low-viscosity, radiopaque liquid polymer compound. Normal and injured coronary segments were scanned using a microscopic computed tomography technique. Three-dimensional reconstructed maximum intensity projection and voxel gradient shading images were displayed at different angles and voxel threshold values, using image analysis software. For quantitation, seven to 10 cross-sectional images (40 normal and 32 balloon injured cross-sections) were captured from each specimen at a voxel size of 21 microm. RESULTS: Normal vasa vasorum originated from the coronary artery lumen, principally at large branch points. Two different types of vasa were found and classified as first-order or second-order according to location and direction. In balloon-injured coronary arteries, adventitial vasa vasorum density was increased (3.16+/-0.17/mm2 vs. 1.90+/-0.06/mm2, p = 0.0001; respectively), suggesting neovascularization by 28 d after vessel injury. Also, in these injured arteries, the vasa spatial distribution was disrupted compared with normal vessels, with proportionally more second-order vasa vasorum. The diameters of first-order and second-order vasa were smaller in normal compared with balloon-treated coronary arteries (p = 0.012 first-order; p < 0.001, second-order; respectively). The density of newly formed vasa vasorum was proportional to vessel stenosis (r = 0.81, p = 0.0001). Although the total number of vasa was increased after injury, the total vascular area comprised of vasa was significantly reduced in injured vessels compared with normals (3.83+/-0.20% to 5.42+/-0.56%, p = 0.0185). CONCLUSIONS: Adventitial neovascularization occurs after balloon injury. The number of new vessels is proportional to vessel stenosis. These findings may hold substantial implications for the therapy of vascular disease and restenosis.

Angioplasty, Balloon, Coronary↗
PubMed1998

Artery size, neointima, and remodeling: time for some standards.

Controversy continues regarding the mechanism of coronary restenosis. While neointimal thickening was initially considered the major cause, recent studies suggest that changes in arterial size, or remodeling, plays an important or even dominant role in late lumen loss. Moreover, neointimal thickness and remodeling may be interrelated. The field has been complicated by the fact that remodeling analyses have not used consistent definitions or methods. In this editorial we thus describe a quantitative paradigm for remodeling analyses: as arterial plaque or neointima forms in an artery, it is accompanied by luminal encroachment, artery expansion or gradations of either. In this manner, remodeling is generally defined as any arterial size change (enlargement or contraction), independent or dependent of neointimal thickening. Standardization of definitions and quantitative methods may improve understanding of the components of restenosis resulting from artery size changes, neointimal thickening and their impact on lumen size.

Animals↗
PubMed1997

Arterial remodeling after experimental percutaneous injury is highly dependent on adventitial injury and histopathology.

BACKGROUND: The extent and nature of unfavorable geometric remodeling, especially related to the adventitia, has not been studied previously. The purpose of this study was to examine two methods of experimental arterial injury, characterize the extent of remodeling, and determine if remodeling is injury-specific. METHODS: Two methods for producing coronary stenoses in pigs were used: heat injury using thermal balloon angioplasty (resulting in adventitial fibrosis), and copper stent implantation (resulting in intense inflammation). Histomorphometric parameters included changes in neointimal thickness (delta neointima) from uninjured to injured sections, and differences in area circumscribed by the internal and external elastic laminas (delta internal elastic lamina area and delta external elastic lamina area, respectively). Remodeling was calculated for each lesion as the enlargement of the external elastic lamina area or internal elastic lamina area for incremental neointimal thickening, expressed as the slopes delta external elastic area/delta neointima and delta internal elastic lamina area/delta neointima. RESULTS: Remodeling indices for the heat lesions for the heat lesions were negative (delta internal elastic lamina area/delta neointima = 0.15, delta external elastic lamina area/delta neointima = 0.64) and indicated little remodeling in contrast to copper stent injury (delta internal elastic lamina area/delta neointima = 0.95, delta external elastic lamina area/delta neointima = 1.20). CONCLUSIONS: Remodeling in fibrotic compared to inflammatory lesions differs markedly, and may explain increased restenosis rates observed in thermal balloon angioplasty in patients. This formulation may be useful to study remodeling and restenosis following interventional technologies.

Angioplasty, Balloon, Coronary↗
PubMed1996

Porcine model of stent thrombosis: platelets are the primary component of acute stent closure.

