Search PubMed⌕ Search

Biomedical subjects

G Bauriedel

Publications and source records attributed to G Bauriedel.

At least 55 records · Page 3Linked to original sources
PubMed1996

Ultrastructural characteristics of human atherectomy tissue from coronary and lower extremity arterial stenoses.

In animal studies, smooth muscle cell phenotype conversion has been suggested to be an essential prerequisite for subsequent migratory and proliferative events leading to (neo)intima formation. To determine ultrastructural characteristics of individual smooth muscle cells and to relate them to specific lesion types and intimal cell density, we compared atherectomy samples from 17 restenotic and 32 primary coronary and peripheral lesions using transmission electron microscopy and histology. Ultrastructural analysis of cell-rich tissue, predominantly of restenotic origin, revealed smooth muscle cells full of synthetic organelles. Moreover, these cells were frequently found to be surrounded by loose extracellular matrix and partially fragmented basement membrane components. In contrast, plaques exhibiting low cell density, as exclusively seen with primary lesions, displayed an extensive buildup of extracellular matrix containing sparse numbers of microfilament-rich smooth muscle cells. The central finding of our study is a morphometrically quantitated, twofold greater (p <0.001) volume fraction of synthetic organelles (VS) within smooth muscle cells in restenotic versus primary plaques, indicating a more dedifferentiated cellular phenotype as a typical feature of restenotic lesions. Equally enhanced VS values were seen for restenotic coronary and peripheral plaques. No VS decrease was observed during time after angioplasty (2.2 to 30 months) regardless of previous revascularization procedures (balloon angioplasty or atherectomy). Despite intra- and interlesional variability, VS and intimal cell density were strongly correlated (r = 0.74; p <0.001). This correlation was observed more often with clinical restenoses and, importantly, in a portion (10% to 15%) of primary lesions. Data from restenotic lesions indicate that a dedifferentiated smooth muscle cell phenotype, pericellular matrix disintegration, and intimal hypercellularity are long-lasting biologic responses to previous smooth muscle cell injury. Similar tissue characteristics expressed in several primary lesions suggest that comparable pathogenic mechanisms are related to the progression and/or acuity of chronic lesions.

Adult↗
PubMed1996

[Incidence and localization of apoptosis bodies in human arteriosclerosis lesions].

Increased density of smooth muscle cells is an accepted feature of human restenosis after angioplasty. In addition to migration and proliferation, deregulated forms of programmed cell death may represent pathogenic mechanisms which lead to increased intimal cellularity. The goal of the present study was (i) to demonstrate programmed cell death in human plaque tissue by the detection of apoptotic bodies and to distinguish it from cellular necrosis, (ii) to evaluate the frequency and the localization of apoptotic bodies, and (iii) to compare restenotic and primary lesions for different expression patterns. To this end, coronary and peripheral atherectomy specimens from 14 restenotic and 25 primary lesions were examined by electron microscopy and morphometric analysis. Apoptotic bodies were distinguished from cellular necroses due to distinct morphological features, and were observed extracellularly, isolated or cell membrane-bound, as well as intracellularly in smooth muscle cells and macrophages. The main finding of this study is that hypercellular restenotic tissue from both coronary and peripheral lesions contains fewer apoptotic bodies than hypocellular plaques from primary lesions (p < 0.01 and p < 0.05, respectively). Most importantly, a highly significant, inverse correlation was seen between the density of apoptotic bodies and intimal cellularity (r = -0.67; p < 0.0001). Especially in the extracellular matrix regions, restenotic lesions showed fewer apoptotic bodies (p < 0.001). Again, these plaques exhibited a smaller number of apoptotic bodies with intracellular or membrane-bound localization; however, this observation was without statistical significance compared to primary lesions. For both plaque types, apoptotic bodies were found more frequently (by the factor 4-10) in the presence of smooth muscle cells than with macrophages. With respect to the cellular composition of the plaques, apoptotic bodies were evenly detected in 15-28% of all smooth muscle cells and macrophages. Our results document a considerable intimal density of apoptotic bodies in high-grade human arteriosclerotic lesions and, in addition, reveal nearby smooth muscle cells and macrophages exhibiting intensive phagocytotic capacity. Differences in the density of apoptotic bodies and in cellularity, coincident with an inverse correlation between these determinants, were observed for restenotic and primary tissue. These findings strongly point to deregulated forms of programmed cell death as important pathogenic mechanisms involved in human restenosis.

