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Biomedical subjects

Gerald Maurer

Publications and source records attributed to Gerald Maurer.

At least 55 records · Page 3Linked to original sources
PubMed2004

Prostaglandin E1 induces vascular endothelial growth factor-1 in human adult cardiac myocytes but not in human adult cardiac fibroblasts via a cAMP-dependent mechanism.

Prostaglandin E(1) (PGE(1)) has been used to treat pulmonary hypertension and peripheral artery occlusive disease and has been successfully employed for pharmacological bridging to transplantation in patients with chronic end-stage heart failure. In addition to its vasoactive effects PGE(1) was shown to stimulate angiogenesis in animal models. Recently we showed that PGE(1)-induced angiogenesis in hearts of patients with ischemic heart disease. We proposed that the angiogenic action of PGE(1) is mediated by vascular endothelial growth factor (VEGF). In the present paper we studied a possible effect of PGE(1) on the expression of VEGF-1 in cultured human adult cardiac myocytes (HACM) and cultured human adult cardiac fibroblasts (HACFB), respectively, to identify a cellular source of VEGF-1 in patients treated with PGE(1). We also aimed to delineate mechanisms involved in a possible regulation of VEGF-1 by PGE(1) in these cells. When HACM, isolated from human myocardial tissue, were treated with PGE(1), a significant up to 3-fold increase in VEGF-1 production could be observed. These results could be confirmed on the level of specific mRNA expression as determined by real-time polymerase chain reaction. The effect of PGE(1) on VEGF-1 expression could be blocked by H089, an inhibitor of cAMP-dependent protein kinase A. In HACFB, also isolated from human myocardial tissue, no effect of PGE(1) on VEGF-1 production was seen. If this effect of PGE(1) is also operative in the in vivo situation, one could speculate that cardiac myocytes could be a cellular source of PGE(1)-induced VEGF-1 expression in patients treated with this drug.

Alprostadil↗
PubMed2004

Pre-existing anticardiolipin antibodies and development of restenosis after coronary balloon angioplasty: predictive value for a complicated course?

Immune mechanisms play a critical role in cardiovascular disease. Cardiolipins are candidate autoantigens with a prothrombotic activity of their corresponding antibodies. We investigated the influence of pre-existing immunoglobulin (Ig)M and IgG anticardiolipin (aCL) antibodies on restenosis after coronary balloon angioplasty and their interaction with tissue plasminogen activator, plasminogen activator inhibitor type-1, von Willebrand factor and lipoprotein (a) in 132 patients with stable angina pectoris using immunoassays. Thirty percent of patients developed angiographically proven restenosis estimated by three independent experienced angiographers; 12% of all patients developed recurrent restenoses at the same site during a follow-up period of 2 years. Circulating IgM aCL antibodies categorized by quartiles predicted recurrent restenoses (logistic regression, for trend P < 0.04) with an increase of relative risk (RR) per quartile of 2.09. The predictive value of IgM aCL antibodies was unchanged adjusting for established cardiovascular risk factors (P = 0.028, RR = 2.69), extent of coronary artery disease (P = 0.014, RR = 2.73) and inflammatory parameters (P = 0.025, RR = 2.79), but lost significance adjusting for other prothrombotic parameters (P = 0.24, RR = 1.76). IgM aCL antibodies positively correlated with lipoprotein (a) (r = 0.23, P = 0.04). However, there was no significant interaction between their influences on recurrent restenoses. The other prothrombotic parameters did not predict single or recurrent restenoses. In conclusion, IgM aCL antibodies may help to identify a group of patients at high risk for recurrent restenoses after coronary balloon angioplasty.

Angina Pectoris↗
PubMed2004

Longitudinal analysis of perfusion lung scintigrams of patients with unoperated chronic thromboembolic pulmonary hypertension.