Acute stent thrombosis remains a major concern of coronary stent implantation. Animal studies using stents do not adequately mimic this clinical problem, since stent placement is rarely associated with acute closure. The purpose of this study was to develop and characterize a porcine model of stent thrombosis. Improved understanding through such a model may be useful toward preventing and treating acute stent closure. Whole blood was drawn from domestic crossbred swine one day before study. Platelets were isolated, labeled with 111-In tropolone, and reinjected within 18 hr of the study. Bilateral carotid arteries were exposed, and severe injury induced by a series of mechanical crushes. This method produced histologic injury similar to human coronary angioplasty, with medial disruption and large dissections protruding into the lumen. Stenting was performed in standard fashion with 3.5-mm JJIS stents. Local platelet deposition was measured and recorded as 111-In radioactivity using a miniaturized scintillation detector (Dosimeter Corp.) mounted directly at the artery injury site. This measurement was made in real time at 1-min intervals. Similarly, volumetric blood flow was measured in real time by Doppler flowmeter. Eighteen arteries of nine pigs were studied. In nine arteries from nine pigs, crush injury only was performed and monitored. In the contralateral artery, crush injury was followed immediately by placement of a 3.5-mm Palmaz-Schatz (coronary) stent. Blood flow decreased rapidly following injury in both groups and followed a cyclic pattern. Eight arteries of the crush alone and two arteries of the crush plus stent groups were totally occluded 1 hr after crush. 111-In counts normalized to baseline were significantly higher at 1 hr in both groups compared to baseline; in the stented group, counts were higher than in the unstented group. Blood flow was higher in the stented group than in unstented group for 1 hr. Histopathologic observation of the thrombi forming in both crush-only and crush-stent injuries showed severe medial dissections with obstructing medial flap formation. The thrombi forming in both groups were highly platelet rich. This model of stent and arterial thrombosis showed rapid formation of platelet-rich thrombus, cyclic blood flow variations, and acute occlusion in 20% of cases. Stent placement at arterial injury sites is associated with thrombus that is predominantly platelet rich. Stent placement at injury sites enhances platelet deposition over crush injury alone. Despite greater numbers of platelets, as shown by increased 111-In counts, stenting improved vessel patency. These were likely due to higher volumetric blood flow, continuous deposition, and embolization of labeled platelets.

Acute Disease↗
PubMed1996

Effect of long-term treatment with propionyl-L-carnitine on smooth muscle cell polyploidy in spontaneously hypertensive rats.

Experimental studies suggest that DNA content is increased in the smooth muscle cells of the arteries of hypertensive animals. It is unclear whether an increase in DNA content occurring in the smooth muscle cells of hypertensive rats represents a pressure-dependent effect. To evaluate the antihypertensive effect of long-term treatment with propionyl-L-carnitine and the possible morphological changes in thoracic smooth muscle cells correlated with this effect, we studied 4-month-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) randomly divided into five groups. One group of SHR was treated with propionyl-L-carnitine for 12 months; the other four groups of SHR and WKY received no treatment and were controls. We used static and flow cytometry to evaluate the polyploid cell content in thoracic aorta smooth muscle cells. Systolic pressure in untreated SHR progressively increased during the experiment. Treatment did not significantly influence pressure values in SHR. In WKY, blood pressure was significantly lower than that in treated and untreated age-matched SHR (2P < .02). The number of polyploid smooth muscle cells was significantly lower in the propionyl-L-carnitine-treated SHR than in the untreated rats (2P < .04) and similar to values for WKY. The reduction of polyploid cells in treated SHR was paralleled by a significant decrease of the aortic total DNA content, whereas no modifications occurred in smooth muscle cell mass. Long-term treatment with propionyl-L-carnitine may interfere with cellular mechanisms regulating the secondary responses involved in DNA synthesis.

Animals↗
PubMed1996

Age-related changes affecting atherosclerotic risk. Potential for pharmacological intervention.

The incidence of cardiovascular diseases that are related to the atherosclerotic process increases exponentially with age. Organ lesions, the clinical manifestation of atherosclerotic disease, are late events due to complications in the plaque (ulceration, thrombosis, calcification) which are the result of an increased vulnerability to disruption of a previously stable plaque. The higher incidence of age-related clinical events could be explained by a rising sensitivity of plaques to destabilising factors, both parietal and humoral. The increased probability that a plaque in an elderly patient will became vulnerable could be related to those destabilising factors that significantly increase with aging, such as advanced glycation end-products. For these reasons, it seems most important that the analysis of these age-related destabilising factors, rather than those factors that promote the development of early atherosclerotic plaques, should be undertaken. Taking the point of view of a pharmacological intervention, this should eventually lead to a more complete understanding of this process.

Age Factors↗
PubMedDate not supplied

Nonbiodegradable expanded polytetrafluoroethylene-covered stent implantation in porcine peripheral arteries: histologic evaluation of vascular wall response compared with uncoated stents.