Aged↗
PubMed1995

[Intra-aortic balloon counterpulsation as percutaneous therapy option in cardiogenic shock].

Six months after sustaining a posterior wall myocardial infarction a 40-year-old man had a further infarction in the anterior wall region. After thrombolysis treatment with recombinant tissue plasminogen activator the patient was at first symptom-free and haemodynamically stable, but 48 hours later another anterior wall re-infarction occurred with cardiogenic shock. Despite infusions of catecholamines at highest dosage and successful coronary angioplasty the circulation became critically unstable and percutaneously introduced intraaortic balloon counterpulsation (IABCP) was commenced. As the haemodynamics improved catecholamine dosage was markedly reduced and then discontinued over the subsequent 24-48 hours and inspiratory oxygen concentration of the ventilated patient was decreased from 100% to 40%. After a total of 5 days the IABCP catheter was removed without complication. The cardiac pump action showed further improvement in the following days. 6 months later the patient's condition was stable in grade II-III (New York Heart Association classification) heart failure. This case illustrates the place of IABPC as a highly effective treatment option in myocardial infarction with cardiogenic shock, especially when combined with interventional revascularisation procedures.

Adult↗
PubMed1995

[Spontaneous hemothorax in dermatomyositis and long-term glucocorticoid treatment].

A 65-year-old woman with dermatomyositis for which she had been treated for ten years with prednisone (latterly 15 mg daily) suddenly experienced severe pain in the left thoracolumbar region. Cardiovascular, pulmonary and vertebral causes of the pain were excluded. But serological tests indicated inflammatory disease and the haemoglobin concentration was low (10.4 g/dl). Left pleural effusions were repeatedly aspirated and some haemorrhagic fluid obtained (haematocrit 0.31 in blood, 0.28 in the pleural effusion). Five days after admission her cardiovascular status became unstable and she developed respiratory failure (haemoglobin 7.6 g/dl). Chest radiograph showed increased pleural effusion. Subsequent thoracotomy revealed a left coagulothorax which was removed and flushed. During this procedure severe bleeding occurred from a covered perforation of the descending aorta, 1.5 x 1.5 cm in size. Although the aortic wall was thin, there was no aneurysm but arteriosclerotic changes and an external erosion near an abscessing mediastinitis, originating from a chronic purulent pleuritis and bronchopneumonia. The severe blood loss caused circulatory failure from which the patient could not be resuscitated.

Aged↗
PubMed1995

[Internal medicine complications of ventriculoatrial shunt].

BACKGROUND: Ventriculo-atrial shunts (VASs) and ventriculo-peritoneal shunts (VPSs) are the symptomatic treatment of choice for hydrocephalus. Bacterial contamination of the atrial part of VASs (usually with Staphylococcus epidermidis) can result in further organ complications, in most instances immune complex mediated glomerulonephritis ("shunt-nephritis") or direct microbial heart valve destruction. PATIENTS AND METHODS: In a retrospective study, we analyzed clinical and laboratory data of 11 patients with VAS associated complications as well as the course of the disease. RESULTS: The following complications were observed: glomerulonephritis (n = 9), glomerulonephritis and aortic valve destruction (n = 1), pulmonary embolism, pulmonary hypertension and tricuspid valve insufficiency (n = 1). Out of the 11 patients, 8 suffered from unexplained fever. All 11 patients had elevated circulating immune complexes. In 3 of 4 patients initially requiring dialysis, renal function improved which allowed to stop hemodialysis. Renal function also improved in 3 of 5 patients who presented with elevated serum creatinine. Unfortunately, the patient with multiple pulmonary embolisms and tricuspid valve insufficiency died of progressive pulmonary hypertension. CONCLUSION: The prognosis for impaired renal function is good only if the VAS infection is diagnosed early and an immediate surgical and antibiotic treatment leads to an eradication of the underlying chronic infection.

Adult↗
PubMed1995

Dislocation of the rotating cutter during directional coronary atherectomy: a note of caution.