Chronic thromboembolic pulmonary hypertension (CTEPH) is the result of single or recurrent pulmonary thromboemboli that are thought to develop into organized pulmonary arterial obstructions by recurrent embolism and in situ thrombosis. Radioisotopic ventilation-perfusion scanning (V/Q scan) is a safe and highly sensitive test for pulmonary thromboembolic disease. The aim was to assess the natural history of thrombus expansion. We performed a prospective quantitative evaluation of ventilation/perfusion scintigrams (V/Q scans) in 20 patients with severe unoperated CTEPH. The baseline V/Q scan of each patient served as a reference for the second scan 21.7 +/- 8.2 months later. Planar images with intravenous 99mTc-labeled human albumin macroaggregates were reconstructed in six standard projections. Perfusion scans were analyzed by a semi-quantitative evaluation. In parallel, hemodynamics and clinical condition were prospectively observed. Lung perfusion scintigrams analyzed by a semi-quantitative method in patients with severe unoperated CTEPH show an apparent decrease of segmental flow abnormalities over time, paralleling right ventricular decline.

Adult↗
PubMed2004

Ultrasound affects distribution of plasminogen and tissue-type plasminogen activator in whole blood clots in vitro.

Ultrasound of 2 MHz frequency and 1.2 W/cm(2) acoustic intensity was applied to examine the effect of sonication on recombinant tissue-type plasminogen activator (rt-PA)-induced thrombolysis as well as on the distribution of plasminogen and t-PA within whole blood clots in vitro. Thrombolysis was evaluated quantitatively by measuring clot weight reduction and the level of fibrin degradation product D-dimer (FDP-DD) in the supernatant. Weight reduction in the group of clots treated both with ultrasound and rt-PA was 35.2% +/-6.9% which is significantly higher (p<0.0001) than in the group of clots treated with rt-PA only (19.9% +/-4.3%). FDP-DD level in the supernatants of the group treated with ultrasound and rt-PA increased sevenfold compared to the group treated with rt-PA alone, (14895 +/-2513 ng/ml vs. 2364 +/-725 ng/ml). Localization of fibrinolytic components within the clots was accomplished by using gel-entrapping technique and immunohistochemistry. Spatial distributions of t-PA and plasminogen showed clearly that ultrasound promoted the penetration of rt-PA into thrombi significantly (p<0.0001), and broadened the zone of lysis from 8.9 +/-2.6 microm to 21.2 +/-7.2 microm. We speculate that ultrasound enhances thrombolysis by affecting the distribution of rt-PA within the clot.

Fibrinolysis↗
PubMed2004

Doppler assessment of mechanical aortic valve prostheses: effect of valve design and size of the aorta.

BACKGROUND AND AIM OF THE STUDY: Discrepancies between Doppler and catheter gradients have been reported for bileaflet aortic valve prostheses. Whether modifications in geometric design of newly developed bileaflet valves lead to a different Doppler-catheter gradient relationship has not been evaluated. Variable results have been reported for tilting-disc prostheses. In addition, the effect of aortic size on the Doppler-catheter gradient relationship remains unclear. METHODS: Various sizes of On-X and Edwards Mira (identical with Sorin Bicarbon) bileaflet valves and Sorin Allcarbon tilting-disc aortic valves (19-25 mm) were studied in a pulsatile flow model. Doppler and catheter gradients were measured simultaneously. Aortic diameters between 1.8 and 4 cm were evaluated. RESULTS: Correlation between Doppler and catheter gradients was excellent (r = 0.98-0.99 for peak and mean gradients), but in bileaflet valves Doppler significantly overestimated the corresponding catheter gradients as reflected by slopes of the regression lines (1.57-1.8). In the range of relevant gradients > or = 10 mmHg, Doppler exceeded catheter gradients by 40 +/- 17% (peak) and 39 +/- 16% (mean) in Mira valves, and by 46 +/- 19% (peak) and 43 +/- 14% (mean) in On-X valves. In the Sorin tilting-disc valve, Doppler accurately reflected catheter gradients (slopes of regression lines 1.05-1.14). The aortic diameter significantly influenced results in only tilting-disc valves, but in absolute terms the effect was clinically less relevant. CONCLUSION: Discrepancies between Doppler and catheter gradients are common to all bileaflet valves, regardless of their specific geometric design, whereas tilting-disc valves must be considered individually. The influence of aortic size on the Doppler-catheter gradient relationship appears clinically to be less relevant in prosthetic valves.

