Eighteen patients had preserved (group A) and 16 abnormal LVEF reserve (group B; range -7 to -32). Group B patients had greater wall thickness than group A, but resting volumes, LVEF, resting and Dip MBF, and myocardial flow reserve were similar. Group B had slightly higher summed stress score and summed difference score in visual analysis than group A, and a significantly higher summed stress wall motion score. In group B, resting TPG was slightly lower (1.31 ± 0.29 vs. 1.37 ± 0.34, p <0.05), and further decreased after Dip, whilst in group A it increased (B = 1.20 ± 0.39, p < 0.0001 vs. rest and vs. A = 1.40 ± 0.43). The number of segments per patient with TPG <1 was higher than in group A (p < 0.001) and was a significant predictor of impaired LVEF reserve (OR 1.86, p < 0.02), together with wall thickness (OR 1.3, p < 0.02).
All patients over 18 years, who attended the stroke unit between 1 October 2002 and 31 December 2002 and were on antiplatelet therapy were included in the study. Data were collected through retrospective chart review and recorded on a standardized data collection form. Continuous and categorical data were expressed as mean and counts respectively. Factors that determine frequency and pattern of antiplatelet therapy were assessed in multiple logistic regression models.
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Dipyridamole, a potent inhibitor of the nucleoside transport into cells, has recently been reported to stimulate the proliferation of capillary endothelial cells in the heart and skeletal muscle of rats following long-term treatment. We tested this drug on cultured calf aortic endothelial cells and obtained no evidence that dipyridamole is able to stimulate directly the proliferation and migration of these cells. By using the chorioallantoic membrane model we observed that the pharmaceutical preparation Curantyl induces vascular responses almost regularly. This effect, however, was found to be dependent on the high concentration of hydrogen ions in this preparation and could be prevented by increasing the pH value. A direct angiogenic effect of dipyridamole could not be demonstrated on the CAM.
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Patients with peripheral arterial disease improve their outcome by receiving aspirin with dipyridamole or ticlopidine after a revascularisation procedure.
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Treatment with the association ASA-DIP was the only one to significantly reduce interaction, as both the size of aggregates and the extent of the covered surface decreased when whole blood was treated, and only the covered surface did when red cells were separately treated. When treating only platelets, the reduction of aggregates had no significance.
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Vascular access grafts implanted in dialysis patients are prone to failure in the long-term because of stenosis and occlusion caused by neointimal hyperplasia. Local delivery of antiproliferative drugs may be effective to prevent this consequence while minimizing the systemic side effects they cause. We developed a combination of poly(lactide-co-glycolide) (PLGA) microspheres with ReGel, an injectable copolymer, as a sustained-release system for perivascular delivery of an antiproliferative drug, dipyridamole. Dipyridamole-incorporated PLGA microspheres with various molecular weights (MWs) of PLGA were prepared by oil-in-water emulsion method. Encapsulation efficiency and surface morphology of microspheres were characterized. In vitro release kinetics of dipyridamole from ReGel or from microspheres/ReGel was experimentally determined. Without microspheres, 40% of the dipyridamole was released from ReGel as an initial burst in the first 3 days followed by continuous release in the subsequent 2 weeks. The use of PLGA microspheres decreased the initial burst and extended dipyridamole release from 23 to 35 days with increasing MW of PLGA. The highest MW PLGA showed a lag time of 17 days before consistent drug release occurred. Mixing microspheres and ReGel with two different MW PLGA achieved a continuous release for 35 days with little initial burst. In vivo release of dipyridamole from microspheres/ReGel exhibited a comparable release pattern to that seen in vitro. This injectable platform is a promising technique for sustained perivascular delivery of antiproliferative drugs.
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To evaluate the prevalence of embolic events and relevant factors in elderly Chinese patients with atrial fibrillation(AF), and to provide evidence on ways to prevent embolic events.