Directional coronary atherectomy (DCA) has received increased attention, especially as a bail-out procedure after failed balloon angioplasty. However, this technique may also be burdened by severe pitfalls. We report a patient with a balloon-resistant left coronary artery lesion subsequently treated with DCA. Despite its over-the-wire guidance, as the rotating cutter was advanced, it deviated from its intra-housing course and intruded into the vascular wall. Dislocation of the rotating blade was due to pressure from hard plaque tissue. After having carefully pulled back the complete catheter system, a severe spasm of the left main stem occurred, which was reversed by intracoronary nitroglycerine. The final angiography showed a left coronary artery without significant, residual stenosis. The case report underscores that DCA passes must be performed under continuous fluoroscopic control, especially for balloon-resistant lesions because of the unpredictability of DCA-imminent complication.

Atherectomy, Coronary↗
PubMed1995

Migration behavior of human smooth muscle cells cultivated from restenotic and primary lesions.

Subintimal smooth muscle cell (SMC) migration is considered an essential determinant of arteriosclerosis and neointimal formation. In this study, a cell culture model was established to characterize migration activity of SMCs originating from restenotic and primary lesions. Plaques from symptomatic stenoses of 32 patients (19 men, 13 women; 4 carotid, 17 peripheral, 11 coronary lesions) were removed by percutaneous atherectomy or direct operative approach. Ten patients suffered from recurrent stenosis. Cell cultures were established by explantation of tissue samples. By indirect immunofluorescence microscopy, SMCs were shown to be the predominant cell type of all advanced lesions irrespective of their origin. The spontaneous cellular motility of SMCs was analyzed in vitro by means of a computer-assisted observation system. Cells of all groups exhibited random motility. SMC migratory velocity was found to be significantly (P < 0.001) greater in cells from restenotic lesions than in those from primary plaques. In conclusion, migration behavior of human SMCs originating from arteriosclerotic lesions may be quantified in vitro as a functional determinant characterizing restenotic versus primary lesions.

Aged↗
PubMed1994

Resection of guide catheter fragments during coronary atherectomy in aorto-ostial lesions: a note of caution.

Angioplasty of coronary aorto-ostial lesions is considered to be troublesome with decreased acute and long-term results and high complication rates. We report a patient with an ostial right coronary artery lesion which was treated after failed PTCA with directional atherectomy as a rescue intervention. After a favorable angiographic and clinical outcome, plastic material was found in the AtheroCath's housing due to resection of the tip of the guide catheter.

Angioplasty, Balloon, Coronary↗
PubMed1994

Role of L-type calcium channels on stimulated calcium influx and on proliferative activity of human coronary smooth muscle cells.

Dihydropyridine (DHP) calcium channel blockers are widely used in treatment of coronary artery disease. To evaluate the specific role of L-type calcium channels in the antianginal and possibly antiatherosclerotic properties of DHP inhibitors, we examined the effects of a 1,4-DHP agonist and antagonist on angiotensin II (ANG II)- and serum-stimulated calcium influx and proliferation of human coronary smooth muscle cells (cSMC). Fluorometry of fura-2 was used to measure changes in free cytosolic Ca2+ concentration ([Ca2+]i) in cSMC after short- and long-term pretreatment with the calcium agonist Bay K 8644 or the antagonist nitrendipine, respectively. Proliferative activity was quantified during exponential growth in serum-supplemented medium with or without both DHPs. Short- and long-term pretreatment with Bay K 8644 increased basal [Ca2+]i significantly in resting cells and augmented ANG II- and serum-induced sustained [Ca2+]i responses. Concordantly, proliferation rate was increased. In contrast, nitrendipine had no significant effect on basal or stimulated [Ca2+]i after short-term treatment, but decreased [Ca2+]i after 24-h incubation, attenuated the plateau phase of ANG II- and serum-evoked [Ca2+]i transients, and reduced proliferative activity of these cells. The results indicate that 1,4-DHPs modulate ANG II- and serum-induced Ca2+ influx in cSMC. Thus, L-type calcium channels may contribute to [Ca2+]i transients evoked by ANG II and serum. Moreover, the modulating effects of both DHPs on proliferative activity suggest involvement of DHP-sensitive calcium channels. Calcium influx through L-type channels may be one of the mechanisms that determine responsiveness to vasoconstrictors and proliferative activity of human cSMC.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1994

[Mechanisms of re-stenosis after angioplasty].