Aorta↗
PubMed2003

Inhibition of restenosis by tissue factor pathway inhibitor: in vivo and in vitro evidence for suppressed monocyte chemoattraction and reduced gelatinolytic activity.

Activation of inflammatory and procoagulant mechanisms is thought to contribute significantly to the initiation of restenosis, a common complication after balloon angioplasty of obstructed arteries. During this process, expression of tissue factor (TF) represents one of the major physiologic triggers of coagulation that results in thrombus formation and the generation of additional signals leading to vascular smooth muscle cell (VSMC) proliferation and migration. In this study, we have investigated the mechanisms by which inhibition of coagulation at an early stage through overexpression of tissue factor pathway inhibitor (TFPI), an endogenous inhibitor of TF, might reduce restenosis. In a rabbit femoral artery model, percutaneous delivery of TFPI using a recombinant adenoviral vector resulted in a significant reduction of the intimamedia ratio 21 days after injury. Investigating several markers of inflammation and coagulation, we found reduced neointimal expression of monocyte chemoattractant protein-1 (MCP-1), lesional monocyte infiltration, and expression of vascular TF, matrix metalloproteinase-2 (MMP-2), and MMP-9. Moreover, overexpression of TFPI suppressed the autocrine release of platelet-derived growth factor BB (PDGF-BB), MCP-1, and MMP-2 in response to factors VIIa and Xa from VSMCs in vitro and inhibited monocyte TF activity. These results suggest that TFPI exerts its action in vivo through not only thrombotic, but also nonthrombotic mechanisms.

Adenoviridae↗
PubMed2003

Glycoprotein 130 ligand oncostatin-M induces expression of vascular endothelial growth factor in human adult cardiac myocytes.

OBJECTIVE: In murine and rat cardiac myocytes the gp130 system transduces survival as well as hypertrophic signals and via induction of the expression of the potent angiogenic factor VEGF in these cells also indirectly contributes to cardiac repair processes through the development of new blood vessels. There are, however, species differences in receptor specificity and receptor crossreactivity in the gp130-gp130 ligand system. We asked whether gp130 signaling is also involved in the regulation of VEGF in human cardiac myocytes and if so which gp130 ligands are critical for such an effect. METHODS: Human adult cardiac myocytes (HACMs) were isolated from myocardial tissue and characterised by positive staining for myocardial actin, troponin-I and cardiotin. HACMs were treated with the gp130 ligands CT-1, IL-6, LIF or OSM and VEGF-1 was determined by a specific ELISA in the conditioned media of these cells. RT-PCR and Western blot analysis was used in order to detect gp130, IL-6-receptor, LIF-receptor or OSM-receptor specific protein and mRNA in human adult cardiac myocytes and for detection of VEGF-1 specific mRNA in cardiac myocytes after incubation with OSM. Pieces of myocardial tissue were incubated ex vivo in the presence and absence of OSM and VEGF was determined in supernatants of these cultures and immunohistochemistry was performed on the tissue using specific antibodies for VEGF-1. Immunohistochemistry was also employed to detect VEGF in sections from a healthy human heart and in a heart from a patient suffering from acute myocarditis. RESULTS: OSM, but not CT-1, IL-6 or LIF increased VEGF-1 production in human adult cardiac myocytes dose-dependently derived from five different donors. This selective stimulation of VEGF by gp130 ligands was also reflected by a specific receptor expression on these cells. We detected high levels of mRNA for gp130 and the OSM receptor in freshly isolated human cardiac myocytes but only low amounts of mRNA for the IL-6 receptor whereas mRNA for the LIF receptor was hardly detectable by RT-PCR. OSM receptor and IL-6 receptor were also detectable by Western blotting whereas LIF receptor was only present as a faint band. OSM also increased the expression of VEGF-1 mRNA in cardiac myocytes. When pieces of human myocardial tissue were incubated with the gp130 ligands in an ex vivo model only OSM resulted in an increase in VEGF-1 in the supernatants of these cultures. Furthermore, VEGF increased in tissue samples treated with OSM in cardiac myocytes as evidenced by immunohistochemistry. In addition, we found increased VEGF-1 expression in myocardial tissue from a patient suffering from acute myocarditis. CONCLUSION: The gp130-gp130 ligand system is also involved in VEGF regulation in human cardiac myocytes and OSM is the gp130 ligand responsible for this effect in the human system whereas LIF and CT-1 which had been shown to regulate VEGF expression in mouse and rat cardiac myocytes had no effect. Thus we have added OSM, which is produced by activated T lymphocytes and monocytes, to the list of regulatory molecules of VEGF production in the human heart. Our results lend further support to the notion that besides hypoxia, inflammation via induction of VEGF through autocrine or paracrine pathways plays a key role in (re)vascularisation of the myocardium.