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Extracellular adenosine in the striatum of adult male rats was measured by the use of a microdialysis fibre inserted transversely in the striatum. The adenosine concentration in samples of perfusate was determined by HPLC coupled to U.V. detection. The adenosine concentration (corrected for recovery) decreased after implantation of the probe. Two hours later it was 1.83 +/- 0.22 in anaesthetized rats, whereas it was 40% higher in rats in which anaesthesia had been discontinued. Twenty-four hours later the adenosine concentration was 0.124 +/- 0.09 microM; the addition of dipyridamole (100 microM), an adenosine uptake blocker, to the perfusate resulted in a 76% increase in adenosine concentration in the effluent, whereas addition of the adenosine deaminase inhibitor erythro-2-(hydroxy-3-nonyl) adenine (100 microM) caused a 260% increase. The addition of tetrodotoxin (1 microM) was followed by a decrease in basal adenosine concentration and a partial inhibition of the increase in adenosine evoked by K+ depolarization. The increase induced by high K+ was markedly inhibited by the NMDA receptor antagonist D(-)-amino-7-phosphoeptanoic acid (1 mM, D-AP7). These findings indicate that the extracellular adenosine level is influenced by neuronal activity, and that under strong depolarizing conditions the increase in adenosine level involves NMDA receptor activation.
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This study was designed to investigate the effects of the cardiovascular drug dipyridamole on fatty acid metabolism in isolated cardiac myocytes. Effects of dipyridamole on the oxidation of long-chain (palmitate) fatty acid, medium-chain (octanoate) fatty acid, and the carbohydrate intermediate (pyruvate) were determined by using isolated cardiac myocytes from both normal and diabetic rats. Dipyridamole increased palmitate oxidation in a concentration-dependent manner in both normal and diabetic myocytes. Maximal stimulation of palmitate oxidation (175% of control) was observed with 100 microM dipyridamole. In contrast, oxidation of octanoate and pyruvate was not affected. The stimulation of palmitate oxidation by dipyridamole persisted despite its removal from the incubation medium. In contrast to the effect in myocytes, palmitate oxidation was not affected by dipyridamole in isolated rat heart mitochondria. Palmitate uptake was increased by 2.5- and 1.6-fold when palmitate concentration was adjusted to 0.05 and 0.2 mM, respectively. Dipyridamole did not affect lipolysis in isolated myocytes. When dipyridamole (100 microM) and L-carnitine (5 mM) were added together to the incubation medium, palmitate oxidation was further increased to 223% of the control. The nucleoside transport inhibitor nitrobenzylthioinosine (NBMPR) failed to increase palmitate oxidation in isolated myocytes. Although palmitate oxidation in diabetic cells is much higher than that in normal myocytes, dipyridamole increased palmitate oxidation by 243% in diabetic myocytes over its baseline oxidation rate in normal cells. These results suggest that increased palmitate oxidation in isolated cardiac myocytes after dipyridamole administration occurs independent of effects on either the phosphodiesterase enzyme or nucleoside transport protein, but it may result from increased palmitate transport across the plasma membrane.
The modulating role played by red cells on platelet function is well known, yet its mechanism of action in the presence of antiaggregating agents is not clearly defined. We tried to assess the influence of aspirin (ASA) or dipyridamole (DIP) treated red cells on platelet aggregation in plasma, with the samples in static conditions and under flow in a perfusion system.
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The antagonist effects of 8-phenyltheophylline (8-PT) and caffeine against the actions of adenosine, (-)-N6-(R-phenyl-isopropyl)-adenosine (PIA), morphine and nalorphine on the guinea pig ileum preparation were examined. Antagonism of both adenosine and PIA by caffeine and 8-PT was concentration dependent. The slopes of Schild plots for both alkylxanthines vs. adenosine were significantly less than -1 unless the adenosine reuptake blocker dipyridamole (0.1 microM) was include in the tissue bath. Under these conditions, the 95% confidence intervals of the Schild plot slopes embraced theoretical unity, suggesting competitive antagonism. The antagonism of PIA by the alkylxanthine was also competitive. Dipyridamole had no effect on the potency of PIA. The pA2 value for caffeine-adenosine was not different from that for caffeine-PIA, and the pA2 values of 8-PT-adenosine and 8-PT-PIA were similar, suggesting that these two agonists interacted with similar receptors. The pA2 values using 8-PT were approximately 1.5-fold higher than those employing caffeine, suggesting higher affinity for 8-PT at these receptors. Caffeine significantly antagonized morphine at all concentrations used (0.5-1.0 mM), but only antagonized nalorphine at the two highest concentrations. After treating ilea with the mu-specific irreversible antagonist beta-FNA (beta-funaltrexamine) (resulting in a preparation with relatively pure kappa receptor population), the antagonist effect of caffeine against morphine was reduced such that only a concentration of 1 mM resulted in significant antagonism, while the effects of caffeine against nalorphine were unchanged. 8-PT did not antagonize morphine or nalorphine.(ABSTRACT TRUNCATED AT 250 WORDS)
Myocardial blood flow was evaluated in 31 subjects with not only visual but also, for the first time, circumferential profile analysis of rubidium 82 (82Rb) images acquired with positron emission tomography. Fifteen were control subjects and 16 subjects had significant coronary artery disease, defined as 50% or greater diameter stenosis in a major coronary artery or a first-order branch. Simultaneous 82Rb images at three myocardial levels were obtained before and after intravenous dipyridamole plus handgrip stress. In patients with significant coronary artery disease, visual analysis correctly identified significant disease in 26 (76%) of 34 arteries and its absence in 12 (86%) of 14 normal arteries. According to circumferential profile analysis, these numbers were 91% and 86%, respectively. Thus circumferential analysis of 82Rb images, obtained before and after intravenous dipyridamole plus handgrip stress, yielded improved sensitivity and comparable specificity compared with visual analysis.