Restenosis post angioplasty is a segmentally limited, wound healing response to a circumscript traumatization of the vascular wall associated with the therapeutic intervention, which also comprises residual or recoiling plaque components at the time of initial revascularization. Studies with animal models and the analysis of human plaque tissue harvested by autopsy or atherectomy indicate a cascade-like course of this wound healing reaction, in which initially different cell types such as thrombocytes, endothelial cells, monocytes/macrophages and smooth muscle cells (SMCs), later predominantly SMCs are involved. In the first phase of inflammation, angioplasty as a multifactorial stimulus induces a sequence of (a) destruction of endothelial and subendothelial structures, (b) traumatization of medial regions with rupture of the internal elastic lamina, (c) exposition of thrombogenic factors such as collagen or tissue factor, (d) stretching of smooth muscle cells with subsequent expression of proto-oncogens (c-fos, c-myc, c-myb), (e) release of growth factors from cells of the bloodstream, endothelial cells and SMCs by direct traumatization and segmental thrombus formation, and (f) thrombin production with autocatalytic activation of the SMC thrombin receptor. Overlapping the inflammation period, granulation begins 3 days after angioplasty. Proteinases such as plasmin as well as collagenases induce the disintegration of extracellular matrix structures, thereby modulating plaque formation, and lead to an organelle-rich SMC phenotype within the intima and media. The phenotypic alteration of SMCs is considered to be the prerequisite for mitogenic and migratory stimulation. This stage shows different expression patterns of growth factors and their receptors; however, there is only limited knowledge about spatiotemporal and maximal expression as well as their coordination for human vascular wall tissue (PDGF, PDGF-R, EGF-R, FGF, FGF-R, TGF-beta). Overlapping with the granulation period, induction of different components of the extracellular matrix occurs 1-2 weeks after angioplasty, possibly mediated by TGF-beta (phase of matrix formation). Smooth muscle cells produce and secrete matrix proteins such as tenascin, fibronectin, collagens and proteoglycans, and thereby induce a marked increase of the neointimal plaque volume. Angiographic restenoses of coronary and peripheral arteries histologically exhibit tissue with high cellularity (> 500 cells/mm2), associated with SMC activity markers such as PCNA or NMMHC-B. Proliferative and migratory activities of these cells in vitro are augmented by a factor of 2 to 3 as compared to those from chronic primary lesions. Transmission electron microscopic analysis proves that within the media a nearly complete re-differentiation of SMCs occurs, whereas intimal SMCs persist in the intermediate phenotype.(ABSTRACT TRUNCATED AT 400 WORDS)

Angioplasty, Balloon, Coronary↗
PubMed1994

Colchicine antagonizes the activity of human smooth muscle cells cultivated from arteriosclerotic lesions after atherectomy.

AIM: Proliferative, migratory, and secretory activities of vascular smooth muscle cells are functional determinants of human atherosclerotic plaque and restenosis formation. The present study was designed to examine the effects of interfering with these processes using drugs. MATERIALS AND METHODS: For in-vitro studies of smooth muscle cell activity, arterial smooth muscle cells were cultivated from human plaque tissue excised from 22 coronary and peripheral lesions and treated with the antitubulin colchicine. Smooth muscle cell migratory activity was analyzed by a standardized semi-automatic video system. Transmission electron microscopy was used to examine cytoplasmic structures. RESULTS: Colchicine caused a concentration-dependent decrease in smooth muscle cell proliferative activity at a half-maximal inhibitory concentration (IC50) of 5 nmol/l. Smooth muscle cell migratory activity was reduced by colchicine in a concentration-dependent manner (IC50, 3 nmol/l). Concordantly, transmission electron microscopy revealed severe disorganization of cytoplasmic structures, especially of organelles, indicating metabolic activation. CONCLUSIONS: In-vitro studies with human smooth muscle cells from arteriosclerotic lesions suggest that the antitubulin principle may be useful in producing anti-arteriosclerotic effects, since a pronounced antagonization of smooth muscle cell proliferative, migratory, and secretory processes, indirectly inferred from ultrastructural analysis, was demonstrated with low concentrations of colchicine.