Adult↗
PubMed2003

Polymorphic membrane protein (PMP) 20 and PMP 21 of Chlamydia pneumoniae induce proinflammatory mediators in human endothelial cells in vitro by activation of the nuclear factor-kappaB pathway.

We tested whether polymorphic membrane proteins (PMPs) of Chlamydia pneumoniae might play a role in triggering an inflammatory response in human endothelial cells. Of 15 purified, recombinant chlamydial PMPs tested, 2 (PMP 20 and PMP 21) dose-dependently increased the production of the inflammatory mediators interleukin (IL)-6 and monocyte chemoattractant protein-1 (MCP-1), in cultured human endothelial cells; production of IL-8 was also increased. When endothelial cells were infected by live C. pneumoniae, an increase in the production of IL-6, IL-8, and MCP-1 was seen. We used adenovirus-induced overexpression of IkappaBalpha-an inhibitor of nuclear factor (NF)-kappaB-to demonstrate that PMP 20 and PMP 21 increase the production of IL-6 and MCP-1 in human endothelial cells by activation of the NF-kappaB pathway, because, in cells overexpressing IkappaBalpha, treatment with the respective PMP did not result in increased production of IL-6 and MCP-1. Thus, C. pneumoniae could, by interactions of its PMPs with the endothelium, contribute to the process of vascular injury during the development and progression of atherosclerotic lesions.

Bacterial Outer Membrane Proteins↗
PubMed2003

Effect of short-term treatment with azithromycin on recurrent ischaemic events in patients with acute coronary syndrome in the Azithromycin in Acute Coronary Syndrome (AZACS) trial: a randomised controlled trial.

BACKGROUND: There is serological and epidemiological evidence of an association between Chlamydia pneumoniae infection and coronary artery disease. Results of previous smaller studies have indicated a reduction of recurrent ischaemic events in patients with acute coronary syndrome when given macrolide antibiotics. We aimed to assess whether short-term treatment with the macrolide antibiotic azithromycin reduces recurrent ischaemic events in patients admitted for unstable angina or myocardial infarction. METHODS: We assessed the effect of azithromycin in a multicentre, double-blind randomised trial in 1439 patients with unstable angina or acute myocardial infarction. Patients were randomly allocated to receive 500 mg azithromycin on the first day after randomisation, followed by 250 mg daily for 4 days or placebo. Patients were followed up for 6 months. The primary endpoints were death, recurrent myocardial infarction, or recurrent ischaemia necessitating revascularisation. Analysis was done by intention to treat. FINDINGS: Treatment with azithromycin did not result in reduction of either individual endpoints or any of the primary endpoints. Of the 716 patients in the azithromycin group, 23 (3%) died, 17 (2%) developed myocardial infarction, 65 (9%) had recurrent ischaemia needing revascularisation, and 100 (14%) had one or more of these endpoints. In the placebo group (n=723) the corresponding numbers of patients were 24 (4%), 22 (3%), 59 (8%), and 106 (15%), respectively (p=0.664, 95% CI 0.72-1.24). 62 (9%) of patients in the azithromycin group and 59 (8%) in the placebo group reached the secondary endpoint of ischaemia or congestive heart failure necessitating admission (difference 0.5%, 95% CI 0.75-1.53; p=0.707). We recorded few side-effects. INTERPRETATION: Short-term treatment with azithromycin does not reduce development of recurrent events in patients with acute coronary syndrome.

