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Biomedical subjects

J Meyer

Publications and source records attributed to J Meyer.

At least 451 records · Page 25Linked to original sources
PubMed1995

Improving the applicability of myocardial densitometry and parametric imaging by extended automated densogram analysis.

In clinical applications the analysis of X-ray contrast densograms acquired in regions of interest (ROI's) over the myocardium is disturbed by many complex factors. For this reason we acquire redundant densogram information for quality control before extracting densitometric parameters. In our approach, initially some stable measures of quality for densograms are used to lower the influence of poor quality densograms by a quality weighted averaging. For example a shape quality measure, Q1, is calculated using regions of optimal and minimal acceptable quality defined with respect to a prototype densogram. Not a few myocardial ROI's yield densograms that differ from single-source densograms (SSD's) due to e.g. superposition of different perfusion beds or the position of the ROI relative to the coronary sinus or stenoses. This might result in a densogram shape with oscillating or plateau behavior. For densograms of a such general shape many parameters defined in the usual way do not depend smoothly on the densogram values. The conventional definitions of some parameters (appearance time, rise time) are therefore extended for application to multi-maxima densograms as well as to SSD's. These new methods are evaluated using digitized clinical angiocardiograms and are applied to parametric imaging (pixeldensograms) in a slightly modified way. Taking into account the densogram quality, its shape and its origin results in a considerable improvement both for densitometry and parametric imaging of myocardial perfusion.

Absorptiometry, Photon↗
PubMed1995

Multiple raters of disruptive child behavior: using a genetic strategy to examine shared views and bias.

Most research on child behavior incorporates information from different individuals. While agreement between informants is generally only modest, there is little understanding of the processes underlying disagreement. In twin studies, differential agreement among raters for MZ and DZ twins is of particular concern. The processes underlying differences among mother, father, and child ratings of oppositional and conduct disorder symptoms are explored. Evidence in favor of a shared parental view of behavior is presented. Parental ratings give higher intrapair correlations, which could be due to either parents rating their twins more similarly or twins contrasting themselves. Rater bias and situational specificity are among the possible explanations of differential ratings. The effects of incorporating multiple raters of behavior on estimates of genetic and environmental effects are explored. These suggest that genetic influences are greater for the shared (multiple-rater) phenotype than for individual ratings; reduction in measurement error is only a partial explanation.

Adolescent↗
PubMed1995

Aspirin therapy: optimized platelet inhibition with different loading and maintenance doses.

Inhibition of cyclooxygenase by aspirin has been shown to be beneficial in clinical situations such as acute myocardial infarction or unstable angina. The precise effect of various doses of aspirin on acute and long-term inhibition of platelet aggregation and thromboxane synthesis remains unclear. In this study we evaluated the effect of oral aspirin (0, 40, 100, 300, or 500 mg) as the initial loading dose in combination with different maintenance doses of aspirin (0, 40, or 100 mg/day) for 14 days on platelet function in healthy men. Bleeding time 2 or 24 hours after the first aspirin administration was significantly increased for 300 and 500 mg aspirin (p < 0.01). Two hours after the first administration of 100, 300, and 500 mg aspirin, a significant inhibition of collagen-induced platelet aggregation (ED50 collagen: from 3 +/- 1 to 17 +/- 2, 24 +/- 3, 22 +/- 3 micrograms/ml, respectively) was seen. At the same time serum thromboxane B2 synthesis was inhibited by more than 99% with 300 and 500 mg aspirin. At the end of the 14-day observation period, bleeding time was significantly prolonged for the different combinations of aspirin doses compared with initial values (p < 0.01). Collagen-induced platelet aggregation and serum thromboxane B2 synthesis were significantly inhibited for all aspirin combinations tested at 14 days (p < 0.05). The 40/40 mg aspirin combination was less effective, because it reached its maximal effect very late at day 7 of the observation period compared with the other combinations.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1995

Guidance of anticoagulation after intracoronary implantation of Palmaz-Schatz stents by monitoring prothrombin and prothrombin fragment 1 + 2.