A visual improvement in anteroseptal and apical myocardial perfusion between stress and rest with Tc-99m MIBI in patients with LBBB probably indicates significant LAD stenosis. In our hands, quantitative software did not aid in the diagnosis. A well-designed, prospective study using a standardized stress protocol (probably dipyridamole or adenosine), which specifically evaluates visual reversibility in the anteroseptal wall and apex, will obviate the need for a Bonferroni correction, and could confirm these findings.
The patients with perfusion abnormalities on ungated rest, ungated stress, or end-systolic stress images had significantly longer minimum QRS duration at rest. These QRS values correlated with SRS and SSS (r: 0.528, P: 0.01 and r: 0.47, P: 0.024, respectively). Analysis of perfusion and functional data demonstrated an inverse correlation between left ventricular ejection fraction (LVEF) and ESS (r: -0.671, P < 0.0001). The patients with end-systolic perfusion abnormalities had significantly lower LVEF rates when compared with the patients with normal perfusion on end-systolic images.
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We have induced the formation of arterial thrombosis in dogs by means of an intima lesion produced by continuous current. The platelets were labeled with 111-In-oxine. Groups of 7 mongrel dogs received treatment for 7 days prior to the trial: Group I, control; Group II, 5 mg/kg body weight/day acetylsalicylic acid; Group III, 20 mg/kg body wt/day acetylsalicylic acid; Group IV, 15 mg/kg body wt/day triflusal + 5 mg/kg body wt/day dipyridamole; Group V, 15 mg/kg body wt/day triflusal; and Group VI, 5 mg/kg body wt/day acetylsalicylic acid + 5 mg/kg body wt/day dipyridamole. The only effective treatment for arterial thrombosis prevention was that employed in Group II (p less than 0.05).
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In November 1976, a 52 year old woman presented with a Moschowitz syndrome with clinical manifestations of continuous fever at 39 degrees and a transient Wernicke type aphasia. Laboratory findings included schizocytosis, a peripheral thrombocytopaenia and functional renal insufficiency. The ethanol tests was positive but there was no frank defibrination syndrome. After corticosteroid therapy failed, the patient was treated with Dipyridamole 400 mg/24 hours IV and acetylsalicylic acid 4 g/24 hours IV. Fever disappeared on the same day and the thrombocytopaenia was corrected in 48 hours. The patient was considered to be cured 15 days later. No precise aetiology to explain the Moschowitz syndrome was discovered apart from the recent ingestion of oestrogens. The authors emphasise the considerable progress which this use of a combination of Dipyridamole and aspirin represents, resulting in the cure of Moschowitz syndrome, a condition considered to be fatal up until a few years ago.
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Peripheral vascular complications are a significant source of morbidity after coronary artery stent implantation. The goal of this study was to assess the incidence, risk factors, and management of vascular complications after stent placement. The study population consisted of 101 consecutive patients who underwent stent placement for either elective or bailout indications. All patients received a standardized anticoagulation regimen of aspirin, dipyridamole, low molecular weight dextran, heparin, and warfarin. Peripheral vascular access sites were examined daily until hospital discharge. Vascular complications occurred in 16 of 101 (16%) patients, including femoral artery pseudoaneurysm (n = 11), hematoma requiring transfusion or surgery (n = 4), and arteriovenous fistula (n = 1). Intervention was required in 14 of 16 (88%) patients with complications. These included transfusion (n = 7), ultrasound-guided compression (n = 8), and/or vascular surgery (n = 7). Length of hospital stay was prolonged in patients with complications (14 +/- 9 vs. 8 +/- 5 d, P < 0.001). The development of peripheral vascular complications did not correlate with clinical or procedural variables such as age, cardiovascular risk factors, arterial sheath size, or elective vs. bailout indication. After the introduction of a pneumatic vascular compression device (FEMOSTOP, C.A. Bard, Billerica, MA), a significant reduction in vascular complications was observed. Complications occurred in only 1 of 41 (2.4%) patients in whom the compression device was used in contrast to 13 of 58 (22.4%) patients compressed manually (P < 0.01). Thus peripheral vascular complications are frequent after coronary artery stent placement and are associated with serious morbidity and prolongation of hospital stay. These complications are significantly reduced by the use of a pneumatic vascular compression device despite intensive systemic anticoagulation.