Aged↗
PubMed2003

Relationship between dobutamine response of dyssynergic myocardium and angiographically documented blood supply.

OBJECTIVE: Because hibernation is considered a down-regulation of contractile function in response to reduced regional myocardial perfusion, hibernating myocardium is expected to be supplied by a critically stenosed or even occluded coronary artery. Thus, high-dose dobutamine has been postulated to cause ischemia and reworsening of myocardial function (biphasic response), whereas myocardium that demonstrates sustained improvement with high-dose dobutamine should not be supplied by a significantly stenosed vessel. This study evaluates the type of dobutamine response-biphasic versus sustained improvement-of dyssynergic myocardium in relation to its angiographically documented blood supply. METHODS: In 38 patients (5 women; mean age 60 +/- 9 years) with chronic coronary artery disease and impaired left ventricular ejection fraction (</=35%), dobutamine echocardiography and quantitative coronary angiography were performed within 4 weeks. Wall-motion response of dyssynergic myocardium to dobutamine, classified as no improvement, biphasic response, or sustained improvement, was compared with the angiographically documented blood supply (presence of coronary stenosis in the corresponding artery, collaterals, and stenoses of the collateral supplying artery) in a segment-by-segment analysis. RESULTS: Of the 465 segments with abnormal wall motion at rest, 201 (47%) showed improvement during dobutamine infusion at low dose. Of these, 145 (72%) were supplied by significantly stenosed epicardial vessels. Only 27 (19%) of these 145 segments showed a biphasic response whereas in the remaining 118 segments wall-motion improvement persisted during high-dose dobutamine infusion. Although mean stenosis severity in the supplying vessel was significantly greater for segments presenting with biphasic response as compared with sustained improvement (95 +/- 7% and 86 +/- 12% luminal diameter reduction, respectively; P <.0001), 69% of segments with sustained improvement were supplied by a critically stenosed artery. Only 7 of 27 segments with biphasic response and 22 of 118 segments with sustained improvement had visible collaterals supplied by a vessel without significant stenosis. The percentage of segments viable by thallium-single photon emission computed tomography imaging was similar for those with sustained and biphasic response (96% and 83%, respectively). CONCLUSIONS: In this group of patients with coronary artery disease and impaired left ventricular function, the great majority of dyssynergic segments that exhibited a sustained, rather than biphasic, dobutamine response were supplied by a critically stenosed artery. Furthermore, the percentage of segments viable by thallium-single photon emission computed tomography did not appear to be different for segments with sustained improvement and those with biphasic response. These findings challenge the hypothesis that biphasic response is the best criterion to identify viable myocardium.

Aged↗
PubMed2003

Pathogenesis of bone loss in heart transplant candidates and recipients.

BACKGROUND: Heart transplantation (HTX) is associated with decreased bone mineral density and changes in bone metabolism. We conducted this study to evaluate the pathophysiology of bone metabolism in HTX candidates and recipients. METHODS: Thirty-six HTX recipients were compared with 36 HTX candidates concerning biochemical parameters of bone metabolism and bone mineral density. RESULTS: Osteocalcin, bone-specific alkaline phosphatase, cross-linked-N-telopeptide of type I collagen, estradiol, serum creatinine, and blood urea nitrogen concentrations were significantly higher, whereas the calcium-creatinine ratio, thyrotropin, thyroxine, and bone mineral density were significantly lower in HTX recipients than in HTX candidates. Compared with a control group, HTX candidates had decreased renal function and increased bone resorption, whereas HTX recipients additionally had increased alkaline phosphatase and osteocalcin levels. In HTX recipients, we found positive correlations between creatinine clearance and bone mineral density; daily and cumulative cortisone doses were not associated with bone mineral density. CONCLUSIONS: In HTX candidates, disturbances in bone metabolism with increased bone resorption may be caused partly by existing low-grade renal insufficiency, regular intake of loop diuretics, and restriction of mobility. In HTX recipients, immunosuppressive therapy-glucocorticoids and cyclosporine-seem to be responsible for changes in bone metabolism.

