As in the main meta-analysis, "serious vascular event": non fatal myocardial infarction, non fatal stroke or vascular death.
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The aim of this study was to determine whether the adenosine receptor that inhibits adrenergic neurotransmission in the rabbit portal vein is of the A1 or the A2 subtype. Isometric contractions of the isolated vein were evoked by electrical field stimulation and by exogenous noradrenaline. Low concentrations of adenosine, and a number of analogues inhibited the response evoked by field stimulation but had no effect on those evoked by noradrenaline. The order of inhibitory potency was: L-N6-phenylisopropyladenosine (L-PIA) = N6-cyclohexyladenosine (CHA) = 5'-N-cyclopropylcarboxamide adenosine (NCPCA) greater than or equal to 5'-N-ethylcarboxamide adenosine (NECA) = 2-chloroadenosine greater than adenosine greater than D-PIA. The difference in potency between the stereoisomers L- and D-PIA was about 60 fold. The purine transport inhibitor dipyridamole potentiated the inhibitory effect of adenosine but not that of its analogues. The inhibitory responses evoked by adenosine and its' analogues were attenuated by the adenosine antagonist theophylline. These results indicate that adenosine selectively inhibits contractions of the rabbit portal vein evoked by adrenergic nerve stimulation via activation of an adenosine A1 receptor.
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Authors report on the revascularization resulted by noninvasive and invasive interferences carried out 6-9 months after surgery and on the improvement of functional status of 56 postinfarction patients with recurrent angina pectoris. They conclude that recoronarography performed in 12 patients revealed diminished patency rate as compared to the estimated rate, especially in those cases, where complete revascularization was considered to have been carried out. Ejection fraction, wall motion score by ventriculography and echocardiography did not seem to improve significantly. However Dipyridamole Thallium scintigraphy showed marked improvement in perfusion in all cases. NYHA functional status noticeably improved in the re-examined patients.
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We have identified a novel human isozyme of 3',5'-cyclic nucleotide phosphodiesterase (PDE), which we designated PDE8B. cDNA of 2844 bp encoding the C-terminal 659 amino acids of PDE8B was cloned following the identification of an expressed sequence tag (EST) obtained through a search of the EST database. The predicted protein sequences of PDE8B showed highest homology (65% identity, 83% similarity) to that of PDE8A. Northern blot analysis indicated that the mRNA encoding PDE8B is expressed specifically and abundantly in thyroid gland as a approximately 4.2 kb mRNA, in contrast to the wide expression of PDE8A mRNA in various tissues. The carboxyl-terminal 584 amino acids of PDE8B were expressed in E.coli as a fusion protein. The recombinant PDE8B exhibited cAMP PDE activity which was not inhibited by various PDE inhibitors including vinpocetine, milrinone, rolipram, and IBMX with the exception of dipyridamole which caused 50% inhibition at a concentration of 40 microM. cAMP hydrolytic activity was unaffected by cGMP and no cGMP PDE hydrolysis were detectable at concentrations up to 100 microM. These findings suggest that PDE8B is a new member of the PDE8 family.
Very low density lipoproteins (VLDL) and low density lipoproteins (LDL) were isolated from serum of hypercholesterolemic guinea-pigs, and the effect of these lipoproteins on guinea-pig platelets was studied. VLDL (greater than 100 microgram/ml) and LDL (greater than 400 microgram/ml) were found to cause aggregation of gel-filtered platelets (GFP), although the extent of GFP aggregation by LDL was smaller than that by VLDL. In platelet-rich plasma, however, lipoproteins could not induce platelet aggregation. VLDL and LDL even at the low concentrations at which lipoproteins alone could not induce aggregation potentiated ADP-induced aggregation of GFP. VLDL-induced aggregation of GFP was inhibited by apyrase (0.2--1.0 mg/ml) in a concentration-related manner. Prostaglandin E1, dipyridamole, potassium cyanide and ethylenediaminetetraacetic acid inhibited VLDL- and ADP-induced aggregation of GFP in the almost same degree. Inhibitions of VLDL-induced GFP aggregation by acetylsalicylic acid and albumin were slightly stronger than that of ADP-induced aggregation. These findings suggest that lipoproteins modulate platelets so that endogenous ADP can be released from platelets.