PURPOSE: To test the vascular wall response to an expanded polytetrafluoroethylene-covered stent, compared with conventional stenting, up to 6 months after deployment in the vascular district of a swine model. METHODS: Fourteen minipigs underwent implantation of expanded polytetrafluoroethylene-covered stents (CS) and bare stents (BS) in five peripheral arteries. Animals were killed at different time points (from 1 to 180 days). Histopathologic assessment by morphologic and morphometric analysis and by scanning electron microscopy (SEM) were used to assess the incorporation characteristics and re-endothelialization extent of the two types of stents. RESULTS: A total of 70 stents (14 CS and 14 BS in the renal arteries; 28 CS in the iliac arteries, and 14 CS in the aorta) were implanted. Microscopic examination confirmed the absence of occlusive thrombi in both the CS and BS groups. Microthrombi were observed in 10 of 13 CS (77% of cases) and in four of four BS (100% of cases, p < 0.05). Inflammation was mild in 69% of segments in which a CS was implanted and in 74% of segments in which a BS was implanted (p = NS), while a severe inflammatory reaction was observed in 6% of CS segments and in 8% of BS segments (p = NS). No differences were detected at the long-term analysis between neointimal thickness in CS compared with BS segments (0.46 +/- 0.18 mm vs 0.42 +/- 0.26 mm at 90 days and 0.36 +/- 0.08 mm vs 0.35 +/- 0.04 mm at 180 days; p = NS, respectively). At SEM analysis, re-endothelization was evident 15 days after the implant in both CS and BS starting from the stent edges. CONCLUSION: CS implantation did not elicit a more severe thrombotic deposition compared with that of BS. A similar inflammatory reaction of the arterial wall was present in the two stent groups 3 and 6 months following the implant. In addition, CS implantation did not stimulate excessive neointimal formation when compared with BS.

Animals↗
PubMedDate not supplied

Intensive care complications in liver and multivisceral transplantation.

The complications concerning liver and intestinal transplant surgery have relevance for the field of intensive care because they share some characteristics with those following complex long-term surgery. Thus, in this article we shall try to describe complications that are specific to liver and multivisceral transplants. A review of the existing literature on this topic reveals a large number of studies dedicated to early as well as late surgical complications, and immunosuppressive treatment, while there are far fewer contributions describing complications exclusively concerning intensive care. We shall thus attempt to focus on certain aspects where, besides the literature data, we have personal experience. In particular we want to underline the implications of failure in the functional recovery of the graft; alterations in water, electrolyte, and glycemic balance; as well as neurological, respiratory, renal, nutritional, and infective complications.

Critical Care↗
PubMedDate not supplied

Pathology of acute and chronic coronary stenting in humans.

BACKGROUND: Despite the increasing use of stents, few reports have described human coronary artery morphology early and late after stenting. METHODS AND RESULTS: Histology was performed on 55 stents in 35 coronary vessels (32 native arteries and 3 vein grafts) from 32 patients. The mean duration of stent placement was 39+/-82 days. Fibrin, platelets, and neutrophils were associated with stent struts </=11 days after deployment. In stents implanted for </=3 days, only 3% of struts in contact with fibrous plaque had >20 associated inflammatory cells compared with 44% of struts embedded in a lipid core and 36% of struts in contact with damaged media (P<0.001). Neointimal growth determined late histological success, and increased neointimal growth correlated with increased stent size relative to the proximal reference lumen area. Neointimal thickness was greater for struts associated with medial damage than struts in contact with plaque (P<0.0001) or intact media (P<0.0001). When matched for time since treatment, neointimal cell density in stented arteries was similar to that in unstented arteries that had undergone balloon angioplasty and showed similar proteoglycan deposition. CONCLUSIONS: Morphology after coronary stenting demonstrates early thrombus formation and acute inflammation followed by neointimal growth. Medial injury and lipid core penetration by struts result in increased inflammation. Neointima increases as the ratio of stent area to reference lumen area increases. Deployment strategies that reduce medial damage and avoid stent oversizing may lower the frequency of in-stent restenosis.

Angioplasty, Balloon, Coronary↗
PubMedDate not supplied

[Fluvial ire].

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Disasters↗
PubMedDate not supplied

Complete regression of iatrogenic Kaposi's sarcoma due to corticosteroid treatment in a patient with tubercular pericarditis. A case report.

We report a case of drug-induced Kaposi's sarcoma (KS) on the sole of the right foot in a 71-year-old man, treated for 6 months with corticosteroid therapy (prednisolone 25 mg/day) for pericardial effusion. After corticosteroid withdrawal, a tuberculin skin test became strongly positive and pericardial effusion was considered to be of tubercular origin. The patient remained constantly HIV negative during 14 months of follow-up. Seven months after continuous antitubercular treatment, the KS nodules regressed spontaneously and finally disappeared. Histological studies confirmed the diagnosis of KS and documented its complete regression. Laboratory investigation confirmed prior exposure to CMV, EBV and HSV and suggested drug-induced immunological suppression. Analysis of the HLA system revealed the positivity of locus DR5, associated with classical KS. This case report underscores the relationship between genetic background, environmental factors, drug-induced immunosuppression and the evolution of this peculiar neoplasm.

Aged↗