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To elucidate feasibility of the absolute myocardial blood flow (MBF), total coronary resistance (TCR), and myocardial blood flow reserve (MBFR) quantification using MRI in patients with coronary artery disease (CAD).
Overall time savings and time savings stratified by operational ability (number of staff, number of SPECT cameras, hours of operation) translate to a more efficient utilization of laboratory resources when using regadenoson compared to adenosine and dipyridamole. Regadenoson is the most efficient pharmacologic stress agent compared to adenosine and dipyridamole.
A 30-year-old right-handed man was admitted for left facial paralysis and dysarthria. He had received oral isotretinoin 45 mg/day for 3 months for treatment of severe acne. A cerebral computed tomography scan showed hypodensity in the right middle cerebral territory corresponding to cerebral ischemia. The patient reported having experienced a similar episode 7 years before, after 3 months' treatment with oral isotretinoin. No risk factors were identified. Isotretinoin was discontinued on admission and the disorders resolved.
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Nine pts, aged 4-20 years (mean 12) with chronic uremic anaemia (mean Hb 5.8 g/dl, range 5.0-7.0 g/dl) on regular thrice-weekly haemodialysis, were treated with human recombinant erythropoietin (rh-uEPO) for a mean of 28.11 weeks (range 4-48). To attain a target Hb concentration (9.6-11.2 g/dl) RH-uEPO (Cilag) was administered i.v. after each dialysis in increasing doses within the range (51-300 U/kg/week). All pts were treated with persantine. Five pts needed iron supplementation. All pts showed increased Hb concentration and none of 6 previously transfusion dependent pts needed further transfusions after the first week of rH-uEPO. Pretreatment long-term dialyzed, polytransfused and iron overloaded pts, even when treated with lower doses of rH-EPO, responded better, reaching target Hb level from the 8th- to the 16th week. Three of 4 highly sensitized pts on rH-EPO treatment had a significant decrease of cytotoxic antibody titre, and 2 were successfully transplanted. rH-EPO also significantly improved the life quality in all pts. No pts developed any serious side affects. There was a transient increase in BP (2 pts) and transaminase with eosinophilia (4 pts).
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Experimental studies have suggested that dipyridamole may inhibit red blood cell labelling with technetium-99m. To evaluate whether this effect is clinically relevant to the performance of radionuclide ventriculography after dipyridamole-thallium stress testing, in vitro red blood cell labelling was compared immediately before and after thallium-201 stress scintigraphy combined with either dipyridamole infusion (30 patients) or exercise stress (20 patients). Modified in vivo red blood cell labelling efficiency was assessed in a further 36 patients following dipyridamole infusion and was compared with that in 15 patients following exercise stress. The importance of a reversal of the dipyridamole effects by aminophylline was evaluated for in vitro and modified in vivo techniques. The red blood cell labelling efficiency was not significantly different in patients following dipyridamole compared with that obtained following exercise stress for both in vitro (93% +/- 4% versus 91% +/- 4%) and modified in vivo (87% +/- 19% versus 90% +/- 6%) techniques. Also, in vitro red blood cell labelling efficiency after dipyridamole was not different to that before stress testing (93% +/- 4% versus 92% +/- 4%). Reversal with aminophylline had no significant effect on the in vitro labelling efficiency with either the in vitro technique (94% +/- 3% with reversal versus 92% +/- 5% without) or the modified in vivo technique (91% +/- 4% with reversal versus 82% +/- 26% without). These results suggest that the red blood cell labelling efficiency is not compromised by the preceding dipyridamole-thallium stress testing but can be optimised by using in vitro labelling.