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The present investigation was undertaken to evaluate the effects of Dilazep, a new antiplatelet and coronary dilating drug, on the exercise tolerance of patients who had suffered previous myocardial infarction and were participating in a cardiac rehabilitation programme. Seventy-two patients were enrolled in the study. They were randomly allocated to two groups of 36 subjects; patients in group A took Dilazep, 300 mg daily; patients in group B took acetylsalicylic acid, 100 mg daily, or dipyridamole, 300 mg daily. Before and after treatment all patients underwent two maximal or symptom limited cycloergometer stress tests, respectively 30 and 60 days after the episode of acute myocardial infarction. Total exercise time, maximum workload reached, heart rate, blood pressure, double product and oxygen pulse were measured. In both groups a significant increase in both total exercise time and maximum workload reached was recorded at the second stress test; this may reflect a greater degree of physical conditioning due to the rehabilitation programme. In group A patients total exercise time increased from 457.12 +/- 5.36 sec to 588.28 +/- 8.24 sec (p less than 0.005), in group B patients it increased from 459.18 +/- 6.11 sec to 547.43 +/- 7.47 sec (p less than 0.005). The mean values of maximum workload reached increased in group A from 4512.14 +/- 116.47 kgm to 5288.57 +/- 145.38 kgm (p less than 0.005), and in group B from 4522.22 +/- 108.42 kgm to 5098 +/- 137.51 kgm (p less than 0.005). Thus the exercise tolerance improved more in patients taking Dilazep than in those taking acetylsalicylic acid or dipyridamole.(ABSTRACT TRUNCATED AT 250 WORDS)
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Adequate Doppler recordings in the LAD were obtained in 92% of patients. A contrast agent was used in the 39% of examinations. No major adverse reaction occurred in any patient. A receiving operating characteristic curve showed that a CFR value < 1.9 had a sensitivity of 85%, a specificity of 87%, a positive predictive value of 71%, a negative predictive value of 94% and a diagnostic accuracy of 86% for identifying a significant LAD stenosis. The area under the receiving operating characteristic curve computed for CFR was significantly higher than for wall motion score index (p < 0.001). In a stepwise forward, multiple logistic regression analysis, both CFR (OR = 4.8, 95% C.I. 3.7-5.3; p < 0.00001) and the wall motion score index for the LAD territory (OR = 4.2, 95% C.I. 2.6-6.8; p < 0.0001) were independent determinants of LAD stenosis > or = 70%.
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We tested the hypothesis that blood flow velocity could be recorded in the left anterior descending coronary artery (LAD) during transthoracic echocardiography by use of second harmonic echo Doppler modality along with contrast enhancement (intravenous Levovist) at rest and after pharmacologically induced maximal vasodilation to assess coronary flow reserve (CFR) with a totally noninvasive approach.
We examined the effect of DP on RTX cytotoxicity in the presence of various physiologic thymidine concentrations in eight colorectal adenocarcinoma cell lines by colony formation assay, and in p53-defective HL60 S and p53-competent HL60 SN3 promyelocytic leukemia cells by a tetrazolium reduction-based assay.
Nine large white pigs were scanned with H(2)(15)O and C(15)O before and after partially occluding the circumflex (n = 4) or the left anterior descending (n = 5) coronary artery at rest and during hyperemia induced by intravenous dipyridamole. Radioactive microspheres labeled with either (57)Co or (46)Sc were injected during each of the H(2)(15)O scans, which allowed comparison between microsphere and PET measurements of regional MBF. PET analyses of 3D acquisition data were performed using filtered backprojection reconstruction and region-of-interest definition by factor and cluster analysis techniques and single-compartment model quantification.
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The hyperaemic response of the hepatic artery to portal vein occlusion (the buffer response) and the action of exogenous adenosine upon hepatic artery blood flow was studied in Asian hybrid minipigs as a potential alternative experimental model to that previously developed in dogs. Adenosine produced a dose-dependent hepatic artery vasodilatation, but of lesser extent than that observed in dogs. A greatly diminished buffer response was observed in the pigs compared to that seen in dogs, and could not be replicated consistently. The adenosine uptake inhibitor dipyridamole did not potentiate responses to adenosine or the buffer response. It is concluded that the minipig is an unsuitable alternative model for the study of the hepatic artery buffer response.
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Adenosine, a known mediator of preconditioning, has been infused into the coronary circulation to induce therapeutic preconditioning, eg, in preparation for angioplasty. However, results have been disappointing. We tested the hypothesis that endothelial nucleoside transporter acts as a barrier impeding the delivery of intravascular adenosine into the underlying myocardium and that this can be overcome with dipyridamole, a nucleoside transporter blocker.