The primary objective of this study was to apply a sophisticated coagulation monitoring system including estimation of the concentration of prothrombin fragment 1 + 2 (PTF 1 + 2) and the activity of prothrombin (coagulation factor II or FII) to cases of stent implantation and to compare the results with those of standard coagulation tests. The secondary objective was to detect the incidence after stenting of subacute thrombosis (SAT) and bleeding complications in these patients and to compare the results with those of a group of patients with stent implantation in whom coagulation was monitored exclusively by standard tests. SAT several days after coronary stenting occurs in up to 20% despite aggressive intravenous and overlapping oral anticoagulation. According to a prospective study protocol 120 consecutive patients with implantation of 155 Palmaz-Schatz stents underwent coagulation monitoring including single daily estimation of the concentration of PTF1 + 2 (target range < 0.5 nmol/L) and of FII activity (15% to 35%) in addition to the standard tests of thrombin time (TT), partial thromboplastin time (aPTT), international normalized ratio (INR), antithrombin III (ATIII), and fibrinogen. Adjustment of heparin and phenprocoumon dosages in this study group was based only on the results of PTF1 + 2 and FII measurements. A control group consisted of 53 patients with implantation of 64 stents who were matched for baseline, angiographic, and procedure-related characteristics. After stenting, anticoagulation was monitored by estimation of TT (target range > 70 seconds), aPTT (> 70 seconds), INR (3.0 to 4.5), AT III (> 80%), and fibrinogen (< 450 mg/dl) in this control group. There was a weak correlation between PTF1 + 2 and aPTT (r = 0.337; PTF1 + 2 = -0.00169aPTT + 0.491) and PTF1 + 2 and TT (r = 0.328; PTF1 + 2 = -0.00142TT + 0.494). A better correlation was found between FII and INR (r = 0.983; FII = -23.8 INR + 134). Stable oral anticoagulation was maintained 2.8 +/- 0.9 days later according to an FII concentration of < 35% compared with an INR > 3. The incidence of SAT was 3.3% with 3.0% for elective versus 3.8% for nonelective stenting. The sensitivity, specificity, and accuracy of the PTF1 + 2 test were 100%, 88%, and 88%, respectively. In the control group the incidence of SAT was 17%, with 16.1% for elective versus 18% for nonelective stenting. Major bleeding complications occurred in 10% (study group) and in 11.3% (control group) of patients (no statistical difference).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1995

Intravascular ultrasound after low and high inflation pressure coronary artery stent implantation.

OBJECTIVES: We sought to characterize the differences seen after low or high pressure coronary artery stent deployment as assessed by intravascular ultrasound. BACKGROUND: Until 1992, the success of stent deployment was assessed by angiographic criteria only, but in 1993 the procedure was expanded to include postprocedural single-use intravascular ultrasound imaging. Ultrasound criteria for successful stent deployment were 1) symmetry, 2) minimal lumen diameter > 3.0 mm, 3) no echo-free spaces between the stent and the vessel, and 4) no uncovered dissections. METHODS: We used mechanical 4.8F or 3.5F 20- or 30-MHz monorail single-use intravascular ultrasound catheters. RESULTS: Fifty-two patients were included, 28 treated in 1991 and 1992 (group A) and 24 treated in 1993 or 1994 (group B); 87% of patients underwent elective stent implantation. The number of echocardiographic studies per patient increased from 1 +/- 0.1 (mean +/- SD) in group A to 2.0 +/- 0.85 in group B. Mean maximal balloon size increased from 3.3 +/- 0.33 to 3.73 +/- 0.24 mm and maximal inflation pressure from 6.9 +/- 1.1 to 15.8 +/- 2.4 bar (p < 0.001). The eccentricity index was 0.915 +/- 0.04 in group B versus 0.87 +/- 0.05 in group A. Minimal lumen diameter measured by echocardiography increased from 2.55 +/- 0.41 mm in group A to 3.14 +/- 0.37 mm in group B. The final mean values per cross-sectional area as a percent of calculated balloon area were similar in group A (67.5 +/- 23%) and group B (66.5 +/- 22.9%). No major acute complications occurred in either group; subacute thrombosis developed in two patients, both in group A. CONCLUSIONS: Intravascular ultrasound data confirm that high pressure stent deployment leads to increased minimal lumen area. Despite high pressure stent deployment, homogeneous stent geometry and optimal stent expansion were not observed in all patients.