Actin Cytoskeleton↗
PubMed1994

[Pathophysiology and pathobiochemistry of restenosis].

The high rate of restenosis after percutaneous transluminal angioplasty obviously depends on multiple factors. Predictors for the clinical outcome seem to be the selection of lesion morphology, the acute result and the biological vessel response in the first months after treatment. Thrombus formation and recoil have been considered to be pivotal events. Thus, anticoagulation and Ca-antagonists were routinely applied after treatment. Multiple studies with medical intervention have been performed, mostly with anticoagulants. However, no effective reduction of restenosis has been achieved so far. Analysis of autopsy tissue obtained after angioplasty indicated the importance of early vascular wall "response to injury" that might as a consequence lead to restenosis formation. This was confirmed by systematic experimental data. With introduction of directional atherectomy "biopsies" of primary and restenotic tissue were obtained. Thus, a subtile diagnostic spectrum including histological, immunohistochemical, electron microscopical, and molecular tissue analysis could be established. In vitro cultures of obtained tissue were performed routinely. They enable a characterization of proliferative and synthetic cellular features. Moreover, the effects of therapeutic measures can be quantified and used for pre-clinical screening. To date, the above described methods indicate as pivotal event the angioplasty induced transformation of contractile myocytes to a synthesizing type of myocytes. The transformation to synthetic active cells is not device dependent, but seems to be a major feature of restenosis. This process is mostly terminated in a period of 3-6 months. To accelerate this physiologic termination would be one interesting therapeutic option. Alternatively, special local drug delivery devices could be used to administer sufficient antiproliferative drugs at the site that needs to be treated.

Angioplasty, Balloon, Coronary↗
PubMed1993

Analysis of atherectomy specimens.

Atherectomy specimens may be regarded as biopsy tissue excised from human vascular target lesions. Proceeding from contrary histologic findings that attribute focal hypercellularity to restenosis, and hypocellularity to chronic lesions, further analysis of atherectomy specimens was performed to study ultrastructural characteristics and functional aspects propagated by both lesion types. Transmission electron microscopy examination showed that intimal smooth muscle cells (SMCs) were the predominant cells in both primary and restenotic lesions. SMCs exhibited variable degrees of metabolic activation, typically higher in SMCs of restenotic lesions. This SMC phenotype was equally expressed when tissue samples were placed in a cell culture model. In an attempt to quantify SMC activity, proliferative as well as migratory activities of cultured cells were measured by growth curves and a computer-assisted motion analysis system, respectively. A 2- to 3-fold increase of both activity determinants was observed with SMCs cultivated from restenotic lesions compared with those from primary lesions, irrespective of their coronary or peripheral origin. Drug-induced interference of human SMC metabolic activation and antagonism to their proliferative and migratory activities may be helpful in evaluation of therapeutic concepts to prevent restenosis. The antitubulin colchicine was studied for its effect on the defined determinants. The data in vitro demonstrate that colchicine decreased proliferative and migratory activity of SMCs and caused disorganization of the cytoplasmic ultrastructure. In conclusion, electron microscopy and cell culture studies may help to shed more light on the structures and mechanisms underlying restenosis and plaque growth. Deliberate counteraction of any of the specific early events implicated in these complex pathobiologic processes may eventually become effective means to suppress restenosis and may thus result in a prophylactic as well as therapeutic treatment of the diseased vascular wall.

Animals↗
PubMed1993

Renal complications of infected ventriculoatrial shunts.