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Patients were stratified according to time after transplantation (group I, up to 2 years after transplantation; group II, 2 to 4 years after transplantation; group III, more than 4 years after transplantation). Changes of the diameter of proximal, mid and distal segments of the left anterior descending coronary artery and the circumflex branch of the left coronary artery were investigated after endothelium-dependent and endothelium-independent stimulation with acetylcholine (ACh, 50 and 100 micrograms i.c.) and nitroglycerin 0.3 mg i.c. Coronary flow changes were assessed endothelium-dependently (ACh 50 and 100 micrograms i.c.) and endothelium-independently (dipyridamole 0.56 mg/kg i.v.) utilizing an 8 F Judkins-style Doppler catheter.
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Six patients with advanced arteriosclerosis obliterans in the lower extremities were subjected to an exercise test on a tread mill with and without dipyridamole treatment. Prostacyclin (PGI2) release was measured by the concentration of its stable metabolite, 6-keto-prostaglandin F1 alpha in plasma. All the patients suffered from ischemic pain during both tests, but no changes were seen in plasma 6-keto-PGF1 alpha. Dipyridamole did not affect the physical performance. Our results suggest that atherosclerotic vessels do not increase PGI2 production in response to ischemia and that a single dose of dipyridamole does not change PGI2 production.
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MFR and EF in patients with OMI were significantly decreased compared with those in patients with AP. Increased baseline MBF and decreased EF were significant factors for the reduced MFR in patients with AP and OMI.
Increased myocardial oxygen demand resulting from hypotension and reflex tachycardia unmasking a reduced endocardial MBF reserve is the primary mechanism of dipyridamole-induced regional dysfunction in chronic coronary artery disease.
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Of 459 consecutive patients with Kawasaki disease, coronary aneurysms were detected in 90 cases by echocardiography during the acute stage. After paired studies of selective CAG and SPECT were conducted, all patients were followed up and monitored for the occurrence of any cardiac events for > or =8 years. During the follow-up interval, there were 15 cardiac events (1 death, 5 infarctions, 2 coronary artery bypass graft operations, and 7 occurrences of unstable angina). Of patients who had some event, thallium redistribution was found on SPECT in 14 (93%, P<0.001). Of the various clinical and scintigraphic image variables, the presence of thallium redistribution was the best multivariate independent predictor of a late cardiac event (chi2=57.8, P<0.0001). The number of aneurysms detected on CAG added minimal statistical improvement to the model (chi2=1.9, P=0.0009).
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The aim of this study was to examine whether myocardial contrast echocardiography (MCE) may be used to study regional myocardial blood flow distribution during dipyridamole-induced hyperemia. MCE was performed before and after dipyridamole infusion in 11 patients with a proximal, significant left anterior descending (LAD) coronary artery stenosis. The relation between contrast-derived parameters and the degree of coronary narrowing and the occurrence of transient regional wall motion abnormalities was also investigated. In the territory supplied by left circumflex coronary artery, mean peak contrast intensity increased after dipyridamole from 50 +/- 18 to 76 +/- 27 IU (p < 0.001). In contrast, a significant reduction in mean peak intensity was observed after dipyridamole in the LAD territory (from 41 +/- 27 to 13 +/- 13 IU, p < 0.01). Similar results were obtained with the use of the area under the time-intensity curve. An increase in peak intensity > or = 10 IU after dipyridamole administration separated normal regions from those supplied by a significant coronary artery lesion with a sensitivity of 91% and a specificity of 91%. Perfusion abnormalities were always detected by contrast echocardiography when septal motion abnormalities developed and, in five patients they were detected in the absence of clinical, electrocardiographic, and echocardiographic signs of ischemia. A weak correlation was found between both peak intensity and area under the curve and percent coronary diameter stenosis and cross-sectional area. In conclusion, dipyridamole MCE can be used during routine coronary angiography to assess myocardial blood flow distribution in patients with coronary artery disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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A prospective randomized study was performed in 137 coronary artery bypass surgery cases to determine if the administration of antiplatelet drugs would improve the patency of coronary artery bypass grafts. The warfarin group received warfarin and thrombotest was controlled to 20% or so. The dipyridamole group received both 300 mg of dipyridamole and 250 mg of aspirin orally each day. These two groups were