Adult↗
PubMed2003

Myocardial involvement in a patient with Burkitt's lymphoma mimicking hypertrophic cardiomyopathy.

Burkitt's lymphoma is a highly aggressive type of non-Hodgkin's lymphoma frequently associated with extranodal or abdominal manifestations. We report the case of a young woman with generalized Burkitt's lymphoma, initially presenting with signs and symptoms of central nervous system involvement. Myocardial infiltration mimicking hypertrophic cardiomyopathy was detected with electrocardiogram, echocardiography, magnetic resonance imaging, and positron emission tomographic scintigraphy with F-18 desoxy-glucose. These abnormalities resolved after high-intensity chemotherapy with a modified B-cell acute lymphoblastic leukemia (B-ALL) protocol.

Adult↗
PubMed2003

Normal values for Doppler echocardiographic assessment of heart valve prostheses.

Assessment of normal and abnormal function of heart valve prostheses remains challenging. Doppler echocardiography has been shown to allow hemodynamic evaluation in various clinical settings and has become the most widely used tool to assess prosthetic valve function. Prosthetic valves, even when they function normally, are to some degree obstructive to the blood flow. The normal values of gradients, pressure half-time, and effective orifice area depend on valve type and valve size. Doppler assessment of prosthetic valve function, thus, requires specification of valve type and valve size, and knowledge of the normal values. This study provides an updated overview on the available data of normal values to facilitate adequate interpretation of Doppler data.

Aortic Valve↗
PubMed2003

Parameters of the tissue factor pathway with coumadin/dipyridamole versus ticlopidine as adjunct antithrombotic-drug regimen in coronary artery stenting.

A different rate and timing of subacute stent thrombosis after percutaneous coronary intervention was reported with various peri-interventional antithrombotic regimens. Next to platelet activation, coagulation triggered by tissue factor (TF) may play a key role in this process. Thirty-one consecutive patients with stable and unstable angina undergoing coronary stenting were randomly assigned to adjunct oral anticoagulation/anti-platelet therapy (coumadin, dipyridamole, aspirin and heparin; n = 16) or adjunct anti-platelet therapy with thienopyridin (ticlopidine, aspirin and heparin; n = 15). Antigen levels of plasma TF, total tissue factor pathway inhibitor (TFPI) and TFPI/ activated factor X (TFPI/FXa) complex were determined before and for up to 6 days after intervention by immunoassay. At baseline, significantly higher levels of plasma TF and TFPI/FXa were found in patients with unstable angina [TF, 161 pg/ml (126-191 pg/ml); TFPI/FXa, 7.8 ng/ml (6.1-9.6 ng/ml)] compared with stable angina [TF, 62 pg/ml (46-82 pg/ml), P < 0.0001; TFPI/FXa, 4.5 ng/ml (3-7.6 ng/ml), P= 0.003]. One hour after intervention, an increase of plasma TF and TFPI/FXa was seen in both treatment groups. In unstable angina patients, plasma levels of TF, TFPI and TFPI/FXa were more efficiently reduced by adjunct ticlopidine therapy compared with adjunct coumadin/dipyridamole. These data suggest reduced release of circulating TF by combined anti-platelet therapy with ticlopidine and aspirin after coronary artery stenting, which may-contribute to the lower incidence of subacute stent thrombosis previously observed.

Adult↗
PubMed2003

Fibrinolytic balance of the arterial wall: pulmonary artery displays increased fibrinolytic potential compared with aorta.