Aged↗
PubMed1995

Platelet receptor desensitization induced by elevated prostacyclin levels causes platelet-endothelial cell adhesion.

OBJECTIVES: The purpose of this study was to investigate the role of platelet prostacyclin receptor desensitization in platelet-endothelial cell adhesion. BACKGROUND: Platelet-endothelial cell adhesion is regulated by endothelial cell-derived mediators, such as prostacyclin and endothelium-derived relaxing factor. Prostacyclin activates platelet adenylate cyclase and augments cyclic adenosine monophosphate formation by way of specific membrane receptors. Platelet exposure to prostacyclin or chemically stable analogs results in a time- and dose-dependent prostacyclin receptor desensitization as it occurs during infusion therapy with prostacyclin analogs or in pathophysiologic situations such as acute myocardial infarction. METHODS: Adhesion of washed and radiolabeled human platelets stimulated with thrombin to cultured umbilical vein endothelial cells was measured under control conditions and under conditions of platelet prostacyclin receptor desensitization induced by incubation with the prostacyclin analog iloprost (10 to 100 nmol/liter) for 3 h. RESULTS: Thrombin (0.08 to 0.2 U/ml) increased platelet adhesion in a dose-dependent manner from 2.7 +/- 0.3% to 6.4 +/- 0.6% (mean value +/- SEM). Preincubation of platelets resulted in a dose-dependent down-regulation of 3H-iloprost binding up to 58.8 +/- 6.7% of control platelets with 100 nmol/liter of iloprost. Co-incubation of prostacyclin receptor-desensitized platelets with endothelial cells resulted in a marked augmentation of thrombin-induced adhesion up to 28.6 +/- 4.5%. Approximately the same increase in platelet adhesion was seen after complete abrogation of endothelial cell prostacyclin synthesis by pretreatment with aspirin. Comparison of iloprost-induced receptor desensitization and increased platelet-endothelial cell adhesion indicated a positive correlation. CONCLUSIONS: Platelet prostacyclin receptor desensitization was observed in humans in vivo during acute myocardial infarction or during therapeutic administration of prostacyclin analogs. In vitro platelet prostacyclin receptor desensitization caused a marked augmentation of platelet-endothelial cell adhesion. This increase in adhesion might result in an enhanced tendency toward thrombus formation in humans.

Blood Platelets↗
PubMed1995

Recombinant hirudin (HBW 023) prevents troponin T release after coronary angioplasty in patients with unstable angina.

OBJECTIVES: This study was performed to evaluate the efficacy of peri-interventional treatment with recombinant hirudin (r-hirudin [HBW 023]) compared with heparin in the prevention of troponin T release in patients with unstable angina. BACKGROUND: Percutaneous transluminal coronary angioplasty in patients with unstable angina is associated with a high risk of acute thrombotic complications. METHODS: Serial troponin T measurements were performed in 61 patients with unstable angina during the 48-h observation period after coronary angioplasty of the ischemia-related lesion. Patients were randomly assigned to peri-interventional intravenous treatment with either r-hirudin (dosage group I: 0.3-mg/kg body weight bolus, 0.12 mg/kg per h for 24 h; dosage group II: 0.5-mg/kg bolus, 0.24 mg/kg per h for 24 h) or heparin (150-IU/kg bolus, 20 IU/kg per h for 24 h). All patients received acetylsalicylic acid before coronary angiography. After 24 h, patients received a constant low dose infusion of either hirudin (0.04 mg/kg per h) or heparin (7 IU/kg per h) for another 24 h. The power of the study to detect a decrease in abnormal troponin T levels from 60% (heparin group) to 20% (combined r-hirudin groups) was 88%. RESULTS: Serial troponin T measurements revealed two peaks within the 48 h after coronary angioplasty in the heparin but not the hirudin groups. An elevated serum troponin T concentration (> 0.2 ng/ml) within 48 h of coronary angioplasty was found in 9 (24%) of 38 patients in the hirudin groups (5 [25%] of 20 in dosage group I; 4 [22%] of 18 in dosage group II) compared with 11 (58%) of 19 in the heparin group (p = 0.01). We observed major cardiac events (death, myocardial infarction, abrupt vessel closure) in 1 (4.8%) of 21 patients in dosage group I, 1 (5.3%) of 19 in dosage group II and 3 (14.3%) of 21 in the heparin group (p = 0.33). CONCLUSIONS: In this pilot trial, hirudin appears to be superior to heparin in preventing troponin T release after coronary angioplasty.