compared for study in grafts patency. Results were analyzed by chi-square. In the warfarin group, 66 patients had three ITA-LAD grafts and 115 saphenous vein grafts (including 4 sequential grafts). In the dipyridamole group, 71 patients underwent 38 ITA grafts and 167 saphenous vein grafts (including 56 sequential grafts). Eighty-eight of the 107 grafts (82%) were patent in the warfarin group, and 190 of 205 grafts (95%) were patent in the dipyridamole group (p less than 0.01). Of the two ITA grafts in the warfarin group, no graft was occluded, a patency of 100%. In the dipyridamole group, 35 of 38 ITA grafts (92%) were patent. In the warfarin group, 86 of 105 saphenous vein grafts (82%) were patent. In the dipyridamole group, 155 of 167 saphenous vein grafts (95%) were patent (p less than 0.01). In the study of grafted coronary vessel, the patency of left anterior descending coronary artery, diagonal branch and right coronary artery was not significant between two groups. In the dipyridamole group, the patency of left circumflex coronary artery was 93%, and that of the warfarin group was 50% (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Due to endothelial dysfunction (ED), coronary vasodilation capacity is reduced in patients with hypercholesterolemia. Cholesterol lowering may largely restore endothelial function. Currently, it is supposed that the onset of this therapeutic effect takes weeks or even months. However, by means of LDL apheresis, a significant LDL reduction may be achieved within hours. Dynamic quantitative positron emission tomography (PET) performed before and after LDL apheresis showed that mean global myocardial perfusion can be measured at rest and after pharmacological vasodilation with dipyridamole using N13 ammonia as tracer.A total of 35 patients (11 women and 24 men) with documented coronary heart disease and hypercholesterolemia underwent PET immediately prior to LDL apheresis and 18-20 hours thereafter. In addition to the decrease in LDL cholesterol (from 175+/-50 to 77+/-25 mg/dl) and fibrinogen (from 287+/-75 to 155+/-52 mg/dl), a significant improvement of myocardial blood flow under dipyridamole (177+/-59 vs 217+/-82 ml/min 100 g, p<0.0001), of coronary flow reserve (2.10+/-0.82 vs 2.62+/-1.02, p<0.0001) and of minimal coronary resistance (0.56+/-0.20 vs 0.44+/-0.17 mmHg 100 g min/ml, p<0.0001) were achieved. Plasma viscosity decreased only by 7.8%. Within 20 hours after single LDL apheresis a 20% improvement of coronary vasodilation capacity was noninvasively demonstrated and quantified.
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Dipyridamole inhibited the proliferation of functionally heterogeneous CD4+ TCR alpha beta+ T-cell clones prepared from CML-patients 4-6 weeks after allogeneic bone marrow transplantation. The effect was seen when testing concentrations corresponding to the therapeutic serum level. Dipyridamole caused a dose-dependent inhibition of PHA-stimulated proliferation both for clones dependent on exogenous IL2 and clones undergoing autocrine proliferation. The inhibition was seen when using different accessory cells (PBM or BCL), and also when dipyridamole was present during IL2- or IL4-dependent proliferation of activated T-cells. The effect of dipyridamole was also investigated for 76 T-cell clones (76 CD4+ and 7 CD8+ clones) prepared by different cloning procedures from three patients. Although these clones were heterogeneous with regard to cytotoxic function, lymphokine production or lymphokine responsiveness, dipyridamole inhibited IL2-dependent proliferation of all clones. In addition dipyridamole inhibited proliferation of CML cells.
1) Antianginal therapy can protect from dipyridamole-induced ischemia and 2) the therapy-induced changes in DET response parallel variations in exercise tolerance and might be useful for the objective, exercise-independent assessment of the therapy efficacy.
Dipyridamole was infused at a rate of 0.56 mg/kg in 4 minutes followed by 3 minutes of low-level cycloergometer exercise. Two mCi of thallium-201 were injected 3 minutes after the end of dipyridamole infusion. Stress and redistribution SPECT acquisitions were performed respectively 5-10 minutes and 4 hours after thallium-201 injection. The cardiac events during a 3-year follow-up were analysed.
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The dorso-lateral medullary syndrome (Wallenberg's syndrome) is produced by infarction of a wedge of lateral medulla posterior to the inferior olivary nucleus and is usually caused by vertebral artery occlusion. Ipsilateral axial lateropulsion as an initial symptom of vertebral artery occlusion is rather rare and the anatomical structure responsible is still uncertain. Here we describe two patients presenting with ipsilateral axial lateropulsion as an initial symptom of vertebral artery occlusion. In one the stroke affected the dorso-lateral aspect of the medulla, in the other more lateral aspects of the medulla were involved. Our data suggest that ipsilateral axial lateropulsion may be caused by lesions of different topography involving either the vestibular nuclei, the cerebellar peduncle or the spinocerebellar tracts.