Classic pulmonary thromboembolism research has documented that large pulmonary thromboemboli lyse spontaneously, suggesting potent fibrinolytic activity in human pulmonary artery (Pa). This concept conflicts with published animal studies in which the proximal Pa was reported to be devoid of tissue plasminogen activator (t-PA) expression. The current study used in situ hybridization protocols to demonstrate t-PA expression in samples of human main Pa (n = 30). Real-time PCR was used to demonstrate quantitatively that the levels of t-PA transcripts were higher than those of its primary regulator [ie, plasminogen activator-inhibitor 1 (PAI-1)] in the Pa samples. Immunologic and functional assays extended these observations by demonstrating that levels of t-PA antigen were higher than PAI-1 antigen, which resulted in the detection of free t-PA activity. This contrasted with the fibrinolytic balance of matched samples of aorta (n = 6) in which PAI-1 transcripts and antigen values were higher than the corresponding t-PA values, and only M(r) 110 kDa t-PA-PAI-1 complexes could be detected in functional assays. To assess the relative fibrinolytic contribution of the endothelial cell layer, Pa endothelial cells and aortic endothelial cells were scraped and propagated in culture for 20 +/- 6 days. Pa endothelial cell-conditioned media revealed increased t-PA/PAI-1 antigen ratios. Taken together, our data indicate that the balance between t-PA and PAI-1 is shifted in human main Pa to favor net PA activity.

Aorta, Thoracic↗
PubMed2003

High prevalence of elevated clotting factor VIII in chronic thromboembolic pulmonary hypertension.

Chronic thromboembolic pulmonary hypertension (CTEPH) is an enigmatic disorder lacking signs, symptoms and classical risk factors for venous thromboembolism. The objective of the prospective case controlled study, carried out at the Pulmonary Hypertension Unit, University Hospital Vienna, Austria, was to investigate whether plasma FVIII is elevated in CTEPH patients. The study examined 122 consecutive patients diagnosed with CTEPH. Plasma FVIII was measured and compared with plasma FVIII of healthy controls (n = 82) and of patients with nonthromboembolic pulmonary arterial hypertension (PAH, n = 88). Results show that CTEPH patients had higher FVIII levels than controls (233 +/- 83IU/dl versus 123 +/- 40IU/dl, p < 0.0001) and PAH patients (158 +/- 61IU/dl, p < 0.0001). Plasma FVIII one year after surgery (212 +/- 94IU/dl) was statistically unchanged compared with preoperative values (FVIII: 226 +/- 88IU/dl, n = 25). FVIII > 230IU/dl was more prevalent in CTEPH patients (41%) than in controls (5%, p < 0.0001) and PAH patients (22%, p = 0.022). We can conclude that elevated plasma FVIII is the first prothrombotic factor identified in a large proportion of CTEPH patients.

Adult↗
PubMed2003

2MHz ultrasound enhances t-PA-mediated thrombolysis: comparison of continuous versus pulsed ultrasound and standing versus travelling acoustic waves.

In addition to fibrinolytic enzymes, ultrasound has the potential to enhance thrombolysis. High frequency ultrasound has the advantage that a combination of diagnostic and therapeutic ultrasound with only one device is possible. Therefore, we investigated the optimal high frequency (2 MHz) ultrasound field characteristics and application mode in vitro. Continuous ultrasound significantly enhanced rt-PA mediated thrombolysis: in a travelling wave field thrombolysis was augmented by 49.0 +/- 14.7% and in a standing wave field by 34.8 +/- 7.3%. In an intermittent application mode (1Hz, 10Hz, 100Hz, 1kHz) most efficient results were obtained for both wave fields using 1 Hz (46.4 +/- 10.7% and 39.1 +/- 6.6%, respectively). Referring to a possible in vivo application our in vitro data suggests that an intermittent application of a 2 MHz high frequency ultrasound using a travelling wave field would be the most potent application for lysing blood clots.

Acoustics↗