Angina, Unstable↗
PubMed1995

Beta-sarcoglycan: characterization and role in limb-girdle muscular dystrophy linked to 4q12.

beta-Sarcoglycan, a 43 kDa dystrophin-associated glycoprotein, is an integral component of the dystrophin-glycoprotein complex. We have cloned human beta-sarcoglycan cDNA and mapped the beta-sarcoglycan gene to chromosome 4q12. Pericentromeric markers and an intragenic polymorphic CA repeat cosegregated perfectly with autosomal recessive limb-girdle muscular dystrophy in several Amish families. A Thr-to-Arg missense mutation was identified within the beta-sarcoglycan gene that leads to a dramatically reduced expression of beta-sarcoglycan in the sarcolemma and a concomitant loss of adhalin and 35 DAG, which may represent a disruption of a functional subcomplex within the dystrophin-glycoprotein complex. Thus, the beta-sarcoglycan gene is the fifth locus identified (LGMD2E) that is involved in autosomal recessive limb-girdle muscular dystrophy.

Amino Acid Sequence↗
PubMed1995

Use of transoesophageal echocardiography in the diagnosis of abscess in infective endocarditis.

Transoesophageal echocardiography is invaluable clinically since it accurately images abscess cavities or aneurysms. It provides the information about the site and extension of abscesses which is needed by surgeons to time and define surgical intervention. Early diagnosis is advantageous, and abscesses should be expected in 5%-30% of patients with echocardiographically discernible vegetations. Since there is no 'abscess typical' organism, transoesophageal echocardiographic examination is helpful at the first indication of infective endocarditis, to identify high-risk patients. Involvement of the aortic valve, growth in the size of vegetations, and the presence of spontaneous echo contrast are echocardiographic indicators of high-risk endocarditis.

Abscess↗
PubMed1995

Clinical predictors of unstable coronary lesion morphology.

We evaluated prospectively clinical and angiographic data in 400 patients, 200 with unstable and 200 with stable angina in order to determine which clinical markers could reliably predict unstable coronary artery lesions. Comparison of the angiogram of 200 patients with unstable and 200 with stable angina revealed a high-grade lesion (42% vs 23%, P < 0.0001), complex lesion morphology (49% vs 20%, P < 0.0001) and thrombus-containing lesions (7% vs 1%, P = 0.006) as typical findings in patients with unstable angina. A high-grade lesion and/or complex lesion (including thrombotic lesions but excluding total occlusion) was found in 61% of unstable and 34% of stable patients (P < 0.0001). Clinical features including the Braunwald classification of unstable angina were then evaluated by means of a multivariate approach with regard to their ability to predict the presence of unstable coronary artery lesions. Multivariate analysis revealed an abnormal ECG as the single most predictive clinical indicator of complex lesion morphology (P < 0.0001, odds ratio 4,2). The clinical presentation of recent onset of angina was highly predictive of a high grade lesion (P = 0.0003, odds ratio 3,2). The endpoint of a high-grade and/or a complex lesion was identified by an abnormal ECG (P = 0.0015, odds ratio 3,0) and recent onset angina (P = 0.0119, odds ratio 2,5). Thus, a high grade and/or complex lesion, typical of patients with unstable angina, was best identified by the clinical feature of recent onset angina and/or abnormal ECG changes.

Aged↗
PubMed1995

The antimalarial drug halofantrine is bound mainly to low and high density lipoproteins in human serum.