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The accuracy of dipyridamole sestamibi SPECT imaging in detecting multivessel disease was similar for men and women. The sensitivity of dipyridamole sestamibi SPECT imaging in detecting disease of the left anterior descending artery was better in women.
Despite predictions that 201Tl imaging would be completely supplanted by the new 99mTc perfusion agents, thallium perfusion imaging is alive and well. In fact, in the past year, important new information on thallium imaging continued to emerge. Among the new data, the reinjection of a "booster" dose of 201Tl after the redistribution images has been heralded as a breakthrough that would equal positron-emission tomography in the prediction of myocardial viability. Pharmacologic coronary vasodilation has been increasingly popular, especially since the approval of intravenous dipyridamole by the Food and Drug Administration and in view of recent studies showing that adenosine is a very attractive alternative to dipyridamole in patients who cannot exercise. Beyond the undisputed diagnostic value of dipyridamole-thallium imaging, data on risk stratification continue to accumulate for patients receiving peripheral vascular surgeries as well as for those recovering from a myocardial infarction. The advent of single-photon emission CT in combination with 201Tl imaging allows improved quantification of jeopardized myocardium. This technique has now been used increasingly to complement the information obtained from coronary angiography by the determination of the functional significance of known coronary stenoses. Recent studies have shown marked heterogeneity in the extent of jeopardized myocardium in patients with coronary artery disease. Equally important have been recent reports on the high prevalence of silent ischemia in patients undergoing 201Tl exercise scintigraphy. Technical progress has also enhanced the diagnostic capability of 201Tl imaging, allowing sharper identification of perfusion defects and quantification of reversible myocardial ischemia precipitated by exertion. Finally, one of the most exciting areas of research in thallium scintigraphy is its established prognostic value in patients with stable angina or those recovering from a myocardial infarction. Recently, these prognostic data have also been extended to patients with unstable angina or those receiving thrombolytic therapy.
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A unique opportunity exists at the drug discovery stage to overcome inherently poor solubility by selecting drug candidates with superior supersaturation propensity. Existing supersaturation assays compare either precipitation-resistant or precipitation-inhibiting excipients, or higher-energy polymorphic forms, but not multiple compounds or multiple concentrations. Furthermore, these assays lack sufficient throughput and compound conservation necessary for implementation in the discovery environment. A microplate-based combination turbidity and supernatant concentration assay was therefore developed to determine the extent to which different compounds remain in solution as a function of applied concentration in biorelevant media over a specific period of time. Dimethyl sulfoxide stock solutions at multiple concentrations of four poorly soluble, weak base compounds (Dipyridamole, Ketoconazole, Albendazole, and Cinnarizine) were diluted with pH 6.5 buffer as well as FaSSIF. All samples were monitored for precipitation by turbidity at 600 nm over 1 h and the final supernatant concentrations were measured. The maximum supersaturation ratio was calculated from the supersaturation limit and the equilibrium solubility in each media. Compounds were rank-ordered by supersaturation ratio: Ketoconazole > Dipyridamole > Cinnarizine ∼ Albendazole. These in vitro results correlated well with oral AUC ratios from published in vivo pH effect studies, thereby confirming the validity of this approach.
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Platelet microparticles (PMP) are submicroscopic membrane vesicles released by platelets during activation. Flow cytometry is the most widely used method for quantifying PMP, but the optimization of the technical method has not yet been fully evaluated. This study was designed to assess the pre-analytical variables including blood sampling conditions, and to evaluate the analytical variations including effect of the platelet-specific antibodies and quantitative beads, precision, linearity and accuracy in comparison with beta-thromboglobulin, which is one of the platelet activation markers. Numbers of PMP collected into citrate-theophylline-adenosine-dipyridamole (CTAD) tubes were increased with time, but to a lesser extent than when collected into sodium citrate tubes. The precision of the PMP assay was relatively high. Excellent linear correlation was observed for dilution linearity. Regarding the platelet-specific antibodies used, anti-CD41a-labeled samples resulted in higher PMP levels than those labeled with anti-CD61 and anti-CD42a. There was no significant difference of PMP counts according to the quantitative beads. The PMP assay is well correlated with beta-thromboglobulin levels. Our findings suggest that blood samples for the PMP assay should be collected in a CTAD tube and delayed measurement is not allowed to avoid artefactual platelet activation. The PMP assay can be used successfully as a useful marker of the detection of in vivo platelet activation, provided that pre-analytical and technical points are optimally taken into consideration.