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Cardiac allograft arteriopathy often limits long-term survival in transplantation recipients but has been difficult to detect by standard diagnostic methods. Because of the diffuse nature of transplantation coronary disease, we postulated that a lung/heart ratio during dipyridamole thallium imaging might better predict arteriopathy-related complications than diagnostic methods that detect discrete luminal stenoses.
Seven days after coronary ligation (MI), rats were randomized to enalapril (n = 8; 500 micrograms.kg-1.d-1), losartan (n = 9; 3 mg.kg-1.d-1), or placebo (n = 8) and treated for 6 weeks. Sham-operated rats (n = 10) served as controls. Coronary blood flow was measured with radiolabeled microspheres during baseline and maximal coronary dilation induced by dipyridamole (2 mg.kg-1.min-1 over 10 minutes). Right and left ventricular (LV) weight was increased in infarcted rats compared with sham-operated animals and enalapril- and losartan-treated MI rats. Minimal LV and right ventricular coronary vascular resistance was increased in MI rats but normalized with enalapril and losartan (LV:sham, 8.9; MI-placebo, 12.7; MI-enalapril, 9.2; MI-losartan, 8.8 mm Hg.mL-1.min-1.g-1, all P < .05 versus MI-placebo). Interstitial fibrosis determined from perfusion-fixed hearts was increased in infarcted rats but reduced by both enalapril and losartan. Myocardial capillary density improved with enalapril and losartan. In separate groups treated as above, plasma and tissue ACE activity was determined and demonstrated significantly higher ACE activity in noninfarcted LV tissue of MI-placebo rats compared with sham (0.64 vs 0.27 nmol.mg protein-1.min-1, P < .05). Enalapril and losartan reduced LV ACE activity (0.39 and 0.29 nmol.mg protein-1.min-1, P < .05 versus MI-placebo).
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The effects of adenosine on long-term potentiation of sympathetic ganglia was studied in the isolated superior cervical ganglion of the rat, using extracellularly recorded compound action potential as an index of synaptic transmission. Adenosine in a small concentration (2 microM) blocked the post-tetanic potentiation without affecting long-term potentiation. Higher concentrations blocked both responses with no significant effect on basal transmission. The inhibitory effect appears to be due to activation of adenosine A1 receptors. This was indicated by results from experiments with the A1 agonist N6-cyclopentyladenosine (1 microM) which caused inhibition of the basal transmission as well as long-term potentiation and post-tetanic potentiation. This inhibition was readily antagonized by 8-phenyltheophylline (1 microM), an A1 receptor antagonist. A small enhancement of basal transmission was seen on treatment with 8-phenyltheophylline. The inhibitory effect of N6-cyclopentyladenosine on long-term potentiation was totally prevented when the Ca2+ concentration in the superfusate was doubled (from 2.2 to 4.4 mM). The adenosine A2 receptor agonist 5'-(N-cyclopropyl)-carboxamidoadenosine (1 microM), although caused a slight potentiation of basal transmission, had no significant effect on the post-tetanic potentiation or long-term potentiation. The adenosine transport inhibitors, dipyridamole (2 microM) and S-(4-nitorobenzyl)-6-thioinosine (2 microM) caused significant inhibition of the basal ganglionic transmission without affecting post-tetanic potentiation or long-term potentiation. The effect of dipyradimole on basal transmission was not antagonized in the presence of 8-phenyltheophylline suggesting a non-specific action. The results suggest that exogenous adenosine can inhibit both post-tetanic potentiation and long-term potentiation in sympathetic ganglia, probably by activation of presynaptic A1 receptors. The results also suggest that endogenous adenosine, which is probably released in minute amounts, may only modulate basal transmission without influencing induction or maintenance of long-term potentiation in the superior cervical ganglion.
Cases having correlating scintigraphy and angiography (n = 425) were selected retrospectively. Immediate poststress and redistribution images were quantified using a circumferential profile analysis with interpolative background subtraction. For each of nine sectors on the left anterior oblique image, multivariate analyses were performed, comparing the relative uptake and net washout of Tl-201 to the exercise workload attained, use of dipyridamole, time to redistribution, gender, and the angiographic presence and severity of stenoses at five key sites. Washout values standardized according to gender, exercise level and time to redistribution, were compared with relative uptake profiles and ST depression using receiver operating curves.