1. The major serum proteins which bind halofantrine were identified by size exclusion chromatography. In addition, the binding affinity of halofantrine to human erythrocytes and serum proteins was measured by an erythrocyte partitioning technique. The influence of serum-drug binding on the distribution of halofantrine in whole blood was estimated by simulating several disease-related changes in the levels of the most important binding proteins. 2. The chromatographic resolution of serum preincubated with halofantrine allowed a quantitative analysis of binding to low density lipoproteins, high density lipoproteins, alpha 1-acid glycoprotein and albumin using the erythrocyte partitioning technique. Very low density lipoproteins did not bind halofantrine to a significant extent. 3. In whole blood halofantrine is bound to serum proteins (83%) and to erythrocytes (17%). Low density lipoproteins (affinity constant nKP = 44.4 l g-1) and high density lipoproteins (nKP = 14.4 l g-1) were the most important binding proteins in serum. alpha 1-acid glycoprotein (nKP = 4.39 l g-1) and albumin (nKP = 0.27 l g-1) had relatively low binding affinities. 4. The concentration of serum proteins influences both the fraction of unbound drug and the fraction of drug associated with the erythrocytes. Changes in serum protein concentrations often encountered in malaria are likely to increase both the unbound fraction and the fraction bound to the erythrocytes.

Animals↗
PubMed1995

Noninvasive visualization of an apparent patent intracoronary stent by transesophageal echocardiography.

In the area of increasing interventional techniques there is a need for noninvasive imaging modalities to provide postinterventional follow-up. We were able to visualize the apparent patency and measure the dimensions of an intracoronary Palmaz-Schatz stent in the left circumflex coronary artery using transesophageal two-dimensional echocardiography. This report indicates the potential of echocardiography to directly assess coronary stents.

Angioplasty, Balloon, Coronary↗
PubMed1995

Has transesophageal echocardiography changed the approach to patients with suspected or known infective endocarditis?

Infective endocarditis is still a great clinical challenge. Its diagnosis is difficult to establish, and mortality has remained around 30%. Early diagnosis and optimal treatment are crucial fo prognosis improvement. Echocardiography plays an indispensable role in the management of this disease, especially with the recently introduced approach, transesophageal echocardiography (TEE). TEE can overcome the limitations of transthoracic echocardiography (TTE) and is superior to TTE in almost every way in providing earlier and more information for the diagnosis and treatment of infective endocarditis. TEE detects valve vegetations with much higher sensitivity and specificity than TTE. It can demonstrate smaller vegetations in the early stage of the disease and vegetations on atypical locations (e.g., mitral valve annulus), and provides detailed characterization of vegetations (e.g., location, size, mobility, and changes during treatment). Such information is of great prognostic value and may help in selecting proper treatment. TEE is more sensitive for detecting complications, such as mitral valve perforation, abscess, and subaortic complications, which respond poorly to medicine and for which timely surgery may be the best treatment. For those with prosthetic valve endocarditis, TEE is especially useful because TTE is greatly limited by the acoustic shadow of prostheses. Both positive and negative results of TEE examination are valuable for confirming or excluding infective endocarditis. TEE also plays a unique role in intraoperative monitoring and can assess surgical results before the chest is closed. TEE has become an invaluable tool for the diagnosis and management of patients with suspected or known infective endocarditis.

Diagnosis, Differential↗
PubMed1995

CD44v6 is a marker for systemic spread in cutaneous T-cell lymphomas. A comparative study between nodal and cutaneous lymphomas.

Adhesion molecules are involved in leukocyte recruitment, lymphocyte recirculation, and in several aspects of tumour biology. Recent discoveries of surface proteins on tumour cells involved in tumour metastasis may explain the invasive behaviour, the migration involving reversible adhesive contacts, the release into the circulation and the extravasation of tumour cells. CD44 is a family of glycoproteins involved in cell-cell and cell-matrix interactions. The v6 (variant exon v6) form of CD44 confers a metastatic potential onto some carcinoma cells. In the present study, the expression of CD44v6 on skin biopsies of 10 inflammatory skin diseases, 30 cutaneous lymphomas (CL), 11 reactive lymph nodes, 10 primary nodal non-Hodgkin's lymphomas (NHL) and 5 secondary nodal NHL was investigated immunohistochemically. None of the 10 nodal NHL were CD44v6 positive for the neoplastic B- or T-cells, whereas 11/12 CL with systemic spread showed a distinct CD44v6 expression in the skin. CD44v6 was not expressed on the tumour cells of skin biopsies of patients without systemic spread (18 cases of CL). In conclusion, CD44v6 expression is connected to an aggressive behaviour of CL.