Contamination of a ventriculoatrial shunt (VAS) with skin organisms that are usually nonpathogenic may be followed by an immunologically mediated renal injury. The bacteria characteristically involved are coagulase-negative Staphylococci (e.g., Staphylococcus epidermidis), which strongly adhere to the plastic surface of the VAS. These bacteria are protected from the body's natural defense mechanisms and respond only poorly to antibiotics. As a result, their growth persists and produces a continuous antigenic stimulation. Circulating immune complexes (CIC) are an appropriate tool to screen for chronically infected VASs. We followed CIC in 138 VAS patients. An infected VAS was seen in 20 of the 24 patients with highly elevated CIC and in 1 of the 19 patients with moderately elevated CIC, but none of the 95 patients with normal CIC had evidence of shunt infection. Of the 21 patients with shunt infections, 8 had renal involvement (4 requiring dialysis, and 4 with proteinuria, hematuria, and/or elevated creatinine). Results from kidney biopsy specimens available from 4 patients confirmed glomerulonephritis. Of the 4 patients requiring dialysis at diagnosis, renal function recovered sufficiently to stop dialysis after successful VAS exchange in all but 1. In the other 4 patients, renal symptoms (proteinuria, creatinine) also improved after VAS revision. Chronic infection with S. epidermidis or other bacteria is a continuing problem in patients with VASs and can lead to an immune-mediated renal injury. However, the prognosis for reversal of the renal injury is relatively good if the VAS infection is treated promptly.

Adolescent↗
PubMed1993

Results of directional peripheral atherectomy with reference to histology, histochemistry, and ultrastructure.

One hundred patients with symptomatic peripheral vascular disease were treated with a directional atherectomy catheter; 153 lesions comprising 98 stenoses and 55 occlusions were located in the iliac (n = 22), superficial femoral (n = 114), popliteal (n = 16), and anterior tibial (n = 1) arteries. The majority of these patients were poor candidates for balloon angioplasty because of the complexity of lesions. There were 70 eccentric and 28 concentric lesions and 55 occlusions (mean length 4.2 +/- 2.9 cm). Acute success rate was 94% for both stenoses and occlusions. Four patients were treated in both lower extremities. The stenoses were reduced from 85 +/- 12% to 12 +/- 10% acutely (occlusions 100% to 9 +/- 9%). Six-month angiographic follow-ups were performed in 81% of treated patients, the others refusing angiography. Mean stenosis after six months was 33 +/- 25% (occlusions 44 +/- 28%). Restenosis (> 50%) was found in 20% of treated lesions: 26% in concentric lesions, 8% in eccentric lesions, and 32% in occluded vessels. Treatment of peripheral vascular disease with the atherectomy device is safe and effective therapy with good long-term results. These results were obtained in complex lesions with 55 occlusions. Atherectomy seems to be particularly beneficial in the treatment of eccentric and complex stenoses and is not limited by occlusion or calcification. Furthermore, insight into the pathogenesis of arteriosclerosis and the development of restenosis is enabled by analysis of removed plaque material.

Aged↗
PubMed1993

[Cellularity and ultrastructural characteristics of human atherectomy specimens: comparison between restenosis and primary stenotic tissue of coronary and peripheral lesions].

Restenosis in patients treated by angioplasty is clinically and angiographically defined. The question remains to which extent each restenotic lesion can be attributed to residual plaque material and/or neointimal tissue formation post primary intervention. In an effort to reveal distinct anatomical characteristics which may allow conclusions to pathogenetic mechanisms involved in restenosis, histopathologic and electron microscopic examinations of human restenotic tissue were performed. To compare tissue samples from clinically restenotic lesions with those from untreated primary lesions for cell number and ultrastructural characteristics, a total of 64 percutaneously excised tissue specimens from coronary (n = 9) and femoral lesions (n = 18) of 27 patients treated by directional atherectomy were analyzed. Semiquantitative assessment of plaque slices for cell number (12 fields of view/lesion; magnification x500) revealed a spectrum of 11.7 to 35.3 cell nuclei/field of view (C/F) for clinical restenoses (n = 10) and of 0.9 to 28.2 C/F for primary lesions (n = 17). When comparing tissue specimens from restenotic origin with those of native lesions, there was a highly significant (p < 0.001) difference in cell number (ave: 22.2 +/- 7.1 versus 8.6 +/- 7.9 C/F; x +/- SD). Hypercellularity (mean cell density defined with > 20 C/F) was observed in 6/10 restenoses, hypocellularity (< 10 C/F) in 0/10 restenoses. For primary lesions, hypocellularity was found in 10/17 lesions, but hypercellularity in 2/17 lesions. Ultrastructural analysis of hypocellular lesions by transmission electron microscopy revealed large extracellular matrix fields with infrequently embedded smooth muscle cells (SMCs). These cells were characterized by a microfilament-rich intermediate phenotype, thereby indicating decreased metabolic activation.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