Adult↗
PubMed1995

Temperate bacteriophages are common among Actinobacillus actinomycetemcomitans isolates from periodontal pockets.

Actinobacillus actinomycetemcomitans is a suspected etiologic agent in destructive periodontal diseases. The detection of bacteriophages in A. actinomycetemcomitans in the subgingival plaque of patients with rapidly destructive forms of periodontitis led to the hypothesis that bacteriophage infection might increase the virulence of this bacterium (19). A. actinomycetemcomitans was isolated from 68 subjects from the Netherlands and Switzerland with localized juvenile periodontitis, rapidly progressing periodontitis, or adult periodontitis, and was tested for the presence of temperate bacteriophage with the overlay plate technique. More than half of the A. actinomycetemcomitans strains were found to release bacteriophage which formed individual plaques on indicator strains. Electron microscopy of preparations from 7 strains revealed virions with an icosahedral head and a contractile tail typical for double-stranded DNA bacteriophages. The presence of A. actinomycetemcomitans carrying temperate bacteriophage was not correlated with the composition of the subgingival microflora nor with the clinical form of periodontal disease. Destructive periodontal disease of subjects with phage-carrying A. actinomycetemcomitans was not more severe than of subjects with phage-free A. actinomycetemcomitans as determined by several clinical parameters. In contrast, the pocket depth and the attachment loss were significantly lower for adult periodontitis subjects with phage-carrying A. actinomycetemcomitans. It seems unlikely that the frequently occurring temperate bacteriophages increase significantly the virulence of A. actinomycetemcomitans.

Adult↗
PubMed1995

Cervical (C2) herpes zoster infection followed by pontine infarction.

This article reports a man who had herpes varicella zoster cervicalis with delayed stroke in the posterior circulation. Empiric treatment was acyclovir, methylprednisolone, and aspirin. Pontine infarction involving migration of the virus via cervicovascular innervation from C2 dorsal root ganglia to the vertebrobasilar circulation with attendant angiitis/angiopathy and thrombosis is proposed.

Basilar Artery↗
PubMed1995

High wall shear stress proximal to myocardial bridging and atherosclerosis: intracoronary ultrasound and pressure measurements.

BACKGROUND: Studies have shown that myocardial bridging may prevent coronary atherosclerosis and that the segment proximal to the bridge is often sclerosed. The underlying mechanism is still unknown. METHODS: Intracoronary ultrasound and pressure measurements were performed in a patient with myocardial bridging in the left anterior descending coronary artery. A 3.5 F, 20 MHz probe was used to measure the change in cross sectional area of the lumen during the cardiac cycle. Intracoronary pressure was measured with a Double tip, end mounted pressure transducer system, the catheter having two pressure sensors located at the end of the catheter 3 cm apart. Intracoronary pressure was recorded as the catheter was slowly advanced and pulled back through the left anterior descending coronary artery. RESULTS: Systolic compression of the bridge segment was clearly visualised on ultrasonography and an eccentric plaque with calcium deposit was found in the segment proximal to the bridge. The pressure in the segment proximal to the bridge (160/26 mm Hg) was higher than that of the proximal normal segment (126/68 mm Hg). The pressure distal to the bridge was 68/30 mm Hg. A highly characteristic "sucking effect" was found in the bridge segment. The pressure in the bridge segment was 102/-40 mm Hg. CONCLUSION: The pressure in the segment proximal to the myocardial bridging was higher than aortic pressure. Disturbance of blood flow and high wall stress proximal to myocardial bridging was a main contributor to the development of atherosclerosis in the segment proximal to the bridge.

Aged↗